Blackwells Five-Minute Veterinary Consult Canine and Feline 7th Edition

Blackwell’s
Five-Minute
Veterinary
Consult:
Canine and Feline
Seventh Edition
Blackwell’s
Five-Minute
Veterinary
Consult
Canine and Feline
Seventh Edition
Edited by
Larry P. Tilley, DVM
Diplomate, American College of Veterinary Internal Medicine
(Small Animal Internal Medicine)
President, VetMed Consultants, Inc.
Santa Fe, New Mexico
USA
Francis W.K. Smith, Jr., DVM

(Small Animal Internal Medicine and Cardiology)
Vice-President, VetMed Consultant, Inc.
Lexington, Massachusetts
USA
Meg M. Sleeper, VMD

(Cardiology)
Professor of Clinical Cardiology
College of Veterinary Medicine
University of Florida, Florida
USA
Benjamin M. Brainard, VMD

Diplomate, American College of Veterinary
Anesthesia and Analgesia and
American College of Veterinary Emergency and
Critical Care
Edward H. Gunst
Professor of Small Animal Critical Care
University of Georgia
Athens, Georgia
USA

This edition first published 2021 © 2021 by John Wiley & Sons, Inc.
Edition History
First Edition 1997 © Lippincott Williams & Wilkins
Second Edition 2000 © Lippincott Williams & Wilkins
Third edition 2004 © Lippincott Williams & Wilkins
Fourth Edition 2007 © Blackwell Publishing Professional
Fifth edition 2011 © John Wiley & Sons, Inc.
Sixth Edition 2016 © John Wiley & Sons, Inc.
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and Medical business to form Wiley-Blackwell.
The right of Larry P Tilley, Francis W Smith, Meg Sleeper, and Benjamin Brainard to be identified as the authors of the editorial material in this work has been
asserted in accordance with law.
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Library of Congress Cataloging-in-Publication Data
Names: Tilley, Lawrence P., editor. | Smith, Francis W. K., Jr., editor. |
Sleeper, Meg M., editor. | Brainard, Benjamin, editor.
Title: Blackwell’s five-minute veterinary consult. Canine and feline /
edited by Larry P. Tilley, Francis W.K. Smith, Jr., Margaret M. Sleeper,
Benjamin Brainard.
Other titles: Five-minute veterinary consult. Canine and feline
Description: Seventh edition. | Hoboken, NJ : Wiley-Blackwell, 2021. |
Includes bibliographical references and index.
Identifiers: LCCN 2020025494 (print) | LCCN 2020025495 (ebook) | ISBN
9781119513179 (hardback) | ISBN 9781119513155 (adobe pdf ) | ISBN
9781119513162 (epub)
Subjects: MESH: Dog Diseases–diagnosis | Cat Diseases–diagnosis | Dog
Diseases–therapy | Cat Diseases–therapy | Veterinary Medicine–methods
| Handbook
Classification: LCC SF991 (print) | LCC SF991 (ebook) | NLM SF 991 | DDC
636.7/0896–dc23
LC record available at https://lccn.loc.gov/2020025494
LC ebook record available at https://lccn.loc.gov/2020025495
Cover Design: Wiley

Cover Image: School children (8-9) at lunch break © Tetra Images - Jamie Grill / Getty Images, Playing Together at School © FatCamera / Getty Images,
Multi-ethnic children at autumn festival © kali9 / Getty Images, WMM - Teenagers hanging out, eating popcorn in urban park © Hero Images / Getty Images
Set in 9/10pt AdobeGarmondPro by SPi Global, Pondicherry, India
10 9 8 7 6 5 4 3 2 1
To my love and joy in life, Ellen Lefkowitz, my son Kyle, and grandson Tucker.
To my late mother Dorothy, who instilled values that have helped me throughout life.
To family and animals who represent the purity of life.
Larry P. Tilley
To my wife, May, my son, Ben, and my daughter, Jade, who are a constant source of
inspiration, love, and joy. To my late father, Frank, who was my perfect role model. To Kaylee
(dog) and Centie (cat) who remind me each day to make time for play.
Francis W.K. Smith, Jr.
To my parents and sister for their stalwart support and to the many animals who have
touched my life and made me a better person.
Meg M. Sleeper
To my family, my mentors, my colleagues; to colleagues and friends who are no longer with
us. “Keep cool, but care”—Thomas Pynchon.
Benjamin M. Brainard
Contents
Topic
5-Fluorouracil (5-FU) Toxicosis 1
Abortion, Spontaneous (Early Pregnancy Loss)—Cats 2
Abortion, Spontaneous (Early Pregnancy Loss)—Dogs 4
Abortion, Termination of Pregnancy 6
Abscessation8
Acetaminophen (APAP) Toxicosis 10
Acidosis, Metabolic 12
Acne—Cats14
Acne—Dogs15
Acral Lick Dermatitis 16
Actinomycosis and Nocardia 17
Acute Abdomen 18
Acute Diarrhea 21
Acute Kidney Injury 23
Acute Respiratory Distress Syndrome 25
Acute Vomiting 27
Adenocarcinoma, Anal Sac 29
Adenocarcinoma, Lung 31
Adenocarcinoma, Nasal 32
Adenocarcinoma, Pancreas 34
Adenocarcinoma, Prostate 35
Adenocarcinoma, Renal 36
Adenocarcinoma, Salivary Gland 37
Adenocarcinoma, Skin (Sweat Gland, Sebaceous) 38
Adenocarcinoma, Stomach, Small and Large Intestine, Rectal 39
Adenocarcinoma, Thyroid—Dogs 40
Aggression—Between Dogs in the Household 42
Aggression to Unfamiliar People and Unfamiliar Dogs—Dogs 44
Aggression Toward Children—Dogs 46
Aggression Toward Familiar People—Dogs 47
Aggression Toward Humans—Cats 49
Aggression, Food and Resource Guarding—Dogs 51
Aggression, Intercat Aggression 53
Aggression, Overview—Cats 56
Aggression, Overview—Dogs 58
Alkaline Hyperphosphatasemia in Dogs 61
331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

for you to download and use in practice
ix
Alkalosis, Metabolic 63
Alopecia—Cats65
Alopecia—Dogs67
Alopecia, Noninflammatory—Dogs 69
Ameloblastoma71
Amphetamine and ADD/ADHD Medication Toxicosis 72
Amyloidosis74
Anaerobic Infections 76
Anal Sac Disorders 77
Anaphylaxis78
Anemia of Chronic Kidney Disease 80
Anemia, Aplastic 82
Anemia, Heinz Body 83
Anemia, Immune-Mediated 84
Anemia, Iron-Deficiency 86
Anemia, Nonregenerative 87
Anemia, Nuclear Maturation Defects (Anemia, Megaloblastic) 89
Anemia, Regenerative 90
Anisocoria92
Anorexia94
Antebrachial Growth Deformities 96
Anterior Uveitis—Cats 98
Anterior Uveitis—Dogs 100
Antidepressant Toxicosis—SSRIs and SNRIs 102
Antidepressant Toxicosis—Tricyclic 104
Aortic Stenosis 106
Aortic Thromboembolism 108
Apudoma111
Arteriovenous Fistula and Arteriovenous Malformation 112
Arteriovenous Malformation of the Liver 113
Arthritis (Osteoarthritis) 115
Arthritis, Septic 118
Ascites120
Aspergillosis, Disseminated Invasive 122
Aspergillosis, Nasal 124
Aspirin Toxicosis 126
Asthma, Bronchitis—Cats 127
Astrocytoma129
Ataxia130
Atlantoaxial Instability 132
Atopic Dermatitis 134
Atrial Fibrillation and Atrial Flutter 136
Atrial Premature Complexes 139
Atrial Septal Defect 141
Atrial Standstill 142
Atrial Wall Tear 144
331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

you to download and use in practice
x
Atrioventricular Block, Complete (Third Degree) 146
Atrioventricular Block, First Degree 148
Atrioventricular Block, Second Degree—Mobitz Type I 150
Atrioventricular Block, Second Degree—Mobitz Type II 152
Atrioventricular Valve Dysplasia 154
Atrioventricular Valvular Stenosis 156
Azotemia and Uremia 159
Babesiosis161
Baclofen Toxicosis 163
Bartonellosis164
Basal Cell Tumor 165
Battery Toxicosis 166
Baylisascariasis167
Benign Prostatic Hyperplasia 168
Benzodiazepine and Other Sleep Aids Toxicosis 169
Beta Receptor Antagonist (Beta Blockers) Toxicosis 171
Beta-2 Agonist Inhaler Toxicosis 172
Bile Duct Carcinoma 173
Bile Duct Obstruction (Extrahepatic) 174
Bile Peritonitis 177
Bilious Vomiting Syndrome 179
Blastomycosis180
Blepharitis182
Blind Quiet Eye 184
Blood Transfusion Reactions 186
Blue‐Green Algae Toxicosis 187
Botulism188
Brachial Plexus Avulsion 189
Brachycephalic Airway Syndrome 190
Brain Injury 192
Brain Tumors 194
Breeding, Timing 196
Bronchiectasis198
Bronchitis, Chronic 200
Brucellosis202
Calcipotriene/Calcipotriol Toxicosis 204
Calcium Channel Blocker Toxicosis 205
Campylobacteriosis206
Candidiasis207
Canine Coronavirus Infections 208
Canine Degenerative Myelopathy 209
Canine Distemper 211
Canine Infectious Diarrhea 213
Canine Infectious Respiratory Disease 215
Canine Parvovirus 217
Canine Schistosomiasis (Heterobilharziasis) 219

xi
Car Ride Anxiety—Dogs and Cats 220
Carbon Monoxide Toxicosis 223
Carcinoid and Carcinoid Syndrome 224
Cardiac Glycoside Plant Toxicosis 225
Cardiomyopathy, Arrhythmogenic Right Ventricular—Cats 226
Cardiomyopathy, Arrhythmogenic Right Ventricular—Dogs 227
Cardiomyopathy, Dilated—Cats 229
Cardiomyopathy, Dilated—Dogs 232
Cardiomyopathy, Hypertrophic—Cats 235
Cardiomyopathy, Hypertrophic—Dogs 238
Cardiomyopathy, Nutritional 239
Cardiomyopathy, Restrictive—Cats 241
Cardiopulmonary Arrest 243
Cataracts245
Cerebellar Degeneration 247
Cerebellar Hypoplasia 248
Cerebrovascular Accidents 249
Ceruminous Gland Adenocarcinoma, Ear 251
Cervical Spondylomyelopathy (Wobbler Syndrome) 252
Chagas Disease (American Trypanosomiasis) 254
Chediak-Higashi Syndrome 255
Chemodectoma256
Cheyletiellosis257
Chlamydiosis—Cats258
Chocolate Toxicosis 260
Cholangitis/Cholangiohepatitis Syndrome 262
Cholecystitis and Choledochitis 265
Cholelithiasis267
Chondrosarcoma, Bone 269
Chondrosarcoma, Nasal and Paranasal Sinus 270
Chondrosarcoma, Oral 271
Chorioretinitis272
Chronic Kidney Disease 274
Chylothorax277
Cirrhosis and Fibrosis of the Liver 279
Claw and Clawfold Disorders 282
Clostridial Enterotoxicosis 284
Coagulation Factor Deficiency 286
Coagulopathy of Liver Disease 288
Cobalamin Deficiency 290
Coccidioidomycosis292
Coccidiosis294
Cognitive Dysfunction Syndrome 295
Cold Agglutinin Disease 297
Colibacillosis298
Colitis and Proctitis 300

xii
Colitis, Histiocytic Ulcerative 303
Compulsive Disorders—Cats 304
Compulsive Disorders—Dogs 306
Congenital and Developmental Renal Diseases 308
Congenital Ocular Anomalies 310
Congenital Spinal and Vertebral Malformations 313
Congestive Heart Failure, Left-Sided 315
Congestive Heart Failure, Right-Sided 317
Conjunctivitis—Cats319
Conjunctivitis—Dogs321
Constipation and Obstipation 323
Contact Dermatitis 325
Coonhound Paralysis (Acute Polyradiculoneuritis) 326
Copper Associated Hepatopathy 328
Coprophagia and Pica 332
Corneal and Scleral Lacerations 334
Corneal Opacities—Degenerations and Infiltrates 336
Corneal Opacities—Dystrophies 337
Corneal Sequestrum—Cats 338
Cough339
Craniomandibular Osteopathy 341
Cruciate Ligament Disease, Cranial 342
Cryptococcosis344
Cryptorchidism346
Cryptosporidiosis347
Crystalluria348
Cutaneous Drug Eruptions 350
Cuterebriasis351
Cyanosis352
Cyclic Hematopoiesis 354
Cylindruria355
Cytauxzoonosis356
Deafness357
Deciduous Teeth, Persistent (Retained) 359
Deep Cutaneous Mycoses 360
Demodicosis362
Dental Caries 364
Dentigerous Cyst 366
Dermatomyositis367
Dermatophilosis369
Dermatophytosis370
Dermatoses, Depigmenting Disorders 372
Dermatoses, Erosive or Ulcerative 374
Dermatoses, Exfoliative 376
Dermatoses, Neoplastic 378
Dermatoses, Papulonodular 380

xiii
Dermatoses, Sterile Nodular/Granulomatous 382
Dermatoses, Sun-Induced 384
Dermatoses, Vesiculopustular 385
Dermatoses, Viral (Non-Papillomatosis) 387
Destructive and Scratching Behavior—Cats 388
Destructive Behavior—Dogs 389
Diabetes Insipidus 391
Diabetes Mellitus With Hyperosmolar Hyperglycemic State 393
Diabetes Mellitus With Ketoacidosis 395
Diabetes Mellitus Without Complication—Cats 397
Diabetes Mellitus Without Complication—Dogs 399
Diaphragmatic Hernia 401
Diarrhea, Antibiotic Responsive 402
Diarrhea, Chronic—Cats 403
Diarrhea, Chronic—Dogs 405
Digoxin Toxicity 407
Diisocyanate Glues 408
Discolored Tooth/Teeth 409
Discospondylitis411
Disseminated Intravascular Coagulation 413
Drowning (Near Drowning) 415
Ductal Plate Malformation (Congenital Hepatic Fibrosis) 416
Dysautonomia (Key-Gaskell Syndrome) 419
Dyschezia and Hematochezia 420
Dysphagia422
Dyspnea and Respiratory Distress 425
Dystocia428
Dysuria, Pollakiuria, and Stranguria 430
Ear Mites 432
Eclampsia433
Ectopic Ureter 434
Ectropion435
Ehrlichiosis and Anaplasmosis 436
Elbow Dysplasia 438
Electric Cord Injury 440
Enamel Hypoplasia/Hypocalcification 441
Encephalitis442
Encephalitis Secondary to Parasitic Migration 444
Endocarditis, Infective 445
Endomyocardial Diseases—Cats 447
Entropion449
Eosinophilia450
Eosinophilic Granuloma Complex 451
Epididymitis/Orchitis453
Epilepsy, Genetic (Idiopathic)—Dogs 454
Epiphora456

xiv
Episcleritis458
Epistaxis459
Erythrocytosis462
Esophageal Diverticula 464
Esophageal Foreign Bodies 465
Esophageal Stricture 467
Esophagitis469
Essential Oils Toxicosis 472
Ethanol Toxicosis 473
Ethylene Glycol Toxicosis 474
Excessive Vocalization and Waking at Night—Dogs and Cats 476
Exercise-Induced Weakness/Collapse in Labrador Retrievers 478
Exocrine Pancreatic Insufficiency 480
Eyelash Disorders (Trichiasis/Distichiasis/Ectopic Cilia) 482
Facial Nerve Paresis and Paralysis 483
False Pregnancy 485
Familial Shar-Pei Fever 487
Fanconi Syndrome 489
Fear and Aggression in Veterinary Visits—Cats 490
Fear and Aggression in Veterinary Visits—Dogs 492
Fears, Phobias, and Anxieties—Cats 494
Fears, Phobias, and Anxieties—Dogs 496
Feline Alveolar Osteitis 498
Feline Calicivirus Infection 499
Feline Herpesvirus Infection 501
Feline Hyperesthesia Syndrome 503
Feline Idiopathic Lower Urinary Tract Disease 504
Feline Immunodeficiency Virus (FIV) Infection 506
Feline Infectious Diarrhea 508
Feline Infectious Peritonitis (FIP) 510
Feline Ischemic Encephalopathy 512
Feline Leukemia Virus (FeLV) Infection 514
Feline Panleukopenia 516
Feline Paraneoplastic Alopecia 518
Feline Stomatitis—Feline Chronic Gingivostomatitis (FCGS) 519
Feline Symmetrical Alopecia 521
Feline Tooth Resorption (Odontoclastic Resorption) 522
Feline (Upper) Respiratory Infections 524
Fever526
Fiber-Responsive Large Bowel Diarrhea 528
Fibrocartilaginous Embolic Myelopathy 530
Fibrosarcoma, Bone 532
Fibrosarcoma, Gingiva 533
Fibrosarcoma, Nasal and Paranasal Sinus 534
Fipronil Toxicosis 535
Flatulence536

xv
Flea Bite Hypersensitivity and Flea Control 538
Food Reactions, Dermatologic 540
Food Reactions (Gastrointestinal), Adverse 542
Gallbladder Mucocele 544
Gastric Dilation and Volvulus Syndrome 546
Gastric Motility Disorders 548
Gastritis, Chronic 550
Gastroduodenal Ulceration/Erosion 552
Gastroenteritis, Acute Hemorrhagic Diarrhea Syndrome 554
Gastroenteritis, Eosinophilic 556
Gastroesophageal Reflux 558
Gastrointestinal Obstruction 559
Gestational Diabetes Mellitus 561
Giardiasis562
Gingival Enlargement/Hyperplasia 563
Glaucoma564
Glomerulonephritis566
Glucagonoma568
Glucosuria570
Gluten Enteropathy in Irish Setters 572
Glycogen Storage Disease 573
Glycogen-Type Vacuolar Hepatopathy 574
Grape and Raisin Toxicosis 577
Hair Follicle Tumors 578
Halitosis579
Head Pressing 581
Head Tilt 583
Head Tremors (Bobbing), Idiopathic—Dogs 585
Heartworm Disease—Cats 586
Heartworm Disease—Dogs 587
Heat Stroke and Hyperthermia 589
Helicobacter spp. 591
Hemangiopericytoma593
Hemangiosarcoma, Bone 594
Hemangiosarcoma, Heart 595
Hemangiosarcoma, Skin 596
Hemangiosarcoma, Spleen and Liver 598
Hematemesis600
Hematuria602
Hemoglobinuria and Myoglobinuria 604
Hemothorax606
Hemotropic Mycoplasmosis 607
Hepatic Amyloid 609
Hepatic Encephalopathy 611
Hepatic Failure, Acute 614
Hepatic Lipidosis 617

xvi
Hepatic Nodular Hyperplasia and Dysplastic Hyperplasia 620
Hepatitis, Chronic 622
Hepatitis, Granulomatous 626
Hepatitis, Infectious (Viral) Canine 628
Hepatitis, Suppurative and Hepatic Abscess 630
Hepatocellular Adenoma 632
Hepatocellular Carcinoma 633
Hepatocutaneous Syndrome 634
Hepatomegaly636
Hepatoportal Microvascular Dysplasia 639
Hepatosupportive Therapies 642
Hepatotoxins643
Hepatozoonosis645
Hiatal Hernia 646
Hip Dysplasia 647
Histiocytic Diseases—Dogs and Cats 650
Histiocytosis, Cutaneous 652
Histoplasmosis653
Hookworms (Ancylostomiasis) 655
Horner’s Syndrome 656
Housesoiling—Cats657
Housesoiling—Dogs661
Hydrocephalus663
Hydronephrosis665
Hyperadrenocorticism (Cushing’s Syndrome)—Cats 667
Hyperadrenocorticism (Cushing’s Syndrome)—Dogs 668
Hypercalcemia672
Hypercapnia674
Hyperchloremia676
Hypercoagulability677
Hypereosinophilic Syndrome (HES) 678
Hyperestrogenism (Estrogen Toxicity) 679
Hyperglycemia681
Hyperkalemia683
Hyperlipidemia685
Hypermagnesemia687
Hypermetria and Dysmetria 689
Hypernatremia691
Hyperosmolarity692
Hyperparathyroidism694
Hyperparathyroidism, Renal Secondary 696
Hyperphosphatemia698
Hypersomatotropism/Acromegaly in Cats 700
Hypertension, Portal 701
Hypertension, Pulmonary 704
Hypertension, Systemic Arterial 706

xvii
Hyperthyroidism709
Hypertrophic Osteodystrophy 711
Hypertrophic Osteopathy 713
Hypertrophic Pyloric Gastropathy, Chronic 714
Hyperviscosity Syndrome 716
Hyphema717
Hypoadrenocorticism (Addison’s Disease) 719
Hypoalbuminemia722
Hypocalcemia724
Hypochloremia726
Hypoglycemia727
Hypokalemia729
Hypomagnesemia731
Hypomyelination733
Hyponatremia734
Hypoparathyroidism736
Hypophosphatemia739
Hypopituitarism741
Hypopyon and Lipid Flare 742
Hyporexia743
Hyposthenuria744
Hypothermia745
Hypothyroidism747
Hypoxemia750
Icterus752
Idioventricular Rhythm 754
Ileus756
Illicit/Club Drug Toxicosis 758
Imidazoline Toxicosis 759
Immunodeficiency Disorders, Primary 760
Immunoproliferative Enteropathy of Basenjis 762
Incontinence, Fecal 763
Incontinence, Urinary 765
Infertility, Female—Dogs 767
Infertility, Male—Dogs 769
Inflammatory Bowel Disease 771
Influenza773
Insoluble Oxalate Plant Toxicosis 775
Insulinoma776
Interstitial Cell Tumor, Testicle 779
Intervertebral Disc Disease—Cats 780
Intervertebral Disc Disease, Cervical 781
Intervertebral Disc Disease, Thoracolumbar 784
Intussusception788
Iris Atrophy 790
Iron Toxicosis 791

xviii
Ivermectin and Other Macrocyclic Lactones Toxicosis 792
Joint Luxations 793
Keratitis, Eosinophilic—Cats 795
Keratitis, Nonulcerative 796
Keratitis, Ulcerative 798
Keratoconjunctivitis Sicca 800
Kitten Behavior Problems 801
Kitten Socialization and Kitten Classes 803
Lactic Acidosis (Hyperlactatemia) 805
Lameness808
Laryngeal and Tracheal Perforation 810
Laryngeal Diseases 812
Lead Toxicosis 814
Left Anterior Fascicular Block 816
Left Bundle Branch Block 818
Legg–Calvé–Perthes Disease 820
Leiomyoma, Stomach, Small and Large Intestine 822
Leiomyosarcoma, Stomach, Small and Large Intestine 823
Leishmaniosis824
Leishmaniosis, Cutaneous 825
Lens Luxation 827
Leptospirosis828
Leukemia, Chronic Lymphocytic 830
Leukocytosis831
Leukoencephalomyelopathy in Rottweilers 833
Lily Toxicosis 834
Lipoma, Infiltrative 835
Liver Fluke Infestation 836
Lower Urinary Tract Infection, Bacterial 838
Lower Urinary Tract Infection, Fungal 840
Lumbosacral Stenosis and Cauda Equina Syndrome 841
Lung Lobe Torsion 843
Lupus Erythematosus, Cutaneous (Discoid) 844
Lupus Erythematosus, Systemic (SLE) 845
Lyme Borreliosis 847
Lymphangiectasia849
Lymphadenopathy/Lymphadenitis851
Lymphedema853
Lymphoma—Cats854
Lymphoma—Dogs856
Lymphoma, Cutaneous Epitheliotropic 858
Lysosomal Storage Diseases 859
Malassezia Dermatitis 860
Malignant Fibrous Histiocytoma 861
Malocclusions—Skeletal and Dental 862

xix
Mammary Gland Hyperplasia—Cats 864
Mammary Gland Tumors—Cats 865
Mammary Gland Tumors—Dogs 867
Marijuana Toxicosis 869
Marking, Roaming, and Mounting Behavior—Cats 870
Marking, Roaming, and Mounting Behavior—Dogs 872
Mast Cell Tumors 874
Mastitis876
Maternal Behavior Problems 877
Maxillary and Mandibular Fractures 879
Megacolon881
Megaesophagus883
Melanocytic Tumors, Oral 886
Melanocytic Tumors, Skin and Digit 888
Melena889
Meningioma—Cats and Dogs 891
Meningitis/Meningoencephalitis/Meningomyelitis, Bacterial 894
Meningoencephalomyelitis, Eosinophilic 896
Meningoencephalomyelitis of Unknown Etiology (MUE) 897
Mesothelioma899
Metabolic, Nutritional, and Endocrine Bone Disorders 900
Metaldehyde Toxicosis 902
Metformin Toxicosis 903
Methemoglobinemia904
Metritis906
Movement Disorders 907
Mucopolysaccharidoses908
Multidrug-Resistant Infections 909
Multiple Myeloma 911
Murmurs, Heart 912
Muscle Rupture (Muscle Tear) 914
Mushroom Toxicoses 916
Myasthenia Gravis 920
Mycobacterial Infections 922
Mycoplasmosis924
Mycotoxicosis—Aflatoxin926
Mycotoxicosis—Tremorgenic Toxins 927
Myelodysplastic Syndromes 928
Myelomalacia, Spinal Cord (Ascending, Descending, Progressive) 929
Myelopathy—Paresis/Paralysis—Cats930
Myeloproliferative Disorders 932
Myocardial Infarction 933
Myocardial Tumors 934
Myocarditis935

xx
Myoclonus937
Myopathy—Hereditary X-linked Muscular Dystrophy 938
Myopathy—Masticatory and Extraocular Myositis 939
Myopathy, Noninflammatory—Endocrine 941
Myopathy, Noninflammatory—Hereditary Labrador Retriever 943
Myopathy, Noninflammatory—Hereditary Myotonia 944
Myopathy, Noninflammatory—Hereditary Scottie Cramp 945
Myopathy, Noninflammatory—Metabolic 946
Myopathy—Polymyositis and Dermatomositis 948
Myxedema and Myxedema Coma 950
Myxomatous Mitral Valve Disease 951
Narcolepsy and Cataplexy 954
Nasal and Nasopharyngeal Polyps 955
Nasal Dermatoses—Canine 956
Nasal Discharge 958
Nasopharyngeal Stenosis 960
Neck and Back Pain 961
Necrotizing Encephalitis 963
Neonatal Mortality and Canine Herpesvirus 964
Neonatal Resuscitation and Early Neonatal Care 966
Neonicotinoid Toxicosis 968
Neosporosis969
Nephrolithiasis970
Nephrotic Syndrome 972
Nephrotoxicity, Drug-Induced 974
Nerve Sheath Tumors 976
Neuroaxonal Dystrophy 977
Neutropenia978
Nocardiosis/Actinomycosis—Cutaneous980
Nonsteroidal Anti-Inflammatory Drug Toxicosis 981
Notoedric Mange 983
Nystagmus984
Obesity986
Odontogenic Tumors 988
Odontoma990
Oliguria and Anuria 991
Ollulanus Infection 993
Ophthalmia Neonatorum 994
Opiates/Opioids Toxicosis 996
Optic Neuritis and Papilledema 998
Oral Cavity Tumors, Undifferentiated Malignant Tumors 1000
Orbital Diseases (Exophthalmos, Enophthalmos, Strabismus) 1001
Organophosphorus and Carbamate Toxicosis 1003
Oronasal Fistula 1005
Osteochondrodysplasia1006

xxi
Osteochondrosis1007
Osteomyelitis1009
Osteosarcoma1011
Otitis Externa and Media 1013
Otitis Media and Interna 1015
Ovarian Remnant Syndrome 1017
Ovarian Tumors 1019
Ovulatory Failure 1020
Pain (Acute, Chronic, and Postoperative) 1021
Palatal Defects 1025
Pancreatitis—Cats1027
Pancreatitis—Dogs1029
Pancytopenia1031
Panniculitis/Steatitis1033
Panosteitis1034
Panting and Tachypnea 1036
Papillomatosis1039
Paralysis1040
Paraneoplastic Syndromes 1042
Paraphimosis, Phimosis, and Priapism 1045
Paraproteinemia1046
Patellar Luxation 1047
Patent Ductus Arteriosus 1049
Pectus Excavatum 1052
Pelger–Huët Anomaly 1053
Pelvic Bladder 1054
Pemphigus1055
Perianal Fistula 1057
Pericardial Disease 1058
Perineal Hernia 1061
Periodontal Disease 1063
Peripheral Edema 1065
Perirenal Pseudocysts 1067
Peritoneopericardial Diaphragmatic Hernia 1068
Peritonitis1069
Petechiae, Ecchymosis, Bruising 1072
Petroleum Hydrocarbon Toxicosis 1074
Pheochromocytoma1076
Phosphofructokinase Deficiency 1078
Physalopterosis1079
Plague1080
Plasmacytoma, Mucocutaneous 1081
Pleural Effusion 1082
Pneumocystosis1084
Pneumonia, Aspiration 1085
Pneumonia, Bacterial 1086

xxii
Pneumonia, Eosinophilic 1088
Pneumonia, Fungal 1090
Pneumonia, Interstitial 1092
Pneumothorax1094
Pododermatitis1096
Poisoning (Intoxication) Therapy 1098
Polioencephalomyelitis—Cats1100
Polyarthritis, Erosive, Immune-Mediated 1101
Polyarthritis, Nonerosive, Immune-Mediated, Dogs 1103
Polycystic Kidney Disease 1105
Polycythemia Vera 1106
Polyneuropathies (Peripheral Neuropathies) 1107
Polyphagia1109
Polypoid Cystitis 1111
Polyuria and Polydipsia 1113
Portosystemic Shunting, Acquired 1115
Portosystemic Vascular Anomaly, Congenital 1118
Poxvirus Infection—Cats 1122
Pregnancy Edema in the Bitch 1123
Pregnancy Toxemia 1125
Premature Labor 1126
Prolapsed Gland of the Third Eyelid (Cherry Eye) 1127
Proptosis1128
Prostate Disease in the Breeding Male Dog 1129
Prostatic Cysts 1131
Prostatitis and Prostatic Abscess 1132
Prostatomegaly1134
Protein-Losing Enteropathy 1136
Proteinuria1138
Protothecosis1141
Pruritus1142
Pseudoephedrine/Phenylephrine Toxicosis 1144
Pseudomacrothrombocytopenia (Inherited Macrothrombocytopenia) 1145
Ptyalism1146
Pulmonary Contusions 1148
Pulmonary Edema, Noncardiogenic 1149
Pulmonary Thromboembolism 1151
Pulmonic Stenosis 1153
Puppy Behavior Problems 1155
Puppy Socialization and Puppy Classes 1157
Puppy Strangles (Juvenile Cellulitis) 1159
Pyelonephritis1160
Pyoderma1162
Pyoderma—Methicillin-Resistant1164
Pyometra1165
Pyothorax1168

xxiii
Pyrethrin and Pyrethroid Toxicosis 1170
Pyruvate Kinase Deficiency 1171
Pythiosis1172
Pyuria1174
Q Fever 1176
Quadrigeminal Cyst 1177
Rabies1178
Rectal and Anal Prolapse 1180
Rectal Stricture 1181
Rectoanal Polyps 1182
Red Eye 1183
Regurgitation1185
Renal Tubular Acidosis 1187
Renomegaly1188
Respiratory Parasites 1190
Retained Placenta 1192
Retinal Degeneration 1193
Retinal Detachment 1195
Retinal Hemorrhage 1197
Rhinitis and Sinusitis 1199
Right Bundle Branch Block 1202
Rocky Mountain Spotted Fever 1204
Rodenticide Toxicosis—Anticoagulants 1206
Rodenticide Toxicosis—Bromethalin 1208
Rodenticide Toxicosis—Cholecalciferol 1209
Rodenticide Toxicosis—Phosphides 1211
Roundworms (Ascariasis) 1212
Sago Palm Toxicosis 1213
Salivary Mucocele 1214
Salmon Poisoning Disease 1216
Salmonellosis1217
Salt Toxicosis 1219
Sarcoptic Mange 1221
Schiff–Sherrington Phenomenon 1222
Schwannoma1223
Sebaceous Adenitis, Granulomatous 1224
Seizures (Convulsions, Status Epilepticus)—Cats 1225
Seizures (Convulsions, Status Epilepticus)—Dogs 1227
Seminoma1230
Separation Anxiety Syndrome 1231
Sepsis and Bacteremia 1235
Sertoli Cell Tumor 1237
Sexual Development Disorders 1238
Shaker/Tremor Syndrome, Corticosteroid Responsive 1240
Shock, Cardiogenic 1241
Shock, Hypovolemic 1243

xxiv
Shock, Septic 1245
Shoulder Joint, Ligament, and Tendon Conditions 1247
Sick Sinus Syndrome 1250
Sinus Arrest and Sinoatrial Block 1252
Sinus Arrhythmia 1254
Sinus Bradycardia 1256
Sinus Tachycardia 1258
Sjögren-Like Syndrome 1260
Skin Fragility Syndrome, Feline 1261
Small Intestinal Dysbiosis 1262
Smoke Inhalation 1264
Snake Venom Toxicosis—Coral Snakes 1265
Snake Venom Toxicosis—Pit Vipers 1266
Sneezing, Reverse Sneezing, Gagging 1268
Soft Tissue Sarcoma 1270
Spermatocele/Sperm Granuloma 1272
Spermatozoal Abnormalities 1273
Spider Venom Toxicosis—Black Widow 1274
Spider Venom Toxicosis—Brown Recluse 1275
Spinal Dysraphism 1276
Splenic Torsion 1278
Splenomegaly1279
Spondylosis Deformans 1281
Sporotrichosis1282
Squamous Cell Carcinoma, Digit 1283
Squamous Cell Carcinoma, Ear 1284
Squamous Cell Carcinoma, Gingiva 1285
Squamous Cell Carcinoma, Lung 1286
Squamous Cell Carcinoma, Nasal and Paranasal Sinuses 1287
Squamous Cell Carcinoma, Nasal Planum 1288
Squamous Cell Carcinoma, Skin 1289
Squamous Cell Carcinoma, Tongue 1290
Squamous Cell Carcinoma, Tonsil 1291
Staphylococcal Infections 1292
Steroid-Responsive Meningitis-Arteritis—Dogs 1294
Stertor and Stridor 1295
Stomatitis and Oral Ulceration 1297
Streptococcal Infections 1299
Stupor and Coma 1300
Subarachnoid Cysts (Arachnoid Diverticulum) 1302
Subinvolution of Placental Sites 1304
Submissive and Excitement Urination—Dogs 1305
Superficial Necrolytic Dermatitis 1306
Supraventricular Tachycardia 1307
Syncope1309
Synovial Cell Sarcoma 1311

xxv
Syringomyelia and Chiari-Like Malformation 1312
Systolic Anterior Motion 1315
Tapeworms (Cestodiasis) 1317
Temporomandibular Joint Disorders 1318
Testicular Degeneration and Hypoplasia 1319
Tetanus1320
Tetralogy of Fallot 1322
Third Eyelid Protrusion 1323
Thrombocytopathies1325
Thrombocytopenia1327
Thrombocytopenia, Primary Immune-Mediated 1329
Thrombocytosis1331
Thunderstorm and Noise Phobias 1333
Thymoma1335
Tick Bite Paralysis 1336
Ticks and Tick Control 1338
Toad Venom Toxicosis 1340
Tooth—Missing1341
Tooth Formation/Structure, Abnormal 1342
Tooth Root Abscess (Apical Abscess) 1343
Torsion of the Spermatic Cord 1345
Toxoplasmosis1346
Tracheal Collapse 1348
Transitional Cell Carcinoma 1350
Transmissible Venereal Tumor 1352
Traumatic Dentoalveolar Injuries (TDI) 1353
Tremors1355
Trichomoniasis1357
Trigeminal Neuritis, Idiopathic 1358
Tularemia1359
Unruly Behaviors: Jumping, Pulling, Chasing, Stealing—Dogs 1361
Ureterolithiasis1363
Urethral Prolapse 1365
Urinary Retention, Functional 1366
Urinary Tract Obstruction 1368
Urinary Tract Parasites 1370
Urolithiasis, Calcium Oxalate 1372
Urolithiasis, Calcium Phosphate 1375
Urolithiasis, Cystine 1376
Urolithiasis, Pseudo (Dried Blood, Ossified Material)1378
Urolithiasis, Struvite—Cats 1379
Urolithiasis, Struvite—Dogs 1381
Urolithiasis, Urate 1383
Urolithiasis, Xanthine 1385
Uterine Inertia 1386
Uterine Tumors 1387

xxvi
Uveal Melanoma—Cats 1388
Uveal Melanoma—Dogs 1389
Uveodermatologic Syndrome (VKH) 1390
Vaginal Discharge 1391
Vaginal Hyperplasia and Prolapse 1393
Vaginal Malformations and Acquired Lesions 1394
Vaginal Tumors 1396
Vaginitis1397
Vascular Ring Anomalies 1399
Vasculitis, Cutaneous 1400
Vasculitis, Systemic (Including Phlebitis) 1401
Ventricular Arrhythmias and Sudden Death in German Shepherds 1404
Ventricular Fibrillation 1405
Ventricular Pre-Excitation and Wolff–Parkinson–White Syndrome 1407
Ventricular Premature Complexes 1409
Ventricular Septal Defect 1411
Ventricular Standstill (Asystole) 1413
Ventricular Tachycardia 1415
Vertebral Column Trauma 1419
Vesicourachal Diverticula 1421
Vestibular Disease, Geriatric—Dogs 1422
Vestibular Disease, Idiopathic—Cats 1424
Vomiting, Chronic 1426
Von Willebrand Disease 1429
Weight Loss and Cachexia 1431
West Nile Virus Infection 1434
Whipworms (Trichuriasis) 1435
Xylitol Toxicosis 1436
Zinc Toxicosis 1437
Appendix I Normal Reference Ranges for Laboratory Tests 1441

Table I-A Normal hematologic values 1441
Table I-B Normal biochemical values 1441
Table I-C Conversion table for hematologic units 1442
Table I-D Conversion table for clinical biochemical units 1443
Appendix II Endocrine Testing 1444
Table II-A Endocrine function testing protocols 1444
Table II-B Tests of the endocrine system 1445
Table II-C Conversion table for hormone assay units 1446
Appendix III Approximate Normal Ranges for Common Measurements
in Dogs and Cats 1447
Appendix IV Normal Values for the Canine and Feline Electrocardiogram 1448
Appendix V Antidotes and Useful Drugs: Methods of Treatment 1449
Appendix VI Toxic Home and Garden Hazards for Pets 1452
Table VI-A Toxic plants and their clinical signs—antidotes and treatment 1452
Table VI-B Herbal toxicities 1457

xxvii
Table VI-C Household cleaners, disinfectants, and solvents—products,
clinical signs, and treatment 1460
Appendix VII Pain Management 1465
Table VII-A Recommended parenteral opioid dosages and indications 1465
Table VII-B Recommended dispensable opioid dosages and indications 1465
Table VII-C Recommended parenteral local anesthetic dosages and indications 1466
Table VII-D Recommended parenteral NSAID dosages and indications 1466
Table VII-E Recommended dispensable NSAID dosages and indications 1467
Table VII-F Dosages and indications for selected drugs used to treat
neuropathic pain 1468
Appendix VIII Medications and Supplements for Osteoarthritis 1469
Table VIII-A Anti-inflammatories and pain medications 1469
Table VIII-B Recommended parenteral NSAID dosages and indications 1470
Table VIII-C Recommended oral NSAID dosages and indications 1471
Table VIII-D Disease-Modifying Drugs (DMOADs) 1472
Appendix IX Glossary of Terminology for Seizures and Epileptic Disorders 1473
Appendix X Common Procedures and Testing Protocols 1475
Abdominocentesis and Fluid Analysis 1476
Arthrocentesis With Synovial Fluid Analysis 1479
Bacterial Culture and Sensitivity 1483
Blood Gas Interpretation 1485
Blood Pressure Determination: Noninvasive and Invasive 1488
Blood Sample Collection 1490
Blood Smear Microscopic Examination 1492
Blood Smear Preparation 1496
Blood Typing 1498
Bone Marrow Aspirate and Biopsy 1501
Bone Marrow Aspirate Cytology: Microscopic Evaluation 1503
Complete Ophthalmologic Exam 1507
Crossmatch1512
Cystocentesis1514
Electrocardiography1517
Fecal Direct Smear and Cytology 1520
Fecal Flotation 1522
Fine-Needle Aspiration 1525
Fluid Analysis 1527
Glucose Curve 1530
Impression Smear 1533
Pericardiocentesis1534
Point of Care Abdominal Ultrasonography 1538
Point of Care Pleural Space and Lung Ultrasonography 1541
Rectal Scraping and Cytology 1547
Saline Agglutination Test 1548
Thoracocentesis and Fluid Analysis 1550
Tracheal Wash 1553
Ultrasound‐Guided Mass or Organ Aspiration 1555

xxviii
Urethral Catheterization 1559
Urinalysis Overview 1563
Urine Sediment 1565
Appendix XI Conversion Tables 1569
Table XI-A Conversion table of weight to body surface area (in square
meters) for dogs 1569
Table XI-B Approximate equivalents for degrees Fahrenheit and Celsius 1569
Table XI-C Weight-unit conversion factors 1570
Appendix XII Important Resources for Veterinarians 1571
Index1573

xxix
Contents by Subject
Topic
Appendices
Appendix I Normal Reference Ranges for Laboratory Tests 1441
Table I-A Normal hematologic values 1441
Table I-B Normal biochemical values 1441
Table I-C Conversion table for hematologic units 1442
Table I-D Conversion table for clinical biochemical units 1443
Appendix II Endocrine Testing 1444
Table II-A Endocrine function testing protocols 1444
Table II-B Tests of the endocrine system 1445
Table II-C Conversion table for hormone assay units 1446
Appendix III Approximate Normal Ranges for Common Measurements
in Dogs and Cats 1447
Appendix IV Normal Values for the Canine and Feline Electrocardiogram 1448
Appendix V Antidotes and Useful Drugs: Methods of Treatment 1449
Appendix VI Toxic Home and Garden Hazards for Pets 1452
Table VI-A Toxic plants and their clinical signs—antidotes and treatment 1452
Table VI-B Herbal toxicities 1457
Table VI-C Household cleaners, disinfectants, and solvents—products,
clinical signs, and treatment 1460
Appendix VII Pain Management 1465
Table VII-A Recommended parenteral opioid dosages and indications 1465
Table VII-B Recommended dispensable opioid dosages and indications 1465
Table VII-C Recommended parenteral local anesthetic dosages
and indications1466
Table VII-D Recommended parenteral NSAID dosages and indications 1466
Table VII-E Recommended dispensable NSAID dosages and indications 1467
Table VII-F Dosages and indications for selected drugs used to treat
neuropathic pain 1468
Appendix VIII Medications and Supplements for Osteoarthritis 1469
Table VIII-A Anti-inflammatories and pain medications 1469
Table VIII-B Recommended parenteral NSAID dosages and indications 1470
Table VIII-C Recommended oral NSAID dosages and indications 1471
Table VIII-D Disease-Modifying Drugs (DMOADs) 1472
Appendix IX Glossary of Terminology for Seizures and Epileptic Disorders 1473

xxxi
Appendix X Common Procedures and Testing Protocols 1475
Abdominocentesis and Fluid Analysis 1476
Arthrocentesis With Synovial Fluid Analysis 1479
Bacterial Culture and Sensitivity 1483
Blood Gas Interpretation 1485
Blood Pressure Determination: Noninvasive and Invasive 1488
Blood Sample Collection 1490
Blood Smear Microscopic Examination 1492
Blood Smear Preparation 1496
Blood Typing 1498
Bone Marrow Aspirate and Biopsy 1501
Bone Marrow Aspirate Cytology: Microscopic Evaluation 1503
Complete Ophthalmologic Exam 1507
Crossmatch1512
Cystocentesis1514
Electrocardiography1517
Fecal Direct Smear and Cytology 1520
Fecal Flotation 1522
Fine-Needle Aspiration 1525
Fluid Analysis 1527
Glucose Curve 1530
Impression Smear 1533
Pericardiocentesis1534
Point of Care Abdominal Ultrasonography 1538
Point of Care Pleural Space and Lung Ultrasonography 1541
Rectal Scraping and Cytology 1547
Saline Agglutination Test 1548
Thoracocentesis and Fluid Analysis 1550
Tracheal Wash 1553
Ultrasound‐Guided Mass or Organ Aspiration 1555
Urethral Catheterization 1559
Urinalysis Overview 1563
Urine Sediment 1565
Appendix XI Conversion Tables 1569
Table XI-A Conversion table of weight to body surface area (in square
meters) for dogs 1569
Table XI-B Approximate equivalents for degrees Fahrenheit and Celsius 1569
Table XI-C Weight-unit conversion factors 1570
Appendix XII Important Resources for Veterinarians 1571
Behavior
Aggression—Between Dogs in the Household 42
Aggression to Unfamiliar People and Unfamiliar Dogs—Dogs 44
Aggression Toward Children—Dogs 46
Aggression Toward Familiar People—Dogs 47

xxxii
Aggression Toward Humans—Cats 49
Aggression, Food and Resource Guarding—Dogs 51
Aggression, Intercat Aggression 53
Aggression, Overview—Cats 56
Aggression, Overview—Dogs 58
Car Ride Anxiety—Dogs and Cats 220
Cognitive Dysfunction Syndrome 295
Compulsive Disorders—Cats 304
Compulsive Disorders—Dogs 306
Coprophagia and Pica 332
Destructive and Scratching Behavior—Cats 388
Destructive Behavior—Dogs 389
Excessive Vocalization and Waking at Night—Dogs and Cats 476
Fear and Aggression in Veterinary Visits—Cats 490
Fear and Aggression in Veterinary Visits—Dogs 492
Fears, Phobias and Anxieties—Cats 494
Fears, Phobias and Anxieties—Dogs 496
Housesoiling—Cats657
Housesoiling—Dogs661
Kitten Behavior Problems 801
Kitten Socialization and Kitten Classes 803
Marking, Roaming, and Mounting Behavior—Cats 870
Marking, Roaming, and Mounting Behavior—Dogs 872
Maternal Behavior Problems 877
Polyphagia1109
Puppy Behavior Problems 1155
Puppy Socialization and Puppy Classes 1157
Separation Anxiety Syndrome 1231
Submissive and Excitement Urination—Dogs 1305
Thunderstorm and Noise Phobias 1333
Unruly Behaviors: Jumping, Pulling, Chasing, Stealing—Dogs 1361
Cardiology
Aortic Stenosis 106
Aortic Thromboembolism 108
Arteriovenous Fistula and Arteriovenous Malformation 112
Ascites120
Atrial Fibrillation and Atrial Flutter 136
Atrial Premature Complexes 139
Atrial Septal Defect 141
Atrial Standstill 142
Atrial Wall Tear 144
Atrioventricular Block, Complete (Third Degree) 146
Atrioventricular Block, First Degree 148
Atrioventricular Block, Second Degree—Mobitz Type I 150

xxxiii
Atrioventricular Block, Second Degree—Mobitz Type II 152
Atrioventricular Valve Dysplasia 154
Atrioventricular Valvular Stenosis 156
Cardiomyopathy, Arrhythmogenic Right Ventricular—Cats 226
Cardiomyopathy, Arrhythmogenic Right Ventricular—Dogs 227
Cardiomyopathy, Dilated—Cats 229
Cardiomyopathy, Dilated—Dogs 232
Cardiomyopathy, Hypertrophic—Cats 235
Cardiomyopathy, Hypertrophic—Dogs 238
Cardiomyopathy, Nutritional 239
Cardiomyopathy, Restrictive—Cats 241
Cardiopulmonary Arrest 243
Congestive Heart Failure, Left-Sided 315
Congestive Heart Failure, Right-Sided 317
Digoxin Toxicity 407
Electric Cord Injury 440
Endocarditis, Infective 445
Endomyocardial Diseases—Cats 447
Fever526
Heartworm Disease—Cats 586
Heartworm Disease—Dogs 587
Heat Stroke and Hyperthermia 589
Hypertension, Pulmonary 704
Hypertension, Systemic Arterial 706
Hypothermia745
Idioventricular Rhythm 754
Left Anterior Fascicular Block 816
Left Bundle Branch Block 818
Lymphedema853
Murmurs, Heart 912
Myocardial Infarction 933
Myocarditis935
Myxomatous Mitral Valve Disease 951
Patent Ductus Arteriosus 1049
Pericardial Disease 1058
Peripheral Edema 1065
Peritoneopericardial Diaphragmatic Hernia 1068
Pleural Effusion 1082
Pulmonary Thromboembolism 1151
Pulmonic Stenosis 1153
Right Bundle Branch Block 1202
Shock, Cardiogenic 1241
Shock, Hypovolemic 1243
Shock, Septic 1245
Sick Sinus Syndrome 1250

xxxiv
Sinus Arrest and Sinoatrial Block 1252
Sinus Arrhythmia 1254
Sinus Bradycardia 1256
Sinus Tachycardia 1258
Supraventricular Tachycardia 1307
Syncope1309
Systolic Anterior Motion 1315
Tetralogy of Fallot 1322
Vascular Ring Anomalies 1399
Vasculitis, Systemic (Including Phlebitis) 1401
Ventricular Arrhythmias and Sudden Death in German Shepherds 1404
Ventricular Fibrillation 1405
Ventricular Pre-Excitation and Wolff–Parkinson–White Syndrome 1407
Ventricular Premature Complexes 1409
Ventricular Septal Defect 1411
Ventricular Standstill (Asystole) 1413
Ventricular Tachycardia 1415
Dentistry
Deciduous Teeth, Persistent (Retained) 359
Dental Caries 364
Dentigerous Cyst 366
Discolored Tooth/Teeth 409
Enamel Hypoplasia/Hypocalcification 441
Feline Alveolar Osteitis 498
Feline Stomatitis—Feline Chronic Gingivostomatitis (FCGS) 519
Feline Tooth Resorption (Odontoclastic Resorption) 522
Gingival Enlargement/Hyperplasia 563
Halitosis579
Malocclusions—Skeletal and Dental 862
Maxillary and Mandibular Fractures 879
Odontogenic Tumors 988
Odontoma990
Oronasal Fistula 1005
Palatal Defects 1025
Periodontal Disease 1063
Stomatitis and Oral Ulceration 1297
Temporomandibular Joint Disorder 1318
Tooth—Missing1341
Tooth Formation/Structure, Abnormal 1342
Tooth Root Abscess (Apical Abscess) 1343
Traumatic Dentoalveolar Injuries (TDI) 1353

xxxv
Dermatology
Acne—Cats14
Acne—Dogs15
Acral Lick Dermatitis 16
Alopecia—Cats65
Alopecia—Dogs67
Alopecia, Noninflammatory—Dogs 69
Anal Sac Disorders 77
Atopic Dermatitis 134
Cheyletiellosis257
Claw and Clawfold Disorders 282
Contact Dermatitis 325
Cutaneous Drug Eruptions 350
Deep Cutaneous Mycoses 360
Demodicosis362
Dermatomyositis367
Dermatophilosis369
Dermatophytosis370
Dermatoses, Depigmenting Disorders 372
Dermatoses, Erosive or Ulcerative 374
Dermatoses, Exfoliative 376
Dermatoses, Neoplastic 378
Dermatoses, Papulonodular 380
Dermatoses, Sterile Nodular/Granulomatous 382
Dermatoses, Sun-Induced 384
Dermatoses, Vesiculopustular 385
Dermatoses, Viral (Non-Papillomatosis) 387
Ear Mites 432
Eosinophilic Granuloma Complex 451
Feline Paraneoplastic Alopecia 518
Feline Symmetrical Alopecia 521
Flea Bite Hypersensitivity and Flea Control 538
Food Reactions, Dermatologic 540
Histiocytosis, Cutaneous 652
Leishmaniosis, Cutaneous 825
Lupus Erythematosus, Cutaneous (Discoid) 844
Lymphoma, Cutaneous Epitheliotropic 858
Malassezia Dermatitis 860
Mycobacterial Infections 922
Nasal Dermatoses—Canine 956
Nocardiosis/Actinomycosis—Cutaneous980
Notoedric Mange 983
Otitis Externa and Media 1013
Panniculitis/Steatitis1033
Papillomatosis1039
Pemphigus1055

xxxvi
Pododermatitis1096
Protothecosis1141
Pruritus1142
Puppy Strangles (Juvenile Cellulitis) 1159
Pyoderma1162
Pyoderma—Methicillin-Resistant1164
Sarcoptic Mange 1221
Sebaceous Adenitis, Granulomatous 1224
Skin Fragility Syndrome, Feline 1261
Sporotrichosis1282
Superficial Necrolytic Dermatitis 1306
Ticks and Tick Control 1338
Uveodermatologic Syndrome (VKH) 1390
Vasculitis, Cutaneous 1400
Endocrinology
and Metabolism
Apudoma111
Carcinoid and Carcinoid Syndrome 224
Diabetes Insipidus 391
Diabetes Mellitus With Hyperosmolar Hyperglycemic State 393
Diabetes Mellitus With Ketoacidosis 395
Diabetes Mellitus Without Complication—Cats 397
Diabetes Mellitus Without Complication—Dogs 399
Glucagonoma568
Hyperadrenocorticism (Cushing’s Syndrome)—Cats 667
Hyperadrenocorticism (Cushing’s Syndrome)—Dogs 668
Hypercalcemia672
Hyperchloremia676
Hyperestrogenism (Estrogen Toxicity) 679
Hyperglycemia681
Hyperkalemia683
Hyperlipidemia685
Hypermagnesemia687
Hypernatremia691
Hyperosmolarity692
Hyperparathyroidism694
Hyperphosphatemia698
Hypersomatotropism/Acromegaly in Cats 700
Hyperthyroidism709
Hypoadrenocorticism (Addison’s Disease) 719
Hypocalcemia724
Hypochloremia726
Hypoglycemia727
Hypokalemia729

xxxvii
Hypomagnesemia731
Hyponatremia734
Hypoparathyroidism736
Hypophosphatemia739
Hypopituitarism741
Hyporexia743
Hyposthenuria744
Hypothyroidism747
Insulinoma776
Lactic Acidosis (Hyperlactatemia) 805
Myxedema and Myxedema Coma 950
Pheochromocytoma1076
Gastroenterology
Acute Abdomen 18
Acute Diarrhea 21
Acute Vomiting 27
Anorexia94
Bilious Vomiting Syndrome 179
Cobalamin Deficiency 290
Colitis and Proctitis 300
Colitis, Histiocytic Ulcerative 303
Constipation and Obstipation 323
Diarrhea, Antibiotic Responsive 402
Diarrhea, Chronic—Cats 403
Diarrhea, Chronic—Dogs 405
Dyschezia and Hematochezia 420
Dysphagia422
Esophageal Diverticula 464
Esophageal Foreign Bodies 465
Esophageal Stricture 467
Esophagitis469
Exocrine Pancreatic Insufficiency 480
Fiber-Responsive Large Bowel Diarrhea 528
Flatulence536
Food Reactions (Gastrointestinal), Adverse 542
Gastric Dilation and Volvulus Syndrome 546
Gastric Motility Disorders 548
Gastritis, Chronic 550
Gastroduodenal Ulceration/Erosion 552
Gastroenteritis, Acute Hemorrhagic Diarrhea Syndrome 554
Gastroenteritis, Eosinophilic 556
Gastroesophageal Reflux 558
Gastrointestinal Obstruction 559
Gluten Enteropathy in Irish Setters 572

xxxviii
Hematemesis600
Hiatal Hernia 646
Hypertrophic Pyloric Gastropathy, Chronic 714
Ileus756
Immunoproliferative Enteropathy of Basenjis 762
Incontinence, Fecal 763
Inflammatory Bowel Disease 771
Intussusception788
Lymphangiectasia849
Megacolon881
Megaesophagus883
Melena889
Obesity986
Pancreatitis—Cats1027
Pancreatitis—Dogs1029
Perianal Fistula 1057
Perineal Hernia 1061
Protein-Losing Enteropathy 1136
Ptyalism1146
Rectal and Anal Prolapse 1180
Rectal Stricture 1181
Rectoanal Polyps 1182
Regurgitation1185
Salivary Mucocele 1214
Small Intestinal Dysbiosis 1262
Vomiting, Chronic 1426
Weight Loss and Cachexia 1431
Hematology/
Immunology
Anaphylaxis78
Anemia, Aplastic 82
Anemia, Heinz Body 83
Anemia, Immune-Mediated 84
Anemia, Iron-Deficiency 86
Anemia, Nonregenerative 87
Anemia, Nuclear Maturation Defects (Anemia, Megaloblastic) 89
Anemia, Regenerative 90
Blood Transfusion Reactions 186
Chediak-Higashi Syndrome 255
Coagulation Factor Deficiency 286
Cold Agglutinin Disease 297
Cyclic Hematopoiesis 354
Disseminated Intravascular Coagulation 413
Eosinophilia450

xxxix
Erythrocytosis462
Familial Shar-Pei Fever 487
Hemotropic Mycoplasmosis 607
Hypercoagulability677
Hypereosinophilic Syndrome (HES) 678
Hyperviscosity Syndrome 716
Immunodeficiency Disorders, Primary 760
Leukocytosis831
Lupus Erythematosus, Systemic (SLE) 845
Lymphadenopathy/Lymphadenitis851
Methemoglobinemia904
Mucopolysaccharidoses908
Neutropenia978
Pancytopenia1031
Paraproteinemia1046
Pelger–Huët Anomaly 1053
Petechiae, Ecchymosis, Bruising 1072
Phosphofructokinase Deficiency 1078
Pseudomacrothrombocytopenia (Inherited Macrothrombocytopenia) 1145
Pyruvate Kinase Deficiency 1171
Sjögren-Like Syndrome 1260
Splenic Torsion 1278
Thrombocytopathies1325
Thrombocytopenia1327
Thrombocytopenia, Primary Immune-Mediated 1329
Thrombocytosis1331
Von Willebrand Disease 1429
Hepatology
Alkaline Hyperphosphatasemia in Dogs 61
Arteriovenous Malformation of the Liver 113
Bile Duct Obstruction (Extrahepatic) 174
Bile Peritonitis 177
Cholangitis/Cholangiohepatitis Syndrome 262
Cholecystitis and Choledochitis 265
Cholelithiasis267
Cirrhosis and Fibrosis of the Liver 279
Coagulopathy of Liver Disease 288
Copper Associated Hepatopathy 328
Ductal Plate Malformation (Congenital Hepatic Fibrosis) 416
Gallbladder Mucocele 544
Glycogen Storage Disease 573
Glycogen-Type Vacuolar Hepatopathy 574
Hepatic Amyloid 609
Hepatic Encephalopathy 611

xl
Hepatic Failure, Acute 614
Hepatic Lipidosis 617
Hepatic Nodular Hyperplasia and Dysplastic Hyperplasia 620
Hepatitis, Chronic 622
Hepatitis, Granulomatous 626
Hepatitis, Infectious (Viral) Canine 628
Hepatitis, Suppurative and Hepatic Abscess 630
Hepatocutaneous Syndrome 634
Hepatomegaly636
Hepatoportal Microvascular Dysplasia 639
Hepatosupportive Therapies 642
Hepatotoxins643
Hypertension, Portal 701
Hypoalbuminemia722
Icterus752
Liver Fluke Infestation 836
Portosystemic Shunting, Acquired 1115
Portosystemic Vascular Anomaly, Congenital 1118
Splenomegaly1279
Infectious
Diseases
Abscessation8
Actinomycosis and Nocardia 17
Anaerobic Infections 76
Aspergillosis, Disseminated Invasive 122
Babesiosis161
Bartonellosis164
Baylisascariasis167
Blastomycosis180
Brucellosis202
Campylobacteriosis206
Candidiasis207
Canine Coronavirus Infections 208
Canine Distemper 211
Canine Infectious Diarrhea 213
Canine Parvovirus 217
Canine Schistosomiasis (Heterobilharziasis) 219
Chagas Disease (American Trypanosomiasis) 254
Chlamydiosis—Cats258
Clostridial Enterotoxicosis 284
Coccidioidomycosis 292
Coccidiosis294
Colibacillosis298
Cryptococcosis344

xli
Cryptosporidiosis347
Cuterebriasis351
Cytauxzoonosis356
Ehrlichiosis and Anaplasmosis 436
Feline Calicivirus Infection 499
Feline Herpesvirus Infection 501
Feline Immunodeficiency Virus (FIV) Infection 506
Feline Infectious Diarrhea 508
Feline Infectious Peritonitis (FIP) 510
Feline Leukemia Virus (FeLV) Infection 514
Feline Panleukopenia 516
Feline (Upper) Respiratory Infections 524
Giardiasis562
Helicobacter spp. 591
Hepatozoonosis645
Histoplasmosis653
Hookworms (Ancylostomiasis) 655
Influenza773
Leishmaniosis824
Leptospirosis828
Lyme Borreliosis 847
Multidrug-Resistant Infections 909
Mycoplasmosis924
Neonatal Mortality and Canine Herpesvirus 964
Neosporosis969
Ollulanus Infection 993
Peritonitis1069
Physalopterosis1079
Plague1080
Pneumocystosis1084
Poxvirus Infection—Cats 1122
Pythiosis1172
Q Fever 1176
Rabies1178
Rocky Mountain Spotted Fever 1204
Roundworms (Ascariasis) 1212
Salmon Poisoning Disease 1216
Salmonellosis1217
Sepsis and Bacteremia 1235
Staphylococcal Infections 1292
Streptococcal Infections 1299
Tapeworms (Cestodiasis) 1317
Tetanus1320
Toxoplasmosis1346
Trichomoniasis1357
Tularemia1359

xlii
West Nile Virus Infection 1434
Whipworms (Trichuriasis) 1435
Musculoskeletal
Antebrachial Growth Deformities 96
Arthritis (Osteoarthritis) 115
Arthritis, Septic 118
Atlantoaxial Instability 132
Craniomandibular Osteopathy 341
Cruciate Ligament Disease, Cranial 342
Discospondylitis411
Elbow Dysplasia 438
Hip Dysplasia 647
Hypertrophic Osteodystrophy 711
Hypertrophic Osteopathy 713
Intervertebral Disc Disease, Cervical 781
Intervertebral Disc Disease, Thoracolumbar 784
Joint Luxations 793
Lameness808
Legg–Calvé–Perthes Disease 820
Metabolic, Nutritional, and Endocrine Bone Disorders 900
Muscle Rupture (Muscle Tear) 914
Myasthenia Gravis 920
Myopathy—Hereditary X-linked Muscular Dystrophy 938
Myopathy—Masticatory and Extraocular Myositis 939
Myopathy, Noninflammatory—Endocrine 941
Myopathy, Noninflammatory—Hereditary Labrador Retriever 943
Myopathy, Noninflammatory—Hereditary Myotonia 944
Myopathy, Noninflammatory—Hereditary Scottie Cramp 945
Myopathy, Noninflammatory—Metabolic 946
Myopathy—Polymyositis and Dermatomositis 948
Osteochondrodysplasia1006
Osteochondrosis1007
Osteomyelitis1009
Panosteitis1034
Patellar Luxation 1047
Polyarthritis, Erosive, Immune-Mediated 1101
Polyarthritis, Nonerosive, Immune-Mediated, Dogs 1103
Shoulder Joint, Ligament, and Tendon Conditions 1247
Nephrology/
Urology
Acidosis, Metabolic 12
Acute Kidney Injury 23

xliii
Alkalosis, Metabolic 63
Amyloidosis74
Anemia of Chronic Kidney Disease 80
Azotemia and Uremia 159
Benign Prostatic Hyperplasia 168
Chronic Kidney Disease 274
Congenital and Developmental Renal Diseases 308
Crystalluria348
Cylindruria355
Dysuria, Pollakiuria, and Stranguria 430
Ectopic Ureter 434
Fanconi Syndrome 489
Feline Idiopathic Lower Urinary Tract Disease 504
Glomerulonephritis566
Glucosuria570
Hematuria602
Hemoglobinuria and Myoglobinuria 604
Hydronephrosis665
Hyperparathyroidism, Renal Secondary 696
Incontinence, Urinary 765
Lower Urinary Tract Infection, Bacterial 838
Lower Urinary Tract Infection, Fungal 840
Nephrolithiasis970
Nephrotic Syndrome 972
Nephrotoxicity, Drug-Induced 974
Oliguria and Anuria 991
Pelvic Bladder 1054
Perirenal Pseudocysts 1067
Polycystic Kidney Disease 1105
Polypoid Cystitis 1111
Polyuria and Polydipsia 1113
Prostatic Cysts 1131
Prostatitis and Prostatic Abscess 1132
Prostatomegaly1134
Proteinuria1138
Pyelonephritis1160
Pyuria1174
Renal Tubular Acidosis 1187
Renomegaly1188
Ureterolithiasis1363
Urethral Prolapse 1365
Urinary Retention, Functional 1366
Urinary Tract Obstruction 1368
Urinary Tract Parasites 1370
Urolithiasis, Calcium Oxalate 1372
Urolithiasis, Calcium Phosphate 1375

xliv
Urolithiasis, Cystine 1376
Urolithiasis, Pseudo (Dried Blood, Ossified Material) 1378
Urolithiasis, Struvite—Cats 1379
Urolithiasis, Struvite—Dogs 1381
Urolithiasis, Urate 1383
Urolithiasis, Xanthine 1385
Vesicourachal Diverticula 1421
Neurology
Ataxia130
Botulism188
Brachial Plexus Avulsion 189
Brain Injury 192
Brain Tumors 194
Canine Degenerative Myelopathy 209
Cerebellar Degeneration 247
Cerebellar Hypoplasia 248
Cerebrovascular Accidents 249
Cervical Spondylomyelopathy (Wobbler Syndrome) 252
Congenital Spinal and Vertebral Malformations 313
Coonhound Paralysis (Acute Polyradiculoneuritis) 326
Deafness357
Dysautonomia (Key-Gaskell Syndrome) 419
Encephalitis442
Encephalitis Secondary to Parasitic Migration 444
Epilepsy, Genetic (Idiopathic)—Dogs 454
Exercise-Induced Weakness/Collapse in Labrador Retrievers 478
Facial Nerve Paresis and Paralysis 483
Feline Hyperesthesia Syndrome 503
Feline Ischemic Encephalopathy 512
Fibrocartilaginous Embolic Myelopathy 530
Head Pressing 581
Head Tilt 583
Head Tremors (Bobbing), Idiopathic—Dogs 585
Hydrocephalus663
Hypermetria and Dysmetria 689
Hypomyelination733
Intervertebral Disc Disease—Cats 780
Leukoencephalomyelopathy in Rottweilers 833
Lumbosacral Stenosis and Cauda Equina Syndrome 841
Lysosomal Storage Diseases 859
Meningioma—Cats and Dogs 891
Meningitis/Meningoencephalitis/Meningomyelitis, Bacterial 894
Meningoencephalomyelitis, Eosinophilic 896
Meningoencephalomyelitis of Unknown Etiology (MUE) 897

xlv
Movement Disorders 907
Myelomalacia, Spinal Cord (Ascending, Descending, Progressive) 929
Myelopathy—Paresis/Paralysis—Cats930
Myoclonus937
Narcolepsy and Cataplexy 954
Neck and Back Pain 961
Necrotizing Encephalitis 963
Nerve Sheath Tumors 976
Neuroaxonal Dystrophy 977
Nystagmus984
Otitis Media and Interna 1015
Pain (Acute, Chronic, and Postoperative) 1021
Paralysis1040
Polioencephalomyelitis—Cats1100
Polyneuropathies (Peripheral Neuropathies) 1107
Quadrigeminal Cyst 1177
Schiff–Sherrington Phenomenon 1222
Seizures (Convulsions, Status Epilepticus)—Cats 1225
Seizures (Convulsions, Status Epilepticus)—Dogs 1227
Shaker/Tremor Syndrome, Corticosteroid Responsive 1240
Spinal Dysraphism 1276
Spondylosis Deformans 1281
Steroid-Responsive Meningitis-Arteritis—Dogs 1294
Stupor and Coma 1300
Subarachnoid Cysts (Arachnoid Diverticulum) 1302
Syringomyelia and Chiari-Like Malformation 1312
Tick Bite Paralysis 1336
Tremors1355
Trigeminal Neuritis, Idiopathic 1358
Vertebral Column Trauma 1419
Vestibular Disease, Geriatric—Dogs 1422
Vestibular Disease, Idiopathic—Cats 1424
Oncology
Adenocarcinoma, Anal Sac 29
Adenocarcinoma, Lung 31
Adenocarcinoma, Nasal 32
Adenocarcinoma, Pancreas 34
Adenocarcinoma, Prostate 35
Adenocarcinoma, Renal 36
Adenocarcinoma, Salivary Gland 37
Adenocarcinoma, Skin (Sweat Gland, Sebaceous) 38
Adenocarcinoma, Stomach, Small and Large Intestine, Rectal 39
Adenocarcinoma, Thyroid—Dogs 40
Ameloblastoma71

xlvi
Astrocytoma129
Basal Cell Tumor 165
Bile Duct Carcinoma 173
Ceruminous Gland Adenocarcinoma, Ear 251
Chemodectoma256
Chondrosarcoma, Bone 269
Chondrosarcoma, Nasal and Paranasal Sinus 270
Chondrosarcoma, Oral 271
Fibrosarcoma, Bone 532
Fibrosarcoma, Gingiva 533
Fibrosarcoma, Nasal and Paranasal Sinus 534
Hair Follicle Tumors 578
Hemangiopericytoma593
Hemangiosarcoma, Bone 594
Hemangiosarcoma, Heart 595
Hemangiosarcoma, Skin 596
Hemangiosarcoma, Spleen and Liver 598
Hepatocellular Adenoma 632
Hepatocellular Carcinoma 633
Histiocytic Diseases—Dogs and Cats 650
Interstitial Cell Tumor, Testicle 779
Leiomyoma, Stomach, Small and Large Intestine 822
Leiomyosarcoma, Stomach, Small and Large Intestine 823
Leukemia, Chronic Lymphocytic 830
Lipoma, Infiltrative 835
Lymphoma—Cats854
Lymphoma—Dogs856
Malignant Fibrous Histiocytoma 861
Mammary Gland Tumors—Cats 865
Mammary Gland Tumors—Dogs 867
Mast Cell Tumors 874
Melanocytic Tumors, Oral 886
Melanocytic Tumors, Skin and Digit 888
Mesothelioma899
Multiple Myeloma 911
Myelodysplastic Syndromes 928
Myeloproliferative Disorders 932
Myocardial Tumors 934
Oral Cavity Tumors, Undifferentiated Malignant Tumors 1000
Osteosarcoma1011
Ovarian Tumors 1019
Paraneoplastic Syndromes 1042
Plasmacytoma, Mucocutaneous 1081
Polycythemia Vera 1106
Schwannoma1223
Seminoma1230

xlvii
Sertoli Cell Tumor 1237
Soft Tissue Sarcoma 1270
Squamous Cell Carcinoma, Digit 1283
Squamous Cell Carcinoma, Ear 1284
Squamous Cell Carcinoma, Gingiva 1285
Squamous Cell Carcinoma, Lung 1286
Squamous Cell Carcinoma, Nasal and Paranasal Sinuses 1287
Squamous Cell Carcinoma, Nasal Planum 1288
Squamous Cell Carcinoma, Skin 1289
Squamous Cell Carcinoma, Tongue 1290
Squamous Cell Carcinoma, Tonsil 1291
Synovial Cell Sarcoma 1311
Thymoma1335
Transitional Cell Carcinoma 1350
Transmissible Venereal Tumor 1352
Uterine Tumors 1387
Vaginal Tumors 1396
Ophthalmology
Anisocoria92
Anterior Uveitis—Cats 98
Anterior Uveitis—Dogs 100
Blepharitis 182
Blind Quiet Eye 184
Cataracts 245
Chorioretinitis 272
Congenital Ocular Anomalies 310
Conjunctivitis—Cats 319
Conjunctivitis—Dogs 321
Corneal and Scleral Lacerations 334
Corneal Opacities—Degenerations and Infiltrates 336
Corneal Opacities—Dystrophies 337
Corneal Sequestrum—Cats 338
Ectropion435
Entropion449
Epiphora 456
Episcleritis 458
Eyelash Disorders (Trichiasis/Distichiasis/Ectopic Cilia) 482
Glaucoma564
Horner’s Syndrome 656
Hyphema717
Hypopyon and Lipid Flare 742
Iris Atrophy 790
Keratitis, Eosinophilic—Cats 795
Keratitis, Nonulcerative 796

xlviii
Keratitis, Ulcerative 798
Keratoconjunctivitis Sicca 800
Lens Luxation 827
Ophthalmia Neonatorum 994
Optic Neuritis and Papilledema 998
Orbital Diseases (Exophthalmos, Enophthalmos, Strabismus) 1001
Prolapsed Gland of the Third Eyelid (Cherry Eye) 1127
Proptosis 1128
Red Eye 1183
Retinal Degeneration 1193
Retinal Detachment 1195
Retinal Hemorrhage 1197
Third Eyelid Protrusion 1323
Uveal Melanoma—Cats 1388
Uveal Melanoma—Dogs 1389
Respiratory
Acute Respiratory Distress Syndrome 25
Aspergillosis, Nasal 124
Asthma, Bronchitis—Cats 127
Brachycephalic Airway Syndrome 190
Bronchiectasis198
Bronchitis, Chronic 200
Canine Infectious Respiratory Disease 215
Chylothorax277
Cough339
Cyanosis352
Diaphragmatic Hernia 401
Drowning (Near Drowning) 415
Dyspnea and Respiratory Distress 425
Epistaxis459
Hemothorax606
Hypercapnia674
Hypoxemia750
Laryngeal and Tracheal Perforation 810
Laryngeal Diseases 812
Lung Lobe Torsion 843
Nasal and Nasopharyngeal Polyps 955
Nasal Discharge 958
Nasopharyngeal Stenosis 960
Panting and Tachypnea 1036
Pectus Excavatum 1052
Pneumonia, Aspiration 1085
Pneumonia, Bacterial 1086
Pneumonia, Eosinophilic 1088

xlix
Pneumonia, Fungal 1090
Pneumonia, Interstitial 1092
Pneumothorax1094
Pulmonary Contusions 1148
Pulmonary Edema, Noncardiogenic 1149
Pyothorax1168
Respiratory Parasites 1190
Rhinitis and Sinusitis 1199
Smoke Inhalation 1264
Sneezing, Reverse Sneezing, Gagging 1268
Stertor and Stridor 1295
Tracheal Collapse 1348
Theriogenology
Abortion, Spontaneous (Early Pregnancy Loss)—Cats 2
Abortion, Spontaneous (Early Pregnancy Loss)—Dogs 4
Abortion, Termination of Pregnancy 6
Breeding, Timing 196
Cryptorchidism346
Dystocia428
Eclampsia433
Epididymitis/Orchitis453
False Pregnancy 485
Gestational Diabetes Mellitus 561
Infertility, Female—Dogs 767
Infertility, Male—Dogs 769
Mammary Gland Hyperplasia—Cats 864
Mastitis876
Metritis906
Neonatal Resuscitation and Early Neonatal Care 966
Ovarian Remnant Syndrome 1017
Ovulatory Failure 1020
Paraphimosis, Phimosis, and Priapism 1045
Pregnancy Edema in the Bitch 1123
Pregnancy Toxemia 1125
Premature Labor 1126
Prostate Disease in the Breeding Male Dog 1129
Pyometra 1165
Retained Placenta 1192
Sexual Development Disorders 1238
Spermatocele/Sperm Granuloma 1272
Spermatozoal Abnormalities 1273
Subinvolution of Placental Sites 1304
Testicular Degeneration and Hypoplasia 1319
Torsion of the Spermatic Cord 1345

l
Uterine Inertia 1386
Vaginal Discharge 1391
Vaginal Hyperplasia and Prolapse 1393
Vaginal Malformations and Acquired Lesions 1394
Vaginitis1397
Toxicology
5-Fluorouracil (5-FU) Toxicosis 1
Acetaminophen (APAP) Toxicosis 10
Amphetamine and ADD/ADHD Medication Toxicosis 72
Antidepressant Toxicosis—SSRIs and SNRIs 102
Antidepressant Toxicosis—Tricyclic 104
Aspirin Toxicosis 126
Baclofen Toxicosis 163
Battery Toxicosis 166
Benzodiazepine and Other Sleep Aids Toxicosis 169
Beta Receptor Antagonist (Beta Blockers) Toxicosis 171
Beta-2 Agonist Inhaler Toxicosis 172
Blue-Green Algae Toxicosis 187
Calcipotriene/Calcipotriol Toxicosis 204
Calcium Channel Blocker Toxicosis 205
Carbon Monoxide Toxicosis 223
Cardiac Glycoside Plant Toxicosis 225
Chocolate Toxicosis 260
Diisocyanate Glues 408
Essential Oils Toxicosis 472
Ethanol Toxicosis 473
Ethylene Glycol Toxicosis 474
Fipronil Toxicosis 535
Grape and Raisin Toxicosis 577
Illicit/Club Drug Toxicosis 758
Imidazoline Toxicosis 759
Insoluble Oxalate Plant Toxicosis 775
Iron Toxicosis 791
Ivermectin and Other Macrocyclic Lactones Toxicosis 792
Lead Toxicosis 814
Lily Toxicosis 834
Marijuana Toxicosis 869
Metaldehyde Toxicosis 902
Metformin Toxicosis 903
Mushroom Toxicoses 916
Mycotoxicosis—Aflatoxin 926
Mycotoxicosis—Tremorgenic Toxins 927
Neonicotinoid Toxicosis 968
Nonsteroidal Anti-Inflammatory Drug Toxicosis 981

li
Opiates/Opioids Toxicosis 996
Organophosphorus and Carbamate Toxicosis 1003
Petroleum Hydrocarbon Toxicosis 1074
Poisoning (Intoxication) Therapy 1098
Pseudoephedrine/Phenylephrine Toxicosis 1144
Pyrethrin and Pyrethroid Toxicosis 1170
Rodenticide Toxicosis—Anticoagulants 1206
Rodenticide Toxicosis—Bromethalin 1208
Rodenticide Toxicosis—Cholecalciferol 1209
Rodenticide Toxicosis—Phosphides 1211
Sago Palm Toxicosis 1213
Salt Toxicosis 1219
Snake Venom Toxicosis—Coral Snakes 1265
Snake Venom Toxicosis—Pit Vipers 1266
Spider Venom Toxicosis—Black Widow 1274
Spider Venom Toxicosis—Brown Recluse 1275
Toad Venom Toxicosis 1340
Xylitol Toxicosis 1436
Zinc Toxicosis 1437
Index1573

lii
Preface
Keeping abreast of advances in veterinary internal medicine is extremely difficult, especially for the
busy general practitioner. To keep current with all the veterinary journals while practicing medicine is
impossible. The veterinarian in practice can be overwhelmed by all of the findings and conclusions of
thousands of studies conducted by veterinary specialists. Blackwell’s Five-Minute Veterinary Consult is
designed to provide the busy veterinary practitioner and student of veterinary medicine with concise
practical reviews of almost all the diseases and clinical problems in dogs and cats. Our goal in creating
this textbook was also to provide up-to-date information in an easy-to-use format. Emphasis is placed
on diagnosis and treatment of problems and diseases likely to be seen by veterinarians.
Our fondest dream was realized when the first six editions of this book were chosen as a comprehensive
reference source for canine and feline medicine by veterinary students, practicing veterinarians, and
board-certified specialists. The format has proven easy to use and very popular with busy practitioners.
The scope of the book and the number of Consulting Editors and authors have been expanded. We
have also increased the number of authors from outside North America, to provide the best advice in
the world. The number of topics has been increased, and every topic has been updated to provide you
with the most current information possible in a textbook. The appendixes have also been expanded to
include more useful tables.
Several good veterinary internal medicine textbooks are available. The uniqueness and value of
Blackwell’s Five-Minute Veterinary Consult as a quick reference is the consistency of presentation, the
breadth of coverage, the contribution of large numbers of experts, and the timely preparation of the
manuscript. The format of every topic is identical, making it easy to find information. An extensive list
of topic headings ensures complete coverage of each topic.
As the title implies, one objective of this book is to make information quickly available. To this end, we
have organized topics alphabetically from A to Z. Most topics can be found without using the index. A
table of contents broken out by organ system and a detailed index are provided. Large volumes of useful
information are summarized in charts in the appendixes. Included in the appendixes are normal labora-
tory values, endocrine testing protocols, common procedures and testing protocols, toxicology tables,
pain management tables, Rx for Osteoarthritis, disease-modifying drugs table, an epilepsy classification
table, conversion tables, and other information pages with important resources for veterinarians. For
this new edition, an appendix has been added to include common procedures and testing protocols
used in veterinary medicine.
We are delighted and privileged to have had the assistance of numerous experts in veterinary internal
medicine from around the world. More than 450 veterinary specialists contributed to this text, allow-
ing each chapter to be written by an expert on the subject. In addition to providing outstanding infor-
mation, this large pool of experts allowed us to publish this major text in a timely manner.
Many large textbooks take several years to write, making some of the information outdated by the time
the book is published. We are indebted to the many contributors and Consulting Editors whose hard
work allowed us to write, edit, and publish this work in 3 years, with most chapters completed within
a year of publication. Our goal is to revise the text every 3–4 years, so that the contents will always be
current.
Blackwell’s Five-Minute Veterinary Consult: Canine and Feline, Seventh Edition is available in a variety of
digital formats. Visit www.wiley.com/go/5MVC for more information. This edition also includes Client
Education Handouts based on the content of Blackwell’s Five-Minute Veterinary Consult. The compli-
mentary Client Education Handouts are available on a companion website at www.fiveminutevet.com/
canineandfeline featuring 331 Client Education Handouts for you to customize and use in practice.
These Handouts can be edited to reflect your practice preferences and then printed on your letterhead
to distribute to your clients.
liii
The book will also be published as an e-book, in downloadable ePub/ePDF formats. Now veterinarians
can quickly access information about necessary clinical skills and new developments in diagnosis and
treatment on their computers or mobile versions. The electronic versions offer fast, affordable access
to much of the accumulated wisdom in veterinary medicine. This technology brings to the clinic
examination room and doctor’s office an easy-to-use resource that will markedly improve the quality of
continuing education and clinical practice, and a companion website offers client education handouts
to be downloaded and used in practice.
The seventh edition of this textbook constitutes an important, up-to-date medical reference source for
your practice and clinical education. We strived to make it complete yet practical and easy to use. Our
dreams are realized if this text helps you to quickly locate and use the “momentarily important” infor-
mation that is essential to the practice of high-quality veterinary medicine. We would appreciate your
input so that we can make future editions even more useful. If you would like to see any changes in
content or format, additions, or deletions, please let us know. Send comments to the following:
Drs. Tilley, Smith, Sleeper and Brainard

c/o John Wiley & Sons
1606 Golden Aspen Dr Ste 104
Ames, IA 50010, USA
liv
Acknowledgments
The completion of this textbook provides a welcome opportunity to recognize in writing the many
individuals who have helped along the way. The Editors gratefully acknowledge the Consulting Editors
and the contributors who, by their expertise, have so unmistakably enhanced the quality of this
textbook.
We would also like to acknowledge and thank our families for their support of this project and the
sacrifices they made to allow us the time to complete the book.
In addition to thanking veterinarians who have referred patients to us, we would like to express our
gratitude to all the veterinary students, interns, and residents who we have had the privilege to teach.
Their curiosity and intellectual stimulation have enabled us to grow and have prompted us to under-
take the task of writing this book.
Finally, a special acknowledgment goes to everyone at Wiley Blackwell. The marketing and sales depart-
ments also must be acknowledged for generating such an interest in this book. They are all meticulous
workers and kind people who have made the final stages of preparing this book both inspiring and fun.
We would also like to thank copy-editors Sally Osborn and Harriet Stewart-Jones, and Erica Judisch,
Executive Editor. A special thank you goes to Mirjana Misina, Editorial Project Manager, who spent
hours and days keeping track of all the contributors and the deadline dates for manuscripts. This edi-
tion would not have taken place without her. An important life goal of ours has been fulfilled: to pro-
vide expertise in small animal internal medicine worldwide and to teach the principles contained in this
textbook to veterinarians and students everywhere.
Larry P. Tilley, Francis W.K. Smith, Jr.,

Meg M. Sleeper and Benjamin M. Brainard
lv
Consulting Editors
MICHAEL AHERNE, MVB, GradDipVetStud, KATE HOLAN, BS, DVM PATTY A. LATHAN, VMD, MS
MS, MANZCVS (Small Animal Surgery) Diplomate ACVIM (Small Animal Internal Diplomate ACVIM (Small Animal Internal
Diplomate ACVIM (Cardiology) Medicine) Medicine)
Clinical Assistant Professor Assistant Professor and Head Associate Professor
Department of Small Animal Clinical Small Animal Internal Medicine Department of Clinical Sciences
Sciences Department of Small Animal Clinical Mississippi State University
College of Veterinary Medicine Sciences Mississippi State, Mississippi, USA
University of Florida Michigan State University Subject: Endocrinology/Metabolism
Gainesville, Florida, USA East Lansing, Michigan, USA
Subject: Cardiology Subject: Hepatology
HEIDI B. LOBPRISE, DVM
Diplomate AVDC (Dentistry)
MELINDA S. CAMUS, DVM LYNN R. HOVDA, RPH, DVM, MS Main Street Veterinary Dental Clinic
Diplomate ACVP (Clinical Pathology) Diplomate ACVIM (Large Animal Internal Flower Mound, Texas, USA
Associate Professor Medicine) Subject: Dentistry
Department of Pathology Director of Veterinary Medicine
College of Veterinary Medicine SafetyCall International & Pet Poison
KATHERN E. MYRNA, DVM, MS
University of Georgia Helpline
Diplomate ACVO
Athens, Georgia, USA Bloomington, Minnesota;
Associate Professor of Ophthalmology
Subject: Hematology/Immunology Assistant Adjunct Professor
Department of Small Animal Medicine and
Department of Veterinary Biomedical
Surgery
Sciences
TIMOTHY M. FAN, DVM, PhD College of Veterinary Medicine
Diplomate ACVIM (Small Animal Internal University of Georgia
University of Minnesota
Medicine, Oncology) Athens, Georgia, USA
St. Paul, Minnesota, USA
Professor Subject: Ophthalmology
Subject: Toxicology
Department of Veterinary Clinical Medicine
MARK P. RONDEAU, DVM
University of Illinois at Urbana-Champaign AMIE KOENIG, DVM
Diplomate ACVIM (Small Animal Internal
Urbana, Illinois, USA Diplomate ACVIM (Small Animal Internal
Medicine)
Subject: Oncology Medicine), Diplomate ACVECC
Professor of Clinical Medicine
Professor of Emergency and Critical Care
Department of Clinical Sciences and
Department of Small Animal Medicine and
J.D. FOSTER, VMD Advanced Medicine
Surgery
Diplomate ACVIM (Small Animal Internal School of Veterinary Medicine
Medicine) University of Pennsylvania
Nephrology/Urology & Internal Medicine Philadelphia, Pennsylvania, USA
Athens, Georgia, USA
Friendship Hospital for Animals Subject: Gastroenterology
Subject: Infectious Diseases
Washington, DC, USA
Subject: Nephrology
ELIZABETH ROZANSKI, DVM
GARY M. LANDSBERG, BSc, DVM
Diplomate ACVECC
Diplomate ACVB, ECAWBM
MATHIEU M. GLASSMAN, VMD Diplomate DACVIM (Small Animal
Veterinary Behaviourist
Diplomate ACVS Internal Medicine)
Vice-President
Chief of Surgery Associate Professor
CanCog Incorporated
Friendship Surgical Specialists Department of Clinical Science
Fergus, Ontario;
Friendship Hospital for Animals Cummings School of Veterinary Medicine
Head
Washington, DC, USA Tufts University
Fear Free Research
Subject: Musculoskeletal North Grafton, Massachusetts, USA
Canada
Subject: Respiratory
Subject: Behavior
lvi
ERIN E. RUNCAN, DVM ALEXANDER H. WERNER RESNICK, VMD Acknowledgment
Diplomate ACT Diplomate ACVD The Book Editors acknowledge the prior
Associate Professor—Clinical Staff Dermatologist contribution of the following Consulting
Theriogenology and Reproductive Medicine Animal Dermatology Center Editors:
Department of Veterinary Clinical Sciences Studio City & Westlake Village Stephen C. Barr (Infectious Diseases)
The Ohio State University California, USA Deborah S. Greco (Endocrinology)
College of Veterinary Medicine Subject: Dermatology Sara K. Lyle (Theriogenology)
Columbus, Ohio, USA Stanley L. Marks (Gastroenterology)
Subject: Theriogenology Paul E. Miller (Ophthalmology)
Joane M. Parent (Neurology)
Carl A. Osborne (Nephrology/Urology)
Alan H. Rebar (Hematology/Immunology)
Walter C. Renberg (Musculoskeletal)
lvii
Contributors
JONATHAN A. ABBOTT, DVM HASAN ALBASAN, DVM, MS, PhD GENNA ATIEE, DVM
Diplomate ACVIM (Cardiology) Associate Veterinarian Diplomate ACVIM (Small Animal Internal
Associate Professor Nephrology & Urology Medicine)
Department of Small Animal Clinical Veterinary Care Specialists Interventional Radiology Fellow
Sciences Milford, Michigan College of Veterinary Medicine
College of Veterinary Medicine USA University of Georgia
University of Tennessee Veterinary Medical Center
Knoxville, Tennessee Athens, Georgia
RACHEL A. ALLBAUGH, DVM, MS
USA USA
Diplomate ACVO (Ophthalmology)
Associate Professor
ANTHONY C.G. ABRAMS-OGG, DVM, DVSc Department of Veterinary Clinical MELISSA J. BAIN, DVM, MS
Diplomate ACVIM (Small Animal Internal Sciences Diplomate ACVB (Behavior)
Medicine) College of Veterinary Medicine Diplomate ACAW (Welfare)
Professor Iowa State University Professor, Clinical Animal Behavior
Department of Clinical Studies Ames, Iowa Department of Veterinary Medicine and
University of Guelph USA Epidemiology
Ontario Veterinary College School of Veterinary Medicine
Guelph, Ontario University of California, Davis
KARIN ALLENSPACH, Dr.med.vet, PhD,
Canada Davis, California
FHEA, AGAF
USA
Diplomate ECVIM-CA
LARRY G. ADAMS, DVM, PhD Professor
Diplomate ACVIM (Small Animal Internal Department of Clinical Sciences TOMAS W. BAKER
Medicine) College of Veterinary Medicine Pound Sound Consulting
Professor of Small Animal Internal Iowa State University Three Rivers, California
Medicine Ames, Iowa USA
Department of Veterinary Clinical USA
Sciences
CHERYL E. BALKMAN, DVM
COLLEEN M. ALMGREN, DVM, PhD Diplomate ACVIM (Small Animal Internal
Purdue University
Diplomate DABT Medicine, Oncology)
West Lafayette, Indiana
Diplomate DABVT Senior Lecturer
USA
Veterinary Toxicologist Department of Clinical Sciences
Pet Poison Helpline/SafetyCall College of Veterinary Medicine
DARCY B. ADIN, DVM International Cornell University
Diplomate ACVIM (Cardiology) Bloomington, Minnesota Ithaca, New York
Clinical Associate Professor USA USA
Department of Large Animal Clinical
SARAH R. ALPERT, DVM GAD BANETH, DVM, PhD
Sciences
Diplomate ABT Diplomate ECVCP
University of Florida
Consulting Veterinarian, Clinical Toxicology Professor
Gainesville, Florida
Pet Poison Helpline & SafetyCall Koret School of Veterinary Medicine
USA
International The Hebrew University
Bloomington, Minnesota Rehovot
MICHAEL AHERNE, MVB, GradDipVetStud, USA Israel
MS, MANZCVS (Small Animal Surgery)
Diplomate ACVIM (Cardiology)
SOPHIE ASCHENBROICH, DVM, PhD KRISTIN M. BANNON, DVM, FAVD
Clinical Assistant Professor
Diplomate ACVP (Anatomic Pathology) Diplomate AVDC
Department of Small Animal Clinical
Assistant Professor Veterinary Dentistry and Oral Surgery of
Sciences
Department of Pathobiological Sciences New Mexico, LLC
School of Veterinary Medicine Algodones, New Mexico
University of Wisconsin-Madison USA
Madison, Wisconsin
USA
USA
lviii
RENEE BARBER, DVM, PhD KRISTEN BARTHOLOMEW, DVM ELSA BELTRAN, Ldo Vet, PGDipVetEd,
Diplomate ACVIM (Neurology) Emergency Clinician MRCVS
Assistant Professor of Neurology and Veterinary Referral Center Diplomate ECVN
Neurosurgery Malvern, Pennsylvania Associate Professor in Veterinary
Department of Small Animal Medicine USA Neurology & Neurosurgery
and Surgery Department of Clinical Science &
College of Veterinary Medicine Services
FIONA L. BATEMAN, BVSc
University of Georgia The Royal Veterinary College
Diplomate ACVD
Athens, Georgia University of London
Assistant Professor of Dermatology
USA North Mymms
Department of Small Animal Medicine
Hatfield, Herts
and Surgery
United Kingdom
LAURA A. BARBUR, DVM College of Veterinary Medicine
Diplomate ACVS (Small Animal) University of Georgia
Small Animal Surgeon Athens, Georgia MARIAN E. BENITEZ, DVM, MS
Department of Surgery USA Diplomate ACVS-SA
Friendship Hospital for Animals Surgeon/Owner
Washington, DC Dogwood Veterinary Surgical Care, PLLC
REBECCA M. BATES, DVM
USA Huntersville, North Carolina
Cardiology Resident
USA
ADRIENNE M. BARCHARD COUTS, DVM and Surgery
Resident ACVECC (SA) College of Veterinary Medicine KIA BENSON, DVM
Westford Veterinary Emergency and University of Georgia Associate Veterinarian, Clinical Toxicology
Referral Center Athens, Georgia SafetyCall International & Pet Poison
Westford, Massachusetts USA Helpline
USA Bloomington, Minnesota
USA
ADRIENNE C. BAUTISTA, DVM, PhD
HEIDI L. BARNES HELLER, DVM Diplomate ABVT
Diplomate ACVIM (Neurology) Scientific Services Veterinarian ELLISON BENTLEY, DVM
Clinical Associate Professor, Neurology/ Royal Canin Diplomate ACVO
Neurosurgery Davis, California Clinical Professor, Comparative
School of Veterinary Medicine USA Ophthalmology
University of Wisconsin-Madison Department of Surgical Sciences
Madison, Wisconsin School of Veterinary Medicine
ASHLEY E. BAVA, BVetMed (Hons) University of Wisconsin-Madison
USA
Emergency Clinician Madison, Wisconsin
Garden State Veterinary Specialists USA
MARGARET C. BARR, DVM, PhD Tinton Falls, New Jersey
Associate Dean for Academic Affairs USA
Professor of Virology and Immunology ALLYSON BERENT, DVM, DACVIM
College of Veterinary Medicine Director, Interventional Endoscopy Services
SARAH S.K. BEATTY, DVM Staff Internal Medicine Specialist
Western University of Health Sciences
Diplomate ACVP (Clincial Pathology) Animal Medical Center
Pomona, California
Clinical Assistant Professor New York, NY
USA
Department of Comparative, Diagnostic, USA
and
CARLA BARSTOW, DVM, MS Population Medicine
JEANNINE BERGER, DVM, CAWA
Diplomate ACT (Theriogenology) College of Veterinary Medicine
Diplomate ACVB (Behavior)
Highland Pet Hospital University of Florida
Diplomate ACAW (Welfare)
Lakeland, Florida Gainesville, Florida
Senior VP of Rescue and Welfare
USA USA
The Society for Prevention of Cruelty to
Animals (SPCA)
JOSEPH W. BARTGES, DVM, PhD JAN BELLOWS, DVM San Francisco, California
Diplomate ACVIM (Small Animal Internal Diplomate AVDC USA
Medicine) Diplomate ABVP
Diplomate ACVN All Pets Dental
MATTHEW R. BERRY, DVM
Professor of Medicine and Nutrition Weston, Florida
Medical Oncology Resident
Department of Small Animal Medicine USA
Department of Veterinary Clinical
and Surgery
Medicine;
PhD Candidate
The University of Georgia
Department of Pathobiology
Athens, Georgia
University of Illinois at Urbana-Champaign
USA
Urbana, Illinois
USA
lix
CHRISTINE F. BERTHELIN-BAKER, DVM LINDSAY BOOZER, DVM MARJORY B. BROOKS, DVM
Diplomate ACVIM (Neurology) Diplomate ACVIM (Neurology) Diplomate ACVIM (Small Animal)
Diplomate ECVN Staff Neurologist Director
Neurologist Friendship Hospital for Animals Comparative Coagulation Section, Animal
Atlanta, Georgia Washington, DC Health Diagnostic Laboratory
USA USA Department of Population Medicine and
Diagnostic Sciences
JEAN M. BETKOWSKI, VMD DWIGHT D. BOWMAN, MS, PhD Cornell University
Diplomate ACVIM (Cardiology) Diplomate ACVM (Parasitology, Honorary) Ithaca, New York
Staff Cardiologist Professor USA
Cape Cod Veterinary Specialists Department of Microbiology and
S. Dennis, Massachusetts Immunology AHNA G. BRUTLAG, DVM, MS
USA College of Veterinary Medicine Diplomate ABT
Cornell University Diplomate ABVT
ADAM J. BIRKENHEUER, DVM, PhD Ithaca, New York Director, Veterinary Services & Senior
Diplomate ACVIM USA Veterinary Toxicologist
Professor of Internal Medicine
Pet Poison Helpline & SafetyCall
Department of Clinical Medicine
SØREN BOYSEN, DVM International
North Carolina State University
Diplomate ACVECC Bloomington, Minnesota;
Raleigh, North Carolina
Professor Adjunct Assistant Professor
USA
Veterinary Emergency and Critical Care Department of Veterinary and Biomedical
Department of Veterinary Clinical and Sciences
KARYN BISCHOFF, DVM, MS
Diagnostic Sciences College of Veterinary Medicine
Diplomate ABVT
Faculty of Veterinary Medicine University of Minnesota
Diagnostic Toxicologist
University of Calgary St. Paul, Minnesota
New York State Animal Health Diagnostic
Calgary, Alberta USA
Laboratory
Canada
Department of Population Medicine and
Diagnostic Sciences JÖRG BUCHELER, DVM, PhD, FTA
College of Veterinary Medicine BENJAMIN M. BRAINARD, VMD Diplomate ACVIM (IM)
Cornell University Diplomate ACVAA and ACVECC Diplomate ECVIM-CA
Ithaca, New York Edward H. Gunst Professor of Small Veterinary Specialty Hospital of Palm
USA Animal Critical Care Beach Gardens
Department of Small Animal Medicine Palm Beach Gardens, Florida
MARIE-CLAUDE BLAIS, DVM and Surgery USA
Diplomate ACVIM (Small Animal Internal College of Veterinary Medicine
Medicine) University of Georgia
ANDREW C. BUGBEE, DVM
Associate Professor Athens, Georgia
Department of Clinical Sciences USA
Medicine)
Faculty of Veterinary Medicine
Associate Clinical Professor of IM
Université de Montréal RANDI BRANNAN, DVM, FAVD Department of Small Animal Medicine &
St-Hyacinthe, Quebec Diplomate AVDC (Dentistry) Surgery
Canada Animal Dental Clinic College of Veterinary Medicine
Portland, Oregon University of Georgia
APRIL E. BLONG, DVM USA Athens, Georgia
Diplomate ACVECC
USA
Assistant Professor
MATT BREWER, DVM, PhD
Diplomate ACVM (Parasitology)
Sciences ANNE E. BUGLIONE, DVM
Associate Professor
College of Veterinary Medicine Postdoctoral Associate
Department of Veterinary Pathology
Iowa State University Department of Neurobiology and
Ames, Iowa Behavior
Iowa State University
USA Cornell University
Ames, Iowa
Ithaca, New York
USA
JOHN D. BONAGURA, DVM, MS USA
Diplomate ACVIM (Cardiology, Internal
Medicine) ALYSSA J. BROOKER, DVM
Resident, Clinical Pathology KARAH BURNS DEMARLE, DVM
Department of Clinical Sciences
Department of Pathology Staff Internist, Small Animal Internal
College of Veterinary Medicine Medicine
University of Georgia Northstar VETS
Raleigh, North Carolina;
Athens, Georgia Robbinsville, New Jersey
Professor Emeritus of Veterinary Clinical
USA USA
Sciences
The Ohio State University
Columbus, Ohio
USA
lx
JENNA H. BURTON, DVM, MS AUDE M.H. CASTEL, DV, MSc BRUCE W. CHRISTENSEN, DVM, MS
Diplomate ACVIM (Oncology) Diplomate ACVIM (Neurology) Diplomate ACT
Associate Professor Clinical Oncology Assistant Professor, Neurology and Kokopelli Assisted Reproductive Services
Department of Surgical and Radiological Neurosurgery Franklin Ranch Pet Hospital
Sciences Department of Clinical Sciences Elk Grove, California
School of Veterinary Medicine Faculty of Veterinary Medicine USA
University of California, Davis University of Montreal
Davis, California St-Hyacinthe, Quebec E’LISE CHRISTENSEN BELL
USA Canada Diplomate ACVB
Owner
Behavior Vets
JULIE K. BYRON, DVM, MS MEGAN N. CAUDILL, DVM, MS
New York and Colorado
Diplomate ACVIM (Small Animal Diplomate ACVP (Clinical Pathology)
USA
Medicine) Department of Comparative, Diagnostic,
Professor—Clinical and Population Medicine
JOHN A. CHRISTIAN, DVM, PhD
Department of Veterinary Clinical College of Veterinary Medicine
Associate Professor of Clinical Pathology
Sciences University of Florida
Department of Comparative Pathobiology
College of Veterinary Medicine Gainesville, Florida
Purdue University
Columbus, Ohio
JULIE T. CECERE, DVM, MS, DACT West Lafayette, Indiana
USA
Clinical Associate Professor, Theriogenology USA
LAURA CAGLE, DVM Sciences RUTHANNE CHUN, DVM
Diplomate ACVECC Virginia-Maryland College of Veterinary Diplomate ACVIM (Oncology)
PhD Candidate – Integrative Pathobiology Medicine Clinical Professor
School of Veterinary Medicine Blacksburg, Virginia Department of Medical Sciences
University of California, Davis USA University of Wisconsin School of
Davis, California Veterinary Medicine
USA Madison, Wisconsin
SHARON A. CENTER, DVM
USA
KAREN L. CAMPBELL, DVM, MS Medicine)
DAVID B. CHURCH, BVSc, PhD, MACVSc,
Diplomate ACVIM (Small Animal Internal Professor
FHEA, MRCVS
Medicine) Department of Clinical Sciences
Professor of Small Animal Studies and
Diplomate ACVD Cornell University
Deputy Principal
Professor Emerita Cornell University Hospital for Animals
The Royal Veterinary College
University of Illinois; Ithaca, New York
Hatfield, Herts
Clinical Professor USA
United Kingdom
Department of Veterinary Sciences
SERGE CHALHOUB, DVM JOHN J. CIRIBASSI, DVM
University of Missouri
Diplomate ACVIM (Small Animal Internal Diplomate ACVB
Veterinary Health Center-Wentzville
Medicine) Chicagoland Veterinary Behavior
Wentzville, Missouri
Senior Instructor, Small Animal Internal Consultants
USA
Medicine Schererville, Indiana
Department of Veterinary Clinical and USA
MELINDA S. CAMUS, DVM Diagnostic Sciences
Diplomate ACVP (Clinical Pathology) Faculty of Veterinary Medicine CÉCILE CLERCX, DVM, PhD
Associate Professor University of Calgary Diplomate ECVIM-CA
Department of Pathology Calgary, Alberta Professor
College of Veterinary Medicine Canada Department of Companion Animal
University of Georgia Clinical Sciences
Athens, Georgia Faculty of Veterinary Medicine
GEORGINA CHILD, BVSc
USA University of Liège
Diplomate ACVIM (Neurology)
Belgium
Consultant
RENEE T. CARTER, DVM Small Animal Specialist Hospital
ANDREANNE CLEROUX
Diplomate ACVO North Ryde;
Associate Professor, Ophthalmology Senior Lecturer
Medicine)
Department of Veterinary Clinical School of Veterinary Science
Lecturer in Internal Medicine &
Sciences University of Sydney
Interventional Radiology
School of Veterinary Medicine Sydney, NSW
Department of Clinical Sciences &
Louisiana State University Australia
Advanced Medicine
Baton Rouge, Louisiana
School of Veterinary Medicine
USA
University of Pennsylvania
Philadelphia, Pennsylvania
USA
lxi
CRAIG A. CLIFFORD, DVM, MS AUDREY K. COOK, BVM&S, MSc VetEd, SUZANNE M. CUNNINGHAM, DVM
Diplomate ACVIM (Oncology) MRCVS Diplomate ACVIM (Cardiology)
Medical Oncologist Diplomate ACVIM (Small Animal Internal Associate Professor
Director of Clinical Trials Medicine) Department of Clinical Sciences
Hope Veterinary Specialists Diplomate ECVIM-CA Cummings School of Veterinary Medicine
Malvern, Pennsylvania Diplomate ABVP (Feline Practice) Tufts University
USA Professor, Small Animal Internal Medicine North Grafton, Massachusetts
Department of Small Animal Clinical USA
JOAN R. COATES, BS, DVM, MS Sciences
Diplomate ACVIM (Neurology) College of Veterinary Medicine and
ELIZABETH A. CURRY-GALVIN, DVM
Professor of Veterinary Neurology & Biomedical Sciences
Barrington Hills, Illinois
Neurosurgery Texas A&M University
USA
Department of Veterinary Medicine and College Station, Texas
Surgery USA
College of Veterinary Medicine TERRY MARIE CURTIS, DVM, MS
University of Missouri Diplomate ACVB
LESLIE LARSON COOPER, DVM
Columbia, Missouri Veterinary Behaviorist
Diplomate ACVB
USA St. Augustine, Florida
Animal Behavior Counseling and Therapy
USA
Davis, California
SUSAN M. COCHRANE, BSc, MSc, DVM, USA
DVSc SARAH L. CZERWINSKI, BSc, DVM
Diplomate ACVIM (Neurology) Diplomate ACVO
EDWARD S. COOPER, VMD, MS
Veterinary Emergency Clinic and Referral Clinical Assistant Professor
Diplomate ACVECC
Centre Department of Small Animal Medicine
Professor—Clinical
Toronto, Ontario and Surgery
Canada College of Veterinary Medicine
Sciences
STEVEN M. COGAR, DVM Athens, Georgia
Ohio State University
Diplomate ACVS-SA USA
Columbus, Ohio
Carolina Veterinary Specialists USA
Winston-Salem, North Carolina RONALDO CASIMIRO DA COSTA, DMV,
USA MSc, PhD
RHIAN COPE, BVSc, BSc(Hon1), PhD,
WILLIAM M. COLE, DVM FACTRA
Professor and Service Head, Neurology
Small Animal Internal Medicine Diplomate ABT
and Neurosurgery
Metropolitan Animal Specialty Hospital Diplomate ABVT
Los Angeles, California Principal Toxicologist
Sciences
USA Australian Pesticides and Veterinary
Medicines Authority
Symonston
AMANDA E. COLEMAN, DVM, DACVIM Columbus, Ohio
Australia
(Cardiology) USA
Associate Professor of Cardiology
Department of Small Animal Medicine JOHN M. CRANDELL, DVM
AUTUMN P. DAVIDSON, DVM, MS
and Surgery Diplomate ACVIM (Small Animal Internal
University of Georgia College of Medicine)
Medicine)
Veterinary Medicine Veterinary Internist
Clinical Professor
Athens, Georgia MedVet Akron
VMTH
USA Akron, Ohio
USA
University of California
HEATHER E. CONNALLY, DVM, MS Davis, California
Diplomate ACVECC SIGNE E. CREMER, DVM, PhD USA
Veterinary Specialty Center on Tucson Associate Professor, Clinical Pathology
(retired) Department of Veterinary Clinical
Associate Veterinarian THOMAS K. DAY, DVM, MS
Sciences
Tucson, Arizona Diplomate ACVAA
Faculty of Health and Medical Sciences
USA Diplomate ACVECC
University of Copenhagen
Emergency and Critical Care Specialist
Frederiksberg
Anesthesiology and Pain Management
FRANCISCO O. CONRADO, DVM, MSc Denmark
Specialist
Diplomate ACVP (Clinical Pathology)
VCA Veterinary Emergency Service and
Assistant Professor
Specialty Center
Department of Biomedical Sciences
Middleton, Wisconsin
Cummings School of Veterinary Medicine
USA
Tufts University
North Grafton, Massachusetts
USA
lxii
ALEXANDER DE LAHUNTA, DVM, PhD NICK DERVISIS, DVM, PhD EDWARD J. DUBOVI, PhD
Retired Professor of Veterinary Anatomy DACVIM (Oncology) Professor of Virology
at Cornell University Medical Oncology Department of Population Medicine and
Ithaca, New York Associate Professor Diagnostic Sciences
USA Department of Small Animal Clinical Animal Health Diagnostic Center
Sciences; College of Veterinary Medicine
Associate Professor Cornell University
HELIO S. AUTRAN DE MORAIS, DVM, PhD
Faculty of Health Sciences Ithaca, New York
Diplomate ACVIM (Internal Medicine and
VA-MD College of Veterinary Medicine USA
Cardiology)
DSACS, Phase II
Director
Blacksburg, Virginia DAVID D. DUCLOS, DVM
Lois Bates Acheson Veterinary Teaching
USA Diplomate ACVD
Hospital
College of Veterinary Medicine Clinical Dermatologist—Animal Skin &
Oregon State University IAN DESTEFANO, DVM Allergy Clinic
Corvallis, Oregon Resident, Emergency & Critical Care Lynnwood, Washington
USA Foster Hospital for Small Animals USA
Tufts University
North Grafton, Massachusetts CEDRIC P. DUFAYET, DVM
JONATHAN D. DEAR, DVM, MAS
USA Associate Veterinarian
Advanced Urinary Disease and
Medicine)
Extracorporeal Therapies Service
Assistant Professor of Clinical Internal SHARON M. DIAL, DVM, PhD
University of California Veterinary
Medicine Diplomate ACVP (Clinical and Anatomic
Medicine Center
Department of Medicine and Pathology)
San Diego, California
Epidemiology Research Scientist
USA
School of Veterinary Medicine College of Veterinary Medicine
University of California, Davis University of Arizona
Davis, California Tucson, Arizona STÉPHANIE DUGAS, DVM, MSc
USA USA Diplomate ACVIM (Neurology)
Medical Neurologist
BluePearl Specialty & Emergency Hospital
TERESA C. DEFRANCESCO, DVM STEPHEN P. DIBARTOLA, DVM Irvine, California
Diplomate ACVIM (Cardiology), ACVECC Diplomate ACVIM (Small Animal Internal USA
Department of Clinical Sciences Medicine)
College of Veterinary Medicine Professor Emeritus of Internal Medicine
North Carolina State University Department of Veterinary Clinical ERIC K. DUNAYER, MS, VMD
Raleigh, North Carolina Sciences Diplomate ABT
USA College of Veterinary Medicine Diplomate ABVT
Ohio State University Senior Toxicologist
Columbus, Ohio ASPCA Animal Poison Control Center
VICTORIA A. DEMELLO, DVM Urbana, Illinois
USA
Nashville Veterinary Specialists USA
Nashville, Tennessee
USA DAVID C. DORMAN, DVM, PhD
CAROLINA DUQUE, DVM, MSc, DVSc
Diplomate ABVT
Diplomate ABT
SAGI DENENBERG, DVM, MRCVS Mississauga Oakville Emergency Hospital
Professor of Toxicology
Veterinary Psychiatrist and Referral Group
Department of Molecular Biomedical
Diplomate ACVB Oakville, Ontario
Sciences
Diplomate ECAWBM Canada
RCVS Recognized Specialist in
Veterinary Behavioural Medicine DAVID DYCUS, DVM, MS, CCRP
North Toronto Veterinary Behaviour Diplomate ACVS (Small Animal)
USA
Specialty Clinic Chief of Orthopedics
Thornhill, Ontario Nexus Veterinary Bone & Joint Center
Canada ELIZABETH R. DRAKE, DVM Medical Director
Diplomate ACVD Nexus Veterinary Specialists
Associate Professor Baltimore, Maryland
THERESA L. DEPORTER, BSc, DVM,
Department of Small Animal Clinical USA
MRCVS
Sciences
Diplomate DECAWBM
Diplomate ACVB (Behavior) HEATHER D. EDGINTON, DVM
University of Tennessee
Veterinary Behaviorist Diplomate ACVD
Knoxville, Tennessee
Behavioral Medicine Department Animal Medical Center of Seattle
USA
Oakland Veterinary Referral Services Shoreline, Washington
Bloomfield Hills, Michigan USA
USA
lxiii
MELISSA N.C. EISENSCHENK, DVM, MS LEAH FERGUSON, DVM, MS J.D. FOSTER, VMD
Diplomate ACVD Diplomate ACVIM (Internal Medicine) Diplomate ACVIM (Small Animal Internal
Owner, Veterinary Dermatologist Veterinary Internist Medicine)
Pet Dermatology Clinic VCA Great Lakes Veterinary Specialists Nephrology/Urology & Internal Medicine
Maple Grove, Minnesota Warrensville Heights, Ohio Friendship Hospital for Animals
USA USA Washington, DC
USA
MARC ELIE, DVM LLUÍS FERRER, BVSc, PhD
Diplomate ACVIM (Internal Medicine) Diplomate ECVD DANIEL S. FOY, MS, DVM
Staff Internist Professor Diplomate ACVIM (Small Animal Internal
Small Animal Internal Medicine Department of Animal Medicine and Surgery Medicine)
BluePearl Veterinary Partners Veterinary School Diplomate ACVECC
Southfield, Michigan Universitat Autònoma de Barcelona, Clinical Assistant Professor
USA Bellaterra, Barcelona College of Veterinary Medicine
Spain Midwestern University
ROBYN ELLERBROCK, DVM, PhD Glendale, Arizona
Diplomate ACT MARIA SOLEDAD FERRER, DVM, MS USA
Assistant Professor Diplomate DACT (Theriogenology)
Department of Large Animal Medicine Associate Professor LINDA A. FRANK, MS, DVM
College of Veterinary Medicine Department of Large Animal Medicine Diplomate ACVD
University of Georgia College of Veterinary Medicine Professor
Athens, Georgia University of Georgia Department of Small Animal Clinical
USA Athens, Georgia Sciences
USA College of Veterinary Medicine
NAHVID M. ETEDALI, DVM University of Tennessee
Diplomate ACVIM (Small Animal Internal TESSA FIAMENGO, DVM, MS Knoxville, Tennessee
Medicine) Diplomate ACT USA
Staff Internist Slade Veterinary Hospital
Head of Hemodialysis and Extracorporeal Framingham, Massachusetts
JONI L. FRESHMAN, DVM MS CVA
Therapies USA
Diplomate ACVIM (Internal Medicine)
Animal Medical Center Owner
New York, New York ANDREA M. FINNEN, DVM, DES, MSc
Canine Consultations
USA Diplomate ACVIM (Neurology)
Peyton, Colorado
Mississauga Oakville Veterinary
USA
Emergency Hospital
TIMOTHY M. FAN, DVM, PhD
Neurology Service
Oakville, Ontario CANNY FUNG, DVM
Medicine, Oncology)
Canada Surgery Intern
Professor Southwest Veterinary Surgical Service
ANDREA FISCHER, DVM, Dr.med.vet., Phoenix Arizona
Dr. habil. USA
University of Illinois at Urbana-Champaign
Urbana, Illinois
Diplomate ECVN EVA FURROW, VMD, PhD
USA
Professor Diplomate ACVIM (Small Animal Internal
Centre for Clinical Veterinary Medicine Medicine)
JUSTIN FARRIS, DVM LMU University of Munich Associate Professor
Clinical Pathology Resident Munich Department of Veterinary Clinical
Department of Pathology Germany Sciences
College of Veterinary Medicine College of Veterinary Medicine
University of Georgia GERRARD FLANNIGAN, DVM, MSc University of Minnesota
Athens, Georgia Diplomate ACVB St. Paul, Minnesota
USA Kernersville, North Carolina USA
USA
RICHARD A. FAYRER-HOSKEN, BVSc, PhD LUIS GAITERO, DVM
LINDA M. FLEEMAN, BVSc, PhD, MANZCVS
Diplomate ACT (Theriogenology) Diplomate ECVN
Animal Diabetes Australia
Diplomate ECAR Associate Professor and Head Neurology
Melbourne, Victoria
Research Scientist and Neurosurgery Service
Australia
Institute for Conservation Research HSC Chief Medical Officer
San Diego Zoo Global Department of Clinical Studies
CHARLOTTE FLINT, DVM, DABT
Escondido, California Ontario Veterinary College
Senior Consulting Veterinarian, Clinical
USA University of Guelph
Toxicology
Guelph, Ontario
Canada
International
Bloomington, Minnesota
USA
lxiv
JOAO FELIPE DE BRITO GALVAO, MV, MS ANNE J. GEMENSKY METZLER, DVM, MS RITA GONÇALVES, DVM, MVM, FHEA,
Diplomate ACVIM (Small Animal Internal Diplomate ACVO MRCVS
Medicine) Professor—Clinical Diplomate ECVN
Internal Medicine Specialist Department of Veterinary Clinical European and RCVS Recognized
VCA Arboretum View Animal Hospital Sciences Specialist in Veterinary Neurology
Downers Grove, Illinois; College of Veterinary Medicine Senior Lecturer in Veterinary Neurology
Adjunct Assistant Professor The Ohio State University Small Animal Clinical Science
The Ohio State University Columbus, Ohio University of Liverpool
Columbus, Ohio USA Neston, Cheshire
USA United Kingdom
KATHERINE GERKEN, DVM, MS
BRIDGET C. GARNER, DVM, PhD Diplomate ACVECC SARA E. GONZALEZ, DVM, MS
Diplomate ACVP (Clinical Pathology) Assistant Clinical Professor Clinical Assistant Professor of Community
Associate Professor Small Animal Emergency and Critical Practice
Department of Pathology Care Department of Small Animal Medicine
College of Veterinary Medicine Department of Clinical Sciences and Surgery
University of Georgia Bailey Small Animal Teaching Hospital University of Georgia College of
Athens, Georgia College of Veterinary Medicine Veterinary Medicine
USA Auburn University Athens, Georgia
Auburn, Alabama USA
USA
LAURENT GAROSI, DVM, FRCVS
Diplomate ECVN JENNIFER GOOD, DVM
RCVS and EBVS® VIRGINIA L. GILL, DVM Diplomate ACVECC (Emergency and
European Specialist in Veterinary Diplomate DACVIM (Oncology) Critical Care)
Neurology Medical Director Assistant Clinical Professor
Clinical Director Vet Oracle Teleneurology Maine Veterinary Medical Center Department of Emergency and Critical
Bedford Scarborough, Maine Care
United Kingdom USA College of Veterinary Medicine
LAURA D. GARRETT, DVM MARGI A. GILMOUR, DVM Athens, Georgia
Diplomate ACVIM (Oncology) Diplomate ACVO USA
Clinical Professor Professor
Department of Veterinary Clinical Department of Veterinary Clinical SHARON FOOSHEE GRACE, M Agric, MS,
Medicine Sciences DVM
College of Veterinary Medicine College of Veterinary Medicine Diplomate ACVIM (Small Animal)
University of Illinois Oklahoma State University Diplomate ABVP (Canine/Feline)
Urbana, Illinois Stillwater, Oklahoma Clinical Professor
USA USA Department of Clinical Sciences
CATHY J. GARTLEY, DVM, DVSc ERIC N. GLASS, MS, DVM Mississippi State University
Diplomate ACT Diplomate ACVIM (Neurology) Mississippi State, Mississippi
Assistant Professor Section Head, Neurology and USA
Department of Population Medicine Neurosurgery
Ontario Veterinary College Red Bank Veterinary Hospital W. DUNBAR GRAM, DVM, MRCVS
University of Guelph Tinton Falls, New Jersey; Diplomate ACVD
Guelph, Ontario Chief of Neurology and Neurosurgery Clinical Associate Professor and
Canada Compassion First Pet Hospital Dermatology Service Chief
Tinton Falls, New Jersey Small Animal Clinical Sciences, University
USA of Florida
ANNA R.M. GELZER, Dr.med.vet., PhD
Diplomate ACVIM Gainesville, Florida
Diplomate ECVIM-CA-Cardiology MATHIEU M. GLASSMAN, VMD USA
Professor of Cardiology Diplomate ACVS
Department of Clinical Sciences & Chief of Surgery JENNIFER L. GRANICK, DVM, PhD
Advanced Medicine Friendship Surgical Specialists Diplomate ACVIM (Small Animal Internal
School of Veterinary Medicine Friendship Hospital for Animals Medicine)
University of Pennsylvania Washington, DC Associate Professor
Philadelphia, Pennsylvania USA Department of Veterinary Clinical
USA Sciences
St. Paul, Minnesota
USA
lxv
GREGORY F. GRAUER, DVM, MS TALIA GUTTIN, VMD EDWARD J. HALL, MA, VetMB, PhD, FRCVS
Diplomate ACVIM (Small Animal Internal Diplomate ACVIM (Small Animal Internal Diplomate ECVIM-CA
Medicine) Medicine) Emeritus Professor of Small Animal
Professor Emeritus Assistant Professor Internal Medicine
Department of Clinical Sciences Small Animal Medicine and Surgery Langford Vets
College of Veterinary Medicine Department Bristol Veterinary School
Kansas State University School of Veterinary Medicine University of Bristol
Manhattan, Kansas St. George’s University Langford
USA True Blue Campus United Kingdom
St. George, Grenada
West Indies
SARAH L. GRAY, DVM STEVEN R. HANSEN, DVM, MS, MBA
Diplomate ACVECC (Emergency and Diplomate ACAW
Critical Care) SHARON GWALTNEY-BRANT, DVM, PhD Diplomate ABVT
Horizon Veterinary Specialist Diplomate ABVT President and CEO
Ventura, California Diplomate ABT Arizona Humane Society
USA Consultant Phoenix, Arizona
Veterinary Information Network USA
Mahomet, Illinois
KURT A. GRIMM, DVM, MS, PhD USA
Diplomate ACVCP TISHA A.M. HARPER, DVM, MS, CCRP
Diplomate ACVAA Diplomate ACVS-SA
TIMOTHY B. HACKETT, DVM, MS
Owner Diplomate ACVSMR
Diplomate ACVECC
Veterinary Specialist Services, PC Clinical Associate Professor
Professor
Conifer, Colorado Department of Veterinary Clinical
USA Medicine
College of Veterinary Medicine and University of Illinois College of Veterinary
Biomedical Sciences Medicine
AMY M. GROOTERS, DVM Colorado State University Urbana, Illinois
Diplomate ACVIM (Small Animal Internal Fort Collins, Colorado USA
Medicine) USA
Professor, Companion Animal Medicine
Veterinary Clinical Sciences JOHN W. HARVEY, DVM, PhD
DEBORAH J. HADLOCK, VMD
Louisiana State University Diplomate ACVP (Clinical Pathology)
Diplomate ABVP (Canine and Feline)
Baton Rouge, Louisiana Professor Emeritus
Certified Veterinary Acupuncturist—CVA
USA Department of Physiological Sciences
(IVAS)
Certified Veterinary Spinal Manipulative
MARGARET E. GRUEN, DVM, PhD Therapist—CVSMT (HOWC)
Diplomate ACVB Owner
USA
Assistant Professor, Behavioral Medicine Hadlock Integrative Veterinary Consulting
Department of Clinical Sciences Salt Lake City, Utah
College of Veterinary Medicine USA LORE I. HAUG, DVM, MS
North Carolina State University Diplomate ACVB
Raleigh, North Carolina JENS HÄGGSTRÖM, DVM, PhD Texas Veterinary Behavior Services
USA Diplomate ECVIM-CA (Cardiology) Sugar Land, Texas
Professor USA
SOPHIE A. GRUNDY, BVSc (Hons), Department of Clinical Sciences
MANZCVS (Small Animal Internal Medicine) Faculty of Veterinary Medicine and ELEANOR C. HAWKINS, DVM
Diplomate ACVIM (Small Animal Internal Animal Science Diplomate ACVIM (Small Animal Internal
Medicine) Swedish University of Agricultural Medicine)
Internal Medicine Consultant Sciences Professor
IDEXX Laboratories, Inc. Uppsala Department of Clinical Sciences
Westbrook, Maine Sweden College of Veterinary Medicine
USA North Carolina State University
FRASER A. HALE, DVM, FAVD Raleigh, North Carolina
Diplomate AVC USA
REBEKAH G. GUNN-CHRISTIE, DVM
Hale Veterinary Clinic
Diplomate ACVP (Clinical Pathology)
Guelph, Ontario
Veterinary Clinical Pathologist CRISTINE L. HAYES, DVM
Canada
Antech Diagnostics Diplomate ABVT
Cary, North Carolina Diplomate ABT
USA Medical Director
ASPCA Animal Poison Control Center
Urbana, Illinois
USA
lxvi
IAN P. HERRING, DVM, MS MASON HOLLAND, VMD TYNE HOVDA, DVM
Diplomate ACVO (Ophthalmology) Diplomate ACVR Anesthesia Intern
Associate Professor Staff Radiologist College of Veterinary Medicine
VA-MD Regional College of Veterinary Port City Veterinary Referral Hospital North Carolina State University
Medicine Portsmouth, New Hampshire Raleigh, North Carolina
Virginia Tech USA USA
Blacksburg, Virginia
USA SUSAN HOLLAND, DVM JUNE C. HUANG, DVM, PhD
Associate Veterinarian, Clinical Toxicology Diplomate ACVP (Clinical Pathology)
MEGHAN E. HERRON, DVM Pet Poison Helpline Veterinary Clinical Pathologist
Diplomate ACVB Bloomington, Minnesota ANTECH Diagnostics
Senior Director Behavioral Medicine, USA Atlanta, Georgia
Education, and Outreach USA
Gigi’s (Shelter for Dogs) FIONA HOLLINSHEAD, BVSc (Hons), PhD,
Canal Winchester, Ohio MANZCVS WAYNE HUNTHAUSEN, DVM
USA Diplomate ACT (Theriogenology) Director
Registered Specialist in Small Animal Animal Behavior Consultations
MILAN HESS, DVM, MS Reproduction Westwood, Kansas
Diplomate ACT (Theriogenology) Glenbred, Matamata Veterinary Services USA
Colorado Veterinary Specialty Group Ltd
Littleton, Colorado Matamata CASSANDRA O. JANSON, DVM
USA New Zealand Diplomate ACVECC
Staff Criticalist
STEVE HILL, DVM, MS STEPHEN B. HOOSER, DVM, PhD Mount Laurel Animal Hospital
Diplomate ACVIM (Small Animal Internal Diplomate ABVT Mount Laurel, New Jersey
Medicine) Professor of Veterinary Toxicology & Head USA
Small Animal Internal Medicine Toxicology Section
Consultant Department of Comparative Pathobiology NICK D. JEFFERY, BVSc, PhD, MSc, FRCVS
Flagstaff Veterinary Internal Medicine & ADDL Diplomate ECVS
Consulting College of Veterinary Medicine Diplomate ECVN
Flagstaff, Arizona Purdue University Professor, Neurology & Neurosurgery
USA West Lafayette, Indiana Department of Small Animal Clinical
USA Sciences
TRACY HILL, DVM PhD
KATE HOPPER, BVSc, PhD Texas A&M University
Diplomate ACVECC College Station, Texas
Medicine)
Associated Professor, Small Animal USA
Assistant Professor
Emergency & Critical Care
Department of Veterinary Surgical & ALBERT E. JERGENS, DVM, PhD, AGAF
and Sur gery
Radiological Sciences Diplomate ACVIM (Small Animal Internal
School of Veterinary Medicine Medicine)
University of California, Davis Professor, Associate Chair for Research
Athens, Georgia
Davis, California and Graduate Studies and Donn E. and
USA
USA Beth M. Bacon Professor in Small Animal
Medicine and Surgery
LORA S. HITCHCOCK, DVM
DEBRA F. HORWITZ, DVM Department of Veterinary Clinical
Diplomate ACVB Sciences
Clinical Cardiologist
Veterinary Behavior Consultations College of Veterinary Medicine
Ohio Veterinary Cardiology, Ltd
St. Louis, Missouri Iowa State University
Metropolitan Veterinary Hospital
USA Ames, Iowa
Akron, Ohio
USA
USA
LYNN R. HOVDA, RPH, DVM, MS
Diplomate ACVIM (Large Animal Internal JEBA R.J. JESUDOSS CHELLADURAI,
KATE HOLAN, BS, DVM Medicine) BVSc, MS, PhD
Diplomate ACVIM (Small Animal Internal Director of Veterinary Medicine Diplomate ACVM (Parasitology)
Medicine) SafetyCall International & Pet Poison Postdoctoral Associate
Assistant Professor and Head Helpline Department of Veterinary Pathology
Small Animal Internal Medicine Bloomington, Minnesota; College of Veterinary Medicine
Department of Small Animal Clinical Assistant Adjunct Professor Iowa State University
Sciences Department of Veterinary and Biomedical Ames, Iowa
Michigan State University Sciences USA
East Lansing, Michigan College of Veterinary Medicine
USA University of Minnesota
St. Paul, Minnesota
USA
lxvii
AIME K. JOHNSON, DVM LISA S. KELLY, DVM, PhD AMIE KOENIG, DVM
Diplomate American College of Diplomate ACVP (Clinical Pathology) Diplomate ACVIM (Small Animal Internal
Theriogenology Veterinary Clinical Pathologist Medicine)
Associate Professor Antech Diagnostics Diplomate ACVECC
Department of Clinical Sciences Atlanta, Georgia Professor of Emergency and Critical Care
Auburn University College of Veterinary USA Department of Small Animal Medicine
Medicine and Surgery
Auburn, Alabama College of Veterinary Medicine
DANIEL E. KEYLER, BS, PharmD, FAACT
USA University of Georgia
Senior Clinical Toxicologist
Athens, Georgia
SafetyCall International
JESSICA JOHNSON, DVM USA
Bloomington, Minnesota;
Senior Dental & Oral Surgery Resident Adjunct Professor
Elevate Your Small Animal Dental Team, Experimental & Clinical Pharmacology CASEY J. KOHEN, DVM
LLC University of Minnesota Diplomate ACVECC
Main Street Veterinary Hospital & Dental Minneapolis, Minnesota Emergency and Critical Care Specialist
Clinic USA MarQueen Veterinary Emergency and
Dallas, Texas Specialty
USA Roseville, California
YUNJEONG KIM, DVM, PhD USA
Diplomate ACVM (Immunology)
LYNELLE R. JOHNSON, DVM, MS, PhD
Associate Professor
Diplomate ACVIM (Small Animal Internal BARBARA KOHN, Prof. Dr. med. vet
Department of Diagnostic Medicine and
Medicine) Diplomate ECVIM-CA
Pathobiology
Professor Clinic for Small Animals
Department of Medicine and Faculty of Veterinary Medicine
Kansas State University
Epidemiology Freie Universität Berlin
Manhattan, Kansas
University of California, Davis Germany
USA
Davis, California
USA MARC S. KRAUS, DVM
SHAWNA L. KLAHN, DVM Professor of Clinical Cardiology
SPENCER A. JOHNSTON, VMD Diplomate ACVIM (Oncology) Diplomate ACVIM (Cardiology, Internal
Diplomate ACVS Associate Professor Medicine)
James and Marjorie Waggoner Professor Department of Small Animal Clinical Diplomate ECVIM-CA (Cardiology)
Head Sciences University of Pennsylvania
Department of Small Animal Medicine Virginia-Maryland College of Veterinary Department of Clinical Sciences and
and Surgery Medicine Advanced Medicine
College of Veterinary Medicine Virginia Tech Philadelphia, Pennsylvania
University of Georgia Blacksburg, Virginia USA
Athens, Georgia USA
USA NATALI KREKELER, Dr. med. vet., PhD
MARY P. KLINCK, DVM, PhD Diplomate ACT
RICHARD J. JOSEPH, DVM Diplomate ACVB Senior Lecturer in Veterinary
Diplomate ACVIM (Neurology) Veterinary Behavioural Medicine Reproduction
Founder, CEO Consultant Melbourne Veterinary School
AnimalMR.com Sainte-Anne-de-Bellevue, Quebec The University of Melbourne
VetsOnCall.org Canada Werribee, Victoria
Katonah, New York Australia
USA
MARGUERITE F. KNIPE, DVM
ERIKA L. KRICK, VMD
RONNIE KAUFMANN, BSc, DVM Diplomate ACVIM (Oncology)
Health Sciences Associate Clinical
Diplomate ECVD (Dermatology) Medical Oncologist and Oncology
Professor, Neurology/Neurosurgery
Head of Dermatology Service Department Head
Department of Surgical and Radiological
The Veterinary Teaching Hospital Mount Laurel Animal Hospital
Sciences
Koret School of Veterinary Medicine Mount Laurel, New Jersey
UC Davis School of Veterinary Medicine
The Hebrew University of Jerusalem USA
Davis, California
Israel
USA
PAULA M. KRIMER, DVM, DVSc
BRUCE W. KEENE, DVM, MSc Diplomate ACVP (Clinical Pathology)
Diplomate ACVIM (Cardiology) JOYCE S. KNOLL, VMD, PhD Professor & Outreach Services Chief
Jane Lewis Seaks Distinguished Diplomate ACVP (Clinical Pathology) Athens Veterinary Diagnostic Laboratory
Professor of Companion Animal Medicine Associate Professor and Interim Chair and Department of Pathology
Department of Clinical Sciences Department of Biomedical Sciences College of Veterinary Medicine
College of Veterinary Medicine Cummings School of Veterinary Medicine University of Georgia
North Carolina State University Tufts University Athens, Georgia
Raleigh, North Carolina North Grafton, Massachusetts USA
USA USA
lxviii
ANNEMARIE T. KRISTENSEN, DVM, PhD CATHY E. LANGSTON, DVM MICHAEL S. LEIB, DVM, MS
Diplomate ACVIM (Small Animal) Diplomate ACVIM (Small Animal Internal Diplomate ACVIM (Small Animal Internal
Diplomate ECVIM-CA & Oncology Medicine) Medicine)
Professor, Companion Animal Clinical Professor - Clinical Emeritus Professor of Internal Medicine
Oncology Veterinary Medical Center Department of Small Animal Clinical
Department of Veterinary Clinical Sciences College of Veterinary Medicine Sciences
Faculty of Health and Medical Sciences The Ohio State University Virginia-Maryland College of Veterinary
University of Copenhagen Columbus, Ohio Medicine
Frederiksberg USA Virginia Tech
Denmark Blacksburg, Virginia
USA
PATTY A. LATHAN, VMD, MS
JOHN M. KRUGER, DVM, PhD Diplomate ACVIM (Small Animal Internal
Diplomate ACVIM- SAIM Medicine) MATTHEW S. LEMMONS, DVM
Professor and Carrigan Chair in Feline Associate Professor Diplomate AVDC
Health Department of Clinical Sciences Dentistry and Oral Surgery
Department of Small Animal Clinical Mississippi State University MedVet
Sciences Mississippi State, Mississippi Carmel, Indiana
College of Veterinary Medicine USA USA
Michigan State University
East Lansing, Michigan
KENNETH S. LATIMER, DVM, PhD JOSE A. LEN, DVM, MS, PhD
USA
Diplomate ACVP (Clinical Pathology) Diplomate ACT
Lanexa Veterinary & Consulting Services, Assistant Professor, Theriogenology
STEPHANIE KUBE, DVM, CCRT, CVPP LLC College of Veterinary Medicine
Diplomate ACVIM (Neurology) Toano, Virginia North Carolina State University
Veterinary Neurology and Pain USA Raleigh, North Carolina
Management Center of New England USA
Walpole, Massachusetts
ROBIN LAZARO, RVT, VTS(ECC)
USA
ICU Supervisor SOPHIE LE PODER, DVM, MS, PhD
North Carolina State Veterinary Hospital Professor in Virology
KAREN A. KUHL, DVM College of Veterinary Medicine Unity of Bacteriology, Immunology and
Diplomate ACVD Raleigh, North Carolina Virology
Midwest Veterinary Dermatology Center USA Ecole Nationale Vétérinaire d’Alfort
Veterinary Specialty Center Maisons-Alfort
Buffalo Grove, Illinois France
USA AMY LEARN, VMD
Resident in Clinical Behavior Medicine
Animal Behavior Wellness Center JOHN R. LEWIS, VMD, FAVD
LEIGH A. LAMONT, DVM, MS
Richmond, Virginia Diplomate AVDC
Diplomate ACVAA
USA Veterinary Dentistry Specialists
Associate Dean of Academic and Student
Silo Academy Education Center
Affairs
Chadds Ford, Pennsylvania
Atlantic Veterinary College MYLÈNE-KIM LECLERC, DMV
USA
University of Prince Edward Island Diplomate ACVIM (Neurology)
Charlottetown, Prince Edward Island Head of the Neurology Service
Canada Centre Veterinaire Rive Sud ELLEN M. LINDELL, VMD
Brossard, Quebec Diplomate ACVB
GARY M. LANDSBERG, BSc, DVM Canada Veterinary Behaviorist
Diplomate ACVB, ECAWBM Central Hospital for Veterinary Medicine
Veterinary Behaviorist North Haven, Connecticut
RICHARD A. LECOUTEUR, BVSc, PhD
Vice-President USA
CanCog Incorporated Diplomate ECVN
Fergus, Ontario; Professor Emeritus MERYL P. LITTMAN, VMD
Head Department of Surgical & Radiological Diplomate ACVIM (Small Animal Internal
Fear Free Research Sciences Medicine)
Canada School of Veterinary Medicine Professor Emerita of Medicine
University of California, Davis Department of Clinical Sciences &
SELENA LANE, DVM Davis, California Advanced Medicine
Diplomate ACVECC USA School of Veterinary Medicine
Clinical Assistant Professor of Small University of Pennsylvania
Animal Emergency and Critical Care Philadelphia, Pennsylvania
Small Animal Medicine and Surgery USA
University of Georgia College of
Veterinary Medicine
Athens, Georgia
USA
lxix
INGRID LJUNGVALL, DVM, PhD VIRGINIA LUIS FUENTES, MA, VetMB, PhD, ORLA MAHONY, MVB
Diplomate ECVIM-CA (Cardiology) CertVR, DVC, MRCVS Diplomate ACVIM (Internal Medicine)
Associate Professor Diplomate ACVIM (Cardiology) Diplomate ECVIM
Department of Clinical Sciences Diplomate ECVIM-CA (Cardiology) Clinical Assistant Professor
Faculty of Veterinary Medicine Professor Department of Clinical Sciences
Swedish University of Agricultural Department of Veterinary Clinical Science Cummings School of Veterinary Medicine
Sciences and Services at Tufts University
Uppsala Royal Veterinary College North Grafton, Massachusetts
Sweden North Mymms USA
United Kingdom
HEIDI B. LOBPRISE, DVM SEAN B. MAJOY, DVM, MS
Diplomate AVDC (Dentistry) JODY P. LULICH, DVM, PhD Diplomate ACVECC
Main Street Veterinary Dental Clinic Diplomate ACVIM (Internal Medicine) Clinical Assistant Professor
Flower Mound, Texas Professor Department of Clinical Sciences
USA Department of Veterinary Clinical Cummings School of Veterinary Medicine
Sciences at Tufts University
Director of the Minnesota Urolith Center North Grafton, Massachusetts
JOHN P. LOFTUS, PhD, DVM
College of Veterinary Medicine USA
Medicine)
St. Paul, Minnesota
Assistant Professor GUILLERMINA MANIGOT, DMV UBA
USA
Department of Clinical Sciences Diplomate CPMV (Dermatology)
College of Veterinary Medicine Dermlink Buenos Aires
Cornell University ALYCEN P. LUNDBERG, DVM Buenos Aires
Ithaca, New York Diplomate ACVIM (Oncology) Argentina
USA Assistant Professor
KATIA MARIONI-HENRY, DMV, PhD,
DAWN E. LOGAS, DVM MRCVS
University of Illinois at Urbana-
Diplomate ACVD Diplomate ACVIM (Neurology) and ECVN
Champaign
Owner/Staff Dermatologist EBVS® European Veterinary Specialist in
Urbana, Illinois
Veterinary Dermatology Center Small Animal Neurology
USA
Maitland, Florida RCVS Specialist in Veterinary Neurology;
USA Senior Lecturer
CANDACE C. LYMAN, DVM Neurology/Neurosurgery Service
Diplomate DACT (Theriogenology) Hospital for Small Animals
JAYME S. LOOPER, DVM
Associate Professor Royal (Dick) School of Veterinary Studies
Diplomate ACVR (Radiation Oncology)
Department of Clinical Sciences University of Edinburgh
Associate Professor
College of Veterinary Medicine Roslin, Midlothian
Auburn University United Kingdom
Sciences
Auburn, Alabama
USA
Louisiana State University STANLEY L. MARKS, BVSc, PhD
Baton Rouge, Louisiana Diplomate ACVIM (Internal Medicine,
USA KASEY E. MABRY, DVM Oncology)
Resident, Small Animal Internal Medicine Diplomate ACVN
Department of Small Animal Medicine Professor
CHERYL LOPATE, MS, DVM
and Surgery Department of Medicine & Epidemiology
Diplomate ACT
College of Veterinary Medicine University of California, Davis
Veterinarian and Owner
University of Georgia School of Veterinary Medicine
Reproductive Revolutions and Wilsonville
Athens, Georgia Davis, California
Veterinary Clinic
USA USA
Wilsonville, Oregon
USA
CATRIONA M. MACPHAIL, DVM, PhD STEVEN L. MARKS, BVSc, MS, MRCVS
Diplomate ACVS Diplomate ACVIM (Small Animal Internal
BIANCA N. LOURENÇO, DVM, MSc, PhD
ACVS Founding Fellow, Surgical Medicine)
Oncology Associate Dean, Director of Veterinary
Medicine)
Professor, Small Animal Surgery Medical Services
Assistant Professor
Department of Clinical Sciences College of Veterinary Medicine
Department of Small Animal and Surgery
Colorado State University NC State University
Fort Collins, Colorado Raleigh, North Carolina
USA USA
Athens, Georgia
USA
lxx
SINA MARSILIO, Dr.med.vet., PhD TERRI L. MCCALLA, DVM, MS KATHRYN M. MEURS, DVM, PhD
Diplomate ACVIM (Small Animal Internal Diplomate ACVO Diplomate ACVIM (Cardiology)
Medicine) Animal HealthQuest Solutions LLC Professor
Diplomate ECVIM-CA Bellingham, Washington Department of Clinical Sciences
Assistant Professor USA North Carolina State University College of
University of California, Davis School of Veterinary Medicine
Veterinary Medicine Raleigh, North Carolina
MEGAN MCCLOSKY, DVM
Department of Veterinary Medicine and USA
Clinical Assistant Professor
Epidemiology
Small Animal Internal Medicine
Davis, California LYNDA M.J. MILLER, DVM, PhD
USA Diplomate ACT
Advanced Medicine
Director of Large Animal Clinical Skills
University of Pennsylvania School of
Associate Professor of Theriogenology
DEBBIE MARTIN, LVT, VTS (Behavior) Veterinary Medicine
Lincoln Memorial University
Veterinary Technician Specialist Philadelphia, Pennsylvania
(Behavior) USA
Harrogate, Tennessee
TEAM Education in Animal Behavior, LLC
USA
Veterinary Behavior Consultations, LLC
PATRICK L. MCDONOUGH, MS, PhD
Spicewood, Texas
Atkinson Center for a Sustainable Future MATTHEW W. MILLER, DVM, MS
USA
Faculty Fellow Diplomate ACVIM (Cardiology)
Professor Emeritus of Veterinary Staff Cardiologist and Cardiology Section
KATY A. MARTIN, DVM, MPH Microbiology Head
USDA Resident in Veterinary Parasitology Animal Health Diagnostic Center VetMed Emergency and Specialty Care
Graduate Research Assistant Department of Population Medicine and Phoenix, Arizona
Department of Veterinary Pathology Diagnostic Sciences USA
Iowa State University Cornell University PAUL E. MILLER, DVM
Ames, Iowa Ithaca, New York Diplomate ACVO
USA USA Clinical Professor of Comparative
Ophthalmology
Department of Surgical Sciences
KENNETH M. MARTIN, DVM KATHRYN M. MCGONIGLE, MPH DVM
Diplomate ACVB (Veterinary Diplomate ACVIM (Internal Medicine)
University of Wisconsin-Madison
Behaviorists) Assistant Professor
Madison, Wisconsin
TEAM Education in Animal Behavior, LLC Clinical Small Animal Internal Medicine
USA
Veterinary Behavior Consultations, LLC Department of Clinical Sciences and
Spicewood, Texas Advanced Medicine
MELISSA L. MILLIGAN, VMD
USA University of Pennsylvania School of
Resident in Internal Medicine
Veterinary Medicine
The Animal Medical Center
PAULA MARTÍN VAQUERO, DVM, PhD New York, New York
USA
Diplomate ACVIM (Neurology) USA
FCB Health Europe
FCB Health Madrid ANNA K. MCMANAMEY, DVM KELLY MOFFAT, DVM
Madrid Cardiology Resident Diplomate ACVB (Behavior)
Spain North Carolina State University Medical Director
Veterinary Hospital VCA Mesa Animal Hospital
Raleigh, North Carolina Mesa, Arizona
KENNETH V. MASON, BSc, MVSc, FACVSc
USA USA
Veterinary Dermatologist
Managing Director
SARAH A. MOORE, DVM
Dermcare-Vet Pty Ltd STEPHEN MEHLER, DVM
Springwood, Queensland Diplomate ACVS
Professor
Australia Chief Medical Officer
Department of Veterinary Clinical Sciences
Veterinarian Recommended Solutions
Blue Bell, Pennsylvania
PHILIPP D. MAYHEW, BVM&S, MRCVS The Ohio State University
USA
Diplomate ACVS Columbus, Ohio
Professor, Small Animal Surgery USA
Department of Surgical and Radiological KRISTINA MEICHNER, DVM
Sciences Diplomate ECVIM-CA (Oncology) ANDREW R. MOORHEAD, DVM, MS, PhD
University of California, Davis Diplomate ACVP (Clinical Pathology) Diplomate ACVM (Parasitology)
Davis, California Assistant Professor Assistant Professor
USA Department of Pathology Department of Infectious Diseases
College of Veterinary Medicine University of Georgia
University of Georgia College of Veterinary Medicine
Athens, Georgia Athens, Georgia
USA USA
lxxi
DANIEL O. MORRIS, DVM, MPH ANTHONY J. MUTSAERS, DVM, PhD NATASHA J. OLBY, Vet MB, PhD, MRCVS
Diplomate ACVD Diplomate ACVIM (Oncology) Diplomate ACVIM (Neurology)
Professor of Dermatology & Allergy Associate Professor Professor of Neurology/Neurosurgery
Department of Clinical Studies Department of Clinical Studies Dr. Kady M. Gjessing and Rahna
School of Veterinary Medicine Department of Biomedical Sciences M. Davidson Distinguished Chair in
University of Pennsylvania Ontario Veterinary College Gerontology
Philadelphia, Pennsylvania University of Guelph Department of Clinical Sciences
USA Guelph, Ontario Member of the Comparative Medicine
Canada Institute
North Carolina State CVM
BRADLEY L. MOSES, DVM
Diplomate ACVIM (Cardiology) KATHERN E. MYRNA, DVM, MS
USA
Staff Clinician Diplomate ACVO
VCA Roberts Animal Hospital and Associate Professor of Ophthalmology
VCA South Shore Animal Hospital Department of Small Animal Medicine GAVIN L. OLSEN, DVM
South Weymouth, Massachusetts and Surgery Diplomate ACVIM (Small Animal Internal
USA College of Veterinary Medicine Medicine)
University of Georgia Staff Internist
Athens, Georgia Carolina Veterinary Specialists
JOCELYN MOTT, DVM
USA Greensboro, North Carolina
USA
Medicine)
VCA TLC Pasadena Veterinary Specialty GEORGINA M. NEWBOLD, DVM
and Emergency Diplomate ACVO JENNIFER L. OWEN, DVM, PhD
South Pasadena, California Assistant Professor- Ophthalmology Diplomate ACVP (Clinical Pathology)
USA Department of Veterinary Clinical Assistant Professor
Sciences Department of Physiological Sciences
CHRISTINE MULLIN, VMD
The Ohio State University University of Florida
Diplomate ACVIM (Oncology)
Columbus, Ohio Gainesville, Florida
Medical Oncologist
USA USA
Hope Veterinary Specialists
Malvern, Pennsylvania
USA REBECCA G. NEWMAN, DVM, MS JOANE M. PARENT, DVM, MVetSc
Diplomate ACVIM (Oncology) ACVIM Neurology
Medical Oncologist Professor
JENNIFER M. MULZ, DVM
Pittsburgh Veterinary Medical Specialist Centre Hospitalier Universitaire
and Emergency Center Vétérinaire
BluePearl Veterinary Partners
Pittsburgh, Pennsylvania Faculté de Médecine Vétérinaire
Sarasota, Florida
USA Université de Montréal
USA
Montréal
Canada
DENNIS P. O’BRIEN, DVM, PhD
KAREN R. MUÑANA, DVM, MS
Professor Emeritus VALERIE J. PARKER, DVM
Professor, Neurology
Department of Veterinary Medicine and Diplomate ACVIM
Surgery Diplomate ACVN
College of Veterinary Medicine Associate Professor, Clinical
University of Missouri Department of Veterinary Clinical
Columbia, Missouri Sciences
USA
USA College of Veterinary Medicine
LISA A. MURPHY, VMD Columbus, Ohio
LINDA K. OKONKOWSKI, DVM
Diplomate ABT USA
Internal Medicine Resident, ACVIM
Associate Professor of Toxicology
(Small Animal Internal Medicine)
Department of Pathobiology
Small Animal Clinical Sciences THOMAS PARMENTIER, DVM
Michigan State University Diplomate ACVIM (Neurology)
College of Veterinary Medicine PhD Candidate
PADLS New Bolton Center Toxicology
East Lansing, Michigan Department of Biomedical Sciences
Laboratory
USA Ontario Veterinary College
Kennett Square, Pennsylvania
University of Guelph
USA
Guelph, Ontario
Canada
lxxii
R. MICHAEL PEAK, DVM DAVID J. POLZIN, DVM, PhD BIRGIT PUSCHNER, DVM, PhD
Diplomate AVCD Diplomate ACVIM (Internal Medicine) Diplomate ABVT
The Pet Dentist at Tampa Bay Professor and Chief of Small Animal Dean and Professor
Largo, Florida Internal Medicine College of Veterinary Medicine
USA University of Minnesota Michigan State University
College of Veterinary Medicine East Lansing, Michigan
KATHERINE L. PETERSON, DVM Department of Veterinary Clinical USA
Diplomate ACVECC Sciences
Diplomate ABT St. Paul, Minnesota
ANDHIKA PUTRA, DVM, MS
Emergency and Critical Care Specialist USA
Dermatology Specialty Intern
Pet Poison Helpline & SafetyCall Department of Small Animal Medicine
International JILL S. POMRANTZ, DVM and Surgery
Bloomington, Minnesota Diplomate ACVIM (Small Animal Internal University of Georgia
USA Medicine) Athens, Georgia
Small Animal Internal Medicine USA
MICHAEL E. PETERSON, DVM, MS Consultant
Gem Veterinary Clinic IDEXX Laboratories, Inc.
Westbrook, Maine BARBARA QUROLLO, MS, DVM
Emmett, Idaho
USA Associate Research Professor
USA
Department of Clinical Sciences-CVM
JASON PIEPER, DVM, MS ERIC R. POPE, DVM, MS Raleigh, North Carolina
Diplomate ACVD Diplomate ACVS USA
Assistant Professor Professor of Surgery
Department of Veterinary Clinical Department of Clinical Sciences
Medicine Ross University School of Veterinary MARYANN G. RADLINSKY, DVM, MS
University of Illinois at Urbana- Medicine Diplomate ACVS
Champaign Basseterre Founding Fellow
Urbana, Illinois St Kitts Minimally Invasive Surgery, Small Animal
USA Soft Tissue Surgeon
Salt River Veterinary Specialists
ROBERT H. POPPENGA, DVM, PhD
SARAH B. PIERARD, BVSc, PgCertVS, MVS Scottsdale, Arizona
Diplomate ABVT
Animal Diabetes Australia USA
Head, Toxicology Section
Melbourne, Victoria California Animal Health and Food Safety
Australia Laboratory LISA RADOSTA, DVM
School of Veterinary Medicine Diplomate ACVB
AMY L. PIKE, DVM University of California Florida Veterinary Behavior Service
Diplomate ACVB Davis, California West Palm Beach, Florida
Owner, Animal Behavior Wellness Center USA USA
Fairfax, Virginia
USA SIMON A. POT, DVM ELEANOR RAFFAN, BVM&S, PhD,
Diplomate ACVO CertSAM, MRCVS
KATHRYN A. PITT, DVM, MS Diplomate ECVO Diplomate ECVIM-CA
Diplomate ACVS-SA Associate Professor of Ophthalmology University Lecturer in Systems Physiology
Assistant Professor of Small Animal Soft Equine Department Department of Physiology, Development
Tissue Surgery Vetsuisse Faculty and Neuroscience
Small Animal Clinical Sciences University of Zurich University of Cambridge
Michigan State University Zurich Cambridge
East Lansing, Michigan Switzerland United Kingdom
USA SILVIA G. PRYOR, DVM MERL F. RAISBECK, DVM, MS, PhD
Diplomate ACVO Diplomate ABVT
Ophthalmology Service Emeritus Professor
AMANDA L. POLDOSKI, DVM
BluePearl Emergency and Specialty Department Veterinary Sciences
Hospital-Irvine University of Wyoming
Toxicology
Irvine, California Laramie, Wyoming
Associate Manager of Veterinary &
USA USA
Regulatory Affairs
DAVID A. PUERTO, DVM LAURA RAYHEL, DVM
International
Diplomate ACVS Assistant Professor
Chief of Surgery Department of Medicine
USA
Center for Animal Referral and College of Veterinary Medicine
Emergency Services Midwestern University
Langhorne, Pennsylvania Glendale, Arizona
USA USA
lxxiii
JONJO REECE, DVM, ECFVG, BSc SHARON L. RIPPEL, DVM RENEE RUCINSKY, DVM
Small Animal Internal Medicine Resident Diplomate ABVT Diplomate ABVP (Feline Practice)
Department of Clinical Sciences Diplomate ABT Medical Director
Cummings School of Veterinary Medicine Clinical Toxicologist Mid Atlantic Cat Hospital
Tufts University Pet Poison Helpline Mid Atlantic Feline Thyroid Center
North Grafton, Massachusetts Bloomington, Minnesota Queenstown, Maryland
USA USA USA
TABATHA J. REGEHR, DVM WESLEY J. ROACH, DVM

Consulting Veterinarian, Clinical Toxicology Diplomate ACVS ELKE RUDLOFF, DVM, CVMA
SafetyCall International & Pet Poison Head of Surgery Department Diplomate ACVECC
Helpline Nashville Veterinary Specialists Clinical Specialist
Bloomington, Minnesota Nashville, Tennessee Emergency and Critical Care
USA USA Lakeshore Veterinary Specialists
Glendale, Wisconsin
MARSHA R. REICH, DVM USA
TRACIE D. ROMSLAND, DVM, MS
Diplomate ACVB Diplomate ACVP (Clinical Pathology)
Veterinary Behaviorist Staff Clinical Pathologist HÉLÈNE L.M. RUEL, DVM, DES, MSc
Maryland-Virginia Veterinary Behavioral Friendship Hospital for Animals Diplomate ACVIM (Neurology)
Consulting Washington, DC PhD Candidate
Silver Spring, Maryland USA Department of Clinical Sciences
USA
Faculty of Veterinary Medicine
KATHRYN A. ROOK, VMD Université de Montréal
JENNIFER M. REINHART, DVM, PhD Diplomate ACVD Saint-Hyacinthe, Québec
Diplomate ACVIM (Small Animal Internal Assistant Professor of Clinical Dermatology Canada
Medicine) Department of Clinical Sciences and
Diplomate ACVCP Advanced Medicine
Assistant Professor School of Veterinary Medicine WILSON K. RUMBEIHA, BVM, PhD, ATS
Department of Veterinary Clinical University of Pennsylvania Diplomate ABT
Medicine Philadelphia, Pennsylvania Diplomate ABVT
College of Veterinary Medicine USA Professor of One Environmental Health
University of Illinois Urbana-Champaign Toxicology
Urbana, Illinois SHERI ROSS, BSc, DVM, PhD Department of Molecular Biosciences
USA Diplomate ACVIM (Internal Medicine) School of Veterinary Medicine
Coordinator University of California, Davis
ILANA R. REISNER, DVM, PhD Advanced Urinary Disease and Davis, California
Diplomate ACVB (Behavior) Extracorporeal Therapies Service USA
Reisner Veterinary Behavior Services, University of California Veterinary Medical
LLC Center - San Diego
Wallingford, Pennsylvania San Diego, California ERIN E. RUNCAN, DVM
USA USA Diplomate ACT
Associate Professor, Clinical
JAMES K. ROUSH, DVM, MS Theriogenology and Reproductive
ALEXANDER M. REITER, Dipl.Tzt., Dr.med.vet Medicine
Diplomate ACVS
Diplomate AVDC, Diplomate EVDC Department of Veterinary Clinical
Doughman Chair Professor
Professor of Dentistry and Oral Surgery Sciences
Department of Clinical Sciences and The Ohio State University
Advanced Medicine College of Veterinary Medicine
School of Veterinary Medicine Columbus, Ohio
Manhattan, Kansas
University of Pennsylvania USA
USA
USA
ELIZABETH ROZANSKI, DVM
Diplomate ACVECC CLARE RUSBRIDGE, BVMS, PhD, FRCVS
LISA RESTINE, DVM Diplomate DACVIM (Small Animal Internal Diplomate ECVN
Associate Veterinarian Medicine) Professor in Veterinary Neurology
Alamo Feline Health Center Associate Professor University of Surrey
San Antonio, Texas Department of Clinical Science School of Veterinary Medicine
USA Cummings School of Veterinary Medicine Faculty of Health & Medical Sciences
Tufts University Guildford, Surrey
AUSTIN RICHMAN, DVM North Grafton, Massachusetts United Kingdom
Diplomate ACVD USA
Los Angeles, California
USA
lxxiv
JOHN E. RUSH, DVM, MS ASHLEY B. SAUNDERS, DVM KARSTEN E. SCHOBER, DVM, MS, PhD
Diplomate ACVIM (Cardiology) Diplomate ACVIM (Cardiology) Diplomate ECVIM-CA (Cardiology)
Diplomate ACVECC Professor of Cardiology Professor
Professor Department of Veterinary Small Animal Head, Cardiology and Interventional
Department of Clinical Sciences Clinical Sciences Medicine
Tufts University College of Veterinary Medicine & Department of Veterinary Clinical
Cummings School of Veterinary Medicine Biomedical Sciences Sciences
North Grafton, Massachusetts Texas A&M University College of Veterinary Medicine
USA College Station, Texas The Ohio State University
USA Columbus, Ohio
USA
KAREN E. RUSSELL, DVM, PhD
Diplomate ACVP (Clinical Pathology) BRIAN A. SCANSEN, DVM, MS
Professor and Associate Department Diplomate ACVIM (Cardiology) GRETCHEN L. SCHOEFFLER, DVM
Head for Clinical Services and Residency Associate Professor and Service Head, Diplomate ACVECC
Programs Cardiology & Cardiac Surgery Chief, Emergency and Critical Care
Department of Veterinary Pathobiology Department of Clinical Sciences Department of Clinical Sciences
College of Veterinary Medicine & Colorado State University College of Veterinary Medicine
Biomedical Sciences Fort Collins, Colorado Cornell University
Texas A&M University USA Ithaca, New York
College Station, Texas USA
USA
MICHAEL SCHAER, DVM
JOHAN P. SCHOEMAN, BVSc,
MMedVet(Med)(Pretoria), PhD(Cantab),
SHERISSE A. SAKALS, DVM Medicine)
DSAM(RCVS-UK)
Diplomate ACVS-SA Diplomate ACVECC
Diplomate ECVIM-CA
VCA Vancouver Animal Emergency & Emeritus Professor
EBVS® European Veterinary Specialist in
Referral Center Adjunct Professor, Emergency and
Internal Medicine
Vancouver, WA Critical Care Medicine
RCVS Recognized Specialist in Small
Canada University of Florida
Animal Medicine;
Professor
CARL D. SAMMARCO, BVSc MRCVS Department of Companion Animal
USA
Diplomate ACVIM (Cardiology) Clinical Studies
Head of Cardiology Chair, Pathobiology Research
Red Bank Veterinary Hospital THOMAS SCHERMERHORN, VMD Faculty of Veterinary Science
Tinton Falls, New Jersey Diplomate ACVIM (Small Animal Internal University of Pretoria
USA Medicine) Onderstepoort
Professor and Jarvis Chair South Africa
SHERRY LYNN SANDERSON, BS, DVM, PhD
Diplomate ACVIM (Small Animal Internal DONALD P. SCHROPE, DVM
Medicine) Diplomate ACVIM (Cardiology)
Manhattan, Kansas
Diplomate ACVN Department of Cardiology
USA
Associate Professor Oradell Animal Hospital
Department of Veterinary Biosciences Paramus, New Jersey
and Diagnostic Imaging PHILIP SCHISSLER, DVM USA
College of Veterinary Medicine Diplomate ACVIM (Neurology)
The University of Georgia Staff Neurologist/Neurosurgeon
Veterinary Neurology Center ERIN M. SCOTT, VMD
Athens, Georgia
Tustin, California Diplomate ACVO
USA
USA Department of Small Animal Clinical
Sciences
DOMENICO SANTORO, DVM, MS, DrSc, College of Veterinary Medicine
RENEE D. SCHMID, DVM
PhD Texas A&M University
Diplomate ABVT
Diplomate ACVD College Station, Texas
Diplomate ABT
Diplomate ECVD USA
Diplomate ACVM (Bacteriology/Mycology/
Toxicology
Immunology)
Pet Poison Helpline & SafetyCall CHRISTOPHER J. SCUDDER, BVSc,
Assistant Professor
International MVetMed, PhD, MRCVS
Bloomington, Minnesota Diplomate ACVIM-SAIM
Sciences
USA Diplomate ECVIM-CA
Head of Internal Medicine
Southfields Veterinary Specialists
Essex
USA
United Kingdom
lxxv
LYNNE M. SEIBERT, DVM, MS, PhD LESLIE SINN, DVM LAIA SOLANO-GALLEGO, DVM, PhD
Diplomate ACVB Diplomate ACVB Diplomate ECVCP
Veterinary Behavior Consultants LLC Specialist in Behavior Professora Agregada (Associate Professor)
Lawrenceville, Georgia Behavior Solutions Departament de Medicina i Cirurgia Animals
USA Hamilton, Virginia Facultat de Veterinària
USA Universitat Autònoma de Barcelona
Barcelona
ASHLEIGH SEIGNEUR, DVM, MVSc
KIM SLENSKY, DVM Spain
Diplomate ACVIM
Associate Veterinarian Diplomate ACVECC
Internal Medicine Department Assistant Professor of Clinical Emergency MITCHELL D. SONG, DVM
South Carolina Veterinary Specialists and and Critical Care Diplomate ACVD
Emergency Care Department of Clinical Sciences and Animal Dermatology, PC
Columbia, South Carolina Advanced Medicine Phoenix, Arizona;
USA School of Veterinary Medicine Adjunct Assistant Clinical Professor
University of Pennsylvania Midwestern University
Philadelphia, Pennsylvania College of Veterinary Medicine
KIM A. SELTING, DVM, MS USA Glendale, Arizona
Diplomate ACVIM (Oncology) USA
Diplomate ACVR (Radiation Oncology) FRANCIS W.K. SMITH, JR., DVM
Associate Professor Diplomate, ACVIM (Small Animal Internal
Department of Veterinary Clinical JASON W. SOUKUP, DVM
Medicine and Cardiology)
Medicine Diplomate AVDC
Vice-President
College of Veterinary Medicine Founding Fellow, AVDC Oral &
VetMed Consultants, Inc.
University of Illinois at Urbana-Champaign Maxillofacial Surgery
Lexington, Massachusetts
Urbana, Illinois Clinical Associate Professor
USA
USA Dentistry and Oromaxillofacial Surgery
Department of Surgical Sciences
MARK M. SMITH, VMD School of Veterinary Medicine
LINDA G. SHELL, DVM Diplomate ACVS University of Wisconsin-Madison
Diplomate ACVIM (Neurology) Diplomate AVDC Madison, Wisconsin
Veterinary Neurology Education and Founding Fellow, ACVS Oral & USA
Consulting Maxillofacial Surgery
Pilot, Virginia Founding Fellow, AVDC Oral &
USA SAMANTHA B. SOUTHER, DVM
Maxillofacial Surgery
Diplomate ACT
Center for Veterinary Dentistry and Oral
Associate Veterinarian, Theriogenology
Surgery
BARBARA L. SHERMAN, MS, PhD, DVM Mohnacky Animal Hospitals
Gaithersburg, Maryland
Diplomate ACVB (Behavior) & ACAW Carlsbad, California
USA
(Animal Welfare) USA
Clinical Professor Emerita
Department of Clinical Sciences PATRICIA J. SMITH, MS, DVM, PhD
CLARISSA P. SOUZA, DVM, MS, PhD
College of Veterinary Medicine Diplomate ACVO
Diplomate ACVD
North Carolina State University PJSmith Animal Eye Consulting
Assistant Professor of Dermatology and
Raleigh, North Carolina Adjunct Ophthalmologist Animal Eye Care
Otology
USA Milpitas, California
USA
Medicine
TRACI A. SHREYER, MA College of Veterinary Medicine
Applied Animal Behaviorist CHRISTOPHER J. SNYDER, DVM University of Illinois
Consultant Diplomate AVDC Urbana-Champaign, Illinois
Department of Comparative Pathobiology Clinical Associate Professor USA
Purdue University Dentistry and Oral Surgery, Department
West Lafayette, Indiana of Surgical Sciences
USA JÖRG M. STEINER, MedVet, DrVetMed,
University of Wisconsin-Madison PhD, AGAF
School of Veterinary Medicine Diplomate ACVIM
DEBORAH C. SILVERSTEIN, DVM Madison, Wisconsin Diplomate ECVIM-CA
Diplomate ACVECC USA University Distinguished Professor
Professor of Critical Care
Dr. Mark Morris Chair in Small Animal
PAUL W. SNYDER, DVM, PhD Gastroenterology and Nutrition
Advanced Medicine
Diplomate ACVP (Anatomical Pathology) Director, Gastrointestinal Laboratory
Fellow, International Academy Toxicologic Department of Small Animal Clinical
Pathologists Sciences
Senior Pathologist College of Veterinary Medicine and
USA
Experimental Pathology Laboratories, Inc. Biomedical Sciences
Bonita Springs, Florida Texas A&M University
USA College Station, Texas
USA
lxxvi
KEVIN S. STEPANIUK, DVM, FAVD WAILANI SUNG, MS, PhD, DVM JAIME L. TARIGO, DVM, PhD
Diplomate AVDC Diplomate ACVB Diplomate ACVP (Clinical Pathology)
Veterinary Dentistry Education and Veterinary Behaviorist Associate Professor
Consulting Services Behavior Service Department of Pathology
Ridgefield, Washington The San Francisco Society for the College of Veterinary Medicine
USA Prevention of Cruelty to Animals (SPCA) University of Georgia
San Francisco, California Athens, Georgia
USA USA
JOSHUA A. STERN, DVM, PhD
Associate Professor STEVEN E. SUTER, VMD, MS, PhD DOMINIC A. TAUER, DVM
Department of Medicine & Epidemiology Diplomate ACVIM (Oncology) Diplomate ABT
School of Veterinary Medicine Professor Consulting Veterinarian in Clinical
University of California, Davis Department of Clinical Sciences Toxicology
Davis, California North Carolina State University College of Pet Poison Helpline and
USA Veterinary Medicine SafetyCall International, PLLC
Raleigh, North Carolina Bloomington, Minnesota
USA USA
VICTOR J. STORA, DVM
Postdoctoral Fellow Transgenesis & Large SUSAN M. TAYLOR, DVM
Animal Model Creation JANE E. SYKES, BVSc(Hons), PhD Diplomate ACVIM
Vite Lab, Referral Center for Animal Diplomate ACVIM (Small Animal Internal Professor Emeritus
Models Medicine) Department of Small Animal Clinical
Department of Clinical Sciences and Professor of Small Animal Internal Sciences
Advanced Medicine Medicine Western College of Veterinary Medicine
School of Veterinary Medicine Department of Medicine & Epidemiology
University of Saskatchewan
University of Pennsylvania University of California, Davis Saskatoon, Saskatchewan
Philadelphia, Pennsylvania Davis, California Canada
USA USA
MICHELLE C. TENSLEY, DVM, MS

JAN S. SUCHODOLSKI, MedVet, DrVetMed, JOSEPH TABOADA, DVM Diplomate ACVIM (Neurology)
PhD, AGAF Diplomate ACVIM Associate Neurologist
Diplomate ACVM (Immunology) Professor and Associate Dean The Animal Neurology and Imaging Center
Associate Professor Department of Veterinary Clinical Algodones, New Mexico
Small Animal Medicine Sciences USA
Associate Director for Research School of Veterinary Medicine
Head of Microbiome Sciences Louisiana State University VINCENT J. THAWLEY, VMD
Gastrointestinal Laboratory Baton Rouge, Louisiana Diplomate ACVECC
Texas A&M University USA Clinical Assistant Professor
College of Veterinary Medicine Emergency and Critical Care Medicine
Department of Small Animal Clinical Department of Clinical Sciences and
LAUREN TALARICO, BS, DVM
Sciences Advanced Medicine
College Station, Texas School of Veterinary Medicine
Section Head Neurology/Neurosurgery
USA University of Pennsylvania
VCA Southpaws Veterinary Specialty &
Emergency Center Philadelphia, Pennsylvania
ALYSSA M. SULLIVANT, DVM, MS Fairfax, Virginia USA
Diplomate ACVIM (Small Animal Internal USA
Medicine) JUSTIN D. THOMASON, DVM
Assistant Professor Diplomate ACVIM (Cardiology; SAIM)
PATRICIA A. TALCOTT, MS, DVM, PhD
Department of Clinical Sciences Clinical Associate Professor
Diplomate ABVT
College of Veterinary Medicine Department of Clinical Sciences
Professor
Mississippi State University College of Veterinary Medicine
Department of Integrative Physiology and
Mississippi State, Mississipi Kansas State University
Neuroscience
USA Manhattan, Kansas
Washington State University USA
ANNIKA SUNDBY, DVM Pullman, Washington
Rotating Intern USA CRAIG A. THOMPSON, DVM
Nashville Veterinary Specialists Diplomate ACVP
Nashville, Tennessee KENDALL TANEY, DVM Clinical Associate Professor - Clinical
USA Diplomate AVDC Pathology
Center for Veterinary Dentistry and Oral Department of Comparative Pathobiology
Surgery Purdue University- College of Veterinary
Gaithersburg, Maryland Medicine
USA West Lafayette, Indiana
USA
lxxvii
JERRY A. THORNHILL, DVM VALARIE V. TYNES, DVM MARIA VIANNA, DVM
Diplomate ACVIM Diplomate ACVB (Veterinary Behavior) Diplomate DACVS
Director, Nephrology & Dialysis Diplomate ACAW (Animal Welfare) Veterinary Specialty Hospital of Palm
Division of Internal Medicine Veterinary Services Specialist Beach Gardens
Veterinary Specialty Center Ceva Animal Health Palm Beach Gardens, Florida
Buffalo Grove, Illinois Lenexa, Kansas USA
USA USA
ALYSHA VINCENT, DVM
MARY ANNA THRALL, BA, DVM, MS YU UEDA, DVM, PhD Internal Medicine Resident (Small Animal
Diplomate ACVP (Clinical Pathology) Clinical Assistant Professor Internal Medicine)
Professor Small Animal Emergency and Critical Care Department of Small Animal Clinical
Department of Biomedical Sciences Department of Clinical Sciences Sciences
Ross University School of Veterinary College of Veterinary Medicine College of Veterinary Medicine
Medicine North Carolina State University Michigan State University
Basseterre, St. Kitts Raleigh, North Carolina East Lansing, Michigan
West Indies USA USA
LARRY P. TILLEY, DVM STEFAN UNTERER, Dr.med.vet., Dr. habil. KAREN A. VON DOLLEN, DVM, MS
Diplomate ACVIM (Small Animal Internal Diplomate ECVIM Diplomate ACT
Medicine) Head of Gastroenterology Service Hagyard Equine Medical Institute
President Clinic of Small Animal Internal Medicine Lexington, Kentucky
VetMed Consultants, Inc. Ludwig-Maximilians-University USA
Santa Fe, New Mexico Munich
USA Germany
DIRSKO J.F. VON PFEIL, Dr.med.vet, DVM
Diplomate ACVS
ANDREA TIPOLD, DVM SHELLY VADEN, DVM, PhD Diplomate ECVS
Diplomate ECVN (Veterinary Neurology) Diplomate ACVIM (Internal Medicine) Diplomate ACVSMR
Department of Small Animal Medicine Professor, Small Animal Nephrology and Sirius Veterinary Orthopedic Center
and Surgery Urology Omaha, Nebraska;
University of Veterinary Medicine Department of Clinical Sciences Small Animal Surgery Locum, PLLC
Hannover College of Veterinary Medicine Dallas, Texas
Hannover North Carolina State University USA
Germany Raleigh, North Carolina
USA
LORI S. WADDELL, DVM
SHEILA M.F. TORRES, DVM, MS, PhD Diplomate ACVECC
Diplomate ACVD (Dermatology) SUZY Y.M. VALENTIN, DVM, MS Professor, Clinical Critical Care
Professor Diplomate ACVIM Department of Clinical Studies and
Department of Veterinary Clinical Diplomate ECVIM-CA (Internal Medicine) Advancement of Medicine
Sciences Internal Medicine Specialist School of Veterinary Medicine
College of Veterinary Medicine Internal Medicine Service University of Pennsylvania
University of Minnesota Centre Hospitalier Vétérinaire Pommery Philadelphia, Pennsylvania
St. Paul, Minnesota Reims USA
USA France
LIORA WALDMAN, BVM&S, MRCVS
SANDRA P. TOU, DVM MEGHAN VAUGHT, DVM CertSAD
Diplomate ACVIM (Cardiology and Diplomate ACVECC Dermatology and Allergy Clinic
Internal Medicine) Staff Criticalist; Haifa
Clinical Assistant Professor of Cardiology ECC Medical Director Israel
Department of Clinical Sciences Maine Veterinary Medicine Center
North Carolina State University Scarborough, Maine
JULIE M. WALKER, DVM
College of Veterinary Medicine USA
Diplomate ACVECC
Clinical Associate Professor
USA
GUILHERME G. VEROCAI, DVM, MSc, PhD Department of Medical Sciences
Diplomate ACVM (Parasitology) School of Veterinary Medicine
WILLIAM J. TRANQUILLI, Bs in Ed, Ms, Clinical Assistant Professor University of Wisconsin-Madison
DVM Director Parasitology Diagnostic Madison, Wisconsin
Diplomate ACVAA Laboratory USA
Professor Emeritus Department of Veterinary Pathobiology
Departments of Clinical Science, College of Veterinary Medicine and
Biological Sciences, and Pathobiology Biomedical Sciences
University of Illinois-Urbana Texas A&M University
Illinois College Station, Texas
USA USA
lxxviii
REBECCA A.L. WALTON, DVM SARA A. WENNOGLE, DVM, PhD R. DARREN WOOD, DVM, DVSc
Diplomate ACVECC Diplomate ACVIM-SAIM Diplomate ACVP (Clinical Pathology)
Clinical Assistant Professor Assistant Professor Associate Professor
Department of Veterinary Clinical Sciences Small Animal Clinical Sciences Department of Pathobiology
College of Veterinary Medicine Michigan State University Ontario Veterinary College
Iowa State University East Lansing, Michigan University of Guelph
Ames, Iowa USA Guelph, Ontario
USA Canada
MICHAEL D. WILLARD, DVM, MS
STUART A. WALTON, BVSc, BScAgr Diplomate ACVIM (Small Animal) J. PAUL WOODS, DVM, MS
MANZCVS (Small Animal Internal Medicine) Senior Professor Diplomate ACVIM (Internal Medicine,
Diplomate ACVIM (Small Animal Internal Department of Small Animal Clinical Oncology)
Medicine) Sciences Professor of Internal Medicine and
Clinical Assistant Professor College of Veterinary Medicine Oncology
Department of Small Animal Clinical Texas A&M University Department of Clinical Studies
Sciences College Station, Texas Ontario Veterinary College;
College of Veterinary Medicine USA Co-Director
University of Florida Institute for Comparative Cancer
Gainesville, Florida LAUREL E. WILLIAMS, DVM Investigation
USA Diplomate ACVIM (Oncology) University of Guelph
Adjunct Professor Guelph, Ontario
Department of Clinical Sciences Canada
ANDREA WANG MUNK, MA, DVM
Medicine) CORRY K. YEUROUKIS, DVM, MS
Raleigh, North Carolina;
Small Animal Internal Medicine Consultant Diplomate ACVP (Clinical)
Oncologist, Medical Director
IDEXX Laboratories, Inc. Clinical Pathologist
Veterinary Specialty Center of Seattle
Westbrook, Maine ANTECH Diagnostics
Lynwood, Washington
USA Annapolis, Maryland
USA USA
KIRSTEN E. WARATUKE, DVM HEATHER M. WILSON-ROBLES, DVM
Diplomate ABT HANY YOUSSEF, BVSc, MS, DVM
Diplomate ACVIM (Oncology)
Toxicologist Diplomate ABT
Professor
ASPCA Animal Poison Control Center Diplomate ABVT
Department of Veterinary Small
Urbana, Illinois Watseka Animal Hospital
Animal Clinical Sciences
USA Watseka, Illinois;
Iroquois County Animal Control Director
Texas A&M University
Watseka, Illinois
BRETT A. WASIK, DVM College Station, Texas
USA
Diplomate ACVIM (Small Animal Internal USA
Medicine)
Antech Diagnostics - Internal Medicine/ TINA WISMER, DVM, MS DANIELLE ZWUESTE, DVM
Endocrinology Consultant Diplomate ABVT Diplomate ACVIM (Neurology)
Veterinary Information Network - Internal Diplomate ABT Vancouver Animal Emergency and
Medicine/Endocrinology Consultant Medical Director Referral Centre
UC Davis Endocrinology Post-doctorate ASPCA Animal Poison Control Center Vancouver
Allen, Texas Urbana, Illinois British Columbia
USA USA Canada
NICOLE M. WEINSTEIN, DVM EWAN D.S. WOLFF, PhD, DVM

Diplomate ACVP (Clinical Pathology) Diplomate ACVIM
Associate Professor Small Animal Internist
Department of Pathobiology BluePearl - Affiliated Veterinary
School of Veterinary Medicine Specialists
University of Pennsylvania USA
USA MICHAEL W. WOOD, DVM, PhD
GLADE WEISER, DVM Medicine)
Diplomate ACVP Emeritus Assistant Professor
Clinical Pathologist Department of Medical Sciences
Loveland, Colorado School of Veterinary Medicine
USA University of Wisconsin-Madison
Madison, Wisconsin
USA
lxxix
About the Companion Website
This book is accompanied by a companion website:
www.fiveminutevet.com/canineandfeline7th
The website includes:
• Videos
• Images
• Client Education Handouts
• Additional references and internet resources
The password for the companion website: pl58ez690xle
lxxx
Canine and Feline, Seventh Edition 1
5-Fluorouracil (5-FU) Toxicosis A
iron, metaldehyde, mushrooms (Amanita, • Antiemetic—maropitant 1 mg/kg IV, SC

Galerina, and Lepiota spp.), sodium fluoroac- q24h; ondansetron 0.1–0.2 mg/kg IV
etate (Compound 1080), strychnine. q6–12h; metoclopramide 0.1–0.5 mg/kg IV,
BASICS • Metabolic—hepatic failure, hepatic SC q6–8h.
OVERVIEW encephalopathy. • GI protection—proton pump inhibitors,
• Antimetabolite, antineoplastic agent; it is • Nervous—idiopathic epilepsy, meningitis, H2 blockers, sucralfate.
metabolized to thymidine, which blocks the neoplasia. • Analgesia—buprenorphine 0.005–0.03 mg/kg
methylation reaction of deoxyuridylic and CBC/BIOCHEMISTRY/URINALYSIS IM or IV q6–12h, butorphanol 0.1–0.5 mg/kg
thymidylic acids, resulting in thymine • CBC—baseline, then continue to monitor
SC, IV, or IM.
deficiency; thymine is critical for DNA and q3–4 days post exposure for 21 days; monitor • Antibiotic—broad-spectrum antibiotic
to a lesser extent RNA replication; the result for echinocytes; leukopenia develops by day 7 therapy if total white blood cell count is
is cell death due to interruption of normal and continues to day 13; thrombocytopenia below 2000.
DNA and RNA synthesis; this mechanism develops by day 7 and can continue for 21 • Bone marrow stimulation—filgrastim
targets rapidly growing cells like bone marrow days; acute anemia due to blood loss can be (Neupogen®) 4–6 μg/kg SQ q24h.
and intestinal crypts; 5-FU has various active secondary to bone marrow suppression by • Transfusion therapy may be indicated if
metabolites resulting in delayed clearance day 9, persisting until day 21. PCV <20%.
from bone marrow and γ-aminobutyric acid • 20% intravenous fat emulsion (IFE)
• Chemistry—baseline; hepatic values may
(GABA) depletion in the brain. increase. unlikely to be effective.
• Labeled for human use only. • Antidote—uridine triacetate has not been
• Electrolytes—baseline; recheck PRN based
• Topical preparation for actinic and solar on GI losses. used in veterinary medicine; must be
keratoses: Efudex® (5% cream, 2% and 5% instituted prior to development of CNS signs;
solution), Carac® (0.5% cream), Fluoroplex® OTHER LABORATORY TESTS cost prohibitive.
(1% cream), Tolak® (4% cream). • Blood gases—metabolic acidosis can occur;
monitor PRN. CONTRAINDICATIONS/POSSIBLE
• IV preparation used for a variety of neoplastic
• Packed cell volume (PCV)/total protein INTERACTIONS
conditions: Adrucil® (50 mg/m: IV solution).
(TP) q6–24h. • Avoid nonsteroidal anti-inflammatory
• Causes acute and severe gastroenteritis and
• Blood glucose q2–4h. drugs (NSAIDs) and CNS depressants.
seizures; seizures can develop within 30 minutes to
6 hours post exposure; bone marrow suppression IMAGING
occurs 7–21 days after acute presentation. N/A
• Patients may survive acute toxicity to
DIAGNOSTIC PROCEDURES
succumb to bone marrow suppression later.
N/A FOLLOW-UP
• Any suspected exposure in animals warrants • CBC q3–4 days for 21 days or more.
immediate veterinary evaluation.
SIGNALMENT
• No species or breed predilection.
TREATMENT
SIGNS • Emesis—not typically indicated due to MISCELLANEOUS
• Cardiovascular—hypotension, myocardial rapid onset of seizures. ABBREVIATIONS
ischemia, arrhythmias. • Single dose activated charcoal with sorbitol • 5-FU = 5-fluorouracil.
• Immune—bone marrow suppression of all in asymptomatic patients; seizures may develop • AC/C = activated charcoal with a cathartic.
cell lines. before opportunity to administer charcoal. • GABA = γ-aminobutyric acid.
• Gastrointestinal (GI)—nausea, salivation, • Gastric lavage can be performed in patients • GI = gastrointestinal.
profuse vomiting, hematemesis, diarrhea, with recent exposure; a single dose of • IFE = intravenous fat emulsion.
hematochezia, abdominal pain, stomatitis. activated charcoal with a cathartic (AC/C) • NSAID = nonsteroidal anti-inflammatory
• Nervous—lethargy, ataxia, depression, can be administered, recovering patient with drug.
disorientation, tremors, seizures (often endotracheal tube in place. • PCV = packed cell volume.
refractory to treatment), death. • Balanced crystalloid IVF to maintain • TP = total protein.
• Ophthalmic—blindness (cats). hydration, aid in elimination, and maintain
• Reproductive—teratogenic, embryotoxic. Suggested Reading
perfusion. Sayre RS, Barr JW, Bailey EM. Accidental
• Respiratory—noncardiogenic pulmonary • Monitor blood pressure q4–6h.
edema, dyspnea, cyanosis, tachypnea. and experimentally induced 5-fluorouracil
toxicity in dogs. J Vet Emerg Crit Care
CAUSES & RISK FACTORS 2012; 22(3):545–549.
• Access to topical preparations in the home. Author Tabatha J. Regehr
• Cats and small dogs may be exposed by
licking pet owner.
MEDICATIONS Consulting Editor Lynn R. Hovda
• Pets in geographic locations of high human DRUG(S) OF CHOICE
UV exposure due to increased human use. • Anticonvulsant—levetiracetam 60 mg/kg
IV loading dose, 20 mg/kg IV q8h; propofol
4–6 mg/kg IV bolus followed by 0.6 mg/kg/
minute CRI; inhalant anesthesia; valium is
typically ineffective; phenobarbital and
DIAGNOSIS pentobarbital have unpredictable efficacy, but
DIFFERENTIAL DIAGNOSIS can be attempted, phenobarbital 5–8 mg/kg
• Other toxins—bromethalin, castor bean, IV slowly to effect.
cycad palms (Cycas and Zamia spp.), disulfoton,
2 Blackwell’s Five-Minute Veterinary Consult
A Abortion, Spontaneous (Early Pregnancy Loss)—Cats
virus (FeLV), feline herpesvirus 1 (FHV-1), • FIP—submit fetal tissue for histopathology
FIP, feline immunodeficiency virus (FIV), and immunohistochemistry. • FIV—ELISA:
feline panleukopenia virus (FPLV). confirm positive results with Western blot.
BASICS • FPLV—viral isolation from fetuses
Noninfectious
DEFINITION • Uterine—cystic endometrial hyperplasia,
submitted for necropsy; document serocon
• Abortion: loss of a pregnancy at any time endometritis, pyometra, anatomic version in queen.
prior to the fetus’s ability to survive outside abnormalities of uterus (e.g., adhesions or Noninfectious Causes
the uterus. • Early pregnancy loss: loss of a strictures), uterine trauma. • Ovarian— • To rule out anovulatory cycle, confirm
pregnancy and death of conceptus within the primary hypoluteoidism is rare in cats, but progesterone >2 ng/mL one week following
first half of gestation secondary hypoluteoidism may result from mating. • Hypoluteoidism—serum
PATHOPHYSIOLOGY prostaglandin exposure, prolonged stress, and progesterone level <1.0 ng/mL prior to
• Noninfectious causes—more common. uterine inflammation. • Fetal—chromosomal abortion indicates luteal failure. • Disorder of
• Infectious causes—direct infection of abnormalities resulting in abnormal or sexual development—evaluate external
embryo, uterus, placenta, or fetuses, or arrested development and embryonic or fetal genitalia, karyotype, and histopathology of
indirectly by systemic infection. death. • Systemic—malnutrition or nutrit- reproductive tract and gonads.
ional disorders (e.g., taurine deficiency, IMAGING
SYSTEMS AFFECTED
vitamin A deficiency or toxicity), severe • Abdominal ultrasound—most specific;
• Reproductive. • Endocrine. • Other
nonreproductive illness, exposure to pregnancy confirmed after 25 days.
systems resulting in debilitating illness.
exogenous estrogens, glucocorticoids, Re-ultrasound every 1–2 weeks for high-risk
GENETICS chemotherapeutic agents, antifungal agents, queens. Confirm fetal heart rates and assess
Higher incidence in purebred or closed some antibiotics (trimethoprim–sulfonamides, fetal fluids and placenta in late gestation
research catteries with closely related tetracyclines, gentamicin), modified live (normal fetal heart rates >200 bpm).
individuals; heritability of susceptibility to vaccines. Visualization of fetal kidney and intestinal
feline infectious peritonitis virus (FIPV)
RISK FACTORS peristalsis indicates fetal maturity.
suspected to be high.
• Cats with high coefficient of inbreeding • Abdominal radiographs—after 45 days, can
INCIDENCE/PREVALENCE (COI). • Previous pregnancy loss. • Previous evaluate fetal number, relative size, and
Difficult to determine, as pregnancy may not history of reduced litter size. • Evidence of position; also assess fetal death (gas pockets)
be diagnosed early. Loss or resorption of one cystic endometrial hyperplasia (CEH) on or fetal malformation.
or two conceptus within a litter is not ultrasound. • Concurrent systemic disease or DIAGNOSTIC PROCEDURES
uncommon. recent trauma. • Older queens (over 6 years). • Submit aborted, stillborn, mummified
GEOGRAPHIC DISTRIBUTION • Malnourishment. • Unsanitary housing fetuses and fetal membranes (fresh or
N/A conditions. • Raw diets. refrigerated on ice) for gross necropsy,
SIGNALMENT histopathology, cultures, and viral isolation.
Increased incidence in queens >5 years old; Submit culture of reproductive tract or entire
increased risk in purebred cats with high tract if removed (uterus, ovaries, oviducts).
inbreeding. DIAGNOSIS Submit samples from aborted and stillborn
fetus for karyotyping. • Pedigree analysis—
SIGNS DIFFERENTIAL DIAGNOSIS
evaluate COI. • Evaluate cattery management
• Early pregnancy loss—failure to ovulate,
General Comments for vaccination protocols, feeding regime,
failure to conceive, chromosomal disorder, or
Frequently no clinical symptoms other than sanitation procedures, and quarantine
disorder of sexual development. • Vaginal
lack of pregnancy or reduced litter size. procedures. • Nutrition—nutritional analysis
discharge—pyometra, uterine stump
of diet: of particular importance when queen
Historical Findings pyometra, mucometra, vaginitis, neoplasia,
is fed homemade and/or raw diet.
Failure to deliver kittens at expected due date, cystitis, active labor or impending abortion,
return to estrus sooner than expected trauma to urogenital tract. • Mass or tissue PATHOLOGIC FINDINGS
(approximately 45 days), discovery of fetal from vaginal vault—dystocia, neoplasia, Variable with etiology.
tissues or placenta, behavior change, systemic hemorrhage/blood clot, uterine prolapse.
illness. CBC/BIOCHEMISTRY/URINALYSIS
Physical Examination Findings • Generally normal. • Inflammatory leuko-
Signs range from normal to dehydration, gram with infection or systemic disease. TREATMENT
fever, abdominal straining, and discomfort to • Anemia of pregnancy; hemoconcentration APPROPRIATE HEALTH CARE
presence of purulent, mucoid, watery, or and azotemia may be seen with dehydration None, for noninfectious, stable queens;
sanguineous vaginal discharge. or hypovolemia. primary hypoluteoidism—managed on
CAUSES OTHER LABORATORY TESTS outpatient basis.
Infectious Infectious Causes NURSING CARE
• Bacterial—organisms implicated in causing • Cytology and bacterial culture of vaginal Inpatient management if systemically ill,
abortion via ascending infection through the discharge, fetus, fetal membranes, or uterine debilitated, severely dehydrated, or for
vaginal vault and cervix include E. coli, contents (aerobic and mycoplasma). medical management of ongoing fetal loss or
Staphylococcus spp., Streptococcus spp., • FeLV—test for antigens in queens using pyometra.
Chlamydia spp., Pasteurella spp., Klebsiella spp., ELISA or indirect fluorescent antibody (IFA). ACTIVITY
Pseudomonas spp., Salmonella spp., Mycoplasma • FHV-1—IFA or PCR from corneal or • Isolation for queens with infectious disease.
spp., and Ureaplasma spp. • Protozoal— conjunctival swabs, viral isolation from • No activity restrictions for most; restrict
Toxoplasma gondii. • Viral— feline leukemia conjunctival, nasal, or pharyngeal swabs. activity as indicated if due to trauma.
(continued) Abortion, Spontaneous (Early Pregnancy Loss)—Cats A
DIET hypertension leading to hemorrhage from CEH. • Fair prognosis for successful
• Feed commercially available diet labeled for placental sites during parturition or at time of pregnancy with treatment for primary
use in pregnancy. • Correct diets with Cesarean section. • Altrenogest can cause hypoluteoidism; significant monitoring
inappropriate taurine or vitamin A concen agalactia and failure of parturition, leading to required for good outcome. • Pregnancy loss
trations. • Avoid feeding raw meats or death of litter; discontinue use 2 days before due to genetic abnormalities likely to recur if
allowing queens to hunt during pregnancy to due date. • Caution with use of altrenogest queen is bred to tom with similar pedigree.
reduce risk for ingestion of pathogenic with infectious processes or necrotic fetuses in
bacteria and T. gondii. uterus; may keep infection within uterus,
CLIENT EDUCATION causing metritis and systemic illness; monitor
pregnancy often with ultrasound. • PGF2α—
• Infectious diseases—verify vaccination
side effects vomiting, hypersalivation,
MISCELLANEOUS
status (vaccinate prior to pregnancy) and
defecation, urination, and tachypnea; dose ASSOCIATED CONDITIONS
disease surveillance measures; ensure use of
dependent and self-limiting. Severe systemic disease otf any kind,
quarantine facilities for pregnant queens and
malnutrition.
new arrivals. • Breeding management—keep POSSIBLE INTERACTIONS
detailed records of reproductive performance, • Progesterone administration during AGE-RELATED FACTORS
pedigree analysis, and social behavior of pregnancy associated with masculinization of Queens >6 years old—higher incidence of
queens (including when not receptive to male). female fetuses; do not administer in first half lower litter size and infertility.
• Nutrition—advise feeding commercial cat of pregnancy and use with informed consent ZOONOTIC POTENTIAL
food during pregnancy. • Genetic disease— thereafter. • Tocolytics associated with T. gondii.
discuss COI and value of introducing new increased risk of dystocia, failure of placental
genetics. • Discuss risk of zoonotic disease separation, lack of milk production, and poor PREGNANCY/FERTILITY/BREEDING
from T. gondii. maternal behavior for first days postpartum. Queens with previous pregnancy loss are at
higher risk of subsequent pregnancy loss or
SURGICAL CONSIDERATIONS ALTERNATIVE DRUG(S) infertility and should be monitored inten-
Ovariohysterectomy (OHE) may be Dopamine agonists (e.g., cabergoline 5 μg/kg sively.
considered if queen is systemically ill from PO q24h) can be used to lower progesterone
uterine infection or deceased fetuses. If and facilitate uterine emptying. Use in SYNONYMS
valuable breeding animal, Cesarean section conjunction with low dose of PGF2α. • Pregnancy loss. • Abortion. • Fetal
can be performed to remove deceased fetuses. mummification. • Early embryonic loss.
SEE ALSO
• Breeding, Timing.
• Sexual Development Disorders.
FOLLOW-UP
MEDICATIONS PATIENT MONITORING ABBREVIATIONS
• CEH = cystic endometrial hyperplasia.
DRUG(S) OF CHOICE • Serial ultrasound—follow pregnancy loss,
uterine emptying, or viability of remaining • COI = coefficient of inbreeding.
• Depends on etiology. • Amoxicillin–
fetuses; initially daily; decrease frequency • FeLV = feline leukemia virus.
clavulanic acid 13.75 mg/kg PO q12h—safe for
when stable, continue until birth (with partial • FHV-1 = feline herpesvirus 1.
pregnancy. • Enrofloxacin 5 mg/kg/day PO—
loss) or uterus is free of fluid (complete • FIPV = feline infectious peritonitis virus.
excellent penetration to uterus; contraindicated
abortion). • Monitor health and attitude of • FIV = feline immunodeficiency virus.
if live fetuses present. • Prostaglandin F2α
queen. • If live fetuses are present—delayed • FPLV = feline panleukopenia virus.
(PGF2α; dinoprost/Lutalyse®) 80–100 μg/kg
parturition my occur with progesterone or • IFA = indirect fluorescent antibody.
IM q8–12h—promotes uterine contractions,
terbutaline treatment; Cesarean section may • OHE = ovariohysterectomy.
loss of corpus luteum, and cervical opening to
be necessary. • PGF2α = prostaglandin F2α.
expulse aborted materials. • Tocolytics—
prevent uterine contractions: terbutaline PREVENTION/AVOIDANCE Suggested Reading
0.03–1.0 mg PO as needed based on tocodyna • Institute infectious disease prevention, Lamm CG. Clinical approach to abortion,
mometry (www.whelpwise.com); 0.03 mg/kg control, and surveillance. • Replace subfertile stillbirth, and neonatal death in dogs and
PO q8h if tocodynamometry not available. queens with more reproductively fit individ cats. Vet Clin North Am Small Anim Pract
• Hypoluteoidism—oral progestogene uals. • Avoid exposure to abortifacient, 2012, (42)3:501–513.
(altrenogest) 0.088 mg/kg PO q24h to teratogenic, or fetotoxic drugs. • Serial Verstegen J, Dhaliwal G, Verstegen-Onclin K.
maintain pregnancy; can monitor queen’s progesterone assays and fetal ultrasound Canine and feline pregnancy loss due to
progesterone, as altrenogest will not interfere during next pregnancy. viral and non-infectious causes: a review.
with progesterone assay. Theriogenology 2008, 70(3):304–319.
POSSIBLE COMPLICATIONS Author Aime K. Johnson
CONTRAINDICATIONS • Loss of entire litter. • Metritis, chronic
• Terbutaline—cardiac disease, pyometra,
Consulting Editor Erin E. Runcan
endometritis, uterine rupture, sepsis, shock. Acknowledgment The author and editors
infectious disease, hypertension. • Uterine pathology. • Masculinization of
• Altrenogest—contaminated uterus with
acknowledge the prior contribution of Milan
female fetuses with progesterone therapy. Hess.
systemically ill queen. • Prostaglandin-cats
with previously diagnosed respiratory disease. EXPECTED COURSE AND PROGNOSIS
• Poor prognosis for live kittens for current
PRECAUTIONS litter, even with aggressive monitoring and Client Education Handout
• Use of tocolytics requires accurate breeding treatment. • May recur in future pregnancies available online
dates to know when to stop treatment; most depending on cause and treatment. • Poor
successful in combination with tocodyna prognosis for normal pregnancy with severe
mometry. • Terbutaline can cause
A Abortion, Spontaneous (Early Pregnancy Loss)—Dogs
CAUSES • Necropsy of aborted fetus, stillborn puppies,
Infectious and placenta(s)—enhance chances of
• Brucella canis.
definitive diagnosis.
BASICS • Systemic or endocrine disease—problems
• Canine herpesvirus.
DEFINITION • Toxoplasma gondii, Neospora caninum.
with maternal environment.
Loss of a fetus because of resorption in early • Mycoplasma and Ureaplasma. CBC/BIOCHEMISTRY/URINALYSIS
stages or expulsion in later stages of pregnancy. • Bacteria—Escherichia coli, Streptococcus, • Usually normal.
PATHOPHYSIOLOGY Campylobacter, Salmonella. • Systemic disease, uterine infection, viral
• Direct—congenital abnormality, infectious • Viruses—distemper, parvovirus, adenovirus. infection, or endocrine abnormalities—may
disease, trauma. Uterine produce changes in CBC, biochemistries, or
• Indirect—infectious placentitis, abnormal • Cystic endometrial hyperplasia and pyometra.
urinalysis.
ovarian function, abnormal uterine environ- • Trauma—acute and chronic. OTHER LABORATORY TESTS
ment. • Neoplasia. • Serologic testing—B. canis, canine
SYSTEMS AFFECTED Ovarian herpesvirus, Toxoplasma, Neospora; collect
• Reproductive. • Hypoluteoidism—abnormal luteal function
serum as soon as possible after abortion;
• Any major body system dysfunction can in absence of fetal, uterine, or placental repeat testing for paired titers for canine
adversely affect pregnancy. disease: progesterone concentrations <1–2 ng/ herpesvirus, Toxoplasma, Neospora.
• B. canis—
GENETICS mL, most commonly 40–45 days’ gestation.
◦ Slide test (D-Tec CB®, Zoetis) very
• No genetic basis for most causes. Exogenous Administration sensitive; negative results reliable;
• Lymphocytic hypothyroidism—single-gene • Embryotoxic drugs. prevalence of false positives as high as 60%.
recessive trait in Borzois. • Chemotherapeutic agents. ◦ PCR best to use on abortive discharge
INCIDENCE/PREVALENCE • Estrogens. (Kansas State Veterinary Diagnostic
• True incidence unknown. • Glucocorticoids. Laboratory).
• Resorption estimated between 11% and • Prostaglandins—lysis of corpora lutea. ◦ Definitive diagnosis made via culture of
13%, up to 30% (at least one resorption). • Dopamine agonists—lysis of corpora lutea abortive discharge or dam serum.
• Incidence of stillbirth 2.2–4.4%; with via suppression of prolactin; bromocriptine, ◦ Tube agglutination—titers >1 : 200
dystocia up to 22.3%. cabergoline. considered positive; titers 1 : 50–1 : 200
SIGNALMENT Hormonal Dysfunction suspicious.
• Hypothyroidism (less common). ◦ Agar gel immunodiffusion—differen
Species tiates between false positives and true
• Hyperadrenocorticism.
Dog positives in agglutination tests; detects
• Endocrine-disrupting contaminants
Breed Predilections documented in human and wildlife fetal loss. cytoplasmic and cell surface antigens.
• Familial lymphocytic hypothyroidism • Baseline T4 serum concentration—
Fetal Defects hypothyroidism possible cause for fetal
(Borzoi)—prolonged interestrus interval,
• Lethal chromosomal abnormality or organ wastage; role in pregnancy loss unclear.
poor conception rate, mid-gestation abortion,
defects. • Serum progesterone concentration
stillbirths.
• Many breeds at risk for hypothyroidism, RISK FACTORS (hypoluteoidism; if no infectious cause); dogs
although evidence of role in abortion unclear. • Exposure of brood bitch to carrier animals. depend on ovarian progesterone production
• Old age. throughout gestation (minimum of 2 ng/mL
Mean Age and Range
• Hereditary factors. required to maintain pregnancy); determine
• Infectious causes, pharmacologic agents
as soon as possible after abortion; in
causing abortion, fetal defects—all ages.
subsequent pregnancies, start weekly
• Cystic endometrial hyperplasia—usually >6
monitoring at week 3 (may be before
years old.
pregnancy documented with ultrasound);
Predominant Sex DIAGNOSIS start biweekly sampling around gestational
Intact bitches. DIFFERENTIAL DIAGNOSIS age of prior loss. Pregnancy loss typically
• Differentiate infectious from noninfectious occurs during seventh week of gestation (see
SIGNS
causes—B. canis immediate and zoonotic Premature Labor).
Historical Findings concern. • Vaginal culture—B. canis with positive
• Failure to whelp on time. • Differentiate resorption from infertility— serologic test; Mycoplasma, Ureaplasma, other
• Expulsion of recognizable fetuses or helped by early diagnosis of pregnancy. bacterial agents; all except B. canis can be
placental tissues. • History of drug use during pregnancy— normal flora, so diagnosis difficult from
• Decrease in abdominal size; weight loss. particularly during first trimester, or use of vaginal culture alone; limited benefit unless
• Anorexia, vomiting, diarrhea. drugs (e.g., dexamethasone, prostaglandins, heavy growth of single organism; Salmonella
• Behavioral changes. ketoconazole, griseofulvin, doxycycline, associated with systemic illness.
Physical Examination Findings tetracycline, dantrolene) known to cause fetal
IMAGING
• Sanguineous or purulent vulvar discharge. death.
• Radiography—identifies fetal structures
• Disappearance of previously documented • Vulvar discharge during diestrus—may
after 45 days of gestation; earlier determines
vesicles or fetuses. mimic abortion; evaluate discharge and origin
uterine enlargement but not uterine contents.
• Abdominal straining, discomfort. to differentiate uterine from distal reproduc
• Ultrasonography—identify uterine size and
• Depression. tive tract disease.
contents; assess fluid and its consistency;
• Dehydration. assess fetal viability (heartbeats: normal,
• Fever. >200 bpm; stress, <150 or >280 bpm).
(continued) Abortion, Spontaneous (Early Pregnancy Loss)—Dogs A
DIAGNOSTIC PROCEDURES • Prostaglandin treatment—discuss side for consistency (increasing mucoid content
• Vaginoscopy—identify source of vulvar effects (e.g., abortion). prognostically good).
discharge and vaginal lesions; use scope of • Infectious disease—establish surveillance • PGF2α—continued for 5 days or until most
sufficient length (16–20 cm) to examine and control measures. of discharge ceases (range 3–15 days).
entire length of vagina. • B. canis—monitor after neutering and
SURGICAL CONSIDERATIONS
• Cytologic examination, bacterial culture— OHE preferred for stable nonbreeding patients. antibiotic therapy; yearly serologic testing
may reveal inflammatory process (e.g., uterine (identify recrudescence).
infection): use guarded swab to ensure anterior • Hypothyroidism—see Hypothyroidism.
sample (distal reproductive tract is heavily PREVENTION/AVOIDANCE
contaminated with bacteria), or collect • Brucellosis, other infectious agents—
secretions by transcervical catheterization. MEDICATIONS surveillance programs to prevent spread to
PATHOLOGIC FINDINGS DRUG(S) OF CHOICE kennel.
Histopathologic examination and culture of • Prostaglandin F2α (PGF2α; Lutalyse®, dinoprost • OHE—for nonbreeding bitches.
fetal and placental tissue—may reveal tromethamine)—uterine evacuation after • Use of modified-live vaccines (e.g., some
infectious organisms; tissue culture, particu- abortion; 0.05–0.1 mg/kg SC q8–24h; distemper, parvovirus), currently unavailable
larly of stomach contents, may identify cloprostenol (Estrumate®, cloprostenol)—1–5 μg/ in United States.
infectious bacteria. kg SC q24h; not approved for use in dogs, but
POSSIBLE COMPLICATIONS
adequate documentation for use; use only if all
• Untreated pyometra—septicemia, death.
living fetuses expelled.
• Brucellosis—discospondylitis, endophthal
• Antibiotics—broad-spectrum agent
mitis, uveitis, zoonotic.
appropriate pending culture and sensitivity of
TREATMENT vaginal tissue or fetus. EXPECTED COURSE AND PROGNOSIS
APPROPRIATE HEALTH CARE • Progesterone (altrenogest) at 0.088 mg/kg • Pyometra—recurrence during subsequent
• Most bitches should be isolated pending (1 mL/25 kg PO q24h); progesterone in oil cycle likely (up to 70%) unless pregnant.
diagnosis. at 2 mg/kg IM q48–72h; progesterone • CEH—recovery of fertility unlikely;
• Hospitalization of infectious patients (Prometrium®; 10 mg/kg PO q24h, adjust pyometra common complication.
preferred. daily dosage based on serum progesterone)— • Hormonal dysfunction—manageable;
• B. canis—highly infective; shed in high for documented hypoluteoidism only to heritability should be considered.
numbers during abortion; suspected dogs maintain pregnancy; must have accurate due • Brucellosis—guarded; extremely difficult to
should be isolated. date to know when to discontinue therapy; eliminate infection even with neutering.
• Outpatient—medically stable patients with inadvertently prolonging gestation results in
noninfectious pregnancy loss. fetal death.
• Partial abortion—attempt to salvage live CONTRAINDICATIONS
fetuses; antibiotics indicated if bacterial Progestogen supplementation contraindicated MISCELLANEOUS
component. with endometrial or mammary gland disease. AGE-RELATED FACTORS
NURSING CARE PRECAUTIONS Older bitches more likely to have CEH.
Dehydration—isotonic crystalloid fluids, • PGF2α—dose-related side effects related to
electrolyte supplementation as indicated. ZOONOTIC POTENTIAL
smooth muscle contraction, diminish with B. canis—can be transmitted to humans
ACTIVITY each injection; panting, salivation, vomiting, (especially if immunosuppressed), particularly
Partial abortion—cage rest, but effect on and defecation common; caution in brachyce when handling bitch and expelled tissues.
reducing further abortion unknown. phalics; dosing critical (LD50 for Notify pathologists if B. canis is suspected.
DIET dinoprost—5 mg/kg).
• Progesterone supplementation will prevent SEE ALSO
No special considerations; abortions have • Brucellosis.
been associated with raw diets. whelping—administration needs to be
discontinued before 2–3 days prior to due • Hypothyroidism.
CLIENT EDUCATION date; risk of masculinization of female fetuses • Infertility, Female—Dogs.
• Critical for B. canis—if confirmed, euthanasia if used before day 45 of gestation. • Premature Labor.
recommended due to lack of successful • Pyometra.
treatment and to prevent spread; may try ALTERNATIVE DRUG(S)
Oxytocin—1 U/5 kg SC q6–24h for uterine ABBREVIATIONS
ovariohysterectomy (OHE) and long-term • CEH = cystic endometrial hyperplasia.
antibiotics with surveillance program for kennel evacuation; consider only where uterine
evacuation solely through uterine contraction • OHE = ovariohysterectomy.
situations (monthly serology, culling any • PGF2α = prostaglandin F2α.
positive animals until three consecutive negative desired.
tests are obtained); discuss zoonotic potential. Suggested Reading
• Primary uterine disease—OHE is indicated Verstegen J, Dhaliwal G, Verstegen-Onclin K.
in nonbreeding patients; cystic endometrial Canine and feline pregnancy loss due to
hyperplasia (CEH) is irreversible. FOLLOW-UP viral and non-infectious causes: a review.
• Infertility or pregnancy loss—may recur in Theriogenology 2008, 70(3):304–319.
PATIENT MONITORING Author Julie T. Cecere
subsequent estrous cycles despite successful
• Partial abortion—monitor viability of Consulting Editor Erin E. Runcan
immediate treatment; pedigree analysis may
remaining fetuses with ultrasonography; monitor
be beneficial in highly linebred animals if
systemic health of dam for rest of pregnancy.
pregnancy loss and small litter size due to
• Vulvar discharges—daily; for decreasing Client Education Handout
inbreeding depression.
amount, odor, and inflammatory component; available online
A Abortion, Termination of Pregnancy
RISK FACTORS • Treatment on day 6–10 of diestrus—may
N/A have reduced efficacy compared to mid-gesta-
tion, but can be less distasteful to client (less
BASICS discharge and recognizable fetuses are not
DEFINITION passed).
Termination of an unwanted pregnancy. May be DIAGNOSIS • Multimodal treatment improves efficacy of
accomplished by drugs that alter embryo • Confirm pregnancy first, ~60% of drugs given alone.
transport in the oviduct, impeding establishment mismated bitches do not become pregnant: NURSING CARE
of a pregnancy, and/or cause luteal regression, ◦ Abdominal palpation—bitch: 31–33 days N/A
terminating an established pregnancy. Due to after luteinizing hormone (LH) surge;
their possible side effects (cystic endometrial ACTIVITY
queen: 21–25 days after breeding.
hyperplasia, aplastic anemia, and bone marrow Normal
◦ Transabdominal ultrasound—bitch: >25 days
suppression), drugs that impair embryonic after LH surge; queen: >16 days after breeding. DIET
transit through the oviduct (estrogens) are not ◦ Abdominal radiographs—bitch: >45 days Avoid feeding prior to each treatment and for
commonly used or recommended. after LH surge; queen: >38 days after breeding. 1–2 hours after treatments (reduces nausea
PATHOPHYSIOLOGY ◦ Serum relaxin concentration in the bitch and vomiting).
After fertilization the embryo travels the (>28 days after LH surge; Witness® Relaxin, CLIENT EDUCATION
oviduct in a timely manner before entering the Synbiotics/Zoetis). • Discuss patient’s reproductive future with
uterus. Impaired embryo transport through DIFFERENTIAL DIAGNOSIS owner. If no litters are desired, then ovario
the oviduct leads to embryonic degeneration • Hydrometra. hysterectomy (OHE) is the best option.
and implantation abnormalities. In the dog • Mucometra. • Discuss with client potential side effects of
and cat, pregnancy maintenance is dependent • Hematometra. treatment options; reach mutual agreement
on progesterone production from the corpora • Pyometra. on treatment plan.
lutea. In dogs and cats, maintenance of the • Pseudopregnancy. SURGICAL CONSIDERATIONS
corpora lutea during the second half of
CBC/BIOCHEMISTRY/URINALYSIS OHE recommended for patients with no
gestation is also supported by prolactin (PRL).
• Within normal limits during first half of reproductive value or when owners do not
Drugs that cause luteal regression, antagonize
pregnancy in healthy patients. desire future litters.
PRL, and/or compete with progesterone
• Decrease in hematocrit during second half
receptors will terminate pregnancy.
of pregnancy in bitches and queens is normal.
SYSTEMS AFFECTED • Recommended as screening tests prior to
• Cardiovascular. treatment in patients with suspected under-
• Digestive.
MEDICATIONS
lying disease.
• Neurologic (caused by drugs used for DRUG(S) OF CHOICE
treatment). OTHER LABORATORY TESTS • Confirmation of pregnancy before initiating
• Vaginal cytology—determines stage of any of treatment protocols suggested below is
• Reproductive.
• Respiratory.
estrous cycle and presence of sperm (absence recommended. Duration of suggested
does not rule out previous breeding). treatment may vary; treatments should be
GENETICS • Serum progesterone concentration deter-
N/A continued until abortion is complete.
mines if female in diestrus and monitors • Prostaglandin F2α (PGF2α)—causes luteal
INCIDENCE/PREVALENCE luteal regression during treatment. regression with subsequent decline in
N/A IMAGING progesterone concentration, cervical relax-
GEOGRAPHIC DISTRIBUTION • Transabdominal ultrasound (method of ation, and uterine contractions. Higher doses
N/A choice)—diagnose pregnancy and monitor necessary prior to day 28 of gestation.
uterine evacuation during treatment. ◦ Bitch low dose protocol—10 μg/kg SC q6h
SIGNALMENT • Abdominal radiographs. for 7–10 days or until pregnancy termination.
Species ◦ Bitch standard dose protocol—100 μg/kg
Dog and cat. N/A SC q8h for 2 days, then 200 μg/kg SC q8h
Breed Predilections
until pregnancy termination.
PATHOLOGIC FINDINGS ◦ Queen low dose protocol—25 μg/kg SC
N/A N/A q6h for 1–2 days, then 50 μg/kg SC q6h for
Mean Age and Range 3–4 days (queen more resistant to luteolytic
Postpubertal bitch and queen. effects of PGF2α than bitches; often higher
Predominant Sex doses for longer periods are required).
Female TREATMENT ◦ Queen standard protocol—0.5–1 mg/kg
SC q12h every other day (>day 40), or
SIGNS APPROPRIATE HEALTH CARE
2 mg/cat SC q24h for 5 days (>day 33).
• Depends on stage of gestation: • Physical examination before initiation of
• Cloprostenol (prostaglandin analogue):
◦ None. treatment.
◦ Bitch—2.5 μg/kg SC q8–12h every 48
◦ Vaginal discharge. • Monitor 30–60 minutes after treatment for
hours until pregnancy termination (~6 days
◦ Fetal expulsion. side effects (vomiting, defecation, hypersaliva-
after start of treatment).
tion, hyperpnea, micturition, tachycardia).
CAUSES • Dexamethasone—mode of action
• Pregnancy status in early diestrus is unknown;
• Impaired oviductal transport. unknown:
ultrasound confirmation of pregnancy not
• Luteal regression. ◦ Bitch—0.2 mg/kg PO q8–12h for 5
possible until ~4 weeks after breeding.
• Progesterone receptor antagonism. days, then decreasing incrementally from
(continued) Abortion, Termination of Pregnancy A
0.16 to 0.02 mg/kg over last 5 days; impaired liver function; side effects may PREVENTION/AVOIDANCE
treatment failures not uncommon. include vomiting and anorexia; prolonged use • OHE for bitches and queens not intended
• Cabergoline (PRL antagonist)—causes (>2 weeks) may cause coat color changes. for breeding.
luteal regression: POSSIBLE INTERACTIONS • Estrus suppression or confinement of
◦ Bitch—1.65 μg/kg SC q24h for 5 days or bitches and queens intended for breeding
• PGF2α and analogues—effect may be reduced
5 μg/kg PO q24h for 5 days (>day 40). by concomitant administration of progestins; during a later cycle to avoid mismating.
◦ Queen—1.65 μg/kg SC for 5 days (>day 30) use may enhance effects of oxytocin. POSSIBLE COMPLICATIONS
or 5 μg/kg PO q24h for 5 days (>day 35). • Cabergoline and bromocriptine—cabergo- Pregnancy termination may not be achieved after
• Bromocriptine (PRL antagonist)—causes line effects may be reduced with concomitant one treatment protocol and continuation or
luteal regression: treatment with dopamine (D2) antagonists; change in treatment protocol may be necessary.
◦ Bitch—50–100 μg/kg IM/PO q12h for avoid concomitant treatment with drugs
4–7 days >day 35 (50% effective); common EXPECTED COURSE AND PROGNOSIS
causing hypotension. • Interestrous interval in bitches treated with
side effect vomiting; reduce dose and give
with meal. ALTERNATIVE DRUG(S) prostaglandins and PRL inhibitors may be
• Cloprostenol and cabergoline combination: • The following drugs are recommended for shortened (~1 month). Queens may resume
◦ Bitch—cabergoline 5 μg/kg PO q24h for use in bitches but are not readily available in estrous behavior 7–10 days after pregnancy
10 days plus cloprostenol 2.5 μg/kg SC at the United States: termination.
start of treatment or 1 μg/kg SC at start of ◦ Aglepristone (progestin and glucocorticoid • Subsequent estrus fertility not affected.
treatment and at day 5 of treatment; receptors antagonist)—10 mg/kg SC q24h
treatment should be initiated >28 days for 2 days >14 days post-LH surge; highly
post-LH surge. effective in preventing pregnancy (>95%
◦ Queen—cabergoline 5 μg/kg PO q24h treatment efficacy); abdominal ultrasound
at 28–30 days essential to insure treatment
MISCELLANEOUS
plus cloprostenol 5 μg/kg SC q48h (>30
days after breeding) until abortion success; if pregnancy still present, repeat ASSOCIATED CONDITIONS
complete (~9 days). injection protocol. Mild reactions at N/A
• Cloprostenol and bromocriptine injection site have been reported; mild AGE-RELATED FACTORS
combination: vaginal discharge may be observed; slight N/A
◦ Bitch—bromocriptine 30 μg/kg PO q8h risk (3.4%) of development of pyometra in
field studies. ZOONOTIC POTENTIAL
for 10 days plus cloprostenol 2.5 μg/kg SC
◦ Aglepristone and cloprostenol combina- N/A
or 1 μg/kg SC at start of treatment and at
day 5 of treatment; treatment should be tion—aglepristone (10 mg/kg SC) combined PREGNANCY/FERTILITY/BREEDING
initiated >28 days post-LH surge. with cloprostenol (1 μg/kg SC) q24h for 2 N/A
days >25 days’ pregnancy; pregnancy
CONTRAINDICATIONS SYNONYMS
terminated within 6 days. Side effects after
• PGF2α and analogues—animals with Induced abortion.
treatment include vomiting and diarrhea;
respiratory disease (bronchoconstriction); do vaginal discharge may be observed. SEE ALSO
not administer intravenously. Use with ◦ Aglepristone (10 mg/kg SC q24h for Breeding, Timing.
caution in brachycephalic breeds. 2 days) with intravaginal misoprostol
• Cabergoline and bromocriptine—avoid ABBREVIATIONS
(200–400 μg depending on body size) daily • CEH = cystic endometrial hyperplasia.
administration in animals hypersensitive to until abortion complete; abortion complete
ergot alkaloids; use with caution in patients • LH = luteinizing hormone.
within 7 days. Vomiting, diarrhea, polydip- • OHE = ovariohysterectomy.
with impaired liver function. sia, anorexia not observed with this regimen.
• Estrogens may cause cystic endometrial • PGF2α = prostaglandin F2α.
hyperplasia (CEH), pyometra, and bone • PRL = prolactin.
marrow suppression leading to pancytopenia. Suggested Reading
PRECAUTIONS Eilts BE. Pregnancy termination in the bitch
• PGF2α and analogues—side effects dose
FOLLOW-UP and queen. Clin Tech Small Anim Pract
dependent and include vomiting, defecation, PATIENT MONITORING 2002, 17:116–123.
dyspnea, tachycardia, salivation, restlessness, In animals treated with luteolytic drugs Fieni F, Dumon C, Tainturier D, Bruyas JF.
and anxiety; side effects subside within 60 (prostaglandins and PRL antagonists), Clinical protocol for pregnancy termination
minutes; use extreme caution in dogs and cats progesterone assays and transabdominal in bitches using prostaglandin F2α. J Reprod
with preexisting cardiopulmonary, liver, and ultrasound examinations should be performed Fertil Suppl 1997, 51:245–250.
renal diseases. to monitor decrease of serum progesterone Author Jose A. Len
• Dexamethasone—polydipsia, polyuria, and concentration and complete evacuation of Consulting Editor Erin E. Runcan
polyphagia are reported side effects; long- uterine contents. In patients treated with
term administration can result in signs of progesterone receptor antagonist drugs,
transabdominal ultrasound examinations are Client Education Handout
hyperadrenocorticism.
recommended to monitor complete evacu available online
• Cabergoline and bromocriptine—should be
administered with caution in patients with ation of the uterus.
A Abscessation
of function), tissue destruction,
and/or organ system dysfunction caused by
accumulation of exudates.
BASICS DIAGNOSIS
Historical Findings
DEFINITION • Often nonspecific signs (e.g., lethargy, DIFFERENTIAL DIAGNOSIS
An abscess is a focal collection of purulent anorexia). Mass Lesions
exudate within a confined tissue space or cavity. • History of trauma or prior infection. • Cyst—transiently painful, slower growing,
PATHOPHYSIOLOGY • Rapidly appearing painful swelling with or no overt signs of inflammation.
• Bacterial organisms may enter tissue by without discharge, if affected area is visible. • Fibrous scar tissue—firm, nonpainful.
penetrating trauma, spread from another Physical Examination Findings • Granuloma—less painful, slower growing,
source of infection (hematogenous or • Determined by organ system or tissue firmer without fluctuant center.
adjacent infected tissues), or migration of a affected. • Hematoma/seroma—variable pain,
contaminated object (e.g., plant awn). • Classic signs of inflammation (heat, pain, nonencapsulated, rapid initial growth but
• Most often, bacteria are inoculated under swelling, and loss of function) associated with slows once full size attained, fluctuant
the skin via puncture or bite wounds. specific anatomic location of abscess. initially, may become more firm over time.
• When bacteria or foreign objects persist in • Inflammation and discharge from fistulous • Neoplasia—variable growth, variable pain.
tissue, purulent exudate accumulates. tract may be visible if abscess has ruptured to Draining Tracts
• If exudate not quickly resorbed or drained, an external surface. • Fungal infection—blastomycosis,
fibrous capsule forms to “wall off ” infection; • Variably sized, painful mass of fluctuant to coccidioidomycosis, cryptococcosis,
abscess may eventually rupture. firm consistency attached to surrounding histoplasmosis, sporotrichosis.
• With fibrous capsule—to heal, the cavity tissues. • Mycobacterial disease.
must fill with granulation tissue from which • Fever common, but may be absent if • Mycetoma—botryomycosis, actinomycotic
causative agent may not be totally eliminated; abscess has ruptured. mycetoma, eumycotic mycetoma.
may lead to chronic or intermittent discharge • Sepsis or infection of body cavity (e.g., • Neoplasia.
of exudate from a draining tract. pyothorax) may be seen if abscess ruptures • Phaeohyphomycosis.
• Sterile abscesses can occur when irritants internally.
(injectable medications, venom) or inflamm CBC/BIOCHEMISTRY/URINALYSIS
atory processes (pancreatitis, immune CAUSES • CBC—normal, neutrophilia with or
mediated, decreased blood supply) lead to • Foreign objects. without left shift, neutropenia and
local collection of purulent exudate. • Pyogenic bacteria—Staphylococcus spp., degenerative left shift (severe infection).
Escherichia coli, β-hemolytic Streptococcus • Serum chemistry profile—depends on
SYSTEMS AFFECTED spp., Pseudomonas, Mycoplasma and severity, system affected. Signs of cholestasis if
• Skin/exocrine—percutaneous (cats > dogs); Mycoplasma-like organisms (l-forms), pancreatic abscess causes obstruction,
anal sac (dogs > cats). Pasteurella multocida, Corynebacterium, hyperglycemia if diabetes mellitus, etc.
• Reproductive—prostate gland (dogs > cats); Actinomyces spp., Nocardia, Bartonella. • Urinalysis—pyuria (prostatic abscess).
mammary gland. • Obligate anaerobes—Bacteroides spp.,
• Ophthalmic—periorbital tissues. OTHER LABORATORY TESTS
Clostridium spp., Peptostreptococcus,
• Hepatobiliary—liver parenchyma. • FeLV, FIV testing—recurrent or slow-
Fusobacterium.
• Gastrointestinal—pancreas (dogs > cats). healing abscesses (cats).
• Noninfectious—pancreatitis, suture
• Respiratory—pulmonary parenchyma. • Cerebrospinal fluid evaluation—increased
reaction, vaccination, other injectable drug
cellularity and protein with brain abscess.
GENETICS administration, stinging insects, snake
• Adrenal function—hyperadrenocorticism.
N/A envenomation, immune-mediated panniculitis,
dermatitis, neoplasia (especially when blood IMAGING
INCIDENCE/PREVALENCE • Radiography—soft-tissue density mass in
supply outgrown).
N/A affected area, may reveal foreign material.
RISK FACTORS
GEOGRAPHIC DISTRIBUTION • Ultrasonography—determine if mass is
• Anal sac—impaction, anal sacculitis.
N/A fluid filled; may reveal foreign object;
• Brain—otitis interna, sinusitis, oral
SIGNALMENT echogenic fluid suggests purulent exudate.
infection.
• Echocardiography—pericardial abscess,
Species • Liver—omphalophlebitis, sepsis.
endocarditis.
Cat and dog. • Lung—foreign object aspiration or
• CT or MRI—pulmonary or brain abscess.
migration, bacterial pneumonia.
Breed Predilections • Mammary gland—mastitis. DIAGNOSTIC PROCEDURES
N/A • Periorbital—dental disease, chewing of Fine-Needle Aspiration
Mean Age and Range wood or other plant material. • Red, white, yellow, or greenish liquid.
N/A • Percutaneous—fighting, trauma, or • Protein content >2.5–3.0 g/dL.
surgery. • Nucleated cell count—3,000–100,000 (or
Predominant Sex
• Prostate gland—bacterial prostatitis. more) cells/μL; primarily degenerate
Mammary glands (female); prostate gland (male).
• Immunosuppression—feline leukemia virus neutrophils, fewer macrophages,
SIGNS (FeLV) or feline immunodeficiency virus lymphocytes.
General Comments (FIV) infection, immunosuppressive chemo- • Bacteria—intra- and extracellular:
• Determined by organ system and/or tissue therapy, acquired or inherited immune system ◦ Gram stain to classify organism for
affected. dysfunctions, underlying predisposing disease empiric therapy.
• Associated with combination of inflamm (e.g., diabetes mellitus, chronic renal failure, ◦ If causative agent not readily identified
ation (pain, swelling, redness, heat, and loss hyperadrenocorticism). with a Romanowsky-type stain, acid-fast
(continued) Abscessation A
stain to detect mycobacteria or Nocardia and • Early drainage—to prevent further tissue POSSIBLE COMPLICATIONS
periodic acid-Schiff stain to detect fungus. damage and abscess wall formation. • Sepsis.
• Remove foreign objects(s), necrotic tissue, • Peritonitis/pleuritis if intra-abdominal or
Biopsy
• Sample should contain both normal and
nidus of infection. intrathoracic abscess ruptures.
abnormal tissue. • Complications to discuss include progressive • Compromise of organ function.
• Impression smears.
tissue damage, necrosis, dehiscence of wound, • Delayed evacuation may lead to chronic,
• Tissue—for histopathologic examination
prolonged healing times in high-motion areas draining fistulous tracts.
and culture. (axillary, inguinal). EXPECTED COURSE AND PROGNOSIS
• Necessary to confirm nodular panniculitis. Depends on cause, organ system involved,
Culture and Susceptibility Testing and amount of tissue destruction.
• Affected tissue and/or exudate—aerobic
and anaerobic bacterial and fungal. MEDICATIONS
• Blood and/or urine if systemic disease. DRUG(S) OF CHOICE
PATHOLOGIC FINDINGS • Antimicrobial drugs that are effective against MISCELLANEOUS
• Exudate-containing mass lesion accom infectious agent and penetrate site of infection. ASSOCIATED CONDITIONS
panied by inflammation. • Broad-spectrum agent—bactericidal with
• FeLV or FIV infection.
• Causative agent may be detectable. both aerobic and anaerobic activity until • Immunosuppression.
results of culture and sensitivity are known;
Gram stain of exudate may guide therapy. AGE-RELATED FACTORS
◦ Dogs and cats—amoxicillin (22 mg/kg N/A
PO q12h); amoxicillin–clavulanic acid ZOONOTIC POTENTIAL
TREATMENT (22 mg/kg PO q12h); clindamycin • Mycobacteria and systemic fungal
APPROPRIATE HEALTH CARE (5–10 mg/kg PO q12h); trimethoprim– infections carry some potential.
• Establish and maintain adequate drainage. sulfadiazine (15 mg/kg PO q12h). • If prostatitis secondary to Brucella canis.
• Surgical removal of nidus of infection or ◦ Cats only—pradofloxacin (7.5 mg/kg
PO q24 for 7 days). PREGNANCY/FERTILITY/BREEDING
foreign object(s) if necessary. N/A
• Initiate appropriate antimicrobial therapy. ◦ Cats with Mycoplasma and L-forms—
• Outpatient—minor abscesses, localized doxycycline (5 mg/kg PO q12h). SEE ALSO
infection, nodular panniculitis. • Aggressive IV antimicrobial therapy— • Actinomycosis and Nocardia.
• Inpatient—sepsis or systemic inflammation, sepsis, peritonitis, pyothorax. • Anaerobic Infections.
extensive surgical procedures, treatment • Antimicrobials not required for confirmed • Colibacillosis.
requiring hospitalization. sterile abscesses. • Mycoplasmosis.
CONTRAINDICATIONS • Nocardiosis/Actinomycosis—Cutaneous.
NURSING CARE • Sepsis and Bacteremia.
• Depends on location of abscess. N/A
• Apply hot packs to inflamed area as needed. PRECAUTIONS ABBREVIATIONS
• Use protective bandaging, Elizabethan N/A • FeLV = feline leukemia virus.
collar as needed. • FIV = feline immunodeficiency virus.
• Accumulated exudate—surgical drainage, POSSIBLE INTERACTIONS
N/A Suggested Reading
debridement of necrotic tissue. Green CE, Goldstein EJC. Bite wound
• Sepsis, peritonitis, pyothorax—fluid ALTERNATIVE DRUG(S) infections. In: Greene CE, ed., Infectious
therapy, antimicrobial therapy, intensive care. Sterile nodular panniculitis—corticosteroids. Diseases of the Dog and Cat, 4th ed. St.
ACTIVITY Louis, MO: Elsevier Saunders, 2012, pp.
Restrict until abscess has resolved and 528–542.
adequate healing occurs. Singh A, Scott Weese J. Wound infections
FOLLOW-UP and antimicrobial use. In: Johnston SA,
DIET Tobias KM, eds., Veterinary Surgery Small
N/A PATIENT MONITORING Animal, 2nd ed. St. Louis, MO: Elsevier,
CLIENT EDUCATION Monitor for progressive decrease in drainage, 2018, pp. 148–155.
• Correct or prevent risk factors. resolution of inflammation, and improvement Author Selena Lane
• Maintain adequate drainage and continue of clinical signs. Consulting Editor Amie Koenig
antimicrobial therapy for adequate period of time. PREVENTION/AVOIDANCE Acknowledgment The author and editors
SURGICAL CONSIDERATIONS • Percutaneous abscesses—prevent fighting; acknowledge the prior contribution of Adam
• Appropriate debridement and drainage— consider castration to reduce roaming or J. Birkenheuer.
may need to leave wound open to external aggressive behavior.
surface; may need drain placement. • Anal sac abscesses—prevent impaction;
consider anal saculectomy for recurrent cases. Client Education Handout
◦ Penrose drains must exit ventrally to
• Prostatic abscesses—consider castration. available online
encourage drainage; may be bandaged, if
bandage is changed regularly. • Mastitis—prevent lactation (spay).
◦ If no ventral drainage, use active drains • Periorbital abscesses—do not allow chewing
(e.g., Jackson-Pratt drain). on foreign objects.
A Acetaminophen (APAP) Toxicosis
SIGNALMENT (alanine aminotransferase [ALT], aspartate
Species transaminase [AST])—characteristic.
• As hepatic function becomes impaired—
BASICS Cats more often than dogs.
decreased blood urea nitrogen (BUN),
DEFINITION SIGNS cholesterol, and albumin, and increased
Results from accidental animal ingestion or General Comments serum bilirubin.
owner administration of over-the-counter Relatively common—owing to widespread • Heinz bodies (cats)—prominent in RBCs
acetaminophen-containing analgesic and human use. within 72 hours.
antipyretic medications. • Anemia, hemoglobinemia, and hemoglob
Historical Findings inuria or hematuria.
PATHOPHYSIOLOGY • Depression.
When the normal biotransformation • Hyperventilation. OTHER LABORATORY TESTS
mechanisms for detoxification (glucuronida- • Darkened mucous membranes. Acetaminophen plasma, serum, or urine
tion and sulfation) are saturated, cytochrome • Signs may develop 1–4 hours after dosing. concentrations.
P450–mediated oxidation produces a toxic IMAGING
Physical Examination Findings
metabolite (N-acetyl-p-benzoquinone imine) N/A
• Progressive depression.
that is electrophilic, conjugates with glutathione,
• Salivation. DIAGNOSTIC PROCEDURES
and binds to sulfhydryl groups, leading to
• Vomiting. N/A
hepatic necrosis.
• Abdominal pain.
Dogs • Tachypnea and cyanosis or muddy mucous
PATHOLOGIC FINDINGS
• Liver is most susceptible to toxicity. • Methemoglobinemia.
membranes—reflect methemoglobinemia.
• Signs commonly observed at exposures • Pulmonary edema.
• Edema—face, paws, and possibly forelimbs;
>75–100 mg/kg. • Centrilobular necrosis and congestion of
after several hours.
• Methemoglobinemia may develop at doses • Chocolate-colored urine—hematuria and
the liver.
>200 mg/kg. • Renal tubular edema and degeneration with
methemoglobinuria; especially in cats.
• Icterus.
proteinaceous tubular casts.
Cats
• Cannot effectively glucuronidate; more • Hypothermia.
limited capacity for acetaminophen • Shock.
elimination than dogs. • Death.
• Saturate glucuronidation and sulfation CAUSES TREATMENT
biotransformation routes. Acetaminophen toxicosis. APPROPRIATE HEALTH CARE
• Red blood cells (RBCs) are most susceptible • With methemoglobinemia—must evaluate
RISK FACTORS
to oxidative injury following glutathione promptly.
• Nutritional deficiencies of glucose and/or
depletion. • With dark or bloody colored urine or
sulfate.
• Develop toxic cytochrome P450 metabolite icterus—inpatient.
• Simultaneous administration of other
at much lower doses than dogs.
glutathione-depressing drugs. NURSING CARE
• Poisoned by as little as 50–60 mg/kg (often
• Gentle handling—imperative for clinically
as little as one half tablet); deacetylation of
acetaminophen to p-aminophenol (PAP) affected patients.
• Induced emesis and gastric lavage—useful
causes oxidative damage to RBCs, rapidly
producing methemoglobinemia by binding to DIAGNOSIS within 4–6 hours of ingestion.
• Anemia, hematuria, or hemoglobinuria—
sulfhydryl groups on hemoglobin. DIFFERENTIAL DIAGNOSIS
• Slower-developing hepatotoxicosis may not
may require whole blood transfusion.
Other Causes of Liver Injury • Fluid therapy—maintain hydration and
be fully expressed before development of fatal
methemoglobinemia. • Hepatotoxic mushrooms. electrolyte balance.
• Blue-green algae. • Oxygen therapy may be needed.
SYSTEMS AFFECTED • Aflatoxins. • Drinking water—available at all times.
• Hemic/lymph/immune—RBCs damaged • Iron, copper, zinc. • Food—offered 24 hours after initiation of
by glutathione depletion, allowing oxidation • Xylitol. treatment.
of hemoglobin to methemoglobin. • Cycad palms.
• Hepatobiliary—liver necrosis (more
ACTIVITY
• Nonsteroidal anti-inflammatory drugs Restricted
common in dogs). (NSAIDs).
• Cardiovascular (primarily cats)—edema of DIET
face, paws, and (to lesser degree) forelimbs Other Causes of Methemoglobinemia N/A
through undefined mechanism. • Onions/garlic.
• Naphthalene.
CLIENT EDUCATION
GENETICS • Chlorates.
• Warn client that treatment in clinically
Cats—genetic deficiency in the glucuronide • Nitrites.
affected patients may be prolonged and
conjugation pathway makes them vulnerable. • Sulfites.
expensive.
• Inform client that patients with liver injury
INCIDENCE/PREVALENCE • Phenol.
Common drug toxicity in cats; less frequent • Benzocaine.
may require prolonged and costly management.
in dogs. • Propylene glycol (cats). SURGICAL CONSIDERATIONS
GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS N/A
N/A • Methemoglobinemia and progressively
rising serum concentrations of liver enzymes
(continued) Acetaminophen (APAP) Toxicosis A
PREVENTION/AVOIDANCE SYNONYMS
• Never give acetaminophen to cats. • Paracetamol.
• Give careful attention to acetaminophen • Tylenol®.
MEDICATIONS dose in dogs. SEE ALSO
DRUG(S) OF CHOICE POSSIBLE COMPLICATIONS Poisoning (Intoxication) Therapy.
• Activated charcoal 1–2 g/kg PO with a Liver necrosis and resulting fibrosis—may
cathartic; immediately after completion of ABBREVIATIONS
compromise long-term liver function in • ALT = alanine aminotransferase.
emesis or gastric lavage. recovered patients.
• N-acetylcysteine (Mucomyst®) 140 mg/kg • AST = aspartate transaminase.
diluted in 5% dextrose injection (D5W) as EXPECTED COURSE AND PROGNOSIS • BUN = blood urea nitrogen.
loading dose PO/IV; then 70 mg/kg diluted • Rapidly progressive methemoglobinemia— • D5W = 5% dextrose injection.
in D5W PO/IV q6h for 7 additional treat- serious sign. • NSAID = nonsteroidal anti-inflammatory
ments. Large overdoses may require up to 17 • Methemoglobin concentrations ≥50%— drug.
treatments. grave prognosis. • PAP = p-aminophenol.
• S-adenosylmethionine (SAMe) as a • Progressively rising serum liver enzymes • RBC = red blood cell.
glutathione donor; 40 mg/kg PO × 1 dose, 12–24 hours after ingestion—serious concern. • SAMe = S-adenosylmethionine.
then 20 mg/kg q24h PO × 7 days. • Expect clinical signs to persist 12–48 hours;
INTERNET RESOURCES
• Added benefit of using methylene blue, death owing to methemoglobinemia possible https://www.aspca.org/pet-care/
cimetidine, and/or ascorbic acid is contro- at any time. animal-poison-control
versial. • Dogs and cats receiving prompt treatment
that reverses methemoglobinemia and Suggested Reading
CONTRAINDICATIONS prevents excessive liver necrosis—may Plumb DC. Acetaminophen. In: Plumb DC,
Drugs that contribute to methemoglobinemia recover fully. ed., Plumb’s Veterinary Drug Handbook,
or hepatotoxicity. • Dogs—death as a result of liver necrosis 9th ed. Ames, IA: Wiley-Blackwell, 2018,
PRECAUTIONS may occur within 72 hours. pp. 6–8.
Drugs requiring extensive liver metabolism or • Cats—death as a result of methemoglobine- Plumlee KH. Hematic system. In: Plumlee
biotransformation—use with caution; expect mia occurs 18–36 hours after ingestion. KH, ed., Clinical Veterinary Toxicology. St.
their half-lives to be extended. Louis, MO: Mosby, 2004, p. 59.
Schell MM, Gwaltney-Brant S. OTC drugs.
POSSIBLE INTERACTIONS In: Poppenga RH, Gwaltney-Brant SM, eds.,
Drugs requiring activation or metabolism by Small Animal Toxicology Essentials. Chichester:
the liver have reduced effectiveness. MISCELLANEOUS Wiley-Blackwell, 2011, pp. 231–233.
ASSOCIATED CONDITIONS Sellon RK. Acetaminophen. In: Peterson ME,
Keratoconjunctivitis sicca may develop in Talcott PA, eds. Small Animal Toxicology,
small-breed dogs as a sequela. 3rd ed. St. Louis, MO: Elsevier, 2013, pp.
FOLLOW-UP 423–429.
AGE-RELATED FACTORS
Stockham SL, Scott MA. Fundamentals of
PATIENT MONITORING Young and small dogs and cats—greater risk
Veterinary Clinical Pathology, 2nd ed.
• Continual clinical monitoring of methemo from owner-given single-dose acetaminophen
Oxford: Blackwell, 2008, p. 186.
globinemia—vital for effective management; medications.
Author Lisa A. Murphy
laboratory determination of methemoglobin PREGNANCY/FERTILITY/BREEDING Consulting Editor Lynn R. Hovda
percentage every 2–3 hours. Imposes additional stress and higher risk on
• Serum liver enzyme activities (ALT, ALP) exposed animals.
every 12 hours; monitor liver damage. Client Education Handout
available online
A Acidosis, Metabolic
effects of catecholamines. In mildly acidemic • Toxins—ethylene glycol, salicylate,
conditions (pH >7.2), effects of increased paraldehyde, methanol intoxication.
sympathetic stimulation predominate and • Hyperphosphatemia (see Hyperphos-
BASICS result in mild increase in heart rate and cardiac phatemia)—raises AG. At a pH of 7.4, each
DEFINITION output. More severe acidemia (pH <7.1), 1 mg/dL increase in phosphate concentration
A process in the body that leads to a decrease especially if acute, may decrease cardiac is associated with a 0.58 mEq/L increase in AG.
in pH below the reference interval. A decline contractility and predispose heart to ventricular
arrhythmias and ventricular fibrillation. RISK FACTORS
in blood pH is specifically termed acidemia.
• Chronic renal failure, diabetes mellitus, and
Associated with a decrease in plasma bicarb- • Respiratory—increased hydrogen ion [H+]
stimulates peripheral and central chemorecep- hypoadrenocorticism.
onate concentration ( HCO3 ; dogs,
tors to increase alveolar ventilation; hyperven- • Poor tissue perfusion or hypoxia—lactic
<18 mEq/L; cats, <16 mEq/L) and base
tilation decreases PCO2, which counters effects acidosis.
excess (BE; –4 mmol/L) with a compensatory
of low plasma HCO3 on pH. In dogs, a • Tumor lysis syndrome or osteosarcoma—
decrease in carbon dioxide tension (PCO2).
decrease of approximately 1 mmHg in PCO2 is hyperphosphatemia.
PATHOPHYSIOLOGY • Trauma, snake envenomation, or malignant
expected for each 1 mEq/L decrease in plasma
• Metabolic acidosis may develop either from hyperthermia—rhabdomyolysis.
HCO3 . Little known about compensation in
a loss of HCO3 (hyperchloremic acidosis) or
cats, but appears to be almost nonexistent.
a gain in acid (high anion gap [AG] acidosis).
• Renal/urologic—kidneys increase net acid
It is usually secondary to an accumulation of
excretion, primarily by increasing excretion of
metabolically produced strong anions (strong
ion gap or high anion gap acidosis), accumu-
NH4+ and Cl–. This compensatory mecha- DIAGNOSIS
nism not very effective in cats.
lation of weak acids (hyperphosphatemia), DIFFERENTIAL DIAGNOSIS
corrected hyperchloremia (hyperchloremic SIGNALMENT Low plasma HCO3 and hyperchloremia may
acidosis), or as a compensatory mechanism Any breed, age, or sex of dog and cat. also be compensatory in animals with chronic
for respiratory alkalosis. SIGNS respiratory alkalosis, in which PCO2 is low
• High anion gap acidosis—increase in the and pH is high or near normal, despite
concentration of other strong anions through Historical Findings decreased HCO3 and increase in Cl– concen-
addition (e.g., ethylene glycol toxicity), excessive Chronic disease processes that lead to tration. Blood gas determination is required
production (e.g., lactate produced by prolonged metabolic acidosis (e.g., renal failure, diabetes to differentiate.
anaerobic metabolism), or renal retention (e.g., mellitus, and hypoadrenocorticism), acute
circulatory shock (hemorrhagic), exposure to LABORATORY FINDINGS
renal failure) of strong anions other than Cl–
causes metabolic acidosis without increasing toxins (e.g., ethylene glycol, salicylate, and Drugs That May Alter Laboratory Results
Cl– concentration (so-called normochloremic or paraldehyde), diarrhea, administration of Potassium bromide measured as Cl– in most
high AG metabolic acidosis). carbonic anhydrase inhibitors (e.g., acetazola- analyzers; administration artificially decreases
• Hyperphosphatemic acidosis—increase in mide and dichlorphenamide). AG.
plasma weak acids (e.g., inorganic phosphate) PHYSICAL EXAMINATION FINDINGS Disorders That May Alter Laboratory
is associated with metabolic acidosis and • Generally relate to underlying disease.
Results
increased AG. At a pH of 7.4, a 1 mg/dL • Depression, stupor, seizures, and/or
• Too much heparin (>10% of sample)
increase in phosphate concentration is generalized muscle weakness in severely decreases HCO3 .
associated with a 0.58 mEq/L decrease in acidotic patients. • Blood samples stored at room temperature
HCO3 and a 0.58 mEq/L increase in AG. • Tachypnea in some patients results from
for >15 minutes have low pH because of
Hyperphosphatemia commonly develops with compensatory increase in ventilation. increased PCO2.
decreased renal phosphorus excretion (e.g., • Kussmaul’s respiration, typically seen in
• Hypoalbuminemia lowers AG; negative
renal failure, hypoparathyroidism), cellular human beings with metabolic acidosis, not charges of albumin are main component of
lysis (e.g., tumor lysis syndrome, trauma, commonly observed in dogs and cats. AG.
rhabdomyolysis), bone neoplasms (increased • Vomiting and/or diarrhea.
bone resorption), and hypervitaminosis D. Valid if Run in Human Laboratory?
CAUSES Yes
• Hyperchloremic acidosis—may be caused by
Cl– retention (e.g., renal failure, renal tubular Associated with Hyperchloremia
CBC/BIOCHEMISTRY/URINALYSIS
acidosis) that typically occurs in response to (Hyperchloremic Metabolic Acidosis) • Low total CO2—total CO2 in serum
HCO3 loss. Cl– and HCO3 are reciprocally • Renal—renal tubular acidosis; carbonic samples handled aerobically closely approxi-
related; loss of HCO3 generally results in anhydrase inhibitors. mates serum HCO3 concentration;
retention of Cl–. Other mechanisms for hyper- • Gastrointestinal—diarrhea. unfortunately, patients with chronic
chloremic acidosis include excessive loss of Na+ • Other: Cl–-rich fluids (e.g., 0.9% NaCl, KCl respiratory alkalosis also have low total CO2,
relative to Cl– (e.g., diarrhea, Addison’s) and supplementation); total parenteral nutrition and distinction cannot be made without
administration of substances containing more with cationic amino acids: lysine, arginine, blood gas analysis.
Cl– than Na+ compared with normal extracel- and histidine; rapid correction of hypocapnia • Metabolic acidoses traditionally divided
lular fluid composition (e.g., administration of (chronic respiratory alkalosis); NH4Cl or HCl. into hyperchloremic and high AG by means
KCl, 0.9% NaCl). Acidemia is usually not Associated with Normochloremia (High of AG. Anion gap, the difference between the
severe in patients with hyperchloremic acidosis. measured cations and the measured anions, is
Anion Gap Metabolic Acidosis)
SYSTEMS AFFECTED • Renal—uremic acidosis, acute renal failure. calculated as AG = [Na+] – ( HCO3 + [Cl–])
• Cardiovascular—fall in pH results in increase • Ketoacidosis—diabetic ketoacidosis, or AG = ([Na+] + [K+]) – ( HCO3 + [Cl–]),
in sympathetic discharge, but simultaneously starvation, liver disease. depending on preference of clinician or
causes decrease in responsiveness of cardiac • Lactic acidosis—impaired perfusion, laboratory. Normal values with potassium
myocytes and vascular smooth muscle to impaired carbohydrate metabolism. included in calculation usually 12–24 mEq/L
(continued) Acidosis, Metabolic A
in dogs and 13–27 mEq/L in cats. Negative affinity of hemoglobin for oxygen, paradoxi-
charges of albumin are major contributors to cal CNS acidosis, overshoot metabolic
normal AG; this should be taken into account alkalosis, hypokalemia.
when evaluating AG in patients with hypo- • Hyperchloremic acidosis—NaHCO3 MISCELLANEOUS
albuminemia. At pH 7.4 in dogs, decrease may be effective and considered whenever ASSOCIATED CONDITIONS
of 1 g/dL in albumin associated with decrease pH <7.1. • Hyperkalemia.
of 4.1 mEq/L in AG. • Uremic acidosis—efficacy of NaHCO3 in • Hyperchloremia.
• Normal AG (i.e., hyperchloremic metabolic acute therapy of uremic acidosis is related to
AGE-RELATED FACTORS
acidosis). shift of phosphate inside cells and consequent
None
• High AG (i.e., normochloremic metabolic amelioration of hyperphosphatemic acidosis.
acidosis). • Lactic acidosis—NaHCO3 increases lactate PREGNANCY/FERTILITY/BREEDING
• Hyperglycemia. production and is of little to no value in lactic N/A
• Azotemia. acidosis. Therapy should be directed at SYNONYMS
• Hyperphosphatemia. augmenting oxygen delivery to tissues and • Dilutional acidosis—metabolic acidosis
• High lactate concentration. reestablishing cardiac output. Small titrated resulting from increased free water in plasma.
• Hyperkalemia (formulas to adjust potassium doses of NaHCO3 can be used as temporizing • Hyperchloremic acidosis—normal anion
concentration based on pH changes should not measure to maintain HCO3 above 5 mEq/L, gap acidosis.
be used). if needed. • Hyperphosphatemic acidosis—metabolic
• Diabetic ketoacidosis—NaHCO3 adversely acidosis resulting from high phosphate
OTHER LABORATORY TESTS
affects outcome in humans with diabetic concentration.
Blood gas analysis reveals low HCO3 , low
ketoacidosis even when pH is <7.0. • Nonrespiratory acidosis.
PCO2, and low pH.
Administration of NaHCO3 to ketoacidotic • Normochloremic acidosis—high anion gap
DIAGNOSTIC PROCEDURES patients cannot be recommended at any pH. acidosis.
None Therapy should be direct at insulin and fluid • Organic acidosis—metabolic acidosis
TREATMENT administration. Reestablishing plasma volume resulting from accumulation of organic
• Acid-base disturbances are secondary and renal perfusion will allow kidneys to anions (e.g., ketoacidosis, uremic acidosis,
phenomena; successful resolution depends on excrete ketoanions, replacing them with Cl–. and lactic acidosis).
diagnosis and treatment of underlying disease CONTRAINDICATIONS SEE ALSO
process. • Avoid NaHCO3 in patients with respiratory • Azotemia and Uremia.
• Restore blood volume and perfusion deficits acidosis because it generates CO2. • Diabetes Mellitus With Ketoacidosis.
before considering sodium bicarbonate • Patients with respiratory acidosis cannot • Hyperchloremia.
(NaHCO3). adequately excrete CO2, and increased PCO2 • Hyperkalemia.
• Treat patients with blood pH ≤7.1 will further decrease pH. • Hyperphosphatemia.
aggressively while pursuing definitive • Avoid diuretics that act in distal nephron • Lactic Acidosis (Hyperlactatemia).
diagnosis. (e.g., spironolactone).
• Discontinue drugs that may cause • Avoid carbonic anhydrase inhibitors (e.g., ABBREVIATIONS
metabolic acidosis. acetazolamide, dichlorphenamide). • AG= anion gap.
• Nursing care—isotonic, buffered electrolyte • Avoid NaHCO3 in acute (<10 mins) cardiac • BE = base excess.
solution is fluid of choice for patients with arrest as it may impair tissue oxygen unloading. • H+ = hydrogen ion.
mild metabolic acidosis and normal liver • HCO3 = bicarbonate.
function. PRECAUTIONS • NaHCO3 = sodium bicarbonate.
Use NaHCO3 cautiously in patients with • PCO2 = carbon dioxide tension.
congestive heart failure because Na+ load may
cause decompensation of heart failure.
Suggested Reading
de Morais HA, Constable PD. Strong ion
POSSIBLE INTERACTIONS approach to acid-base disorders. In:
MEDICATIONS None DiBartola SP, ed., Fluid, Electrolyte and
DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) Acid-Base Disorders, 4th ed. St. Louis, MO:
• NaHCO3 may help patients with hyper None Saunders, 2012, pp. 316–330.
chloremic, hyperhosphatemic, or uremic de Morais HA, Leisewitz AL. Mixed acid-base
acidosis, but not patients with lactic acidosis disorders. In: DiBartola SP, ed., Fluid,
or diabetic ketoacidosis. Electrolyte and Acid-Base Disorders, 4th ed.
• NaHCO3 may be considered for alkaline St. Louis, MO: Saunders, 2012, pp. 302–315.
diuresis in salicylate toxicity. ° Estimation of FOLLOW-UP DiBartola SP. Metabolic acid-base disorders.
HCO3 dose—dogs, 0.3 × body weight (kg) In: DiBartola SP, ed., Fluid, Electrolyte and
PATIENT MONITORING
× (21 – patient HCO3 ); cats, 0.3 × body Acid-Base Disorders, 4th ed. St. Louis, MO:
Recheck acid-base status; frequency dictated
weight (kg) × (19 – patient HCO3 ). Give Saunders, 2012, pp. 271–280.
by underlying disease and patient response to
half of this dose slowly IV and reevaluate Hopper K. Traditional acid-base analysis. In:
treatment.
blood gases before deciding on need for Silverstein DC, Hopper K, eds., Small
additional administration. Empirical dose of POSSIBLE COMPLICATIONS Animal Critical Care Medicine, 2nd ed. St.
1–2 mEq/kg followed by reevaluation of • Hyperkalemia in acute hyperchloremic Louis, MO: Elsevier, 2015, pp. 289–299.
blood gas status is safe in most patients. acidosis. Author Helio S. Autran de Morais
° Potential complications of NaHCO3 • Myocardial depression and ventricular Consulting Editor J.D. Foster
administration—volume overload resulting arrhythmias. Acknowledgment The author and book
from administered Na+, tetany from low editor acknowledge the prior contribution of
ionized calcium concentration, increased Lee E. Palmer.
A Acne—Cats
(bacterial, yeast, or dermatophytes), or to • Severe cases may warrant treatment with
diagnose neoplasia. isotretinoin (Accutane) or cyclosporine,
PATHOLOGIC FINDINGS modified (Atopica®).
BASICS • Demodicosis—isoxazoline parasiticides.
• Mild disease—follicular distention with
OVERVIEW keratin (comedo), hyperkeratosis, and CONTRAINDICATIONS/POSSIBLE
• Inflammatory dermatitis affecting the chin follicular plugging, most often associated INTERACTIONS
and lips. with allergic dermatitis. • Benzoyl peroxide and salicylic acids—can
• Symptoms may be recurrent or persistent. • Severe disease—mild to severe folliculitis be irritating.
SIGNALMENT and perifolliculitis with follicular pustule • Some wipes contain alcohols that can be
• Cats. formation leading to furunculosis and irritating.
• Prevalence for sex, age, or breed not pyogranulomatous dermatitis. • Systemic isotretinoin—use with caution, if
reported. • Bacteria and Malassezia in these lesions are animal will not allow application of topical
considered secondary invaders and not medications; potential deleterious side effects
SIGNS
causative agents. in human beings (drug interactions and
• Cats may have a single episode, a life-long
• Demodex mites can be primary agents of teratogenicity); container should be labeled
recurrent problem, or a continual disease.
this disease. for animal use only and kept separate from
• Frequency and severity of each occurrence
vary with the individual. human medications to avoid accidental use;
• Comedones, mild erythematous papules, currently difficult to obtain for animal
serous crusts, and dark keratin debris develop patients.
on the chin and less commonly on the lips. TREATMENT
• Swelling of the chin. • Initial treatment—gentle clipping and
• Severe cases—nodules, hemorrhagic crusts, soakings to soften crusts.
pustules, cysts, fistulae, severe erythema, • Food elimination diet. FOLLOW-UP
alopecia, and pain. • Intradermal allergy testing. • Monitor for relapses.
• Pain often associated with bacterial • Continue one or a combination of the • Maintenance cleansing programs can be
furunculosis. therapies listed below until all lesions have used to reduce relapses; affected cats are likely
CAUSES & RISK FACTORS resolved. to have variable numbers of comedones
• Discontinue treatment by tapering life-long, which often are just cosmetic, and
Precise etiology unknown; often is associated
with allergic skin diseases; may be a disorder medication over a 2- to 3-week period. treatment is not necessary.
• Recurrent episodes—once the recurrence
of keratinization, poor grooming, abnormal
sebum production, immunosuppression, viral rate is determined, an appropriate maintenance
infection, or stress. protocol can be designed for each individual.
• Continual episodes—life-long maintenance
treatment necessary. MISCELLANEOUS
PREGNANCY/FERTILITY/BREEDING
Systemic isotretinoin should not be used on
DIAGNOSIS breeding animals.
DIFFERENTIAL DIAGNOSIS MEDICATIONS Suggested Reading
• Hypersensitivity (atopy, flea bite, food, Jazic E, Coyner KS, Loeffler DG, Lewis TP.
contact). DRUG(S) OF CHOICE
An evaluation of the clinical, cytological,
• Bacterial folliculitis. Topical infectious and histopathological features of
• Demodicosis. • Shampoo—once or twice weekly with feline acne. Vet Dermatol 2006,
• Malassezia infection. antiseborrheic (sulfur-salicylic acid, benzoyl 17(2):134–140.
• Dermatophytosis. peroxide, or ethyl lactate). Miller WH, Griffin CE, Campbell KL. Acne.
• Neoplasia of sebaceous or apocrine glands. • Cleansing agents—benzoyl peroxide, salicylic In: Muller & Kirk’s Small Animal
• Eosinophilic granuloma. acid, chlorhexidinephytosphingosine. Dermatology, 7th ed. St. Louis, MO:
• Medicated wipes. Elsevier, 2013, pp. 640–642.
• Antibiotic ointment—mupirocin 2%. Rosencrantz WS. The pathogenesis,
N/A
• Other topicals—clindamycin or erythro diagnosis, and management of feline acne.
OTHER LABORATORY TESTS mycin solution or ointment. Vet Med 1993, 5:504–512.
N/A • Combination topicals—benzoyl peroxide- Werner AH, Power HT. Retinoids in
IMAGING antibiotic gels (e.g., Benzamycin). veterinary dermatology. Clin Dermatol
N/A • Topical retinoids—tretinoin (e.g., Retin-A® 1994, 12(4):579–586.
0.01%): gel more effective because of better White SD. Feline acne and results of
DIAGNOSTIC PROCEDURES penetration.
• Skin scrapings—demodicosis.
treatment with mupirocin in an open
• In severe inflammatory periods 10–14 days clinical trial: 25 cases (1994–96). Vet
• Bacterial culture—resistant infection. of oral prednisolone (1–2 mg/kg q24h) may
• Fungal culture—dermatophytosis.
Dermatol 1997, 8:157.
help to reduce scar tissue formation. Author David D. Duclos
• Cytology—bacteria, Malassezia.
• Biopsy—rarely needed; necessary in Systemic Consulting Editor Alexander H. Werner
selected cases to characterize changes such as • Antibiotics—amoxicillin with clavulanate, Resnick
cystic follicles, to differentiate acne from cephalosporin, or fluoroquinolone.
other diseases such as demodicosis, infections
Acne—Dogs A
IMAGING • Gentamicin/steroid-containing ointments

N/A for the ears can be applied to localized lesions
DIAGNOSTIC PROCEDURES twice daily; most useful for lesions on the
BASICS chin, as the pet cannot lick this area. Constant
• Impression cytology will help determine if
OVERVIEW bacteria or yeast are present. long-term use over months may cause alopecia
• Also (more correctly) muzzle folliculitis and • Skin scrape—demodicosis.
and cutaneous atrophy: limit frequency and
furunculosis. • Dermatophyte culture—dermatophytosis.
duration of application.
• Chronic inflammatory disorder of the chin • Bacterial culture and sensitivity testing—in Systemic
and lips of mostly young animals. patients with suppurative folliculitis and • Antibiotics based on culture and sensitiv-
• Characterized by folliculitis and furunculo- furunculosis that are nonresponsive to initial ity—when indicated (e.g., cephalexin,
sis; almost never comedogenic as seen in “true antibiotic selection. 22–30 mg/kg PO q12h for 2–4 weeks).
acneiform” lesions of human beings. • Biopsy—histologic confirmation for cases • Oral corticosteroids: tapering dosages of
• Recognized almost exclusively in short- in which diagnosis is in question. prednisolone (initial 0.5 mg/kg/day) to
coated breeds. reduce significant inflammation; not for
• Genetic predisposition, local trauma, and PATHOLOGIC FINDINGS
• Clinical signs and histopathologic findings
continued use.
allergic disease often play a role. • Evaluate for and manage concurrent
are diagnostic.
SIGNALMENT • Characterized histopathologically by
allergic/atopic skin disease.
• Dogs, often younger, sometimes puppies. folliculitis and furunculosis. CONTRAINDICATIONS/POSSIBLE
• Predisposed short-coated breeds—boxer, • Bacteria—not always isolated from lesions INTERACTIONS
Doberman pinscher, English bulldog, Great in early stages. • Topical steroids—may cause adrenal
Dane, Weimaraner, mastiff, Rottweiler, • As disease progresses, papules enlarge and suppression and thinning of skin with
German shorthaired pointer, pit bull terrier. rupture, promoting a suppurative folliculitis frequent or constant use.
SIGNS and furunculosis.
• Ventral chin and lip margins may have few
to numerous erythematous papules and
sometimes bullae. These may coalesce to form
plaques. FOLLOW-UP
TREATMENT
• Initial lesions are inflammatory and sterile; • Reduce behavioral trauma to the chin (e.g.,
PATIENT MONITORING
bacteria may not be isolated and lesions may • Continue antibiotics until lesions have
rubbing on the carpet, chewing bones that
not respond to antibiotics. increase salivation). healed.
• Advanced lesions may contain pus or blood, • Repeat bacterial culture/sensitivity if lesions
• Frequent cleaning with chlorhexidine-
indicating secondary deep bacterial folliculitis containing pads, shampoos, or solutions can worsen.
and furunculosis. • Discontinue topical corticosteroids when
be helpful, but instruct owners not to scrub at
• Lesions may be pruritic, some are painful the area. possible.
on palpation, but most are nonpainful and • Gentamicin/steroid-containing ointments EXPECTED COURSE AND PROGNOSIS
nonpruritic. for the ears work well on the chin when • Long-term topical treatment may be
• Chronic and pruritic lesions may become applied twice daily. required.
hyperpigmented, lichenified, scarred, and • If topicals are not helpful by themselves, • Chronic scarring may be prevented by early
alopecic. add oral antibiotics based on positive cytology and aggressive therapy.
CAUSES & RISK FACTORS and culture and sensitivity testing.
Several short-coated breeds appear to be • Severe cases may necessitate short courses of
genetically predisposed to acne. Lesions may oral steroids.
be worse in allergic individuals. • Evaluate for underlying allergic/atopic
disease and institute proper therapy for
MISCELLANEOUS
diagnosis and control of these diseases; control ASSOCIATED CONDITIONS
of allergic disease may permit resolution of Allergic/atopic disease may cause and
muzzle folliculitis and furunculosis. exacerbate this condition.
DIAGNOSIS • Instruct owners to avoid squeezing the Suggested Reading
DIFFERENTIAL DIAGNOSIS lesions; trauma may make inflammation Miller WH, Griffin CE, Campbell KL.
• Dermatophytosis. worse. Muzzle folliculitis and furunculosis. In:
• Demodicosis. Muller & Kirk’s Small Animal Dermatology,
• Juvenile cellulitis. 7th ed. St. Louis, MO: Elsevier, 2013, pp.
• Contact dermatitis. 201, 640.
• With other symptoms, consider allergic/
atopic disease as playing a role. MEDICATIONS Author Melissa N.C. Eisenschenk
Consulting Editor Alexander H. Werner
CBC/BIOCHEMISTRY/URINALYSIS DRUG(S) Resnick
N/A Topical Acknowledgment The author and editors
OTHER LABORATORY TESTS • Daily cleaning with chlorhexidine-containing acknowledge the prior contribution of Karen
N/A pads, shampoos, or solutions can be helpful; Helton Rhodes.
instruct owners not to scrub at the areas.
A Acral Lick Dermatitis
• Bacterial culture and sensitivity—tissue • Combine/withdraw administration of these
cultures may differ from surface culture. medications carefully.
• Food elimination diet—determine food
BASICS Topical
allergy. Pruritus—flunixin meglumine and fluo-
OVERVIEW • Intradermal allergy testing—atopy. cinolone in dimethyl sulfoxide (combined),
• Compulsion to lick limb/s resulting in • Biopsy—to rule out neoplasia, other topical capsaicin products; intralesional
plaque formation. infections. corticosteroids rarely helpful; wear gloves
• Skin/exocrine affected. • Behavioral history (additional behavioral when applying; prevent licking of area for
signs typical). 10–15 minutes.
SIGNALMENT
• Neurologic and orthopedic evaluation.
• Dogs. CONTRAINDICATIONS/POSSIBLE
• Most common in large breeds—Labrador PATHOLOGIC FINDINGS
Histopathology—epidermal hyperplasia, INTERACTIONS
retrievers, Doberman pinschers, Great Danes,
• Doxepin—caution using with monoamine
Irish setters, golden retrievers, German plasmacytic dermal inflammation, folliculitis,
furunculosis, perihidradenitis, hidradenitis, oxidase inhibitors, clonidine, anticonvulsants,
shepherd dogs, boxers, and Weimaraners.
epitrichial gland dilation/rupture, vertical oral anticoagulants, steroid hormones, anti-
• Median age 4 yrs, range 1–12 yrs; no sex
streaking fibrosis. histamines, or aspirin.
predilection.
• Antihistamines—may cause sedation.
SIGNS • Psychotropic medications should be
• Excessive licking of affected area. combined and/or withdrawn carefully.
• Alopecic, eroded/ulcerated, thickened, and • Cardiotoxicity and hepatoxicity—rare cases
raised firm plaques with scabs and exudation, TREATMENT in animals on TCAs. Routine monitoring
usually located on dorsal aspect of carpus, • Rule in/out bacterial, fungal, ectoparasitic, recommended.
metacarpus, tarsus, or metatarsus. endocrine causes and treat accordingly along
• Single or multiple lesions. with pruritus control.
• If infection resolves and pruritus and/or
CAUSES & RISK FACTORS
lesions persist, consider biopsy, allergy
• Anything causing local irritation or lesion
workup, neurologic/orthopedic exam, FOLLOW-UP
may initiate lick–itch cycle. • Monitor level of licking and chewing closely.
• Associated diseases: staphylococcal
radiographs, behavioral modification.
• Treat underlying disease to prevent
• Physical restraints—to permit healing.
furunculosis, hypersensitivity, endocrinopathy, recurrence.
• Limited research to support effectiveness:
demodicosis, dermatophytosis, foreign body • If no underlying disease detected, psycho-
reaction, neoplasia, underlying joint disease radiation, acupuncture, CO2 laser, cryosurgery,
standard surgery. genic causes possible (compulsive or self-
or arthritis, trauma, neuropathy, psychogenic, mutilation disorder); prognosis is guarded.
• Difficult to treat, especially if no underlying
or sensory nerve dysfunction.
cause found; warn owner that patience and
time are necessary.
MISCELLANEOUS
DIAGNOSIS
AGE-RELATED FACTORS
DIFFERENTIAL DIAGNOSIS MEDICATIONS Dogs <5 years old—strongly consider allergy.
• Neoplasia.
• Bacterial furunculosis.
DRUG(S) OF CHOICE ZOONOTIC POTENTIAL
• Focal demodicosis. Antibiotics Dermatophytosis (rare) and methicillin-resist-
• Focal dermatophytosis. Based on bacterial culture/susceptibility. ant Staphylococcus aureus may have zoonotic
Administer until resolution of infection plus implications.
Usually normal. 2 weeks. ABBREVIATIONS
• ACTH = adrenocorticotropin hormone.
Systemic
OTHER LABORATORY TESTS • LDDST = low-dose dexamethasone
• Pruritus—antihistamines (2 weeks for
Endocrinopathy—total T4/free T4/thyroid- suppression test.
stimulating hormone (TSH); adrenocortico- response typically), e.g., hydroxyzine (2.2 mg/
kg PO q8h); chlorpheniramine (4–8 mg/dog • SSRI = selective serotonin reuptake
tropin hormone (ACTH) stimulation test or inhibitor.
low-dose dexamethasone suppression test PO q8–12h; maximum of 0.5 mg/kg q12h);
amitriptyline (1–2 mg/kg PO q12h), also • TCA = tricyclic antidepressant.
(LDDST). • TSH = thyroid-stimulating hormone.
tricyclic antidepressant (TCA); corticoster-
IMAGING oids, e.g., prednisolone 1 mg/kg PO q24h Suggested Reading
Radiology (entire limb +/– neck/lumbar and taper based on response (or other steroid Shumaker AK. Diagnosis and treatment of
region)—neoplasia; local trauma; radiopaque equivalent). canine acral lick dermatitis. Vet Clin North
foreign bodies; bony proliferation may be • Behavioral—selective serotonin reuptake Am Small Anim Pract. 2019, 49:105–123.
seen secondary to chronic irritation; evidence inhibitors (SSRIs), e.g., fluoxetine (1 mg/kg Author Heather D. Edginton
of underlying arthritis if over a joint. PO q24h); TCAs, e.g., amitriptyline Consulting Editor Alexander H. Werner
DIAGNOSTIC PROCEDURES (1–2 mg/kg PO q12h, also antihistamine); Resnick
• Skin scrapings—demodicosis. doxepin (3–5 mg/kg PO q12h; maximum Acknowledgment The author acknowledges
• Dermatophyte PCR and/or culture—fungal 150 mg q12h); clomipramine (2–4 mg/kg the prior contribution of Alexander H.
infection. PO q24h); dopamine antagonists, e.g., Werner Resnick.
• Epidermal cytology—bacterial infection. naltrexone (2.2 mg/kg PO q24h).
Actinomycosis and Nocardia A
• Nonregenerative anemia.
• Leukocytosis with a left shift and mono-
BASICS cytosis. MEDICATIONS
OVERVIEW • Hyperglobulinemia. DRUG(S) OF CHOICE
• Opportunistic bacterial infections caused • Ionized hypercalcemia (nocardiosis). • Important to distinguish between
by branching Gram-positive bacteria that OTHER LABORATORY TESTS Actinomyces and Nocardia for appropriate
cause clinically similar suppurative-to- N/A antimicrobial selection.
granulomatous inflammation: • Antibiotics—protracted course of therapy
◦ Actinomyces spp. (anaerobic-to- IMAGING (weeks to months) usually required; continue
microaerophilic, normal flora of mucous • Dependent on systems affected. for several weeks after resolution of all signs.
membranes, gastrointestinal and urogenital • Thoracic radiographs—alveolar and • Actinomycosis—penicillins considered drug
tracts). interstitial lung pattern with possible alveolar of choice; amoxicillin: 20–40 mg/kg PO q8h.
◦ Nocardia spp. (aerobic soil saprophytes). disease, pleural effusion (pyothorax), peri- • Nocardiosis—potentiated sulfonamides at
• Organ systems affected may include: cardial effusion, subcutaneous masses. 15–30 mg/kg PO q12h are usually first choice.
◦ Skin and subcutaneous. • Abdominal radiographs—peritoneal
effusion, abdominal mass effect. CONTRAINDICATIONS/POSSIBLE
◦ Respiratory.
◦ Cardiovascular. • Radiographs of infected bone—periosteal INTERACTIONS
◦ Musculoskeletal. new bone, reactive osteosclerosis, osteolysis. • Dogs can develop toxic or hypersensitivity
◦ Nervous. adverse reactions to sulfonamides.
◦ Disseminated (Nocardia). • Metronidazole and aminoglycosides are
• Gram staining, cytology, and acid-fast
ineffective against Actinomyces spp.
SIGNALMENT staining are helpful, but do not preclude the
• Dogs and cats (uncommon). need for culture; acid-fast stain—Actinomyces
• Dogs with outdoor access (Actinomyces); negative, Nocardia variable; sulfur granules
young dogs (Nocardia); male cats (both). suggest Actinomyces.
• Exudates or osteolytic bone fragments FOLLOW-UP
SIGNS submitted in aerobic and anaerobic
• Depends on whether infection is localized PATIENT MONITORING
specimen containers for culture can provide Monitor closely for recurrence after therapy
or disseminated (Nocardia) and on organ a definitive diagnosis (see Anaerobic
systems involved. discontinued.
Infections).
• Cutaneous and subcutaneous swellings • Nocardia may require speciation if not PREVENTION/AVOIDANCE
(cervicofacial—Actinomyces), abscesses, or responding to empiric therapy. Avoid areas with grass awns; prevent bites and
nonhealing wounds with draining tracts; scratches.
localized draining cutaneous lesions are PATHOLOGIC FINDINGS
Histopathologic examination— POSSIBLE COMPLICATIONS
common in cats. Difficult to fully clear infection.
• Poor body condition, pain, fever, weight loss. pyogranulomatous or granulomatous cellulitis
• Exudative pleural or peritoneal effusions. with colonies of filamentous bacteria; special EXPECTED COURSE AND PROGNOSIS
• Cough, dyspnea, decreased ventral lung stains may enhance visualization. Sulfur • Redevelopment of infection after discontinu-
sounds (empyema). granules are a useful diagnostic tool, but can ation of antibiotics is possible.
• Lameness due to osteomyelitis. be difficult to find. • Actinomyces—up to 90% cure reported in
• Motor and sensory deficits. dogs after appropriate therapy.
• Retroperitonitis (Actinomyces)—lumbar • Nocardia—up to 50% mortality reported.
pain, rear limb paresis or paralysis.
CAUSES & RISK FACTORS TREATMENT
Scratches and bite wounds, traumatic • Prolonged antimicrobial therapy is
inoculation, foreign body migration (e.g., required. MISCELLANEOUS
grass awn), immunosuppression (Nocardia). • Surgical debridement or excision of infected
AGE-RELATED FACTORS
tissue (e.g., lung lobe, body wall mass) may
Young outdoor dogs.
improve outcome.
• Exudative fluid (thorax, abdomen, subcut ZOONOTIC POTENTIAL
aneous tissue) should be drained and the No reports of humans being infected by
DIAGNOSIS infected cavity lavaged. either organism through direct contact. Bite
DIFFERENTIAL DIAGNOSIS • A thoracostomy tube with intermittent or and scratch wounds can cause human disease.
• Actinomyces and Nocardia appear similar continuous drainage is usually needed for cats SEE ALSO
and are not reliably distinguished by Gram with pyothorax; dogs may benefit from Anaerobic Infections.
staining, cytology, or clinical signs. surgical exploration of thorax prior to
Actinomyces is usually accompanied by thoracostomy tube placement to attempt Suggested Reading
foreign body removal. Sykes JE. Actinomycosis and nocardiosis. In:
multiple other coinfective bacteria.
Greene CE, ed., Infectious Diseases of the
• Other causes of similar clinical signs must
Dog and Cat, 4th ed. St. Louis, MO:
be considered, including other bacterial or
Saunders Elsevier, 2011, pp. 484–495.
fungal infections, neoplasia, and other
Author Sharon Fooshee Grace
diseases that cause effusions.
Consulting Editor Amie Koenig
A Acute Abdomen
Predominant Sex Urinary Tract
Male cats and dogs are at higher risk for • Distention is main cause of pain in urinary
urethral obstruction. tract.
BASICS • Obstruction due to tumors of trigone area
SIGNS
DEFINITION of bladder or urethra, urinary calculi, or
An emergency condition characterized by General Comments granulomatous urethritis.
historical and physical examination findings Clinical signs vary greatly, depending on type • Traumatic rupture of ureters or bladder.
of a tense, painful abdomen. May represent a and severity of underlying disease. • Urethral tear associated with pelvic fractures
life-threatening condition. Historical Findings from acute trauma.
• Trembling, reluctance to move, inappetence, • Uroabdomen leads to chemical peritonitis.
PATHOPHYSIOLOGY • Acute pyelonephritis, acute kidney injury,
• An affected patient has pain associated with vomiting, diarrhea, vocalizing, and abnormal
postures (tucked up or praying position). nephroliths, and ureteroliths are uncommon
either distention of an organ, inflammation, causes of acute abdomen.
traction on the mesentery or peritoneum, or • Question owner carefully to ascertain what
ischemia. system is affected; for example, melena with a Genital Tract
• Abdominal viscera are sparsely innervated, history of nonsteroidal anti-inflammatory • Prostatitis and prostatic abscess, pyometra;
and diffuse involvement is often necessary to drug (NSAID) treatment may suggest GI a ruptured pyometra or prostatic abscess can
elicit pain; nerve endings also exist in the mucosal ulceration. cause endotoxemia, sepsis, and cardiovascular
submucosa-muscularis of the intestinal wall. Physical Examination Findings collapse.
• Inflammation produces abdominal pain by • Abdominal pain, splinting of abdominal • Uncommon—rupture of gravid uterus after
releasing vasoactive substances that directly musculature, gas- or fluid-filled abdominal blunt abdominal trauma, uterine torsion,
stimulate nerve endings. organs, abdominal mass, ascites, pyrexia or ovarian tumor or torsion, and intra-
hypothermia, tachycardia, and tachypnea. abdominal testicular torsion (cryptorchid).
SYSTEMS AFFECTED
• Behavioral—trembling, inappetence, vocalizing, • Pain may be localizable to cranial, middle, Abdominal Wall/Diaphragm
lethargy, and abnormal postural changes such as or caudal abdomen. • Umbilical, inguinal, scrotal, abdominal,
the praying position to achieve comfort. • Perform rectal examination to evaluate or peritoneal hernia with strangulated
• Cardiovascular—ischemia, severe inflamm colon, pelvic bones, urethra, and prostate, as viscera.
ation, systemic inflammatory response well as for presence of melena. • Organ displacement or entrapment in
syndrome and sepsis may lead to shock. • Rule out extra-abdominal causes of pain by hernia will lead to abdominal pain if vascular
Tachycardia or other arrhythmia may affect careful palpation of kidneys and thoracolumbar supply of organ(s) involved becomes impaired
capillary refill time and mucous membrane vertebrae. or ischemic.
color. Pain may cause arrhythmias. • Pain associated with intervertebral disc
disease often causes referred abdominal RISK FACTORS
• Gastrointestinal (GI)—vomiting, diarrhea, • Exposure to NSAIDs or corticosteroid treat-
inappetence, generalized functional ileus; guarding and may be mistaken for true
abdominal pain. Renal pain can be associated ment (increased risk when used concurrently)—
pancreatic inflammation, necrosis, and gastric, duodenal, or colonic ulcers.
abscesses may lead to cranial abdominal pain, with pyelonephritis.
• Garbage or fatty food ingestion—pancreatitis.
vomiting, and ileus. CAUSES • Foreign body ingestion—intestinal
• Hepatobiliary—jaundice associated with obstruction.
GI
cholestasis from biliary obstruction (including • Stomach—gastritis, ulceration, perforation, • Abdominal trauma—hollow viscus rupture.
pancreatitis) or bile peritonitis. Hyperbili foreign body, gastric dilatation-volvulus. • Hernia—intestinal obstruction/strangulation.
rubinemia may occur secondary to sepsis. • Intestine—obstruction (foreign body,
• Renal/urologic—azotemia due to prerenal
intussusception, mass, etc.), enteritis, ulcer-
(dehydration, hypovolemia, and shock), renal ation, perforation.
(acute pyelonephritis and acute kidney injury), • Rupture after obstruction, ulceration, or
and postrenal causes (ureteral obstruction, DIAGNOSIS
blunt or penetrating trauma, or due to tumor
urethral obstruction, and uroperitoneum growth. DIFFERENTIAL DIAGNOSIS
from bladder rupture). • Vascular compromise from infarction, • Renal-associated pain, retroperitoneal pain,
• Respiratory—increased respiratory rate due spinal or paraspinal pain, and disorders
mesenteric volvulus, or torsion.
to pain or metabolic/acid-base disturbances. causing diffuse muscle pain may mimic
Pancreas abdominal pain; careful history and physical
SIGNALMENT • Inflammation, abscess, ischemia. examination are essential in pursuing the
Species • Mass or inflammation obstructing common appropriate problem.
• Dogs and cats. bile duct may cause jaundice. • Parvoviral enteritis can present similarly to
• Dogs more commonly; often challenging to intestinal obstructive disease; fecal parvoviral
Hepatic and Biliary System
identify abdominal pain in feline patients. • Acute hepatitis—rapid distention of the antigen assay and CBC (leukopenia) are
Breed Predilections liver and its capsule can cause pain. helpful differentiating diagnostic tests.
• Male Dalmatians have a higher risk of • Biliary obstruction, rupture, or necrosis CBC/BIOCHEMISTRY/URINALYSIS
urethral obstruction because of the high may lead to bile leakage and peritonitis. • Inflammation or infection may be
incidence of urate urolithiasis. • Gallbladder mucocele. associated with leukocytosis or leukopenia.
• German shepherds with pancreatic atrophy • Hepatic abscess. • Active inflammation may be characterized
have a higher risk of mesenteric volvulus. Spleen by a neutrophilic left shift.
Mean Age and Range Torsion, mass, thrombus, abscess. • Anemia may be seen with blood loss
Any associated with GI ulceration.
(continued) Acute Abdomen A
• Azotemia is associated with prerenal, renal, DIAGNOSTIC PROCEDURES vention with surgery is important when
and postrenal causes. Abdominocentesis/Abdominal Fluid indicated.
• Electrolyte abnormalities can help to • Aggressive therapy and prompt identification
evaluate GI disease (i.e., hypochloremic Analysis of underlying cause are very important.
metabolic alkalosis with gastric outflow • Perform abdominocentesis on all patients • Many causes of acute abdominal pain
obstruction) and renal disease (i.e., hyper presenting with acute abdomen. Four- require emergency surgical intervention.
kalemia with acute kidney injury or postrenal quadrant approach may improve yield. Fluid
can often be obtained for diagnostic evalu NURSING CARE
obstruction). • Keep patient NPO if vomiting, until a
• Hyperbilirubinemia and increased hepatic ation, even when only a small amount of free
abdominal fluid exists, well before detectable definitive cause is determined and addressed.
enzyme activity help localize a problem to • Intravenous fluid therapy usually required
liver or biliary system. radiographically. Ultrasound is much more
sensitive than radiography for detection of because of large fluid loss associated with
• Urine specific gravity (before fluid therapy) acute abdomen; goal is to restore normal
is needed to help differentiate prerenal, renal, fluid and can be used to direct
abdominocentesis. Blind abdominocentesis circulating blood volume.
and postrenal azotemia. • If shock exists, supplement initially with
• Urine sediment may be helpful in acute can be performed safely without ultrasound
guidance. Abdominal fluid analysis with isotonic crystalloid fluids (up to 90 mL/kg,
kidney injury, ethylene glycol intoxication, dogs; 70 mL/kg, cats) to restore volume;
and pyelonephritis. elevated white blood cell (WBC) count,
degenerate neutrophils, and intracellular hypertonic fluids or colloids may also be
OTHER LABORATORY TESTS bacteria is consistent with septic peritonitis beneficial if refractory to isotonic crystalloids
• Venous blood gas analysis including lactate and is an indication for immediate surgery. or hypoproteinemic.
concentration may indicate acid-base • Diagnostic peritoneal lavage can be performed • Evaluate hydration and electrolytes (with
abnormalities, and increased lactate may be by introducing sterile saline (10–20 mL/kg) and appropriate treatment adjustments) frequently
associated with hypoperfusion. performing abdominocentesis, with or without after commencement of treatment.
• Canine and feline pancreatic lipase immuno ultrasound guidance. ACTIVITY
reactivity can be useful in evaluating • Measurement of glucose concentration in N/A
pancreatitis. abdominal effusion in comparison with
peripheral blood may aid in diagnosis of DIET
IMAGING Early nutritional support is important.
septic abdomen. A blood-to-abdominal fluid
Abdominal Radiography glucose difference of >20 mg/dL is consistent Nutritional support can be enteral (oral,
• May see abdominal mass or changes in nasoesophageal, esophageal tube, gastrostomy
with septic effusion.
shape or shifting of abdominal organs. • Pancreatitis patients may have abdominal
tube, enterostomy tube) or parenteral.
• Loss of abdominal detail suggests
effusion characterized as nonseptic (sterile) CLIENT EDUCATION
abdominal fluid accumulation. peritonitis. Acute abdomen may represent a life-threatening
• Free abdominal gas suggests ruptured GI
• Creatinine concentration higher in condition. Prompt diagnosis and appropriate
viscus or infection with gas-producing bacteria abdominal fluid than in serum indicates treatment essential to a favorable outcome.
and is indication for emergency surgery. urinary tract leakage.
• Use caution when interpreting radiographs SURGICAL CONSIDERATIONS
• Similarly, higher bilirubin concentration in • Many different causes of acute abdomen
following abdominocentesis with an open abdominal fluid than in serum indicates bile
needle. Free gas may be introduced with this exist; make definitive diagnosis whenever
peritonitis. possible prior to surgical intervention.
technique.
• Use caution when evaluating postoperative Sedation and Abdominal Palpation • Definitive diagnosis prior to surgery can
radiographs; free gas is a normal postoperative Because of abdominal splinting associated prevent both potentially unnecessary and
finding. with pain, thorough abdominal palpation is expensive surgical procedures and associated
• Diffuse GI distension is a consistent finding often not possible without sedation; this is morbidity and mortality.
with peritonitis. particularly useful for detecting intestinal • Also allows surgeon to prepare for task and
• Foreign bodies may be radiopaque. foreign bodies that do not appear on survey educate owner on prognosis and financial
• Upper GI barium contrast radiographs are radiographs. investment.
useful in evaluating the GI tract, particularly Exploratory Laparotomy
for determination of GI obstruction. Surgery may be useful diagnostically (as well
• Loss of contrast or radiographic detail in as therapeutically) when ultrasonography (or
the area of the pancreas can be observed with other advanced imaging) is not available, or MEDICATIONS
pancreatic inflammation. when no definitive cause of acute abdomen
DRUG(S) OF CHOICE
Abdominal Ultrasound has been established with appropriate
• A sensitive diagnostic tool for detection of diagnostics. Analgesics
GI obstruction, pancreatitis, abdominal • Pain medication may be indicated for
PATHOLOGIC FINDINGS
masses, abdominal fluid, abscesses, cysts, control of abdominal discomfort.
Varies with underlying disease.
lymphadenopathy, and biliary or urinary • Opioids are good choices.
calculi. ◦ Fentanyl—2–5 μg/kg as initial IV bolus,
• Focused Assessment with Sonography in 2–10 μg/kg/h as CRI.
Trauma (FAST) may be used for rapid ◦ Hydromorphone—0.05–0.2 mg/kg SC/
assessment. TREATMENT IM/IV q4–6h.
◦ Morphine—0.5–2 mg/kg SC/IM, q4–6h.
Abdominal CT APPROPRIATE HEALTH CARE
◦ Buprenorphine—0.01–0.02 mg/kg SC/
May provide superior information to • Inpatient management with supportive care
until decision about whether problem to be IM/IV q4–6h.
ultrasound in large patients; useful when ◦ Methadone—0.1–0.4 mg/kg SC/IM/IV
surgeon requires additional information. treated medically or surgically. Early inter-
q6h.
A Acute Abdomen (continued)
Histamine H2 Antagonists hypovolemic patients and those with renal and acquired diet- and infection-related
• Reduce gastric acid production. impairment. diseases; older animals have higher incidence
• Famotidine 0.5–1 mg/kg IV/SC/IM q12h. • NSAIDs may also cause GI of malignancies.
• Ranitidine 2 mg/kg IV q12h. complications. SYNONYMS
Proton Pump Inhibitor POSSIBLE INTERACTIONS Colic
Pantoprazole 0.5 mg/kg IV q12h or 0.05– N/A SEE ALSO
0.1 mg/kg/hr as CRI. ALTERNATIVE DRUGS • Gastric Dilation and Volvulus Syndrome.
Protectants N/A • Gastroduodenal Ulceration/Erosion.
Sucralfate 0.25–1 g PO q8h. • Gastrointestinal Obstruction.
Antiemetics • Intussusception.
• Metoclopramide 0.2–0.4 mg/kg IV q6–8h • Pancreatitis—Cats.
• Pancreatitis—Dogs.
(or 24-hour CRI at 1–2 mg/kg/24h). FOLLOW-UP • Prostatitis and Prostatic Abscess.
• Maropitant: dogs 2–4 months of age, 1 mg/
kg SC q 24h; dogs >4 months of age and cats, PATIENT MONITORING • Pyelonephritis.
1 mg/kg SC/IV q24h. Patients usually require intensive medical care • Urinary Tract Obstruction.
and frequent evaluation of vital signs and
• Ondansetron 0.2–0.5 mg/kg IV slowly ABBREVIATIONS
q6–12h. laboratory parameters.
• FAST = Focused Assessment with
Antibiotics
PREVENTION/AVOIDANCE Sonography in Trauma.
• Antibiotics may be indicated if signs of
Avoidance of indiscriminate eating may • GI = gastrointestinal.
infection are seen or hemorrhagic diarrhea prevent GI foreign body obstruction and • NSAID = nonsteroidal anti-inflammatory
is present. decrease incidence of pancreatitis. drug.
• Broad-spectrum coverage pending culture POSSIBLE COMPLICATIONS • WBC = white blood cell.
results. Varies with underlying cause. Suggested Reading
• Obtain cultures prior to treatment if EXPECTED COURSE AND Beal MW. Approach to the acute abdomen.
possible, but do not delay intervention if Vet Clin North Am Small Anim Pract 2005,
indicated. PROGNOSIS
35:375–396.
Varies with underlying cause; guarded until
CONTRAINDICATIONS Heeren V, Edwards L, Mazzaferro EM. Acute
this is determined.
• Do not use metoclopramide if GI abdomen: diagnosis. Compend Contin
obstruction is suspected. Educ Pract Vet 2004, 26:350–363.
• Do not use barium if GI perforation is Heeren V, Edwards L, Mazzaferro EM. Acute
suspected; use iodinated contrast agent instead. abdomen: treatment. Compend Contin
MISCELLANEOUS Educ Pract Vet 2004, 26:3566–3673.
PRECAUTIONS Author Steven L. Marks
• Gentamicin and NSAIDs can be AGE-RELATED FACTORS
Younger animals have higher incidence of Consulting Editor Mark P. Rondeau
nephrotoxic and should be avoided in
trauma-related problems, intussusceptions,
Acute Diarrhea A
Historical Findings
• Dietary history, dietary indiscretion,
medication/toxin history, and general
BASICS husbandry should be investigated. ◦ Special DIAGNOSIS
DEFINITION care should be taken to identify potentially DIFFERENTIAL DIAGNOSIS
Nonepisodic diarrhea of fewer than 7 days’ contagious causes of diarrhea, and isolate Unlikely to be confused with other conditions;
duration. these patients early. ◦ Patients that should be however, rarely intestinal bleeding or expulsion
isolated for further diagnostics include of liquid in constipated patient can mimic
PATHOPHYSIOLOGY unvaccinated, raw diet consumption, housing
Excess water and/or solid content of feces is acute diarrhea.
with many other cats/dogs, or multiple cats/
caused by five main mechanisms: dogs from same household affected. CBC/BIOCHEMISTRY/URINALYSIS
• Osmotic—from maldigestion, ingestion of • Extra-GI etiologies—may reflect etiology:
• Varying activity levels can be seen, from
poorly absorbable compounds, toxins. normal to lethargic. • Character of diarrhea ◦ Increased hepatic enzyme activity in
• Decreased absorption—mucosal damage hepatobiliary diseases. ◦ Increased hepatic
can help localize etiology: ◦ Small intestinal
causing loss of absorptive cells from infection, diarrhea characteristics: large volume, normal enzyme activity, hypoalbuminemia,
inflammation, or toxins. • Increased secretion frequency, concurrent weight loss and/or inflammatory leukogram in pancreatitis.
(secretory)—mediated by toxins, inflamma- vomiting. ◦ Melena, if present, points to ◦ Hypoalbuminemia, decreased Na : K ratio
tion, parasympathetic stimulation. gastric or upper small intestinal bleed. in hypoadrenocorticism. • Intra-GI causes
• Increased permeability/exudative—severe of diarrhea—often normal. • Parvoviral
◦ Steatorrhea, if present, points to maldigestive
mucosal, lacteal, and vessel damage, due to disorder like exocrine pancreatic insufficiency enteritis causes significant neutropenia.
inflammation, ulceration, or direct damage. (EPI). ◦ Large intestinal diarrhea • As result of diarrhea, following may be
• Dysmotility—increased or decreased present: ◦ Hemoconcentration. ◦ Prerenal
characteristics—small volume, increased
motility alters digestion, absorption, frequency, tenesmus, mucus, hematochezia. azotemia. ◦ Hypokalemia. ◦ Hypoalbuminemia,
secretion, and therefore water regulation. hypocholesterolemia. ◦ Hypoglycemia—toy
Physical Examination Findings breed puppies with GI signs predisposed.
SYSTEMS AFFECTED • Patients can vary from stable to unstable.
• Cardiovascular—fluid losses can be significant,
• Common findings—dehydration,
with progressive dehydration to hypovolemia. hypovolemia, abdominal pain, nausea, • Extra-GI interrogation: ◦ Baseline cortisol
• Gastrointestinal (GI)—colitis can develop or adrenocorticotropic hormone (ACTH)
fluid–gas interface on intestinal palpation,
secondary to orad causes of diarrhea. increased borborygmi. • Rectal examination stimulation test in dogs. ◦ T4 in cats.
• Immune—with enterocyte loss, the mucosal ◦ Quantitative pancreatic lipase immunore-
may reveal melena, hematochezia, steatorrhea.
barrier can be compromised, leading to trans- activity. ◦ Trypsin-like immunoreactivity if
location of GI bacteria and sepsis. • Metabolic— CAUSES EPI suspected. • Intra-GI interrogation:
electrolyte losses, especially bicarbonate and • Extra-GI causes: ◦ Common—hepatobiliary ◦ Parvovirus ELISA should be immediately
potassium. Hypokalemia is common with disease, pancreatitis, neoplasia (non-GI). performed in any suspect so isolation
concurrent hyporexia. • Vascular—albumin and ◦ Uncommon—endocrine (hypoadrenocorti- protocols may be initiated as soon as possible.
globulin losses via increased permeability can be cism, hyperthyroidism), peritonitis, sepsis. ◦ Fecal flotation, fecal direct smear cytology,
significant and lead to hypoalbuminemia, • Intra-GI causes: ◦ Infectious—bacterial: Giardia ELISA. ◦ Diarrhea PCR panel may
decreased vascular oncotic pressure, and edema Campylobacter spp., E. coli, Salmonella spp., be useful for specific pathogens (i.e., Salmonella),
or cavitary effusion. Clostridial enterotoxins; parasitic: many species but note there is controversy about some
of ascarids, cestodes, hookworms, whipworms; bacteria on this panel causing clinical signs.
GENETICS protozoal: giardiasis, tritrichomoniasis,
N/A coccidiosis; viral: parvovirus, canine distemper IMAGING
INCIDENCE/PREVALENCE virus, corona virus; rickettsial: salmon Abdominal Radiography
Increased incidence due to dietary indiscretion poisoning (Neorickettsia); fungal: histoplasmo- • Survey abdominal radiographs interrogate
or infectious etiologies in young patients. sis, mycotoxins. ◦ Inflammatory (most mainly extra-GI causes of diarrhea. • Acute
GEOGRAPHIC DISTRIBUTION common cause)—acute enteritis/enterocolitis enteritis/enterocolitis—mild gas and/or fluid
Some infectious etiologies have specific due to dietary indiscretion or sudden diet dilation of stomach/intestine. • Pancreatitis—
geographic distributions. change, acute hemorrhagic diarrhea syndrome. widened gastroduodenal angle, focal decreased
◦ Medications/toxins—antibiotics, chemo- serosal detail at proximal duodenal flexure.
SIGNALMENT therapeutic agents, methimazole, nonsteroidal
• Species—dog and cat. • Breed predilec- Abdominal Ultrasonography
anti-inflammatory drugs (NSAIDS), toxins • Abdominal ultrasonography may be useful
tions—none. • Mean age and range—com- (corrosive, heavy metals). ◦ Motility—obstruc-
mon in puppies and kittens due to dietary in interrogation of intra- and extra-GI causes
tive or nonobstructive foreign bodies, intussus- of diarrhea, such as pancreatitis. • Emergency
indiscretion and infectious etiologies. ception, mesenteric torsion. ◦ Neoplasia—
• Predominant sex—N/A.
cage-side focused ultrasonographic examina-
primary neoplasia including adenocarcinoma, tion of abdomen is indicated in patients with
SIGNS lymphoma (small cell and large cell) leiomy- acute abdominal pain, to evaluate for etiologies
oma/leiomyosarcoma, mast cell tumor (cats), that are surgical emergencies, such as septic or
General Comments metastatic.
• Acute diarrhea common, and usually self- bile peritonitis. • If peritoneal effusion is
limiting. Most animals stable, and require RISK FACTORS seen, abdominocentesis and immediate
minimal diagnostics/treatment. • In patients • Dietary—abrupt diet change or dietary in-house cytology are indicated (+/– culture).
that are unstable, with cardiovascular or indiscretion. • Medications—many medica- DIAGNOSTIC PROCEDURES
metabolic compromise, more aggressive tions can cause acute diarrhea (see Causes). Endoscopy rarely indicated in acute diarrhea,
diagnostic and treatment approach is warranted. • Infectious—geographic distribution effect. except for patients with melena where gastro-
duodenal ulceration is suspected.
A Acute Diarrhea (continued)
PATHOLOGIC FINDINGS acute diarrhea, as usually self-limiting; if AGE-RELATED FACTORS

Dependent on underlying etiology. diarrhea persists beyond 5–7 days, further Younger patients more likely to have
etiologic investigation and appropriate infectious etiologies.
treatment are warranted. • Anthelmintics ZOONOTIC POTENTIAL
(e.g., fenbendazole 50 mg/kg PO q24h for 5 Parasitic, protozoal, and bacterial etiologies
days) are recommended for empiric treatment
TREATMENT of parasitic enteritis. • Antiprotozoal or
(e.g., Ancylostoma, Campylobacter, Giardia,
Salmonella).
APPROPRIATE HEALTH CARE coccidiostatic medication should be used if
• Stable patients, mild diarrhea—outpatient fecal analysis warrants. PREGNANCY/FERTILITY/BREEDING
medical care. Careful assessment of young Varies with treatment.
CONTRAINDICATIONS
patients should be made, as they can become SYNONYMS
• Prokinetic medications should not be given
unstable with mild signs. • Unstable patients, N/A
to patients with diarrhea. • Anti-diarrheal
hypovolemic or acute abdominal pain—inpa-
medications like loperamide should not be SEE ALSO
tient medical care.
given to breeds with possible ABCB-1/ • Acute Vomiting. • Diarrhea, Chronic—
NURSING CARE MDR-1 mutation. Cats. • Diarrhea, Chronic—Dogs.
• Isolation protocols should be instituted • Gastroenteritis, Acute Hemorrhagic
PRECAUTIONS
immediately for any patient that may have a Diarrhea Syndrome. • Pancreatitis—Cats.
• For puppies and kittens, see manufacturer’s
contagious etiology of diarrhea, i.e., patients • Pancreatitis—Dogs.
instructions regarding age and safety labeling.
that are unvaccinated, fed raw diets, come
• Many drugs such as antibiotics and anti- ABBREVIATIONS
from housing situations with many other
diarrheal medications can perpetuate diarrhea. • ACTH = adrenocorticotropic hormone.
animals, or if multiple animals in same
• Metronidazole can cause neurologic toxic • EPI = exocrine pancreatic insufficiency.
household are exhibiting same clinical signs.
effects with high dose and/or chronic use. • GI = gastrointestinal. • NSAID = non-
• Fluid therapy as mandated by hydration/
perfusion status and ongoing losses. • Most POSSIBLE INTERACTIONS steroidal anti-inflammatory.
hyporexic patients with dehydration/hypo- N/A INTERNET RESOURCES
volemia need isotonic crystalloids to replenish ALTERNATIVE DRUG(S) • https://www.avma.org/practicemanagement/
losses and provide maintenance. • Potassium N/A clientmaterials/pages/default.aspx • https://
supplementation may be needed. veterinarypartner.vin.com
ACTIVITY Suggested Reading
Activity restriction only required in post Hall J. Physiology of gastrointestinal
operative care of surgical patients. FOLLOW-UP disorders. In: Hall J, ed., Guyton and Hall’s
DIET Textbook of Medical Physiology, 13th ed.
PATIENT MONITORING Philadelphia, PA: Elsevier, 2016, 843–852.
Feeding bland, highly digestible diet is • Continuation of diarrhea for 3–5 days is to
indicated for 3–5 days, then gradual Marks SL, Kook PH, Papich MG, et al.
be expected, but should be continual improve ACVIM consensus statement: Support for
reintroduction of patient’s routine diet. ment in signs. • If diarrhea not improving, or rational administration of gastrointestinal
CLIENT EDUCATION getting more severe, further diagnostics are protectants to dogs and cats. J Vet Intern
Client education on dietary indiscretion, warranted. • If diarrhea persists beyond 7 Med 2018, 32:1823–1840.
gradual diet changes, routine deworming, and days or recurs despite appropriate therapy, Marks SL, Rankin SC, Byrne BA, Weese JS.
vaccination may be appropriate. consider chronic diarrhea etiologies. Enteropathogenic bacteria in dogs and cats:
SURGICAL CONSIDERATIONS PREVENTION/AVOIDANCE diagnosis, epidemiology, treatment, and
Surgery rarely may be indicated to treat Avoid rapid diet changes and dietary control. J Vet Intern Med 2011, 25:
etiology, such as mechanical obstruction. indiscretion, and institute prophylactic 1195–1208.
deworming and vaccinations. Weese JS, Giguère S, Guardabassi L, et al.
ACVIM consensus statement on therapeu-
tic antimicrobial use in animals and
• Dehydration and hypovolemia.
antimicrobial resistance. J Vet Intern Med
MEDICATIONS • Hypoalbuminemia and subsequent cavitary
2015, 29:487–498.
effusion.
DRUG(S) OF CHOICE Willard MD. Diarrhea. In: Ettinger SJ, ed.,
• In acute diarrhea caused by stress or EXPECTED COURSE AND PROGNOSIS Textbook of Veterinary Internal Medicine,
antibiotics, veterinary-grade probiotics may • Mild acute diarrhea usually self-limiting. 8th ed. St. Louis, MO: Elsevier, 2017, pp.
be useful. • Antibiotics not indicated in acute • Other prognoses etiology dependent. 164–166.
diarrhea patients, and should be avoided in Author Talia Guttin
accordance with antibiotic stewardship, unless Consulting Editor Mark P. Rondeau
specifically indicated with known bacterial Acknowledgment The author and editor
etiology, or in cases where bacterial transloca- MISCELLANEOUS acknowledge the prior contribution of
tion and sepsis are of concern (e.g., parvoviral Erin Portillo.
enteritis with neutropenia). Gastric antacids ASSOCIATED CONDITIONS
not indicated unless concurrent vomiting • Acute vomiting. • Hyporexia.
and/or regurgitation. • Anti-diarrheal Client Education Handout
medications like loperamide not indicated in available online
Acute Kidney Injury A
CAUSES • Urine specific gravity (USG) ≤1.020, mild

Hemodynamic/Hypoperfusion to moderate proteinuria, glucosuria, casts,
Shock, trauma, thromboembolism pyuria, hematuria, and tubular epithelial cells;
BASICS variable bacteriuria and crystalluria.
(e.g., disseminated intravascular coagulation
DEFINITION [DIC]), vasculitis, transfusion reaction), OTHER LABORATORY TESTS
• Acute kidney injury (AKI) represents a heatstroke, excessive vasoconstriction (e.g., • Metabolic acidosis—mixed disorders may
continuum of renal injury, from mild, administration of nonsteroidal anti-inflammatory occur.
clinically inapparent, nephron loss to severe drugs [NSAIDs]), adrenal insufficiency, • Leptospirosis testing.
acute renal failure. excessive vasodilation (e.g., angiotensin- • Ethylene glycol testing.
• AKI is likely underrecognized. Any increase converting enzyme inhibitors [ACEIs] or • Canine pancreatic lipase immunoreactivity
in serum creatinine >0.3 mg/dL from antihypertensive drugs), prolonged anesthesia, (cPLI) for pancreatitis.
hydrated baseline is considered an AKI. significant hypertension, heart failure.
• The spectrum of injury is highly variable IMAGING
and may range from mild subclinical to Nephrotoxic • Survey and contrast radiography—kidneys
severe damage, requiring renal replacement Grape or raisin ingestion (dogs), lily ingestion normal to large with smooth contours;
therapy. (cats), ethylene glycol, aminoglycoside, asymmetric in cats (“big kidney–little kidney”
• Patients with AKI have the potential for amphotericin B, chemotherapeutic agents, syndrome) with ureteral obstruction, uroliths
recovery of renal function. NSAIDs, radiographic contrast agents, heavy may be seen.
metals, insect or snake venom, heme pigment, • Antegrade nephropyelography for ureteral
PATHOPHYSIOLOGY and many others. Patients with ethylene obstruction.
• AKI may be categorized as prerenal, glycol toxicity may be exposed from other • Ultrasonography—evidence of pancreatitis,
intrinsic renal, or postrenal based on under sources than antifreeze, such as some paints, marked cortical hyperechogenicity may suggest
lying etiology. Pre- and postrenal causes may freezer packs, catering heat sources, etc. ethylene glycol toxicity. Moderate cortical
progress to intrinsic renal damage. hyperechogenicity suggests glomerulonephritis
• Patients with preexisting chronic kidney Intrinsic and Systemic Disease
Leptospirosis, immune-mediated or nephrosis. Pelvic and/or ureteral dilation
disease (CKD) are very predisposed to develop may suggest outflow obstruction.
ment of clinical AKI due to decreased renal glomerulonephritis, pancreatitis, septicemia,
reserve. Special care must be taken in patients DIC, hepatic failure, heat stroke, transfusion DIAGNOSTIC PROCEDURES
with existing CKD to minimize predisposing reaction, bacterial endocarditis, pyelonephritis, • Monitor urine output (UOP): anuria
factors: volume depletion, nephrotoxic lymphoma, and ureteral obstruction. (≤0.25 mL/kg/h), oliguria, polyuria (≥2 mL/
medications, etc. RISK FACTORS kg/h). Avoid urinary catheterization due to
• Endogenous—preexisting CKD,
infection risk. Assess UOP with serial body
SYSTEMS AFFECTED weights, ultrasound bladder assessment,
• Renal/urologic. pancreatitis, dehydration, sepsis, hypovolemia,
hypotension, advanced age, concurrent disease. weigh bedding, etc.
• Uremia may affect all body systems. • Fine-needle aspiration may diagnose
• Exogenous—drugs, prolonged anesthesia,
INCIDENCE/PREVALENCE trauma, multiple organ disease, high lymphoma.
• Prevalence is lower than for CKD. • Renal biopsy may help identify underlying
environmental temperature.
• Prevalence may increase in environments cause and prognosticate recovery.
that support Leptospira. PATHOLOGIC FINDINGS
• Ureteral obstruction is most common cause Nephrosis or nephritis, glomerulonephritis,
of severe acute uremia in cats. calcium oxalate crystals, interstitial edema,
DIAGNOSIS and lack of interstitial fibrosis, variable
SIGNALMENT
DIFFERENTIAL DIAGNOSIS tubular regeneration.
Species • Prerenal azotemia—oliguria correctable
Dog and cat. with fluid repletion. Typically hypersthenuric,
Breed Predilections but consider ability to concentrate urine:
None preexisting kidney disease, endocrine
disorders, medications, and diet may all affect TREATMENT
Mean Age and Range
• 6–8 years peak prevalence.
concentrating ability. APPROPRIATE HEALTH CARE
• Older animals at greater risk due to
• Postrenal azotemia—anuria, dysuria, Inpatient management—eliminate inciting
decreased renal reserve (AKI on CKD). stranguria, painful or asymmetric kidneys, causes; discontinue nephrotoxic drugs;
ureteral/urethral obstruction, enlarged maintain hemodynamic stability; ameliorate
SIGNS prostate, urethral tear, uroperitoneum. life-threatening fluid imbalances, biochemical
Historical Findings • CKD—polyuria, polydipsia, history of abnormalities, and uremic complications.
Sudden onset of anorexia, listlessness, chronic illness, loss of body condition, anemia. NURSING CARE
depression, vomiting or diarrhea (± blood), • Hypoadrenocorticism—hyponatremia, • Hypovolemia—correct estimated fluid
halitosis, ataxia, seizures, known toxin or drug hyperkalemia, low serum cortisol. deficits with balanced isotonic solution
exposure, recent medical or surgical • Pancreatitis—cranial abdominal pain, within 2–4 hours if patient condition
procedure. hyperbilirubinemia, increase in liver enzyme permits; once hydrated, ongoing fluid
activity. requirements are provided by 5% dextrose for
Normal body condition and hair coat, CBC/BIOCHEMISTRY/URINALYSIS insensible losses (~20–25 mL/kg/day) and
depression, dehydration (or iatrogenic • Variable packed cell volume (PCV), balanced electrolyte solution equal to sensible
overhydration), scleral injection, oral leukocytosis, or lymphopenia. losses; avoid overhydration.
ulceration, necrosis of tongue, uremic breath, • Variable increases in blood urea nitrogen • Hypervolemia—stop fluid administration
hypothermia, fever, tachypnea, bradycardia, (BUN), creatinine, phosphorus, potassium, and eliminate excess fluid by diuretics or
nonpalpable urinary bladder, and asymmetric, and glucose; and variably low bicarbonate and dialysis.
enlarged, painful, or firm kidneys. calcium.
A Acute Kidney Injury (continued)
• Monitor body weight and blood pressure give half IV over 30 minutes and remainder signaled by sudden (and often excessive) polyuria
several times daily and adjust fluids to over 2–4 hours, then reassess. and sluggish and possibly incomplete return of
maintain stable weight once rehydrated. Hyperkalemia renal function over 4–12 weeks; dialysis extends
DIET • Correct dehydration with potassium-free
potential for renal regeneration and repair.
• Anuric AKI—poor prognosis without
• Nutritional support should be provided fluids.
within 3 days using moderately protein- • Minimize potassium intake.
dialysis. Anuria is not prognostic and does
restricted diets. • Discontinue medications that promote
not impact ability for renal recovery, if
• Caloric and protein requirements supplied hyperkalemia. hemodialysis is available to maintain patient
by blended renal diets, liquid enteral solutions, • Loop diuretics—furosemide 1–2 mg/kg IV.
during recovery period.
or formulated diets delivered by enteral • Sodium bicarbonate—correct bicarbonate
feeding tube. Parenteral nutrition may be deficit, if bicarbonate status unknown
needed in some cases. 1–2 mEq/kg IV.
CLIENT EDUCATION • Dextrose ± insulin—1–2 mL/kg of 50% MISCELLANEOUS
• Depending on inciting cause, prognosis for
dextrose diluted to 25% IV or regular insulin
ZOONOTIC POTENTIAL
recovery of renal function is variable. Average 0.1–0.2 U/kg IV bolus followed by 1–2 g
Leptospirosis
recovery for all causes of AKI is 50%. Likelihood dextrose/unit insulin.
• Calcium gluconate 10%—0.5–1.0 mL/kg PREGNANCY/FERTILITY/BREEDING
of some degree of persistent kidney damage.
IV over 10–15 minutes (cardioprotective, A rare complication of pregnancy; promoted
• Potential for complications of treatment
does not alter serum potassium). by acute metritis, pyometra, and postpartum
(e.g., fluid overload, pancreatitis, sepsis, and
• Refractory hyperkalemia—dialysis. sepsis or hemorrhage.
multiple organ failure); expense of prolonged
hospitalization; options for continued care if Vomiting SYNONYMS
conventional medical management fails • Reduce gastric acid production— • Acute renal failure.
(hemodialysis, peritoneal dialysis); zoonotic pantoprazole (1 mg/kg IV q12h), • Acute tubular necrosis.
potential of leptospirosis. famotidine CRI. • Acute uremia.
SURGICAL CONSIDERATIONS • Mucosal protectant for gastrointestinal (GI) SEE ALSO
• See Ureterolithiasis.
ulceration—sucralfate (0.25–1 g PO q6–8h). • Azotemia and Uremia.
• Antiemetics—maropitant (1 mg/kg SC/IV • Hyperkalemia.
• Renal transplantation may provide long-
term survival for cats with severe, nonrecov q24h); ondansetron (0.2–1 mg/kg IV q8–12h). • Hypertension, Systemic Arterial.
ered AKI. PRECAUTIONS • Leptospirosis.
Modify dosages of drugs requiring renal • Ureterolithiasis.
Peritoneal or Hemodialysis
• Dialysis can stabilize the patient to allow metabolism or elimination. ABBREVIATIONS
time for renal recovery. Without, most • ACEI = angiotensin-converting enzyme
oliguric patients die before sufficient renal inhibitors.
repair occurs. • AKI = acute kidney injury.
• Indications—oliguria or anuria, life-threat FOLLOW-UP • BUN = blood urea nitrogen.
ening fluid overload or acid-base/electrolyte • CKD = chronic kidney disease.
PATIENT MONITORING • cPLI = canine pancreatic lipase
disturbances, BUN ≥100 mg/dL, serum
Fluid, electrolyte, and acid-base balances; body immunoreactivity.
creatinine ≥5 mg/dL, clinical course
weight; blood pressure; UOP; and clinical status. • DIC = disseminated intravascular
refractory to conservative treatment, peri-
operative stabilization, and poisoning/ PREVENTION/AVOIDANCE coagulation.
overdosage with dialyzable toxin/drug. • Anticipate AKI in aged patients or those • GI = gastrointestinal.
with systemic disease, sepsis, trauma, hemo- • NSAID = nonsteroidal anti-inflammatory
dynamic instability, receiving nephrotoxic drug.
drugs, multiple organ failure, or undergoing • PCV = packed cell volume.
prolonged anesthesia. • UOP = urine output.
MEDICATIONS • Monitor urine production, BUN, and • USG = urine specific gravity.
DRUG(S) OF CHOICE creatinine in high-risk patients. Suggested Reading
Inadequate Urine Production POSSIBLE COMPLICATIONS Cowgill LD, Langston C. Acute kidney
• Avoid overhydration. Once fluid replete, Seizures, coma, cardiac arrhythmias, hypo- or insufficiency. In: Bartges J, Polzin DJ, eds.,
administer diuretics. hypertension, congestive heart failure, pulmonary Nephrology and Urology of Small Animals.
• Hypertonic mannitol (20%)—0.5 g/kg IV edema, uremic pneumonitis, GI bleeding, sepsis, Ames, IA: Wiley-Blackwell, 2011,
over 15–30 minutes; if effective, continue IV cardiopulmonary arrest, and death. pp. 472–523.
bolus q6h. EXPECTED COURSE AND PROGNOSIS Sykes JE, Hartmann K, Lunn KF, et al. 2010
• Furosemide—1–4 mg/kg IV; if effective, • Prognosis depends on underlying cause,
ACVIM small animal consensus statement
continue at 0.5 mg/kg/h or 2 mg/kg q6h. extent of renal injury, concomitant disease or on leptospirosis: diagnosis, epidemiology,
• Dopamine—potential side effects and lack organ failure, and response to therapy. treatment, and prevention. J Vet Intern
of efficacy contraindicate its use except for • Survival rate ~50%, but depends on cause:
Med 2011, 25(1):1–13.
pressor control. Fenoldopam may be more <20% for advanced ethylene glycol toxicosis, Authors Sheri Ross and Cedric P. Dufayet
efficacious. >80% for acute leptospirosis. Consulting Editor J.D. Foster
• Dialysis for refractory cases. • Polyuric AKI—typically milder than
Metabolic Disorders, Acid-Base oliguric; recovery may occur over 2–6 weeks,
Client Education Handout
Disorders but prognosis remains guarded.
available online
Administer bicarbonate if serum bicarbonate • Oliguric AKI—extensive kidney injury,
≤16 mEq/L; bicarbonate replacement: mEq = difficult to manage, and has poor prognosis
bicarbonate deficit × body weight (kg) × 0.3; for recovery without dialysis; recovery may be
Acute Respiratory Distress Syndrome A
GENETICS 0.21–1.0). Normal PF ratio = 500; comparison

Certain humans are more prone to develop of this ratio allows evaluation of severity of lung
ing ARDS than others due to specific gene disease and direct comparison of blood gases
BASICS polymorphisms. This has not been investi taken at different FiO2. PaCO2 is often low;
DEFINITION gated in the veterinary population. hypercapnia tends to be late (preterminal)
• Acute respiratory distress syndrome (ARDS) development. • Total protein of airway edema
INCIDENCE/PREVALENCE
is a syndrome of acute onset of respiratory fluid compared with serum total protein—ratio
Unknown
failure typified by diffuse bilateral pulmonary of edema fluid to serum total protein <0.5
infiltrates on a dorsoventral thoracic radiograph, SIGNALMENT supportive of low‐protein hydrostatic pressure
with no clinical evidence of left atrial Species pulmonary edema (e.g., heart failure, fluid
hypertension or volume overload. ARDS Dog and cat. overload); edema fluid/serum total protein ratio
results from an overwhelming inflammatory >0.7 suggests high‐protein, increased permeability
Breed Predilections pulmonary edema such as ARDS and
reaction in the alveolocapillary membrane in
response to a systemic or pulmonary inflamm A familial form of ARDS has been reported pneumonia. • Coagulation panel may reveal
atory insult. The end result is increased in a group of related Dalmatian dogs; it is hypocoagulable state supportive of
vascular permeability leading to edema. • The clinically indistinguishable from ARDS. disseminated intravascular coagulation (DIC)
2012 Berlin Definition of ARDS defines three Mean Age and Range or cause of pulmonary hemorrhage.
categories of severity based on PaO2/FiO2 (PF) Unknown IMAGING
ratio and level of positive end‐expiratory
SIGNS Thoracic Radiographs
pressure (PEEP) employed during ventilation,
with mild ARDS defined by a PF ratio of Historical Findings • Bilateral/diffuse pulmonary infiltrates.
200–300 mmHg with PEEP ≥5 mmHg, • Acute onset of respiratory distress in patient • Severity of radiographic signs can lag behind
moderate ARDS as a PF ratio of 100– with significant underlying disease or exposure to clinical disease by 12–24 hours. • Can be
200 mmHg with PEEP ≥5 mmHg, and severe known risk factors. • Patient often hospitalized difficult to distinguish from cardiogenic edema;
ARDS as a PF ratio <100 mmHg with PEEP for primary disease when develops ARDS. cardiac silhouette and pulmonary vascular size
≥5 mmHg. usually normal in ARDS.
PATHOPHYSIOLOGY • Severe respiratory distress. • Crackles (if Echocardiography
• ARDS is due to a diffuse inflammatory insult present) heard bilaterally on auscultation. • Attempt to rule out cardiogenic cause for
that causes widespread damage to alveolar • Fever—depends on underlying disease. pulmonary edema. • May be able to estimate
endothelial and epithelial cells, resulting in • Cyanosis in more severe cases. • Signs degree of pulmonary hypertension.
thickening of the membrane and impaired gas relevant to primary disease process. DIAGNOSTIC PROCEDURES
exchange. This inflammatory insult can be CAUSES Pulmonary artery catheter to measure
triggered by primary pulmonary disease or it pulmonary artery occlusion pressure can be used
can be of nonpulmonary origin, and leads to Primary Pulmonary Causes to rule out cardiogenic cause for edema; by
exudative, proliferative, and fibrotic changes • Aspiration pneumonia. • Pneumonia. definition, ARDS is associated with pulmonary
within the lung. • First, excessive accumulation • Pulmonary contusion. • Near drowning. artery occlusion pressure (PAOP) ≤18 mmHg.
and activation of neutrophils, monocytes, and • Chemical or smoke inhalation. • Idiopathic
platelets in the pulmonary microvasculature form of ARDS associated with acute interstitial PATHOLOGIC FINDINGS
lead to increased alveolar endothelial pneumonia or idiopathic pulmonary fibrosis Gross Pathology
permeability. This causes protein‐rich edema has been reported in humans and dogs. Lungs are dark, heavy, and ooze fluid when cut.
fluid and inflammatory cells to leak into the Nonpulmonary Causes Histopathology
interstitial and alveolar spaces. • Alveolar • Systemic inflammatory response syndrome • Acute phase—pulmonary vascular congestion
epithelial injury results from release of cytokines (SIRS). • Sepsis. • Neoplasia. • Pancreatitis. with edema fluid and inflammatory cell
and other inflammatory mediators from • Severe trauma and shock. • Severe bee sting accumulation in interstitium and alveoli;
leukocytes and platelets. • Epithelial injury envenomation. epithelial cell damage, hyaline membrane
involves both type I and type II alveolar formation, microthrombi, microatelectasis.
epithelial cells, and results in alveolar flooding RISK FACTORS
• SIRS. • Sepsis. • Severity of illness. • Multiple • Proliferative phase—hyperplasia of type 2
and surfactant dysfunction. This causes collapse pneumocytes, interstitial mononuclear
and consolidation of alveoli with development transfusions.
infiltration, organization of hyaline membranes,
of severe hypoxemia, and hyaline membrane and fibroproliferation.
formation in the alveolar spaces.
• Microthrombi in the pulmonary vasculature,
hypoxic pulmonary vasoconstriction, and DIAGNOSIS
release of endogenous vasoconstrictors lead to
pulmonary arterial hypertension, which can DIFFERENTIAL DIAGNOSIS TREATMENT
lead to right‐sided heart failure. • Proliferation • Left‐sided congestive heart failure. • Fluid
overload. • Diffuse pneumonia. • Pulmonary APPROPRIATE HEALTH CARE
of type 2 alveolar epithelial cells and pulmonary • No specific therapy; general aims to maintain
fibrosis occurs in the late stages of ARDS. hemorrhage.
tissue oxygenation and minimize iatrogenic lung
SYSTEMS AFFECTED CBC/BIOCHEMISTRY/URINALYSIS injury while treating underlying disease.
• Respiratory. • Cardiovascular—right‐sided • Leukocytosis or leukopenia. • Other changes • Oxygen therapy—no more than required to
heart failure secondary to pulmonary hyper- dependent on underlying disease process. maintain PaO2 >60–80 mmHg to minimize
tension; hemodynamic compromise may be OTHER LABORATORY TESTS oxygen toxicity. • Positive‐pressure ventilation
associated with aggressive mechanical • Arterial blood gases—low PF ratio (where (PPV) essential in management of ARDS patients;
ventilator settings. PaO2 is measured in mmHg and FiO2 is indicated in patients that are hypoxemic despite
A Acute Respiratory Distress Syndrome (continued)
oxygen therapy, patients requiring high levels of • Vasoactive drugs to maintain blood
inspired oxygen for prolonged periods, or pressure. • Anesthetic drugs to allow PPV.
patients working so hard to breathe that at risk • Analgesia as appropriate. • Low‐dose
of exhaustion. • ARDS thought to be corticosteroid—use remains controversial, MISCELLANEOUS
exacerbated by ventilator‐induced lung injury with conflicting reports of efficacy for low‐ ASSOCIATED CONDITIONS
associated with alveolar overdistension dose steroids in early or late ARDS. SIRS, multiple organ dysfunction syndrome,
compounded by cyclic opening and collapse of sepsis.
ALTERNATIVE DRUG(S)
atelectatic alveoli; therefore, lung‐protective
Furosemide may produce pulmonary venous SYNONYMS
strategies of PPV with moderate to high PEEP,
dilation and improve lung function, as • Acute hypoxemic respiratory failure. • Acute
low tidal volumes, and permissive hypercapnia
intermittent bolus of 1 mg/kg IV q6–12h or interstitial pneumonia. • Adult respiratory
recommended to minimize ventilator‐induced
as CRI of 0.2 mg/kg/h IV. Beware dehydra distress syndrome. • High‐protein pulmonary
lung injury; tidal volumes of 6 mL/kg have been
tion and effects on organ function. edema. • Shock lung.
found to increase survival significantly in human
ARDS patients compared to tidal volumes of SEE ALSO
12 mL/kg. • Recruitment maneuvers and high • Dyspnea and Respiratory Distress. • Panting
levels of PEEP can both cause significant and Tachypnea. • Pulmonary Edema,
hemodynamic compromise and patients should FOLLOW‐UP Noncardiogenic. • Sepsis and Bacteremia.
have constant direct arterial blood pressure PATIENT MONITORING ABBREVIATIONS
monitoring. • Intensive supportive care of Arterial blood gases, pulse oximetry, end‐tidal • ARDS = acute respiratory distress syndrome.
cardiovascular system and other organ systems is carbon dioxide, thoracic radiographs, arterial • DIC = disseminated intravascular coagulation.
vital, as these patients at high risk for development blood pressure, ECG, temperature, urine • PAOP = pulmonary artery occlusion pressure
of multiple organ dysfunction. output, CBC, coagulation profiles, serum (formerly pulmonary capillary wedge pressure).
NURSING CARE chemistry, blood cultures, monitoring for • PEEP = positive end‐expiratory pressure.
• Monitor temperature closely, especially if other organ dysfunction. • PF ratio = PaO2/FiO2 ratio. • PPV =
using an oxygen cage, as animals with excessive positive‐pressure ventilation. • SIRS = systemic
PREVENTION/AVOIDANCE
work of breathing can easily become hyper- inflammatory response syndrome.
• Appropriate therapy of primary disease
thermic. • Ventilator patients require frequent processes to reduce inflammatory insult INTERNET RESOURCES
position changes and physical therapy; regular to lung. • Intensive cardiovascular www.ardsnet.org
oral care with dilute chlorhexidine solution is monitoring and support of critically ill
important to reduce oral colonization with animals to ensure adequate tissue perfusion.
Suggested Reading
bacteria as source of sepsis, and frequent ARDS Definition Task Force, Ranieri VM,
• Careful management of recumbent animals
endotracheal tube suctioning needed to prevent Rubenfeld GD, et al. Acute respiratory
to reduce chance of aspiration, especially if
occlusion; inflate cuff carefully and change distress syndrome: the Berlin Definition.
patient has neurologic disease or upper
endotracheal cuff position regularly to prevent J Am Med Assoc 2012,
airway disorders that reduce ability to protect
tracheal damage. • Blood pressure monitoring, 307(23):2526–2533.
airway. • Judicious use of blood products in
as septic patients prone to hypotension. • Fluid Balakrishnan A, Drobatz KJ, Silverstein DC.
patients with inflammatory or severe
therapy important to support cardiovascular Retrospective evaluation of the prevalence,
systemic disease.
system and maintain normovolemia while risk factors, management, outcome, and
avoiding fluid overload, as this will negatively POSSIBLE COMPLICATIONS necropsy findings of acute lung injury and
affect lung function. • Multiorgan dysfunction syndrome—acute acute respiratory distress syndrome in dogs
kidney injury, DIC, and gastrointestinal and cats: 29 cases (2011–2013). J Vet
ACTIVITY disease are more common forms of organ Emerg Crit Care 2017, 27(6):662–673.
If not anesthetized for ventilation, strict cage dysfunction seen. • Barotrauma—can result Matthay MA, Ware LB, Zimmerman GA.
confinement. in pneumothorax; incidence thought to be The acute respiratory distress syndrome.
DIET less with lower tidal volume ventilation J Clin Invest 2012, 122(8):2731–2740.
Nutritional support important but challenging. strategies. • Ventilator‐associated pneumonia— Parent C, King LG, Van Winkle TJ, Walker
Enteral feeding desired over parenteral nutrition, patients on PPV have increased risk of LM. Respiratory function and treatment in
but must consider high risk of regurgitation and pneumonia that may be difficult to dogs with acute respiratory distress
aspiration in recumbent patient. differentiate from worsening of initial lung syndrome: 19 cases (1985–1993). J Am Vet
injury; airway cultures should be considered Med Assoc 1996, 208:1428–1433.
CLIENT EDUCATION in deteriorating patients. • Oxygen toxicity Ware LB, Matthay MA. The acute respiratory
Clients need to be aware of the guarded may be unavoidable due to severity of distress syndrome. N Engl J Med 2000,
prognosis and high costs of therapy. hypoxemia in spite of PPV; oxygen toxicity 342:1334–1349.
SURGICAL CONSIDERATIONS indistinguishable from ARDS on Wilkins PA, Otto CM, Baumgardner JE, et al.
Underlying disease may require surgery. histopathology, making incidence of this Acute lung injury and acute respiratory distress
problem impossible to determine. syndromes in veterinary medicine: consensus
EXPECTED COURSE AND PROGNOSIS definitions: The Dorothy Russell Havemeyer
• Mortality in human patients remains at Working Group on ALI and ARDS in
MEDICATIONS 40–60%. • Mortality in veterinary patients is Veterinary Medicine. J Vet Emerg Crit Care
likely greater than 90%. (San Antonio) 2007, 17(4):333–339.
DRUG(S) OF CHOICE Author Casey J. Kohen
• No specific drug therapy. • Antibiotics for
Consulting Editor Elizabeth Rozanski
underlying disease where indicated.
Acute Vomiting A
toxin history should be investigated. • Nausea regurgitation via esophagitis, so if both signs are
and hypersalivation. • Varying amounts, present, it is important to establish chronology.
frequency, and severity of vomiting. • Varying • In cats, vomiting can be mistaken for coughing.
BASICS activity levels can be seen, from normal to ◦ Coughing involves extension of neck and
DEFINITION lethargic. • Hematemesis may be seen. elbows. ◦ Physical exam findings may differenti-
Vomiting of fewer than 7 days’ duration. Physical Examination Findings ate. ◦ Videos can be helpful to differentiate.
PATHOPHYSIOLOGY • Dehydration/hypovolemia, cranial CBC/BIOCHEMISTRY/URINALYSIS
• Vomiting is a reflex initiated by the abdominal pain, nausea, fluid–gas interface • Extra-GI causes: ◦ Increased hepatic enzyme
vomiting center in the medulla, triggered by on intestinal palpation, increased borborygmi. activity in hepatobiliary diseases. ◦ Renal
three major mechanisms—gastric/duodenal • Careful sublingual examination for azotemia in kidney disease. ◦ Increased
mucosal irritation, gastric/duodenal distention, anchored linear foreign bodies. • Careful hepatic enzyme activity, hypoalbuminemia,
or the chemoreceptor trigger zone (CRTZ). abdominal palpation for mechanical inflammatory leukogram in pancreatitis.
• Mucosal irritation or gastric/duodenal obstruction. • Rectal examination for melena ◦ Hypoalbuminemia, decreased Na : K ratio
distention signal the vomiting center via or concurrent diarrhea. in hypoadrenocorticism. • Intra-GI causes—
sympathetic and vagal afferent innervation. CAUSES often normal. • As result of vomiting,
Anti-peristaltic waves force intestinal contents • Extra-GI causes: ◦ Common—hepatobiliary
following may be present: ◦ Hemoconcentration.
back to the duodenum, then distention disease, kidney disease, pancreatitis, neoplasia ◦ Prerenal azotemia. ◦ Hypokalemia,
becomes the main trigger for the vomiting (non-GI). ◦ Uncommon—CNS, cardiac, hypochloremia. ◦ Hypoalbuminemia,
reflex. • The CRTZ can directly trigger the endocrine (hypoadrenocorticism, hyper hypocholesterolemia. ◦ Hypoglycemia—
vomiting center via receptor activation or thyroidism, diabetic ketoacidosis), respiratory toy-breed puppies predisposed.
vestibular input; known receptors are α2, D2, disease, peritonitis, sepsis. ◦ Intra-GI causes: OTHER LABORATORY TESTS
H1, M1, NK1, 5HT3. • Cerebral cortex and ◦ Congenital/genetic—hiatal hernia. • Extra-GI interrogation—baseline cortisol or
vestibular apparatus can also directly stimulate ◦ Infectious—parasitic, protozoal, viral adrenocorticotropic hormone (ACTH)
the vomiting center. • The vomiting center (parvovirus, canine distemper virus, corona stimulation test in dogs, T4 in cats, quantitative
initiates an autonomic motor reaction via virus), fungal, bacterial (Campylobacter, pancreatic lipase immunoreactivity. • Intra-GI
spinal nerves to diaphragmatic and abdominal Salmonella). ◦ Inflammatory (most common interrogation—fecal flotation, fecal direct
muscles, and cranial nerves 5, 7, 9, 10, and 12 cause)—acute gastritis/gastroenteritis due to smear cytology.
to the upper gastrointestinal (GI) tract. • The dietary indiscretion or sudden diet change,
reflex involves a deep breath, opening the IMAGING
acute hemorrhagic diarrhea syndrome.
upper esophageal sphincter, closing the glottis, ◦ Mechanical obstruction—foreign body, Abdominal Radiography
strong diaphragmatic and abdominal muscle intussusception, obstructive mass (granuloma, • Survey abdominal radiographs indicated in
contractions, and lower esophageal sphincter neoplasia, pyloric hypertrophy, trichobezoar), most acutely vomiting patients to evaluate
relaxation, leading to expulsion of contents. torsion/volvulus (gastric, mesenteric). potential surgical emergencies, like mechanical
SYSTEMS AFFECTED ◦ Medications/toxins—α2 agonists, antibiotics, obstructions and sepsis. Survey abdominal
• Cardiovascular—fluid losses can be significant, apomorphine, chemotherapeutic agents, radiographs also interrogate many extra-GI
with progressive dehydration to hypovolemia; methimazole, nonsteroidal anti-inflammatory causes of vomiting. • Acute gastritis/gastro-
vagal stimulation can lead to bradycardia, and drugs (NSAIDS), opioids, toxins (corrosive, enteritis—mild gas and/or fluid dilation of
rarely syncope. • GI—esophagitis. • Metabolic— heavy metals). ◦ Neoplasia—primary such as stomach/intestine. • Mechanical obstruction—
vomiting of mixed small intestinal and gastric adenocarcinoma, lymphoma, leiomyoma/ foreign body may be radiopaque, or two
contents results in isotonic electrolyte losses; leiomyosarcoma, gastrointestinal stromal populations of bowel may be seen, one
pyloric obstruction results in metabolic alkalosis; tumor, mast cell tumor (cats), metastatic. distended orad to the obstruction, and one
hypokalemia is common with concurrent ◦ Ulcers—gastric and/or duodenal ulceration is normal aborad to the obstruction. • If foreign
hyporexia. • Respiratory—aspiration usually secondary: NSAIDS, neoplasia (primary body is suspected, but no radiographic
pneumonitis/pneumonia. GI, mast cell tumor, gastrinoma), hypoadreno evidence, serial radiographs every 6 hours or
corticism, uremia, infectious (controversial— contrast radiography may be considered.
GENETICS • Gastric dilatation and volvulus—
Helicobacter), stress.
N/A malpositioned pylorus on right lateral
RISK FACTORS radiograph. • Pancreatitis—widened gastro
• Dietary—abrupt diet change or dietary duodenal angle, focal decreased serosal detail at
Increased incidence of infectious causes and
indiscretion. • Medications—many medic proximal duodenal flexure.
dietary indiscretion in young patients.
ations can cause acute vomiting. • Infectious—
GEOGRAPHIC DISTRIBUTION geographic distribution effect. Abdominal Ultrasonography
Some infectious etiologies have specific • Abdominal ultrasonography may be useful
geographic distributions. in interrogation of intra- and extra-GI causes
of vomiting, such as pancreatitis and
SIGNALMENT
intussusception. • Emergency cage-side
• Species—dog and cat. • No breed, age, or DIAGNOSIS focused ultrasonographic examination of
sex predilections.
DIFFERENTIAL DIAGNOSIS abdomen is indicated in patients with acute
SIGNS • Vomiting can be mistaken for regurgitation. abdominal pain, to evaluate for etiologies that
Historical Findings ◦ Vomiting—prodromal nausea (hypersaliva- are surgical emergencies, such as septic or bile
• Care should be taken to differentiate tion), retching, abdominal contractions. peritonitis. • If peritoneal effusion seen,
vomiting from regurgitation. • Dietary ◦ Regurgitation—no prodromal nausea, passive abdominocentesis and immediate in-house
indiscretion, foreign body, and medication/ expulsion of fluid/food. ◦ Vomiting can lead to cytology are indicated (+/- culture).
A Acute Vomiting (continued)
DIAGNOSTIC PROCEDURES SC/PO q6–8h, or 1–2 mg/kg/day as CRI),

• Endoscopy rarely indicated in acute phenothiazine derivative chlorpromazine
vomiting, except for gastric foreign bodies or (0.5 mg/kg SC q8h). • Refractory vomiting
gastric ulceration. • Exploratory celiotomy patients (i.e., pancreatitis) may need multi MISCELLANEOUS
may be considered with high suspicion for modal anti-emetics that act on different ASSOCIATED CONDITIONS
mechanical obstruction, even when not receptors. • Gastric/duodenal ulcers—proton Acute diarrhea, hyporexia.
confirmed with imaging. pump inhibitor such as pantoprazole IV or
AGE-RELATED FACTORS
PATHOLOGIC FINDINGS omeprazole PO (1 mg/kg IV/PO q12h) is
Younger patients more likely to have ingested
Dependent on underlying etiology. preferred treatment. Sucralfate, while used
foreign body or have infectious etiologies.
conventionally in ulcers, has only been shown
to help cats with esophagitis, and due to ZOONOTIC POTENTIAL
impaired absorption of concurrently given Parasitic, protozoal, and bacterial etiologies
medications, and q8 dosing, is of questionable (Ancylostoma, Campylobacter, Giardia, Salmonella).
TREATMENT efficacy. • NSAID-induced ulceration— PREGNANCY/FERTILITY/BREEDING
consider misoprostol. • Vestibular mediated— Misoprostol for treatment of NSAID-induced
APPROPRIATE HEALTH CARE
H1 antagonist like diphenhydramine (2–4 mg/ ulcers is contraindicated in pregnant animals
• Stable patients, mild vomiting—outpatient
kg PO/IM q6–8h). and humans.
medical care. Careful assessment of young
patients should be made, as they can become CONTRAINDICATIONS SYNONYMS
unstable with mild signs. • Unstable patients, • Prokinetic medications should not be given to Emesis
hypovolemic or acute abdominal pain— patients with mechanical obstruction.
SEE ALSO
inpatient medical care. • Emergency surgery • Phenothiazine derivatives—caution in patients
• Acute Diarrhea. • Gastroduodenal
may be indicated—mechanical obstruction, with seizures or hypovolemia/hypotension.
Ulceration/Erosion. • Gastroenteritis, Acute
septic or bile peritonitis, volvulus. • Anticholinergics should not be given, as
Hemorrhagic Diarrhea Syndrome.
exacerbation of signs from ileus can result.
NURSING CARE • Pancreatitis – Cats. • Pancreatitis – Dogs.
• Fluid therapy as mandated by hydration/ PRECAUTIONS • Vomiting, Chronic.
perfusion status. • Most patients with Anti-emetic medications should not be given ABBREVIATIONS
dehydration/hypovolemia need isotonic to patient receiving outpatient care, unless • ACTH = adrenocorticotropic hormone.
crystalloids to replenish losses and provide mechanical obstruction has been ruled out. • CRTZ = chemoreceptor trigger zone.
maintenance. • Nothing PO—only indicated POSSIBLE INTERACTIONS • GI = gastrointestinal. • NSAID =
in patients with mechanical obstruction, Ondansetron IV can react with other nonsteroidal anti-inflammatory drug.
severe intractable vomiting, or patients with medications and precipitate.
high risk of aspiration. INTERNET RESOURCES
ALTERNATIVE DRUGS • https://www.avma.org/practicemanagement/
ACTIVITY Dolasetron, famotidine. clientmaterials/pages/default.aspx • https://
Activity restriction only required in veterinarypartner.vin.com
postoperative care of surgical patients.
Suggested Reading
DIET Gallagher A. Vomiting and regurgitation. In:
Once vomiting resolves, gradual FOLLOW-UP Ettinger SJ, ed., Textbook of Veterinary
reintroduction of small amounts of water, Internal Medicine, 8th ed. St. Louis, MO:
then small, frequent meals of bland, highly PATIENT MONITORING Elsevier, 2017, pp. 158–164.
digestible diet is indicated for 3–5 days, then • If patient receives anti-emetic with
Hall J. Physiology of gastrointestinal
gradual reintroduction of patient’s routine outpatient medical care, and continues to disorders. In: Hall J, ed., Guyton and Hall’s
diet and feeding schedule. vomit—hospitalize for further diagnostics Textbook of Medical Physiology, 13th ed.
and inpatient medical care. • If vomiting not Philadelphia, PA: Elsevier, 2016, 843–852.
CLIENT EDUCATION improving, or getting more severe, further
Client education on dietary indiscretion, Marks SL, Kook PH, Papich MG, et al.
diagnostics are warranted. • If vomiting ACVIM consensus statement: support for
gradual diet changes, and foreign body persists beyond 7 days or recurs despite
avoidance may be appropriate. rational administration of gastrointestinal
appropriate therapy, consider chronic protectants to dogs and cats. J Vet Intern
SURGICAL CONSIDERATIONS vomiting etiologies. Med 2018, 32:1823–1840.
Surgery may be indicated to treat etiology, PREVENTION/AVOIDANCE Unterer S, Busch K, Leipig M, et al.
such as mechanical obstruction. Avoid rapid diet changes and dietary Endoscopically visualized lesions, histologic
indiscretion, and institute prophylactic findings, and bacterial invasion in the
deworming and vaccinations. gastrointestinal mucosa of dogs with acute
POSSIBLE COMPLICATIONS hemorrhagic diarrhea syndrome. J Vet
MEDICATIONS • Aspiration pneumonia. • Esophagitis. Intern Med 2014, 28:52–58.
• Dehydration and hypovolemia. Author Talia Guttin
DRUG(S) OF CHOICE Consulting Editor Mark P. Rondeau
• Anti-emetics not usually needed for mild EXPECTED COURSE AND PROGNOSIS Acknowledgment The author and editor
acute vomiting, but may be needed in more • Mild acute vomiting from acute gastritis/ acknowledge the prior contribution of Erin
severe cases—5HT3 antagonists such as gastroenteritis usually self-limiting. Portillo.
ondansetron (0.2–1 mg/kg SC/IV q8h), NK1 • Mechanical obstruction from foreign bodies
antagonist maropitant (1 mg/kg SC q24h or has good prognosis with rapid recognition
2 mg/kg PO q24h), dopamine antagonist and and treatment. • Other prognoses etiology Client Education Handout
prokinetic metoclopramide (0.2–0.5 mg/kg dependent. available online
Adenocarcinoma, Anal Sac A
• Mast cell tumor.

• Melanoma.
• Lymphoma.
BASICS • Squamous cell carcinoma. TREATMENT
• Perineal hernias. • Surgical resection is treatment of choice.
DEFINITION
Malignant neoplasm derived from the • Resection of primary tumor and enlarged
CBC/BIOCHEMISTRY/URINALYSIS lymph nodes prolongs survival—both at
apocrine glands of the anal sac. • Hypercalcemia—15–30% of cases; initial diagnosis and upon relapse.
PATHOPHYSIOLOGY associated hyposthenuria. • If mass is large and locally invasive at
• Locally invasive. • Secondary renal failure may develop with diagnosis, surgery will be palliative, not
• High metastatic rate (~50–80% at diagnosis), longstanding and severe hypercalcemia. curative.
often to locoregional lymph nodes including Beware of interpreting urine specific gravity • Debulking all disease present may control
medial iliac (MILN), internal iliac, sacral, less to differentiate prerenal versus renal azotemia hypercalcemia until tumor recurrence.
frequently to distant sites including liver, in hypercalcemic patients. Hypercalcemia • Surgery may not be possible if primary
spleen, or lungs. inhibits concentrating abilities of kidneys, mass is very large.
• Frequently associated with hypercalcemia, thus azotemia with dilute urine may be seen • Adjuvant radiation for microscopic disease
secondary to parathyroid hormone–related with both prerenal and renal azotemia. may help delay local recurrence and evidence
peptide (PTH-rP) secretion. Treatment of disease to resolve hypercalce- of lymph node metastases.
• Prognosis good to guarded with appropriate mia and fluid therapy is needed to determine • Hypofractionated radiation can provide
treatment intervention. if underlying renal pathology is present. benefit in cases of advanced or inoperable
SYSTEMS AFFECTED OTHER LABORATORY TESTS disease, with about one-third of dogs showing
• Gastrointestinal. If hypercalcemia is present, and tumor cannot partial response to radiation, and about
• Endocrine/metabolic. be identified, parathyroid hormone and two-thirds of dogs having improvement or
• Hemic/lymphatic/immune. PTHrP levels can be assessed—high PTHrP resolution of their clinical signs.
supports neoplasia as cause of hypercalcemia.
GENETICS
This ancillary screening test is not commonly
English cocker spaniels significantly over-
required, as anal gland tumors are easily
represented, springer and Cavalier King
palpable.
Charles spaniels also overrepresented. MEDICATIONS
IMAGING
INCIDENCE/PREVALENCE DRUG(S) OF CHOICE
• Abdominal radiography—to evaluate
Relatively uncommon—17% of perianal • Saline diuresis (200–300 mL/kg/day)
medial iliac lymph nodes and lumbar and
tumors, 2% of all skin/subcutaneous tumors. preoperatively if hypercalcemia is severe. Also
pelvic bones.
can consider bisphosphonate (zoledronate,
SIGNALMENT • Thoracic radiography—to evaluate for
pamidronate) or low-dose (0.25 mg/kg BID)
• Older dogs; extremely rare in cats. pulmonary metastasis.
prednisone to increase calciuresis, if corticos-
• Females overrepresented in some studies. • Abdominal ultrasonography—may
teroids not contraindicated.
• Breed predilection as stated above. identify enlarged locoregional lymph nodes
• Low-dose prednisone can also be used to
SIGNS not visible radiographically, and also
manage hypercalcemia palliatively in dogs
metastatic lesions involving visceral organs
Historical Findings that are not receiving any other therapy.
(liver/spleen).
Signs may be due to physical presence of • No controlled studies showing improved
• CT scan—identifies lymphadenopathy with
primary tumor (visible mass near anus, outcomes with adjuvant chemotherapy
greater sensitivity than ultrasound. In one
tenesmus, scooting behaviors) or lymph postoperatively; however, such studies fraught
study ultrasound found all affected lymph
nodes enlarged due to metastasis (tenesmus, with challenges, including range of stages of
nodes in only 30.8% of cases where CT
obstipation, stranguria), or systemic presenting dogs and retrospective nature of
identified multiple nodes involved.
manifestations due to hypercalcemia most publications. Theoretically, systemic
(polyuria/polydipsia, anorexia). DIAGNOSTIC PROCEDURES therapy needed to address the highly metastatic
• Fine-needle aspiration and cytology of anal biologic behavior of this tumor.
Physical Examination Findings sac mass to rule out conditions other than • Limited reports of partial responses to
• Mass associated with anal sac; may be quite adenocarcinoma; while differentiation of platinum compounds in dogs—cisplatin
small relative to significant metastatic disease benign versus malignant neoplasm of perianal (70 mg/m2 IV with 6h saline diuresis—
burdens. masses is difficult, apocrine gland adenocarci- 18.3 mL/kg/h), carboplatin (300 mg/m2 IV
• Caudal abdominal lymphadenopathy—on noma of anal sac will have neuroendocrine as slow bolus) every 3 weeks.
rectal or abdominal palpation. appearance and can be differentiated from • Mitoxantrone (5 mg/m2 IV every 3 weeks
CAUSES & RISK FACTORS perianal gland tumors. for five treatments) in combination with
None definitively identified. • Fine-needle aspiration and cytology of radiation therapy used in one small case
enlarged lymph nodes, liver, or splenic series.
nodules to confirm metastasis. • Possible role for melphalan after debulking
• Histopathology required for definitive surgery (7 mg/m2 PO q24h for 5 days every 3
diagnosis. Incisional biopsy can be consid- weeks).
DIAGNOSIS ered, but excisional biopsy appropriate if • Toceranib phosphate reported to have some
DIFFERENTIAL DIAGNOSIS location of mass and cytology supportive of benefit (partial response or stable disease) in
• Anal sac abscess. anal sac neoplasia. 28 dogs with measurable tumor. In 15 dogs
• Perianal adenoma/adenocarcinoma. with stage 4 (distant metastasis) disease,
A Adenocarcinoma, Anal Sac (continued)
toceranib phosphate led to stable disease and EXPECTED COURSE AND PROGNOSIS Suggested Reading
modest improvement in clinical signs in 13 • Wide ranges of survivals reported. Many Barnes DC, Demetriou JL. Surgical manage-
dogs, with median progression-free interval dogs do well with multiple surgeries with or ment of primary, metastatic and recurrent
and survival time of 1 year. without adjuvant therapies (chemotherapy, anal sac adenocarcinoma in the dog: 52
• Phase 1 trial combining carboplatin and radiation therapy). Long-term prognosis is cases. J Small Anim Pract 2017; 58:263–268.
toceranib phosphate in 11 dogs, 4 of which fair, with both local progression and Elliott JW. Response and outcome following
had apocrine adenocarcinoma of anal sac, identi- metastasis occurring. toceranib phosphate treatment for stage
fied combination of carboplatin (200 mg/m2 • Cures may occur if tumor is found early four anal sac apocrine gland adenocarci-
IV every 3 weeks) and toceranib phosphate and treated aggressively—median survival noma in dogs: 15 cases (2013–2017). J Am
(~2.75 mg/kg PO every other day) to be well time for nonmetastatic tumors <3.2 cm in Vet Med Assoc 2019; 254:960–966.
tolerated. Neutropenia was dose-limiting largest diameter was 1,237 days. McQuown B, Keyerleber MA, Rosen K, et al.
toxicity. All dogs with anal sac tumors • Growth of tumor may be slow and Treatment of advanced canine anal sac
responded, with 1 partial response and 3 debulking lymph node metastatic disease adenocarcinoma with hypofractionated
stable disease. Further studies are warranted. burdens may significantly prolong survival. radiation therapy: 77 cases (1999–2013).
CONTRAINDICATIONS/POSSIBLE • Hypercalcemia variably associated with Vet Comp Oncol 2017; 15:840–851.
poor prognosis, with some studies showing it Palladino S, Keyerleber MA, King RG, et al.
INTERACTIONS as negative factor. Utility of computed tomography versus
• Use caution with platinum chemotherapeu-
• Four papers (involving 200 dogs) showed abdominal ultrasound examination to
tic agents in dogs with renal insufficiency. median survival times of 6–20 months, identify iliosacral lymphadenomegaly in
• Do not use cisplatin in cats.
depending on stage and treatment. dogs with apocrine gland adenocarcinoma
• Dogs with lymph node metastasis lived of the anal sac. J Vet Intern Med 2016;
significantly longer if nodes were extirpated. 30:1858–1863.
• Ultimately, dogs that cannot have their Pradel J, Berlato D, Dobromylskyj M, et al.
FOLLOW-UP tumors excised completely succumb to Prognostic significance of histopathology in
hypercalcemia-related complications or mass canine anal sac gland adenocarcinomas:
PATIENT MONITORING
effect from primary tumor or regional nodal preliminary results in a retrospective study
• If complete resection was achieved—physi-
metastases. of 39 cases. Vet Comp Oncol 2018;
cal examination, thoracic radiography,
abdominal ultrasonography, or abdominal 16:518–528.
+/– thoracic CT and serum biochemistry at Author Laura D. Garrett
3, 6, 9, and 12 months postoperatively, then Consulting Editor Timothy M. Fan
every 6 months thereafter. MISCELLANEOUS
• Incomplete resection—frequency of and
ASSOCIATED CONDITIONS Client Education Handout
modalities for monitoring dependent on Hypercalcemia as paraneoplastic syndrome. available online
ancillary treatments selected. If further
therapies declined, at minimum monitor ABBREVIATIONS
tumor size, blood calcium, and renal values. If • MILN = medial iliac.
using adjuvant therapy, monitor based on • PTHrP = parathyroid hormone-related
specifics of therapy. peptide.
Adenocarcinoma, Lung A
OTHER LABORATORY TESTS chemotherapy may be superior. ◦ Toceranib

N/A phosphate (Palladia) has shown some anecdotal
IMAGING success. • Chemotherapy can be toxic; seek
BASICS advice if unfamiliar with cytotoxic drugs.
• Thoracic radiography—usually demonstrates
OVERVIEW focal, solitary, well‐circumscribed mass in dogs, CONTRAINDICATIONS/POSSIBLE
• Comprises >75% of primary pulmonary often in caudal lung lobes; caudal lobes most INTERACTIONS
tumors in dogs and cats. • Strongest predictors common in cats, though radiographic patterns • Doxorubicin—cardiotoxic, avoid in dogs
of outcome: tumor grade, node involvement, vary more and can include diffuse interstitial with myocardial disease (arrhythmias);
clinical signs. • May metastasize. • May be disease; radiographs must be performed in cats nephrotoxic in cats. • Cisplatin—do not give
associated with hypertrophic osteopathy. presenting with multiple digit tumors to screen to cats (fatal); do not use in dogs with
SIGNALMENT for primary lung tumor (lung‐digit syndrome). preexisting renal disease; never use without
• Ultrasonography—to obtain aspirate or biopsy appropriate and concurrent diuresis.
Dogs
specimen if mass in contact with chest wall, or
• 1% of all tumors. • Mean age of affected
evaluate abdomen for primary tumor. • CT—to
animals 10 yrs. • No sex predilection, though
assess surgical feasibility, lymphadenopathy (93%
more females in some reports. • Medium to
accuracy), metastatic disease; can see cavitated
large breeds overrepresented.
areas, irregular margins, bronchial invasion. FOLLOW‐UP
Cats PATIENT MONITORING
• Rarer than in dogs. • Mean age of affected • Serial thoracic radiographs—every 3 mths;
• Thoracocentesis with cytologic examination
animals 11 yrs. • No breed predilection. administer minimum two cycles of chemo
(for pleural effusion). • Cytology—transthoracic
SIGNS fine‐needle aspiration (83% agreement with therapy before evaluating response. • Perform
histopathology). • Percutaneous tissue biopsy— CBC (with any chemotherapy), biochemical
Historical Findings analysis (cisplatin), and urinalysis (cisplatin)
• Related to presence of lung mass: use Tru‐Cut instrument, not commonly
performed. • Open lung biopsy—via thoraco before each chemotherapy.
◦ Nonproductive cough (>50% dogs, ~40%
cats). ◦ Dyspnea (may be related to pneumo tomy, or minimally invasive thoracoscopy. POSSIBLE COMPLICATIONS
thorax or pleural effusion). ◦ Tachypnea. PATHOLOGIC FINDINGS • Following diagnostic procedures or
◦ Hemoptysis. • Paraneoplastic signs: • Adenocarcinoma—classified by location thoracotomy—pneumo‐ or hemothorax.
◦ Lameness—bone metastasis or hypertrophic (bronchial, bronchiolar, bronchiolar‐alveolar, • Resulting from chemotherapy—myelo
osteopathy (dogs or cats), weight‐bearing lytic or alveolar) and degree of differentiation. suppression, fever, sepsis, nausea.
digit metastasis (cats). ◦ Polyuria or polydipsia— • Immunohistochemistry on biopsy for thyroid EXPECTED COURSE AND PROGNOSIS
hypercalcemia or hyperadrenocorticism from transcription factor‐1 (TTF‐1), surfactant • Metastasis to tracheobronchial lymph
ectopic production of adrenocorticotrophic protein A, and napsin A to confirm pulmonary nodes—single best prognostic indicator;
hormone (ACTH). ◦ Fever. carcinoma, especially adenocarcinoma. TTF‐1 median survival without metastasis approaches
Physical Examination Findings and napsin A can also be seen in thyroid tumors. 1 yr and with metastasis, 60 days. More
• May be asymptomatic or lack respiratory • Cats tend to have less differentiated tumors, common (75%) in cats. • Postoperative
signs (~25% dogs, 9% cats). • Tachypnea, corresponding to more aggressive behavior. survival around 2 yrs in both cats and dogs if
dyspnea. • Fever. • Limb swelling. • Ascites, positive prognostic factors present, and ~1 yr
pleural effusion. overall in dogs, 4 mths overall in cats.
• Other patient, tumor, and treatment factors
Some (controversial) evidence correlates risk TREATMENT positively influencing prognosis—complete
• Surgery—mainstay of treatment: partial or surgical excision; size of primary tumor (<5 cm);
to urban environment; secondhand environ lack of metastasis; well‐differentiated cellular
mental tobacco smoke not definitively linked complete lobectomy with tracheobronchial
lymph node biopsy or removal; thoracoscopic morphology on histopathology, lack of
to primary lung cancer in dogs, though weak clinical signs prior to surgery. • Poor
association seen in dogs with short and removal possible at limited centers and offers
less postoperative morbidity. • Radiotherapy— prognosis for cats with lung‐digit syndrome
medium‐length noses. poor (~1 mth).
reports anecdotal, but certain patients may
benefit. • Chemotherapy should be considered
following surgery for tumors that are high
grade, undifferentiated, and/or have nodal
DIAGNOSIS involvement, though no benefit confirmed. MISCELLANEOUS
• Cytology of mass aspirate. • Tissue biopsy/ Intracavitary chemotherapy can be used to
definitive resection. treat malignant pleural effusion. PREGNANCY/FERTILITY/BREEDING
Chemotherapy not advised in pregnant animals.
DIFFERENTIAL DIAGNOSIS
• Granulomatous lesion (fungal, foreign body, ABBREVIATIONS
parasitic). • Pulmonary abscess. • Other • ACTH = adrenocorticotrophic hormone.
primary lung tumor: ◦ Squamous cell MEDICATIONS • TTF‐1 = thyroid transcription factor‐1.
carcinoma. ◦ Sarcomas (osteo‐, chondro‐, DRUG(S) OF CHOICE Suggested Reading
lipo‐). • Metastatic lung tumor. • Pneumonia. • Chemotherapy—vinorelbine concentrates Rissetto KC, Lucas P, Fan TM. An update on
• Asthma. • Pulmonary thromboembolism. in lungs and responses have been seen. diagnosing and treating primary lung
• Congenital cyst. • Lung torsion/hematoma. ◦ Doxorubicin, cisplatin, carboplatin, tumors. Vet Med 2008, 103(3):154.
CBC/BIOCHEMISTRY/URINALYSIS mitoxantrone, vinorelbine, and/or vindesine: Author Kim A. Selting
No specific abnormalities. rational choices for primary or adjuvant Consulting Editor Timothy M. Fan
therapy. ◦ Platinum‐based or gemcitabine
A Adenocarcinoma, Nasal
• Abnormal mentation or other neurologic biopsy instrument including retroflex
findings (rare). rhinoscopic biopsy of nasopharynx, cannula
CAUSES (closed suction), or hydropulsion techniques.
BASICS • Cytologic evaluation of regional lymph
Dolichocephalic morphology, p53 mutations,
DEFINITION and cyclooxygenase-2 (COX-2) overexpression nodes to detect regional metastatic disease.
Malignant neoplasm involving the nasal may all play a role. PATHOLOGIC FINDINGS
cavity and paranasal sinuses. • Bilateral involvement and osteolysis common.
RISK FACTORS
PATHOPHYSIOLOGY • Regional lymph node metastasis <10% at
Urban environment and secondhand smoke
Progressive local and regional invasion of the may be risk factors. time of diagnosis, but up to 45% at necropsy.
nasal cavity, paranasal sinuses, and surrounding
tissues by neoplastic epithelial and glandular
epithelial cells.
SYSTEMS AFFECTED DIAGNOSIS TREATMENT
• Respiratory—congestion, epistaxis, APPROPRIATE HEALTH CARE
mucopurulent nasal discharge, obstruction, DIFFERENTIAL DIAGNOSIS
• Radiation therapy is standard of care.
dyspnea. • Other sinonasal tumors (e.g., squamous cell
carcinoma, lymphoma, sarcomas, olfactory • Radiation therapy can be administered with
• Ophthalmic—exophthalmos, epiphora. curative intent (conventional definitive or
• Musculoskeletal—facial deformity. neuroblastoma).
• Intracranial neoplasia (in dogs or cats with
stereotactic radiotherapy) or for palliation of
• Nervous—seizures, altered mentation. clinical signs.
neurologic signs).
INCIDENCE/PREVALENCE • Viral infection—cats. • Conventional definitive radiation involves
• In dogs, less than 2% of all tumors are nasal • Fungal infections, including aspergillosis
multiple fractions for high total dose; usually
tumors. (dogs) and cryptococcosis (cats). 10–20 fractions to allow normal tissue
• In dogs, adenocarcinoma more common • Bacterial sinusitis.
recovery with goal of minimizing risk of late
than squamous cell carcinoma, chondro • Parasites (e.g., nasal mites).
permanent radiation side effects.
sarcoma, and other histologies, comprising • Stereotactic radiation therapy is newer
• Foreign body.
31.5% of all nasal tumors. • Trauma.
technique that allows more conformal
• In cats, nasal tumors comprise <1% of all • Tooth root abscess and oronasal fistula.
treatment than conventional techniques to
tumors. In cats, adenocarcinoma and • Coagulopathies (nasal tumors most often
avoid toxicity to normal tissue without
lymphoma are most common. tend to be unilateral epistaxis; coagulopathy sacrificing tumor control; comparable dose
GEOGRAPHIC DISTRIBUTION tends to be bilateral epistaxis). delivered over much shorter time than with
Nasal adenocarcinomas are more commonly • Systemic hypertension (nasal tumors most
conventional techniques; stereotactic radio-
reported in urban areas. often tend to be unilateral epistaxis; hypertension therapy involves 1–5 consecutive daily
tends to be bilateral epistaxis). fractions.
SIGNALMENT • Palliative radiation involves much lower
• Dog and cat. CBC/BIOCHEMISTRY/URINALYSIS total dose than definitive to minimize toxicity
• Median age in dogs is 10 years and in cats • Usually normal. while improving quality of life through
is 13 years. • Occasional blood loss anemia. reduction of tumor size; usually 4–6 fractions.
• In dogs, medium to large breeds affected OTHER LABORATORY TESTS • Combining radiation therapy with novel
more commonly, with possible overrepres • Cytologic examination—occasionally drug therapy (toceranib phosphate—Palladia®,
entation of mesocephalic and dolichocephalic helpful (e.g., aspirates of subcutaneous mass if and others) appears safe and well tolerated.
breeds. facial deformity). • Radiation therapy followed by surgery to
SIGNS • Coagulation profile to rule out coagulopathy. debulk residual mass may improve local
• Blood pressure to rule out systemic control time, but results in higher rate of
Historical Findings complications.
• Intermittent and progressive history of
hypertension.
• Surgery alone considered ineffective, with
unilateral to bilateral epistaxis and/or IMAGING most tumors relapsing within 6 months.
mucopurulent discharge that initially • Survey skull radiography—not sensitive;
responds to antibiotic therapy (median may show asymmetric destruction of NURSING CARE
duration 3 months). turbinates accompanied by soft tissue mass • During radiation therapy, supportive care
• Sneezing and increased upper respiratory effect; may see fluid density in frontal sinuses for radiation-related mucositis may involve
noises, including reverse sneezing. secondary to outflow obstruction. softening food; rinsing mouth with “magic
• Open-mouth breathing. • Thoracic radiography—evaluate for lung mouthwash” (topical anesthetic), saline, or
• Halitosis. metastasis (uncommon). dilute black tea; and administration of
• Anorexia (more frequent in cats). • CT or MRI best imaging method for local medications to control discomfort.
• Seizures (rare—secondary to invasion of staging and observing integrity of cribriform • These side effects temporary, but may cause
cranial vault). plate or orbital invasion; also used for discomfort for 10–14 days.
therapeutic planning. ACTIVITY
• Nasal discharge (blood, mucopurulent). DIAGNOSTIC PROCEDURES • Limit activity to minimize risk of epistaxis
• Decreased or absent airflow in nasal • Oral examination under anesthesia. and dyspnea.
passages (unilateral or bilateral). • Rhinoscopy may permit visual observation • Using harness instead of collar during walks
• Facial deformity, exophthalmos, epiphora. of mass and aid biopsy. may help minimize epistaxis.
• Pain upon nasal or paranasal sinus • Tissue biopsy necessary for definitive DIET
palpation or upon opening mouth. diagnosis—biopsies may be performed blind, • Soften food if needed during radiation therapy.
• Regional lymphadenomegaly (rare). following advanced imaging, using pinch
(continued) Adenocarcinoma, Nasal A
• Avoid extremes of temperatures and salty ALTERNATIVE DRUG(S)

foods with radiation therapy–related • Palladia, a tyrosine kinase inhibitor, may
mucositis. have anticancer activity in some carcinomas,
including nasal adenocarcinomas. It is MISCELLANEOUS
CLIENT EDUCATION
• Nasal adenocarcinoma may be painful currently being investigated alone and in PREGNANCY/FERTILITY/BREEDING
even though pet not showing visible signs combination with radiation therapy. Chemotherapeutic drugs and general
of pain. • Objective responses have been documented anesthesia are a risk to the fetus and would
• Consider use of medications for discomfort, with use of Palladia alone. not be recommended in pregnant animals.
epistaxis, and congestion. • Yunnan Baiyao, a Chinese herbal medication,
SYNONYMS
• Radiation therapy most effective option is often prescribed for epistaxis.
• Nasal carcinoma.
and well tolerated using modern radiotherapy • Nasal tumor.
techniques, with fewer side effects than
SEE ALSO
previously reported.
• Chondrosarcoma, Nasal and Paranasal Sinus.
• Radiation side effects may impact patient’s FOLLOW-UP • Squamous Cell Carcinoma, Nasal and
quality of life during treatment, but most pets
PATIENT MONITORING Paranasal Sinus.
enjoy relatively normal quality of life following
• Clinical response is usually observed within • Squamous Cell Carcinoma, Nasal Planum.
treatment.
2–3 weeks from start of radiation therapy. ABBREVIATIONS
• Intermittent congestion, nasal discharge,
Reductions in epistaxis, nasal discharge, • COX-2 = cyclooxygenase-2.
and sneezing may occur post therapy due to
congestion, and sneezing are expected.
increased sensitivity from tumor’s destruction INTERNET RESOURCES
• CT or MRI is needed to assess objective
of nasal turbinates. • https://veterinarymedicine.dvm360.com/
tumor response to therapy and is recommended
SURGICAL CONSIDERATIONS 2–3 months post radiation treatment. vetmed/Medicine/Canine-and-feline-
Anesthetic recovery—ensure airway is • Other staging tests, including thoracic nasaltumors/ArticleStandard/Article/
maintained until animal is sternal and alert, imaging (radiography or CT) and lymph detail/735167
to prevent apnea in patients with bilateral node evaluation, are generally recommended • https://www.ncbi.nlm.nih.gov/pubmed?ter
nasal obstruction. at 3-month intervals during/following m=dog+nasal+carcinoma+radiotherapy&cmd
therapy. =DetailsSearch
• Routine staging with CT/MRI and Suggested Reading
monitoring of recurrent clinical signs can Adams WA, Bjorling DE, McAnulty JF, et al.
MEDICATIONS detect early recurrence. Outcome of accelerated radiotherapy alone
POSSIBLE COMPLICATIONS or accelerated radiotherapy followed by
DRUG(S) OF CHOICE exenteration of the nasal cavity in dogs with
• Chemotherapy is considered ineffective for • Pain.
• Dyspnea. intranasal neoplasia: 53 cases (1990–2002).
durable tumor control, but may benefit some J Am Vet Med Assoc 2005, 227:936–941.
patients if radiation therapy is not viable • Epistaxis.
• Secondary infections. Adams WA, Kleiter MM, Thrall DE, et al.
option. Various drugs have been described, Prognostic significance of tumor histology
including cisplatin (dogs only), carboplatin, • Weight loss.
• Anorexia. and computed tomographic staging for
doxorubicin, and piroxicam. Toceranib radiation treatment response of canine nasal
phosphate (Palladia) exerts therapeutic • Chemotherapy or radiation toxicity.
tumors. Vet Radiol Ultrasound 2009,
activity against nasal carcinoma. EXPECTED COURSE AND PROGNOSIS 50(3):330–335.
• Consult with oncologist for more details. • Untreated—median survival around 2–6
Geiger TL, Nolan MW. Linac-based
• Adequate analgesic therapy should be months. stereotactic radiation therapy for canine
employed as needed in patients suffering from • Definitive conventional and stereotactic
non-lymphomatous nasal tumors: 29 cases
invasive disease with bone destruction, signs radiation therapy—median survival times (2013–2016). Vet Comp Oncol 2018,
of pain, or radiation therapy side effects. reported at 12–18 months in dogs and 12–20 16:E68–E75.
CONTRAINDICATIONS months in cats; 1-year survival rate 20–57% Henry CJ, Brewer WG, Tyler JW, et al.
Cisplatin—never use in cats. (dogs and cats); 2-year survival rate 20–48% Survival in dogs with nasal adenocarcinoma:
(dogs and cats). 64 cases (1981–1995). J Vet Intern Med
PRECAUTIONS • Presence of cribriform lysis, brain involve
• Most chemotherapeutics have risk of 1998, 12:436–439.
ment, or metastatic disease (advanced stage) LaDue TA, Dodge R, Page RL, et al. Factors
gastrointestinal, hematologic, and other are poor prognostic indicators.
potential side effects, and should be influencing survival after radiotherapy of
• Ophthalmic complications of radiation
administered and monitored by an nasal tumors in 130 dogs. Vet Radiol
therapy—more likely in dogs than cats. Ultrasound 1999, 40:312–317.
oncologist. • Incidence and severity of ophthalmic
• Piroxicam can cause gastric ulceration, so Author Jayme S. Looper
toxicity have dramatically decreased with Consulting Editor Timothy M. Fan
careful monitoring of appetite, vomiting, and advanced radiation therapy techniques now
stool color (melena) is recommended. commonly used.
POSSIBLE INTERACTIONS • Chronic rhinitis is possible following
Concurrent radiation therapy and chemo radiation therapy for sinonasal tumors and
therapy will increase risk of side effects, but may require periodic symptomatic therapy.
have not shown to significantly improve
tumor control.
A Adenocarcinoma, Pancreas
IMAGING
• Abdominal radiographs may reveal a mass
or loss of serosal detail associated with
BASICS concurrent pancreatitis or peritoneal effusion. FOLLOW-UP
OVERVIEW • Ultrasonography may reveal one or more POSSIBLE COMPLICATIONS
• Malignant tumor of ductal or acinar origin masses or concurrent pancreatitis (mixed • Intestinal obstruction
arising from the exocrine pancreas. echogenicity, large pancreas, hyperechoic • Biliary obstruction
• Usually metastatic by the time of diagnosis, peripancreatic fat). Pancreatic thickening, • Pancreatic abscess
affecting regional lymph nodes and visceral abdominal effusion, and single to multiple • Peritonitis
abdominal organs (liver) and associated nodules of varying size may be identified. • Metastasis
peritoneal cavity. Sonographic findings may be impossible to
EXPECTED COURSE AND
distinguish from pancreatic nodular hyper-
SIGNALMENT PROGNOSIS
plasia. Rarely the ultrasound of the pancreas
• Rare in dogs—0.5–1.8% of all tumors. Progression to death is often rapid given that
may appear normal except for dilation of the
• Rare in cats—2.8% of all tumors. there is no successful curative treatment
pancreatic duct.
• Older female dogs and Airedale terriers at available. Despite the grave prognosis,
• Abdominal CT will allow for therapeutic
higher risk than others. individual patients treated with complete
decisions regarding surgical resectability and
• Median age (dogs)—9.2 years. resection of their tumor and chemotherapy, in
approach, which can affect the owner’s
• Mean age (cats)—11.6 years. the absence of systemic metastasis, may have
willingness to treat.
SIGNS prolonged survival.
• Nonspecific—fever; vomiting; weakness;
• Surgical biopsy—definitive.
anorexia; icterus; malabsorption syndrome;
• Fine-needle aspirate cytology—supportive.
weight loss.
In many cases, where the tumor is not
• Abdominal pain—variable.
resectable, the fine-needle aspirates may MISCELLANEOUS
• Abdominal effusion—malignant.
provide strong enough evidence to start ASSOCIATED CONDITIONS
• Metastasis to bone and soft tissue common.
medical treatment. Gastrin-secreting pancreatic carcinoma
• Pathologic fractures secondary to metastasis
reported. (gastrinoma) has been reported in dogs and
• Palpable abdominal mass (cats). cats. Clinical signs are associated with
• Paraneoplastic syndromes of epidermal hypergastrinemia, which results in inapprop
necrosis, hyperinsulinemia, and hypergluca- TREATMENT riate hydrochloric acid secretion by the
gonemia may be present. • None reported curative. stomach, leading to gastroduodenitis.
• Average duration of clinical signs (cats): 41 • Palliation of pain with aggressive analgesic Suggested Reading
days, range 2–180 days. combinations is necessary. Cave T, Evans H, Hargreavest J, et al.
• Surgical intervention to alleviate intestinal Metabolic epidermal necrosis in a dog
Unknown and biliary obstruction, if necessary. associated with pancreatic adenocarcinoma,
• Surgery is typically not a good option in hyperglucagonaemia, hyperinsulinaemia,
many cases, due to the extent of the disease at and hypoaminoacidaemia. J Small Anim
the time of diagnosis. Pract 2007, 48:522–526.
• If surgery is an option, partial or total Hecht S, Penninck DG, Keating JH. Imaging
DIAGNOSIS pancreatectomy may prolong survival. A findings in pancreatic neoplasia and nodular
DIFFERENTIAL DIAGNOSIS Whipple procedure (pancreaticoduodenectomy) hyperplasia in 19 cats. Vet Radiol Ultrasound
• Primary pancreatitis; may be concurrent
and/or partial colon resection may be required 2006, 48:45–50.
and complicate or delay early diagnosis. for tumor resection. This can influence the Linderman MJ, Brodsky EM, de Lorimier LP,
• Pancreatic pseudocyst.
perisurgical morbidity and mortality risk. et al. Feline exocrine pancreatic carcinoma:
• Treat concurrent pancreatitis. a retrospective study of 34 cases. Vet Comp
• Pancreatic nodular hyperplasia.
• Antiemetics and supportive care (hydration Oncol 2013, 11(3):208–218.
• Hepatic neoplasia.
• Other causes of vomiting and icterus.
and caloric requirements). Author Nick Dervisis
• Peritoneal carcinomatosis. Consulting Editor Timothy M. Fan
• Other causes of abdominal effusion in cats.
• Usually nonspecific changes (e.g., mild MEDICATIONS
anemia and neutrophilia). DRUG(S) OF CHOICE
• Hyperamylasemia less reliable than • Gemcitabine is used in humans for the
hyperlipasemia. treatment of pancreatic carcinoma, and while
• Lipase concentrations are often markedly used in dogs with cancer, it has not been
elevated and may serve as a noninvasive established as the standard of care for dogs
biochemical marker of neoplasia in dogs. with pancreatic adenocarcinoma.
OTHER LABORATORY TESTS • Always consult a veterinary oncologist for
Rarely there may be significant metabolic updates in treating this rare neoplasm.
alterations that affect glucagon, insulin, and CONTRAINDICATIONS/POSSIBLE
amino acid concentrations. INTERACTIONS
N/A
Adenocarcinoma, Prostate A
OTHER LABORATORY TESTS PREVENTION/AVOIDANCE

Serum and seminal plasma markers such as Keeping dogs sexually intact may decrease risk.
acid phosphatase, prostate-specific antigen, POSSIBLE COMPLICATIONS
BASICS and canine prostate-specific esterase are not • Urethral obstruction.
OVERVIEW elevated in dogs with PAC. • Metastasis to regional lymph nodes, skeleton,
• Prostatic adenocarcinoma (PAC) is a IMAGING and lungs.
malignant tumor that occurs in both neutered • Thoracic radiography—metastases may
and intact male dogs. EXPECTED COURSE AND PROGNOSIS
appear as pulmonary nodules or increased Guarded to poor, survival of 2–6 months
• Although this neoplasm represents <1% of interstitial markings.
all canine malignancies, it is the most common depending upon presenting clinical
• Abdominal radiography—sublumbar
prostatic disorder in neutered male dogs. symptoms.
lymphadenomegaly, mineralization of the
• Metastases to regional lymph nodes, lungs, prostate, and lytic lesions to the lumbar
and the lumbosacral skeleton are common. vertebrae or pelvis may be seen.
SIGNALMENT • Abdominal ultrasonography—focal to
• Dogs and rarely cats. multifocal hyperechogenicity with asymmetry MISCELLANEOUS
• Medium- to large-breed intact or neutered and irregular prostatic outline, ± prostatic ZOONOTIC POTENTIAL
male dogs. mineralization. None
• Median age of 9–10 years. • Contrast cystography may help differentiate
prostatic from urinary bladder disease. PREGNANCY/FERTILITY/BREEDING
SIGNS N/A
Historical Findings ABBREVIATIONS
• Prostatic aspirate (percutaneous or trans-
• Tenesmus (with the production of • NSAID = nonsteroidal anti-inflammatory
rectal).
ribbon-like stool). drug.
• Prostatic wash.
• Weight loss. • PAC = prostatic adenocarcinoma.
• Prostatic biopsy performed percutaneously
• Stranguria and dysuria.
or surgically. Suggested Reading
• Rear limb lameness.
• Percutaneous biopsy has been associated Axiak SM, Bigio A. Canine prostatic
• Lethargy.
with tumor seeding along the biopsy tract. carcinoma. Compend Contin Educ Vet
• Exercise intolerance.
2012, 34(10):E1–E4.
Physical Examination Findings Author Ruthanne Chun
• A firm, asymmetric, and immobile prostate Consulting Editor Timothy M. Fan
gland.
• Prostatomegaly is common, but is not TREATMENT
always present. • Prostatectomy if local disease (success of
• Pain may be elicited in response to this procedure depends on skill of surgeon
abdominal or rectal palpation. and extent of disease).
• Caudal abdominal mass, cachexia, pyrexia, • Radiation therapy may palliate signs and
and dyspnea may also be identified. prolong survival.
• Neutering—however, most tumors are not
CAUSES & RISK FACTORS androgen responsive.
Neutered males are at increased risk for • Stenting of the prostatic urethra will resolve
prostatic neoplasia. urinary outflow obstruction and thereby
prolong survival.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS MEDICATIONS
• Other primary neoplasia (i.e., squamous DRUG(S) OF CHOICE
cell carcinoma, transitional cell carcinoma). • Chemotherapy—carboplatin, cisplatin, or
• Metastatic or locally invasive neoplasia (i.e., doxorubicin; may offer short-term benefit.
transitional cell carcinoma). • Pain relief with nonsteroidal anti-inflamma-
• Acute or chronic prostatitis, benign prostatic tory drugs (NSAIDs), morphine-derived drugs.
hypertrophy, and prostatic cysts are possible • Stool softeners to relieve tenesmus.
differentials in intact male dogs, but are
highly unlikely in neutered dogs. CONTRAINDICATIONS/POSSIBLE
CBC/BIOCHEMISTRY/URINALYSIS INTERACTIONS
• Inflammatory leukogram possible.
N/A
• Alkaline phosphatase may be high.
• Postrenal azotemia may be present if
urethral obstruction exists.
• It is prudent to evaluate urine samples via FOLLOW-UP
cystocentesis and free-catch techniques, as
hematuria, pyuria, and malignant epithelial cells PATIENT MONITORING
may be observed in free-catch samples, but are Ability to urinate and defecate, pain secondary
unusual in samples obtained by cystocentesis. to skeletal metastases, quality of life.
A Adenocarcinoma, Renal
DIAGNOSTIC PROCEDURES neutrophilic leukocytosis have been reported
• Renal biopsy (ultrasound guided or in isolated cases.
surgical) for definitive diagnosis. • Renal failure.
BASICS • Mitotic index found to be prognostic in 70 • Nodular dermatofibrosis and uterine
OVERVIEW dogs treated with nephrectomy. leiomyomas are commonly associated with
• Accounts for <1% of all reported neoplasms cystadenocarcinoma.
in dogs. ABBREVIATIONS
• Renal tumors tend to be highly metastatic, • GGT = gamma-glutamyltransferase.
locally invasive, and often bilateral.
• Renal cystadenocarcinoma, a rare heritable
TREATMENT • hpf = high-power field.
• Aggressive surgical excision is the treatment Suggested Reading
syndrome with a less aggressive behavior and
of choice for unilateral disease. Bryan JN, Henry CJ, Turnquist SE, et al.
better long-term prognosis than renal adeno-
• Successful chemotherapeutic management Primary renal neoplasia of dogs. J Vet Intern
carcinoma, has been described in German
of either disease has not been described. Med 2006, 20:1155–1160.
shepherd dogs.
• Supportive management for patients in De Lorimier LP, Bernard S. Marked serum
SIGNALMENT renal failure may be necessary. GGT elevations in two dogs with renal
• Adenocarcinoma—older (8–9 years) dogs, carcinoma. Letter to the Editor. J Small
1.6 : 1 male-to-female ratio, no breed Anim Pract 2017, 58:187.
predilection. Edmondson EF, Hess AM, Powers BE.
• Cystadenocarcinoma—German shepherd Prognostic significance of histologic features
dogs, often female. MEDICATIONS
in canine renal cell carcinomas: 70
SIGNS DRUG(S) OF CHOICE nephrectomies. Vet Pathol 2015, 52:260–268.
• Adenocarcinoma—insidious, nonspecific None Knapp DW. Tumors of the urinary system.
signs such as weight loss, inappetance, CONTRAINDICATIONS/POSSIBLE In: Withrow SJ, Vail DM, eds., Small
lethargy, hematuria, and pale mucous INTERACTIONS Animal Clinical Oncology, 4th ed.
membranes. N/A Philadelphia, PA: Saunders, 2007, pp.
• Cystadenocarcinoma—may present for 649–658.
nodular dermatofibrosis, a syndrome of Author Ruthanne Chun
painless, firm, fibrous lesions of the skin and Consulting Editor Timothy M. Fan
subcutaneous tissues.
FOLLOW-UP
• Adenocarcinoma—unknown. PATIENT MONITORING
• Cystadenocarcinoma—heritable in German • Renal failure—measure serum urea
shepherd dogs. nitrogen and creatinine; urinalysis.
• Quality of life if bilateral or otherwise
nonsurgical disease.
DIAGNOSIS N/A
DIFFERENTIAL DIAGNOSIS POSSIBLE COMPLICATIONS
• Other primary neoplasia (i.e., lymphoma, • Renal failure.
nephroblastoma). • Metastatic disease.
• Metastatic neoplasia (i.e., hemangiosarcoma). • Invasion of local vital structures (vena cava,
• Renal adenoma or cyst. aorta).
• Pyelonephritis. EXPECTED COURSE AND PROGNOSIS
CBC/BIOCHEMISTRY/URINALYSIS • Adenocarcinoma—median reported
• CBC may show paraneoplastic poly- survival of 49 dogs was 16 months (range
cythemia or leukocytosis, or anemia. 0–59).
• Biochemistry may be normal, or may reveal • Cystadenocarcinoma—few large studies of
azotemia. Marked gamma-glutamyltransferase this rare disease, reported median survival of
(GGT) elevation may be prognostic. 12+ months with no definitive therapy.
• Urinalysis may show hematuria, proteinu- • Based on mitotic index: >30 mitotic
ria, bacteriuria, or casts. figures/10 high-power fields (hpf; median
survival of 187 days) vs. 10–30/10 hpf
OTHER LABORATORY TESTS (median survival of 452 days) vs. <10/hpf
Urine culture and sensitivity. (median survival of 1184 days).
IMAGING
• Thoracic radiographs—metastatic disease
reported in up to 16% of patients.
• Abdominal radiographs—mass visualized in
81% of patients.
MISCELLANEOUS
• Abdominal ultrasonography, CT, or ASSOCIATED CONDITIONS
contrast radiography—useful in identifying • The paraneoplastic syndromes of hyper-
and staging the disease. trophic osteopathy, polycythemia, and a
Adenocarcinoma, Salivary Gland A
• MRI or CT imaging allows superior • Median survival 550 days for dogs and 516
discrimination of tumor for surgery and/or days for cats in retrospective study.
radiation treatment planning. • Local control obtained through radiation
BASICS • Thoracic radiographs indicated to check for and/or surgery is critical to outcome.
OVERVIEW lung metastases.
• Tumor arising from major (e.g., parotid, DIAGNOSTIC PROCEDURES
mandibular, sublingual, or zygomatic) or • Cytologic examination of aspirate may
minor salivary glands.
• Mandibular or parotid glands constitute
differentiate salivary adenocarcinoma from MISCELLANEOUS
mucocele and abscess.
80% of cases. • Biopsy for histopathology is required for Suggested Reading
• Mandibular gland most frequently affected definitive diagnosis. Hammer A, Getzy D, Ogilvie G, et al.
in dogs. Salivary gland neoplasia in the dog and cat:
• Parotid gland most frequently affected in survival times and prognostic factors.
cats. JAAHA 2001, 37:478–482.
• Locally invasive. Blackwood L, Harper A, Elliot J, Gramar I.
• Cats typically have more advanced disease TREATMENT External beam radiotherapy for the
than dogs at time of diagnosis. • Aggressive surgical resection—when treatment of feline salivary gland carcinoma:
• Metastasis—regional lymph node in 39% possible; most are invasive and difficult to six new cases and a review of the literature. J
of cats and 17% of dogs at diagnosis; distant excise completely. Feline Med Surg 2019, 21(2):186–194.
metastasis reported in 16% of cats and 8% of • Radiotherapy—good local control and Author Anthony J. Mutsaers
dogs at diagnosis, but may be slow to develop. prolonged survival may be possible. Consulting Editor Timothy M. Fan
• Epithelial malignancies—constitute roughly • Aggressive local resection (usually histologi-
85% of salivary gland tumors. cally incomplete) followed by adjuvant
• Adenomas comprise only 5% of salivary radiation can achieve local control and
tumors. long-term survival in some cases, but further
studies are needed to determine the most
SIGNALMENT
effective treatment, including the possible
• Dogs and cats.
role for chemotherapy.
• Mean age, 10–12 years.
• Siamese cats may be at relatively higher risk.
• Male cats affected twice as often as female cats.
• No other breed or sex predilection has been
determined. MEDICATIONS
SIGNS DRUG(S) OF CHOICE
• Unilateral, firm, painless swelling of the Chemotherapy efficacy is largely unreported;
upper neck (mandibular and sublingual), ear however, it may be indicated for treatment/
base (parotid), upper lip or maxilla (zygo- palliation of metastatic disease.
matic), or mucous membrane of lip (acces-
CONTRAINDICATIONS/POSSIBLE
sory or minor salivary tissue).
• Other signs may include halitosis, weight INTERACTIONS
loss, anorexia, dysphagia, exophthalmus, N/A
Horner’s syndrome, sneezing, and dysphonia.
Unknown
FOLLOW-UP
PATIENT MONITORING
Evaluations—physical examination and
DIAGNOSIS thoracic radiographs every 3 months
reasonable if aggressive surgery and/or
DIFFERENTIAL DIAGNOSIS radiation therapy employed.
• Squamous cell carcinoma.
• Mucocele. POSSIBLE COMPLICATIONS
• Abscess. Temporary acute side effects (e.g., moist
• Soft tissue sarcoma, e.g., fibrosarcoma. dermatitis and alopecia) expected with
• Lymphoma. radiation therapy. Consultation with a
radiation oncologist is recommended
CBC/BIOCHEMISTRY/URINALYSIS regarding specific, anatomic site–related side
Results often normal. effects associated with planned dose and field
OTHER LABORATORY TESTS size.
N/A EXPECTED COURSE AND PROGNOSIS
IMAGING • Improved survival time in dogs without
• Regional radiographs usually are normal; evidence of nodal or distant metastasis at
may see periosteal reaction on adjacent bones diagnosis; clinical stage not prognostic
or displacement of surrounding structures. for cats.
A Adenocarcinoma, Skin (Sweat Gland, Sebaceous)
PATHOLOGIC FINDINGS improve survival. A study reported a
• Apocrine gland adenocarcinomas are postexcisional median survival time of
divided into multiple subtypes based on the 30 months in dogs.
BASICS anatomic location they arise in. They typically
OVERVIEW are invasive into the underlying stroma and
• Malignant growth originating from blood vessels, and often show poorly
sebaceous or apocrine sweat glands of the skin. demarcated borders and a high mitotic index.
• Approximately 2% of all skin tumors in • Sebaceous gland adenocarcinomas often MISCELLANEOUS
dogs. reveal lymphatic vessel invasion. Suggested Reading
Carpenter JL, Andrews LK, Holzworth J.
SIGNALMENT
Tumors and tumor like lesions. In:
• Apocrine sweat gland—rare in dogs,
Holzworth J, ed. Diseases of the Cat:
uncommon in cats.
Medicine and Surgery. Philadelphia, PA:
• Sebaceous gland—rare in both dogs and TREATMENT Saunders, 1987, pp. 406–596.
cats. • Aggressive en bloc surgical excision, Hauck ML. Tumors of the skin and subcuta-
• Middle-aged to older pets. including resection of draining lymph node, neous tissues. In: Withrow SJ, Vail DM,
• Male intact dogs overrepresented for recommended for both types. Page RL, eds., Small Animal Clinical
sebaceous gland adenocarcinomas. Histopathologic analysis of lymph nodes Oncology, 5th ed. St. Louis, MO: Elsevier
• Female dogs overrepresented for apocrine assists with determining prognosis and Saunders, 2013, pp. 305–320.
adenocarcinoma in one study. establishing adjuvant treatment plan. Haziroglu R, Haligur M, Keles H.
SIGNS • Margins of entire tissue specimen must be Histopathological and immunohistochemi-
• May appear as solid, firm, raised, superficial evaluated histologically to assess completeness cal studies of apocrine sweat gland
skin lesions. of resection. adenocarcinomas in cats. Vet Comp Oncol
• May be ulcerated and bleeding and • Radiation therapy may be recommended 2014, 12(1):85–90.
accompanied by inflammation of the for treatment of draining lymph nodes after Kycko A, Jasik A, Bocian L, et al.
surrounding tissue. resection to prevent recurrence and develop- Epidemiological and histopathological
• Apocrine sweat gland—often poorly ment of regional metastasis; radiation therapy analysis of 40 apocrine sweat gland
circumscribed, ulcerated and potentially of primary tumor site recommended when carcinomas in dogs: a retrospective study. J
purple in color; very invasive into underlying wide and complete resection not possible. Vet Res 2016, 61:331–337.
tissue; may occur anywhere on the body, Pakhrin B, Kang MS, Bae IH, et al.
frequently affecting the limbs and trunk in Retrospective study of canine cutaneous
dogs and head, limbs, and abdomen in cats. tumors in Korea. J Vet Sci 2007,
• Sebaceous gland—often nodular, ulcerated MEDICATIONS 8:229–236.
and inflamed, moderate risk of lymph node Simko E, Wilcock BP, Yager JA. A retrospec-
involvement; frequently found on head and DRUG(S) OF CHOICE tive study of 44 canine apocrine sweat gland
neck in dogs and on the head, thorax, and • Chemotherapy has been used anecdotally adenocarcinomas. Can Vet J 2003,
perineum in cats. for the treatment of both tumor types, in 44(1):38–42.
• Dermal and lymphatic tracking can be both species. Author Jason Pieper
observed early in disease course. • Contact a veterinary oncologist for any Consulting Editor Timothy M. Fan
updated treatments that may be available. Acknowledgment The author and book
CAUSES & RISK FACTORS • Nonsteroidal anti-inflammatory drugs and
Unknown editor acknowledge the prior contribution of
other analgesics are recommended, as Louis-Philippe de Lorimier.
indicated, for pain control.
INTERACTIONS
DIAGNOSIS None
• Other more frequent skin tumors.
• Cutaneous histiocytic diseases.
• Immune-mediated skin diseases.
• Deep bacterial/fungal infections.
FOLLOW-UP
• Sebaceous gland adenocarcinoma—little is
CBC/BIOCHEMISTRY/URINALYSIS known about the metastatic potential of this
Normal malignancy, but it may be rapidly metastatic
OTHER LABORATORY TESTS to regional lymph nodes in some patients;
N/A long-term prognosis is anecdotally good with
multimodal therapy combining aggressive
IMAGING surgery, chemotherapy, and radiation therapy.
Thoracic radiographs recommended at time • Apocrine gland adenocarcinoma—fair to
of diagnosis to assess for distant metastases. good long-term prognosis; the histologic
DIAGNOSTIC PROCEDURES finding of vascular invasion is a negative
• Biopsy for histopathology and definitive prognostic factor predicting systemic
diagnosis. metastases; aggressive surgical resection (local
• Cytologic examination or biopsy of and regional tumor control) followed by
draining lymph nodes. adjuvant chemotherapy is recommended to
Adenocarcinoma, Stomach, Small and Large Intestine, Rectal A
IMAGING EXPECTED COURSE AND PROGNOSIS

• Ultrasound—may reveal a thickened Dogs
stomach or bowel wall; may see mass in the • Overall poor; pedunculated rectal tumors
BASICS gastrointestinal tract, enlarged lymph nodes. do best; most cases recur locally, develop
OVERVIEW • Positive contrast radiography—filling defect metastasis, or do both rapidly.
• Uncommon tumor arising from the (stomach); intraluminal space-occupying or • Median survival gastric—2 months.
epithelial lining of the gastrointestinal tract. annular constriction (small bowel); gastric • Median survival small intestinal—10
• Prognosis guarded to poor. neoplasm most often found in distal two- months.
thirds of stomach. • Mean survival large intestinal—annular
SIGNALMENT
• Double contrast radiography—large 1.6 months vs. pedunculated 32 months.
• Dog more commonly affected than cat.
intestine and rectum; polypoid or annular
• Middle-aged to older (>6 years) animals; Cats
space-occupying masses.
age range 3–13 years. • Guarded.
• Advanced imaging with contrast CT can
• No breed predisposition. • Few reported cases, but may have
provide highest-quality images of gastrointes-
• Possible male predisposition. prolonged survival (>1 year).
tinal tract and assessment for presence and
SIGNS extent of lymphadenopathy.
Historical Findings DIAGNOSTIC PROCEDURES
• Stomach—vomiting, anorexia, weight loss, • Ultrasound-guided fine-needle aspirate of
hematemesis, and melena. bowel mass or enlarged lymph node may MISCELLANEOUS
• Small intestine—vomiting, weight loss, provide definitive cytologic diagnosis. Suggested Reading
borborygmus, flatulence, and melena. • Endoscopic biopsy may be nondiagnostic
Crawshaw J, Berg J, Sardinas JC, et al.
• Large intestine and rectum—mucus, because tumors are frequently deep to the Prognosis for dogs with nonlymphomatous
blood-tinged feces, and tenesmus. mucosal surface; thus surgical biopsy often small intestinal tumors treated by surgical
Physical Examination Findings required. excision. J Am Anim Hosp Assoc 1998,
• Stomach—nonspecific, melena on rectal • Presence of signet ring cells and/or
34:451–456.
exam. cytoplasmic microvacuolation on cytologic Riondato F, Miniscalco B, Berio E, et al.
• Small intestine—may feel mid-abdominal evaluation of gastric biopsy squash prep Diagnosis of canine gastric adenocarcinoma
mass; distended, painful loops of small bowel. samples correlated well with diagnosis of using squash preparation cytology. Vet J
• Large intestine and rectum—palpable mass gastric adenocarcinoma in one study. 2014, 201(3):390–394.
per rectum, may form annular ring, may have Seim-Wikse T, Jorundsson E, Nodtvedt A,
multiple nodular lesions protruding into the et al. Breed predisposition to canine gastric
colon; bright red blood on rectal exam. carcinoma: a study based on the Norwegian
CAUSES & RISK FACTORS TREATMENT canine cancer register. Acta Vet Scand 2013,
• Unknown. • Surgical resection—treatment of choice; 55:25.
• Possible genetic cause—gastric adenocarci- seldom curative. Swann HM, Holt DE. Canine gastric
nomas in related Belgian shepherds and • Gastric—usually nonresectable. adenocarcinoma and leiomyosarcoma: a
Dutch Tervuren shepherds. • Small intestine—remove by resection and retrospective study of 21 cases (1986–1999)
anastomosis; metastasis to regional lymph and literature review. J Am Anim Hosp
nodes and liver common. Assoc 2002, 38:157–164.
• Large intestine and rectal—may occasionally von Babo V, Eberle N, Mischke R, et al.
be resected via pull-through surgical procedure; Canine non-hematopoietic gastric
DIAGNOSIS metastasis common; transcolonic debulking neoplasia: epidemiologic and diagnostic
DIFFERENTIAL DIAGNOSIS may provide palliation of obstruction. characteristics in 38 dogs with post-surgical
• Foreign body. outcome of five cases. Tierarztl Prax Ausg K
• Inflammatory bowel disease. Kleintiere Heimtiere 2012, 40(4):243–249.
• Lymphoma. Author Laura D. Garrett
• Parasites. MEDICATIONS Consulting Editor Timothy M. Fan
• Leiomyoma.
DRUG(S) OF CHOICE
• Leiomyosarcoma.
• Chemotherapy—only anecdotal reports,
• Pancreatitis.
usually unsuccessful.
CBC/BIOCHEMISTRY/URINALYSIS • Piroxicam 0.3 mg/kg PO q24h can provide
• Stomach and small intestine—may see palliation for large intestinal and rectal tumors.
microcytic, hypochromic, nonregenerative
anemia (iron-deficiency anemia). Mild and
persistent elevations in blood urea nitrogen in INTERACTIONS
the face of normal creatinine can support GI Seek advice before initiating treatment with
protein or blood loss. cytotoxic drugs.
• Large intestine and rectum—no characteristic
changes.
Fecal occult blood may be positive; diet FOLLOW-UP
affects results—can recheck to confirm after Physical examination, thoracic radiographs,
3 days of non-meat diet. and abdominal ultrasound—at 1, 3, 6, 9, and
12 months post surgery.
A Adenocarcinoma, Thyroid—Dogs
Historical Findings Cytology
• Palpable mass/swelling in cervical neck, • Examination of fine-needle aspirates from
coughing, dyspnea, dysphagia, dysphonia, tumor and palpable regional lymph nodes.
BASICS facial edema, neck pain. • If functional • Specimen almost always heavily
DEFINITION thyroid tumor—may see polyuria, polydipsia, contaminated with blood owing to highly
A malignant tumor arising from the follicular polyphagia, weight loss, restless behavior, vascular nature of tumor. • Homogeneous
or parafollicular cells (medullary/C-cells) of diarrhea (symptoms associated with hyperthy- population of epithelial cells, sometimes
the thyroid gland. roidism). • If hypothyroid—may see poor with colloid and/or tyrosine-containing
hair coat, weight gain, lethargy. granules. Often, cell fragility leads to cell
PATHOPHYSIOLOGY rupture and free nuclei. • Unable to
• About 60% of patients are euthyroid, 30% Physical Examination Findings
• Freely movable or fixed cervical mass,
differentiate malignant from benign thyroid
hypothyroid, and 10% hyperthyroid. cells; but almost all thyroid neoplasms in
• Typically very invasive tumors with high unilateral or bilateral. • Rarely may see
Horner’s syndrome, or cranial vena cava dogs are malignant.
rate of metastasis (lungs, retropharyngeal
lymph nodes, liver), with up to 35–40% of syndrome. • If hyperthyroid—cardiac PATHOLOGIC FINDINGS
dogs having metastasis at time of diagnosis. arrhythmias or murmurs. Gross
• Animals with bilateral tumors have a 16 CAUSES • Characterized by high vascularity with areas
times greater risk of developing metastatic Unknown of hemorrhage and necrosis. • Usually poorly
disease than animal with unilateral tumors. encapsulated; often invade adjacent tissues
RISK FACTORS
SYSTEMS AFFECTED • Breed predilection.
(e.g., trachea and esophagus, and surrounding
• Cardiovascular—hyperthyroid dogs are • Iodine deficiency.
vasculature); may adhere to jugular vein,
usually tachycardic and may have systemic carotid artery, and vagosympathetic trunk.
hypertension. • Endocrine/metabolic—affected Histopathology
dogs may be hypothyroid, euthyroid, or • Thyroid follicular carcinomas are
hyperthyroid; hypercalcemia may be seen as a subclassified as well differentiated (follicular,
paraneoplastic syndrome or secondary to DIAGNOSIS compact, follicular–compact, or papillary),
concurrent parathyroid hyperplasia or para- DIFFERENTIAL DIAGNOSIS poorly differentiated, or undifferentiated—
thyroid adenocarcinoma. • Respiratory—dogs • Other primary neoplasms—lymphoma; with follicular–compact and compact tumors
may be dyspneic owing to a space-occupying soft tissue sarcoma; salivary gland adeno most common in dogs. • C-cell (e.g.,
mass adjacent to the trachea; metastasis to the carcinoma; parathyroid carcinoma; carotid parafollicular, medullary) carcinomas less
lungs common. Large compressive masses can body tumor. • Secondary tumors—metastatic common. May need special stains to
result in caval syndrome manifested as facial oral/tonsillar squamous cell carcinoma; oral differentiate between C-cell and follicular
edema. Compression and/or deviation of the melanoma. • Inflammatory—abscess or carcinomas.
trachea can lead to nonproductive cough. granuloma. • Salivary mucocele.
GENETICS CBC/BIOCHEMISTRY/URINALYSIS
Unknown • Usually normal. • May see nonregenerative
INCIDENCE/PREVALENCE normocytic normochromic anemia of chronic TREATMENT
Accounts for 1.2–3.8% of all canine tumors disease, leukocytosis. • Rare—hypercalcemia;
isosthenuria. APPROPRIATE HEALTH CARE
and represents 10–15% of all primary head • Definitive treatment dependent on tumor
and neck tumors. OTHER LABORATORY TESTS stage (tumor size, mobility, and evidence of
GEOGRAPHIC DISTRIBUTION Thyroid hormone (T4 and/or free T4 levels) metastatic disease). • Complete surgical
May be more common in iodine-deficient and endogenous thyroid-stimulating excision recommended for freely movable
areas. hormone (TSH) levels. thyroid tumors. • Full course external beam
SIGNALMENT IMAGING radiation therapy recommended preopera-
• Thoracic radiography (three-view)— tively for large tumors, as sole therapy for
Species nonresectable tumors, or postoperatively for
evaluation of lungs and other thoracic
Dog structures for metastasis. • Cervical incompletely surgically removed tumors.
Breed Predilections ultrasonography, CT, and MRI—evaluation • Palliative radiation and/or chemotherapy
Boxers, golden retrievers, Siberian huskies, of tissue of origin, vascularity, invasion, and recommended for tumors that are metastatic
and beagles at increased risk, but seen in any cervical lymph nodes. • Technetium-99m at presentation. • Functional thyroid
breed. scintigraphy to evaluate for ectopic and carcinomas can be treated with iodine-131,
functional thyroid tissue or metastatic but doses are very large (60–100 mCi) and
Mean Age and Range
lesions. • Radioiodine studies—may provide therefore there are limited facilities that offer
Older dogs (median 9–15 years; range 4–18 this therapy. • Toceranib phosphate (Palladia®)
years). information about the tumor’s ability to
produce thyroid hormone. can exert cytoreductive activity. • Isotretinoin
Predominant Sex 9-cis postoperatively may improve median
No sex predilection. DIAGNOSTIC PROCEDURES survival time (MST) in follicular–compact
SIGNS Biopsy and compact thyroid carcinoma.
Tru-Cut® not recommended owing to NURSING CARE
General Comments high risk of severe hemorrhage; open
• Usually not diagnosed until a large mass is Varies with signs on examination.
biopsy usually required and allows for
palpable. • Approximately 65% are unilateral, controlled hemostasis in the event of ACTIVITY
35% are bilateral. bleeding. Restrict activity if dyspneic.
(continued) Adenocarcinoma, Thyroid—Dogs A
CLIENT EDUCATION PRECAUTIONS removal of unilateral thyroid tumors is 1,462

• Warn owners of importance of controlling Chemotherapy can cause gastrointestinal, days vs. 365 days for patients undergoing
heart rate and rhythm in hyperthyroid bone marrow, cardiac, and other toxicities— bilateral thyroidectomy. • For animals treated
patients and of possibility of episodes of seek advice from medical oncologist if with full course external beam radiation
collapse. • Warn owners of possible postop- unfamiliar with cytotoxic drugs. therapy—progression-free survival at 1 year
erative laryngeal paralysis and intraoperative POSSIBLE INTERACTIONS 80% and 72% at 3 years in one study, and in
hemorrhage. • Warn owners of acute Verapamil—may potentiate doxorubicin- another study MST 24.5 months. • Palliative
radiation therapy toxicities—moist desqua- induced cardiotoxicity. radiation therapy in 13 dogs—MST 24
mation, laryngitis, tracheitis, esophagitis. months vs. 170 days in dogs with advanced
ALTERNATIVE DRUG(S) disease. • 131I therapy in combination with
SURGICAL CONSIDERATIONS N/A
See Appropriate Health Care. surgery—MST 34 months, or 131I alone MST
30 months. • Animals treated with cisplatin
Risks alone (13 dogs)—overall response rate 53%,
• Marked hemorrhage—tumors highly median progression-free interval for
vascular and invasive into surrounding responders 202 days, and overall MST
structures, including vasculature; may need FOLLOW-UP
98 days.
blood transfusion and intensive postoperative PATIENT MONITORING
care. • Laryngeal paralysis—owing to trauma • Serum calcium concentration—if bilateral
to recurrent laryngeal nerve. • Damaged thyroidectomy was performed; signs of
parathyroid glands—may occur during hypocalcemia (agitation, panting, muscle
surgery. tremors, tetany, and seizures) may be MISCELLANEOUS
observed. ◦ Treat with 10% calcium ASSOCIATED CONDITIONS
gluconate (1–1.5 mL/kg IV over 10–20 • Nonthyroidal malignancies common.
minutes). ◦ Maintain serum calcium with • Multiple endocrine neoplasia reported.
dihydrotachysterol (vitamin D) orally and/or
MEDICATIONS oral calcium supplementation if necessary. AGE-RELATED FACTORS
DRUG(S) OF CHOICE • Thyroid hormone—supplementation with
None
• Chemotherapeutic agents: ◦ Chemotherapy thyroxine may be necessary after bilateral PREGNANCY/FERTILITY/BREEDING
recommended as sole therapy, or possibly in thyroidectomy. • TSH concentration—a goal It is not recommended to breed animals with
combination with surgery and/or radiation of thyroxin supplementation is to down cancer. Chemotherapy is teratogenic—do not
therapy. ◦ Cisplatin (60 mg/m2 every 3 regulate the body’s secretion of TSH. • Site of give to pregnant animals.
weeks), carboplatin (300 mg/m2 every 3 primary tumor—physical examination and SYNONYMS
weeks), or doxorubicin (30 mg/m2 every 3 cervical ultrasound; thoracic radiographs Thyroid carcinoma.
weeks)—reported to effect partial remission every 3 months to detect pulmonary
in approximately 50% of cases. ◦ Toceranib metastasis. ABBREVIATIONS
(2.5–3 mg/kg 3 times a week)—had biologic • MST = median survival time.
PREVENTION/AVOIDANCE • TSH = thyroid stimulating hormone.
activity in 80% of cases (26% partial Unknown
remission, 53% stable disease). ◦ Isotretinoin Suggested Reading
9-cis (2 mg/kg/day)—potentially difficult to POSSIBLE COMPLICATIONS Lunn KF, Page RL. Tumors of the endocrine
obtain in United States due to prescribing • Tumor—anemia; thrombocytopenia; system. In: Withrow SJ, Vail DM, Page RL,
restrictions. • Thyroid management: hypercalcemia; respiratory distress. eds., Small Animal Clinical Oncology,
◦ Thyroxine—maintenance doses to decrease • Chemotherapy—dilated cardiomyopathy; 5th ed. Philadelphia, PA: Saunders, 2013,
TSH production have been recommended; renal failure; pancreatitis; sepsis; gastro pp. 513–515.
some tumors contain TSH receptors; value of intestinal upset. • Surgery—hemorrhage; Nadeau ME, Kitchell BE. Evaluation of the
hormone replacement therapy in affected hypothyroidism; hypoparathyroidism leading use of chemotherapy and other prognostic
dogs not determined. ◦ Methimazole 5 mg to hypocalcemia; laryngeal paralysis. variables for surgically excised canine
PO q8h for medium to large dogs; may be • Radiotherapy—acute side effects: moist thyroid carcinoma with and without
beneficial for hyperthyroid patients. ◦ Beta desquamation, pharyngeal mucositis, metastasis. Can Vet J 2011,
blockers—may be indicated for tachycardia or esophagitis, tracheitis; late side effects: 52(9):994–998.
hypertension in hyperthyroid patients. hypothyroidism, alopecia, and skin or coat Pack L, Roberts RE, Davson SD, Dookwah
color change (at radiation site). HD. Definitive radiation therapy for
CONTRAINDICATIONS
• Doxorubicin is cumulatively toxic to EXPECTED COURSE AND PROGNOSIS infiltrative thyroid carcinoma in dogs. Vet
cardiac myocytes, causing decreased • Prognosis—related to grade and stage of Radiol Ultrasound 2001, 42:471–474.
myocardial function; do not give to animals disease (tumor size, mobility, and evidence of Author Rebecca G. Newman
with poor cardiac function or dilated cardio- metastatic disease) with small, low-grade, Consulting Editor Timothy M. Fan
myopathy. • Cisplatin is nephrotoxic; do not nonattached unilateral, nonmetastatic tumors
give to animals with renal disease. having best prognosis. • MST after surgical
A Aggression—Between Dogs in the Household
read or respond appropriately to other dog’s Safety Recommendations
body language. • Aggression likely to be more • Never allow dogs to “fight it out,” as serious
severe between dogs of equal size, age, and sex. injuries may occur. • Owners must ensure
BASICS • Owner’s inability to read early signs of safety by identifying and avoiding all situations
OVERVIEW conflict between household dogs. • Owner’s that may trigger aggressive interactions, such as
• Aggression toward other dog(s) within a failure to create or maintain social stability and when dogs are walking past each other in a
household or with dogs that are familiar and predictability in dogs’ interactions and relation- confined space or being given attention or
spend time together regularly. • Dogs can form ship with each other. high‐valued treats; the dogs may at least initially
stable social relationships quickly, sometimes need to be kept physically separated to prevent
within minutes of being introduced. Aggression agonistic encounters. • Owners must be
usually revolves around resources (e.g., food, instructed in methods of safely breaking up
toys, owner attention, resting places), but may fights by never reaching toward the dogs’ heads
DIAGNOSIS or necks to physically pull them apart; preferred
be fear related or can occur at times of
excitement/arousal (e.g., visitors or other dogs DIFFERENTIAL DIAGNOSIS methods include physical barrier deterrent
on the property). • Usually within the range of • Status‐related aggression. • Conflict‐related (e.g., noise distractor, water, or deterrent spray)
normal behavior, but may be excessive, aggression. • Play behavior/nonaggressive or leashes left constantly attached when dogs
abnormal, or related to underlying medical arousal. • Possessive aggression. • Protective are together. • Owners should be advised of
conditions. aggression. • Fear aggression. • Pain‐related their liability for bites. • For treatment to be
aggression. • Irritable aggression. • Generalized effective, aggression‐provoking stimuli should
SYSTEMS AFFECTED anxiety disorder. be prevented prior to behavior modification.
Behavioral • At any time or place an aggression‐evoking
INCIDENCE/PREVALENCE To rule out underlying medical conditions situation could arise (e.g., around food/valued
Approximately 11%. and as baseline prior to drug use. resources), dogs must be confined away from
SIGNALMENT each other or under direct physical control of a
OTHER LABORATORY TESTS responsible adult; dogs can be separated by
Breed Predilections As needed to rule out underlying medical placing in separate rooms, with pet gates,
• No breed or sex predilection. • Although conditions; thyroid screening. exercise pens, or crates, or securely tethered
genetic factors contribute, environment may play IMAGING short term to hooks installed in walls. • Tools
a stronger role in degree of aggression exhibited. As needed to rule out underlying medical for safety and management include head
Mean Age and Range conditions, (e.g., pain); MRI if CNS disease halters, basket muzzles, or harnesses with
Signs usually develop at social maturity suspected. leashes attached for prevention, and to safely
(approximately 18–36 months of age). remove dogs from situations that may elicit
DIAGNOSTIC PROCEDURES aggression. • If safety cannot be ensured, it may
Predominant Sex N/A be necessary to rehome dog to a single‐dog
May be more common/intense between intact household, where all triggers can be avoided.
males and females.
Behavior Therapy
SIGNS • Structured interaction programs (such as
• Barking, growling, lip‐lifting, snarling, TREATMENT “Learn to earn” or “Say please by sitting”),
snapping, lunging, biting, directed toward where dog is taught to consistently perform a
CLIENT EDUCATION
other dogs in the home. • Subtle commun desired behavior (e.g., sit) before receiving
ication signals between dogs may include General Comments
anything it values (e.g., attention, food), give
blocking access to rooms or other resources, • Treatment requires a multifaceted approach,
the dog control of its resources by being calm,
hard stare, taller stance, tail elevated, ears including immediate management to ensure
provide structure and predictability in all
perked forward, and approaching/direct safety and prevent recurrence, behavior
interactions, teach impulse control, and train
contact with other dog. • May be accompanied modification, and medication (if indicated).
dog using positive interactions (e.g., good
by fearful/submissive body postures/facial • Successful treatment requires owner
things happen by sitting calmly). • Separately,
expressions (e.g., crouching, backing away, understanding of canine social behavior and
teach each dog behaviors that will serve as a
ears back, tail tucked, looking away, lip‐ communication, identification of all aggression‐
foundation for management and control when
licking). • Dogs fighting in a household may eliciting stimuli, risks involved in living with an
together including sit and relax, down‐settle,
get along well except in specific trigger aggressive dog(s), willingness and ability to
go to mat or crate, focus on owner (e.g.,
situations, especially resources, access to follow safety and management recommen
watch/look), and leave it; private sessions with
passageways/doorways, and at times of dations, and effective implementation of
force‐free trainer can be the best option for
arousal. • Predictors of aggression—presence reward‐based behavior modification. • Realistic
achieving success. • Once each dog can reliably
of owner; access to resources such as food, expectation is for managing triggers, most often
perform foundation and relaxation exercises,
toys, spaces, and beds; periods of high arousal for rest of dog’s life and gradually improving,
then owners can work with dogs together,
such as people entering the house. not resolving. • Owners must be aware that the
separated by distance to ensure both dogs can
only way to entirely prevent future injuries may
CAUSES & RISK FACTORS remain focused or engaged in desirable
be to continually separate dogs when no one is
• Underlying medical conditions including behaviors (e.g., mat) that can be reinforced.
home, remove one of the dogs from the home,
pain, endocrinopathies, neurologic, and sensory • During times together, close supervision is
or use of safety equipment and constant
decline. • May be normal canine behavior; can needed; owners must be able to recognize body
supervision to safely manage when dogs are in
be strongly influenced by previous experience language and be vigilant for stimuli that might
same space. • Positive punishment and
(e.g., early socialization, previous aggressive incite aggression; verbal cues should be used to
dominance‐based training can lead to increased
encounters with other dogs, inappropriate prevent or interrupt undesirable behaviors and
aggression, fear, and injuries, and must be
punishment) and other behavioral disorders teach what is desirable; use of a leash attached
avoided.
such as anxiety; in some cases, one dog may not to each dog with head halter or while wearing
(continued) Aggression—Between Dogs in the Household A
basket muzzle will increase safety when dogs For Situational or Adjunctive Use PREVENTION/AVOIDANCE
are in close proximity. • Use positive reinforce Alpha‐2 Agonists Safety and management recommendations are
ment (e.g., treats, toys, petting) to teach • Clonidine 0.01–0.05 mg/kg PO PRN lifelong.
behaviors incompatible with those that lead to 1.5–2 hours before eliciting trigger, up to POSSIBLE COMPLICATIONS
aggression (e.g., response substitution, q8–12h. • Side effects—transient hyper Injuries to dogs and humans.
differential reinforcement of alternative glycemia, anticholinergic, hypotension,
behavior). • Systematic desensitization and EXPECTED COURSE AND PROGNOSIS
collapse, bradycardia, and agitation. • Lifelong management likely necessary.
counter‐conditioning to triggers—desensiti
zation is a process by which dogs will be Serotonin 2a Antagonist/Reuptake Inhibitors • Prognosis for improvement depends on
exposed to their triggers under their threshold; • Trazodone 2–5 mg/kg PO PRN prior to severity of aggression; motivation; whether
food, toys, verbal praise, or physical attention eliciting trigger, up to q8h—may titrate up to triggers can be identified, avoided, and safely
(e.g., petting) can be used to reward calm 8–10 mg/kg if no adverse effects; use cautiously managed; and owner compliance; prognosis
behavior. Counter‐conditioning is a process in at higher doses and when combining with other more favorable if triggers are predictable and
which positive associations are paired with drugs that increase serotonin due to risk of preventable, and aggression occurs at low
each stimulus exposure, (e.g., most‐valued serotonin syndrome. • Side effects—sedation, intensity. • Aggression may recur with change in
treats); dogs should be exposed to each other anorexia, ataxia, GIT effects, cardiac conduction routine, housing, or health, and increasing age.
under control of handlers and at distance at disturbances, agitation.
which they can remain calm and focused on Benzodiazepines
their handlers while performing cued behaviors • Might be used to reduce anxiety prior to
for rewards; gradually dogs can be moved eliciting trigger. • Side effects—sedation, MISCELLANEOUS
closer in proximity to each other and in varied lethargy, ataxia, paradoxical excitement; may
situations while focusing on handlers. disinhibit aggression. ASSOCIATED CONDITIONS
Other fear‐ or anxiety‐related conditions;
SURGICAL CONSIDERATIONS CONTRAINDICATIONS possessive, redirected, and territorial aggression.
Castration reduced intermale aggression in Corticosteroids may cause or contribute to
62% of dogs. polyphagia, increased food guarding, and ZOONOTIC POTENTIAL
irritability. Human injury/bite wounds.
PRECAUTIONS PREGNANCY/FERTILITY/BREEDING
Use caution, as any psychotropic medication Do not breed dogs that exhibit aggressive
MEDICATIONS may cause undesirable changes in behavior, behavior.
DRUG(S) OF CHOICE including increased irritability and aggression. SEE ALSO
• Aggression, Food and Resource Guarding—
• No medications licensed for treatment of POSSIBLE INTERACTIONS
canine aggression; owners must have Do not combine SSRIs, TCAs, or monoamine Dogs.
informed consent of potential side effects and • Aggression, Overview—Dogs.
oxidase (MAO) inhibitors (e.g., amitraz,
risks, and that use is off‐label. • Owners need • Fears, Phobias, and Anxieties—Dogs.
selegiline) and use cautiously or avoid with
to understand that medication will not ensure opioids, tramadol, or other medications that ABBREVIATIONS
safety and to follow all safety procedures. increase serotonin—can result in serotonin • GIT = gastrointestinal tract.
• Medications may be indicated for moderate syndrome. • MAO = monoamine oxidase.
to intense fear and anxiety, impulsivity, and ALTERNATIVE DRUG(S) • SSRI = selective serotonin reuptake inhibitor.
reactivity. • Proper diagnosis with behavioral Natural products—dog‐appeasing pheromones, • TCA = tricyclic antidepressant.
modification plan, including appropriate supplements containing alpha‐casozepine or Suggested Reading
selection of behavioral drugs, leads to most l‐theanine, or a calming probiotic might be Herron ME, Shofer SS, Reisner IR. Survey of the
successful outcomes. considered for mild to moderate anxiety or use and outcome of confrontational and non‐
Selective Serotonin Reuptake Inhibitors used adjunctively. confrontational training methods in client‐
(SSRIs) owned dogs showing undesired behaviors. Appl
• Fluoxetine 0.5–2 mg/kg PO q24h. Anim Behav Sci 2009, 117:47–54.
• Paroxetine 0.5–1 mg/kg PO q24h. Landsberg G, Hunthausen W, Ackerman L.
• Sertraline 1–3 mg/kg PO q24h. • Side Behavior Problems of the Dog and Cat,
FOLLOW‐UP 3rd ed. St. Louis, MO: Saunders Elsevier,
effects—sedation, irritability, gastrointestinal
tract (GIT) effects, agitation; decreased appetite PATIENT MONITORING 2013, pp. 320–324.
common and usually transient. • Clients will need ongoing assistance and Pike A. Managing canine aggression in the
should receive at least one follow‐up within home. Vet Clin N Am Small Anim Pract
Tricyclic Antidepressants (TCAs) first 1–3 weeks after consultation. Provisions 2018, 48:387–402.
• Clomipramine 1–3 mg/kg q12h (label‐ for further follow‐up should be made at that Authors Jeannine Berger and Wailani Sung
restricted for aggression). • Side effects— time. • Drugs should only be prescribed Consulting Editor Gary M. Landsberg
sedation, GIT effects, anticholinergic effects, under direct supervision and monitoring of Acknowledgment The authors and editors
cardiac conduction disturbances if veterinarian. acknowledge the prior contributions of
predisposed, agitation. Meredith E. Stepita and Laurie Bergman.
A Aggression to Unfamiliar People and Unfamiliar Dogs—Dogs
during leash (walk) training. Owner responses ensure safety, prevent further repetition and
including leash corrections, verbal and/or potential intensification of the problem,
physical punishment may increase fear, address pet welfare, and provide an environ
BASICS anxiety, and arousal, and condition further ment in which pet can learn and desired
OVERVIEW negative associations. • Owner’s inability to outcomes can be achieved, prior to
• Aggression directed toward person or dog read early signs of fear or conflict. • Owner’s implementing behavior modification.
that does not live in the household. • Variety failure to create or maintain predictable • Decrease or avoid visitors and unfamiliar
of motivations including fear, territoriality, pattern of positive interactions with unfamiliar dogs to the home. • Avoid walks at times or in
conflict, and possessiveness. • Usually within people and dogs. • Fear of strangers. locations where stimulus exposure might occur.
range of normal behavior, but may be excessive On walks, maintain a 15 ft distance from other
or abnormal due to learning, early experiences, people and dogs. • Confine dog away from
genetics, or underlying medical conditions. potential targets; stay below threshold, (e.g.,
distance, location); and ensure direct physical
SYSTEMS AFFECTED DIAGNOSIS control of adult together with safety products if
Behavioral DIFFERENTIAL DIAGNOSIS any possible exposure. • Confine territorial
INCIDENCE/PREVALENCE • Fear aggression. • Territorial aggression. dogs to where they cannot see/hear visitors
Stranger‐directed aggression represents 32.5% • Possessive aggression. • Protective approaching territory before they become
of canine behavioral referral caseload. May be aggression. • Conflict‐related aggression. alerted or aggressive. Confine dogs for duration
skewed as many cases may go unreported. • Generalized anxiety disorder. • Pain‐related of visitor’s stay inside house. • Safety measures
SIGNALMENT aggression. • Irritable aggression. include training dogs to wear a basket muzzle,
CBC/BIOCHEMISTRY/URINALYSIS use of head collars or harnesses with leashes
Breed Predilections attached, and confinement training (e.g., safe
None To rule out underlying medical conditions
and as baseline prior to any drug use. haven, closed doors, barricades) away from
Mean Age and Range potential triggers. • Owners should be advised
• Any age. • Signs may begin to emerge as
OTHER LABORATORY TESTS of their liability for bites. • Ensure that dog
primary socialization wanes (12–16 weeks of As needed to rule out underlying medical cannot escape through fencing or unlatched
age) or may arise or intensify at social conditions, including thyroid screening. gates or doors. • If safety cannot be ensured,
maturity (18–36 months). • Genetic IMAGING dog should be removed from household.
concerns and more guarded prognosis when As needed to rule out underlying medical Behavior Therapy
signs arise before 12 weeks. conditions, (e.g., pain); MRI if CNS disease • Structured interaction programs (such as
Predominant Sex
suspected. “Learn to earn” or “Say please by sitting”),
• May be overrepresented in males. where dog is taught to consistently perform
• Territorial aggression more common in desired behavior (e.g., to sit) before receiving
intact males—initial signs usually present by anything it values (e.g., attention, petting,
1 year. TREATMENT feeding, going for a walk), give dog control of
its resources for being calm, provide structure
SIGNS CLIENT EDUCATION and predictability in all interactions, teach
• Barking, growling, lip‐lifting, snarling,
General Comments impulse control, and train dog using positive
snapping, lunging, biting, directed toward
• Treatment requires a multifaceted approach interactions (e.g., good things happen by
other dogs or people. • Subtle communication
including management to ensure safety and sitting calmly). • Use positive reinforcement
signals may include blocking access to
prevent recurrence, behavior modification, to train alternative desirable behaviors (e.g.,
resources, hard stare, taller stance, tail elevated,
and medication. • Treatment must focus on response substitution) that can be used during
ears perked forward, and approaching or
managing the problem and gradually modifying stimulus exposure. • Train each behavior in
direct contact. • May be accompanied by
behavior to reduce fear, anxiety, and aggres neutral situations with most motivating
fearful/submissive body postures/facial
sion, not cure/full resolution. • Successful rewards (e.g., treats, food, toys, petting) to
expressions (e.g., crouching, backing away, ears
treatment requires owner understanding of achieve outcomes immediately and success
back, tail tucked, looking away, lip‐licking).
canine social behavior and communication, fully in absence of stimuli, including a calm
• Territorial aggression arises in familiar
risks, identification of all aggression‐eliciting sit; go to bed or crate to settle; walk on loose
locations or spaces (e.g., home, yard, car) with
stimuli, how to implement safe management, leash; focus on owner for guidance using eye
confident body language. • Fear aggression
and effective implementation of reward‐based contact (e.g., watch, look); find it (e.g., move
more likely when dog is cornered or cannot
behavior modification. • Owners must be away for a reward); and hand target (e.g.,
escape. • May be more frequent or severe on‐
aware that the only certain way to prevent touch nose to owner’s hand). • Private
than off‐leash, on own property, or when
future injuries is avoidance of stimuli. sessions with force‐free trainer are often
behind barrier (e.g., fence, pet gate, crate).
• Educate owners that use of physical or recommended to achieve foundation basics
CAUSES & RISK FACTORS verbal punishment, confrontation, or before any exposure. • Behavior modification—
• Underlying medical conditions, including establishing dominance (such as alpha rolls), desensitization (DS) is process by which dogs
pain, endocrinopathies, neurologic, sensory and corrections with choke chains or prong will be exposed to their triggers under their
decline. • May be normal canine behavior. collars, can lead to human injury, further threshold and rewarded if remain calm.
Strongly influenced by previous experience, negative associations with stimuli, increased Counter‐conditioning (CC) is process in
(e.g., socialization, unpleasant outcomes/ fear, anxiety, and aggression, and disruption of which trigger or stimulus is paired with
associations) such as previous fear‐evoking or human–animal bond. positive outcomes with each exposure.
aggressive encounters with dogs or people, • When owner can effectively keep dog calm
Safety Recommendations
punishment, and other behavior disorders and under control, and get desirable outcomes
• Preventing or avoiding stimuli/triggers that
including fear, anxiety, and reactivity. • May on cue in absence of stimuli, begin exposure
evoke fear, anxiety, or aggression is essential to
begin as unruly or exuberant behavior or by determining limit (e.g., distance, location,
(continued) Aggression to Unfamiliar People and Unfamiliar Dogs—Dogs A
person, dog) at which dog will orient but not q8–12h. • Side effects—transient hyperglyce EXPECTED COURSE AND PROGNOSIS
yet react. Pair highest‐value rewards with each mia, anticholinergic, hypotension, bradycar • Resolution may not be achievable and
exposure. • Gradually (baby steps) increase dia, and agitation. lifelong management may be necessary.
stimulus intensity, staying below threshold Serotonin 2a Antagonist/Reuptake • Prognosis based on whether triggers can be
that will result in fear and/or aggression by avoided to ensure safety and prevent recurrence,
decreasing distance, increasing distractions, or Inhibitors and whether improvement can be achieved
moving to more challenging environments. • Trazodone 2–5 mg/kg PO PRN prior to
with behavior modification and medication.
• Progress is slow (typically weeks to months).
eliciting trigger, up to q8h—may titrate up to • Prognosis more favorable if aggression occurs
Carefully monitor body language to avoid 8–10 mg/kg if no adverse effects. Use at low intensity and in predictable situations.
setbacks. • Owners must always be vigilant cautiously at higher doses and when combin • Prognosis dependent on owner compliance.
for approach of stimuli that might incite fear ing with other drugs that increase serotonin • Approximately 75% of dogs aggressive
or aggression. • Discuss whether referral to due to risk of serotonin syndrome. • Side toward unfamiliar dogs could be around other
veterinary behavior specialist is recommended effects—sedation, anorexia, ataxia, GIT effects, dogs on leash after treatment.
for counseling on risk assessment, prognosis, cardiac conduction disturbances, agitation.
behavioral management, behavior modific Benzodiazepines
ation, and medication use. • May be used to reduce anxiety prior to
eliciting trigger. • Side effects—sedation,
lethargy, ataxia, paradoxical excitement, may
MISCELLANEOUS
Castration reduced aggression by at least 50%
disinhibit aggression. ASSOCIATED CONDITIONS
toward unfamiliar dogs in <20% of dogs and
Other fear‐ or anxiety‐related conditions;
toward human territorial intruders in <10% CONTRAINDICATIONS
possessive, redirected, and territorial aggression.
of dogs. Castration reduced intermale Corticosteroids can be contraindicated in food‐
aggression in 62% of dogs. aggressive dogs; could cause or contribute to ZOONOTIC POTENTIAL
polyphagia, resource guarding, and irritability. Human/dog injury and bite wounds.
PRECAUTIONS PREGNANCY/FERTILITY/BREEDING
Use caution—any psychotropic medication Do not breed dogs that exhibit aggressive
MEDICATIONS may cause undesirable changes in behavior, behavior.
including increased irritability or aggression. SEE ALSO
DRUG(S) OF CHOICE
• No medications licensed for treatment of POSSIBLE INTERACTIONS • Aggression, Food and Resource Guarding—
canine aggression. Owners must have Do not combine selective serotonin reuptake Dogs.
informed consent of risks, potential side inhibitors (SSRIs), tricyclic antidepressants • Aggression, Overview—Dogs.
effects, and that medication use is off‐label. (TCAs), and monoamine oxidase (MAO) • Fear and Aggression in Veterinary Visits—
• Medications may be indicated for moderate inhibitors (e.g., amitraz, selegiline) and use Dogs.
to intense fear, anxiety, impulsivity, and cautiously or avoid with opioids, tramadol, • Fears, Phobias, and Anxieties—Dogs.
reactivity. • Ensure that owners understand and other medications that increase seroto ABBREVIATIONS
risks of owning aggressive dog, that medication nin—can result in serotonin syndrome. • GIT = gastrointestinal tract.
will not ensure safety, and that they follow ALTERNATIVE DRUG(S) • MAO = monoamine oxidase.
safety procedures. • Proper diagnosis with Natural products—dog‐appeasing • SSRI = selective serotonin reuptake
behavioral modification plan, including pheromones, supplements containing inhibitor.
appropriate selection of behavioral drugs, alpha‐casozepine or l‐theanine, or a calming • TCA = tricyclic antidepressant.
leads to most successful outcome. probiotic might be considered for mild to Suggested Reading
For Ongoing Use moderate anxiety or used adjunctively. Herron ME, Shofer SS, Reisner IR. Survey of
Selective Serotonin Reuptake Inhibitors the use and outcome of confrontational and
• Fluoxetine 0.5–2 mg/kg PO q24h. non‐confrontational training methods in
• Paroxetine 0.5–1 mg/kg PO q24h. client‐owned dogs showing undesired
• Sertraline 1–3 mg/kg PO q24h. • Side FOLLOW‐UP behaviors. Appl Anim Behav Sci 2009,
effects—sedation, irritability, gastrointestinal 177:47–54.
PATIENT MONITORING Horwitz D, ed. Blackwell’s 5 Minute Consult
tract (GIT) effects, agitation; decreased • Clients will need ongoing assistance with at
appetite common and usually transient. Clinical Companion: Canine and Feline
least one follow‐up within the first 1–3 weeks Behavior, 2nd ed. Hoboken, NJ: Wiley‐
Tricyclic Antidepressants after consultation. Provisions for further Blackwell, 2018, pp. 58–69, 89–99.
• Clomipramine 1–3 mg/kg q12h (label‐ follow‐up should be made at that time. Landsberg G, Hunthausen W, Ackerman L.
restricted for aggression). • Side effects— • Drugs should only be prescribed under the
Behavior Problems of the Dog and Cat, 3rd
sedation, GIT effects, anticholinergic effects, supervision and monitoring of a veterinarian. ed. St. Louis, MO: Saunders Elsevier, 2013,
cardiac conduction disturbances if predis PREVENTION/AVOIDANCE pp. 320–324.
posed, and increased agitation. Safety and management recommendations Authors Jeannine Berger and Wailani Sung
For Situational or Adjunctive Use are lifelong. Consulting Editor Gary M. Landsberg
Alpha‐2 Agonists POSSIBLE COMPLICATIONS Acknowledgment The authors and editors
• Clonidine 0.01–0.05 mg/kg PO PRN Injuries to dogs and humans. acknowledge the prior contributions of
1.5–2 hours before eliciting trigger, up to Meredith E. Stepita and Laurie Bergman.
A Aggression Toward Children—Dogs
Selective Serotonin Reuptake
Inhibitors (SSRIs)
• Fluoxetine 0.5–2.0 mg/kg q24h.
BASICS DIAGNOSIS • Sertraline 0.5–4 mg/kg q24h or divided
OVERVIEW DIFFERENTIAL DIAGNOSIS q12h. • Paroxetine 0.5–1.5 mg/kg q24h.
Children are the most frequently reported See Causes & Risk Factors. Tricyclic Antidepressants (TCAs)
victims of dog bites and tend to be injured CBC/BIOCHEMISTRY/URINALYSIS • Clomipramine 1–3 mg/kg q12h.
more severely than adults. To rule out medical contributing factors. Natural products containing alpha‐
SIGNALMENT OTHER LABORATORY TESTS casozepine, l‐theanine, calming probiotic,
Dogs of any breed, age, sex, and neuter status. Anecdotal evidence correlates hypothyroidism or a dog‐appeasing pheromone may aid in
Breed with increased aggression; however, no data‐ reducing anxiety.
• Breeds vary with demographics. Breed based evidence exists. CONTRAINDICATIONS/POSSIBLE
identification may be unreliable. • Breeds IMAGING INTERACTIONS
most commonly presenting to a behavior N/A • Psychotropic medication can increase
referral service that had bitten a child agitation and anxiety or disinhibit aggression.
include English springer spaniel, German DIAGNOSTIC PROCEDURES Use with safety recommendations to prevent
shepherd, Labrador retriever, Golden • Detailed history of the bite event and the
bites. • Avoid SSRI or TCA in combination.
retriever, and American cocker spaniel. behavior of both dog and child to determine ◦ Use cautiously or avoid with any drugs that
• Most fatal attacks (rare) are attributed to motivation or trigger. • Pain assessment. increase serotonin. ◦ Avoid use of SSRI or
Rottweilers, pit bulls, and their mixes. TCA + monoamine oxidase inhibitor (MAOI),
• Larger dogs may be more likely to inflict including amitraz.
severe injury. • Smaller breeds can also be
dangerous and may invite inappropriate TREATMENT
handling by children.
SAFETY WITH FAMILIAR DOGS
Sex • Never leave infants or young children FOLLOW‐UP
• More frequent in males than females. unsupervised with dogs. Securely separate infants
• Unneutered males are overrepresented in PREVENTION/AVOIDANCE
from dogs when alone, even if both asleep. • If • Do not rely on training alone to eliminate
severe bites. • Neutering will not significantly one adult is present, separate dog from young
reduce the risk. aggression. • Preventive measures are most
children. • If more than one adult is present, important in management of aggression to
Age assign responsibility for one adult to dog, and one children. • Even well‐trained, socialized dogs
• Any age, but more frequent at or beyond to child. • Educate owners to read and recognize may bite.
social maturity (2+ years). • Risk may canine communication signals and triggers. • Do
increase in geriatric dogs because of pain, not allow child to approach or interact with dog POSSIBLE COMPLICATIONS
sensory impairment, or cognitive decline. when dog is lying down or in possession of • Family may not recognize or acknowledge
resources. • Separate dog when eating or chewing risks. • Disease may aggravate aggression.
SIGNS • Family may not be compliant. • Psychotropic
valued items. • Do not allow child to hug, kiss,
Aggression drug may be unrealistically relied upon or
bend over, or lie down beside dog.
CAUSES & RISK FACTORS ineffective. • Access of young children to dog
SAFETY WITH UNFAMILIAR DOGS may be difficult to control.
Clinical Categories/Motivation • Do not tether unsupervised. • Do not allow
• Fear related. • Pain related. • Play related. young children to interact with unfamiliar EXPECTED COURSE AND PROGNOSIS
• Conflict related. • Predatory behavior. dogs. • Securely lock gates in yards. • Avoid • Aggressive behavior can often be reduced
• Territorial. • Resource guarding. underground electric fences that do not prevent and controlled, but not “cured.” Lifetime
entry of children into yard or escape of dogs. compliance is needed. • Prognosis is poor if
Dog‐Associated Risk Factors
social/physical environment cannot be
• Disease and associated irritability. BEHAVIOR MODIFICATION controlled. • In some cases it may be necessary
• Pain‐related aggression and resource • Establish secure, separate “safe haven” for dog.
to rehome or euthanize dog, while in some
guarding are the most common reasons for • Restrict fearful or reactive dog on lead and
dogs behavior may improve as child grows older.
bites to familiar children <6 years old. offer food at safe distance from children, to turn
• Anxiety. • Fear. • Dog lying down, a negative situation into a positive one. • Do not
particularly under or on furniture. • Parent/ rely on training alone; safety requires prevention.
littermate aggression. • History of growling, • Redirect dog’s attention: teach “look” or
snapping, biting. “touch” cues. • Consider positive conditioning MISCELLANEOUS
Environmental/Social Risk Factors to basket muzzle; however, supervised inter ABBREVIATIONS
• Younger children most likely bitten by the actions are still essential, as muzzles do not • MAOI = monoamine oxidase inhibitor.
family pet or other familiar dogs. • Presence insure safety. • Avoid punishment, which may • SSRI = selective serotonin reuptake
of infants (risk of predatory attacks). increase anxiety and aggression. inhibitor. • TCA = tricyclic antidepressant.
• Presence of young children. • Presence of
Suggested Reading
food, edible toys. • Punishment‐based
Reisner IR, Shofer FS, Nance ML. Behavioral
training triggering defensiveness. • Inadequate
assessment of child‐directed canine aggression.
supervision by parents/caregivers. • Hugging, MEDICATIONS Inj Prev 2007, 13:348–351.
kissing, or bending over anxious, fearful,
DRUG(S) OF CHOICE Author Ilana R. Reisner
conflict‐aggressive, or resource‐guarding dogs.
May be indicated for dogs with generalized Consulting Editor Gary M. Landsberg
or situational anxiety or fearful behavior.
Aggression Toward Familiar People—Dogs A
or offensive and more likely to occur when rolls, and corrections with choke chains or
cornered or cannot escape. prong collars, can lead to human injury,
CAUSES & RISK FACTORS further negative associations with the stimuli,
BASICS increased fear, anxiety and aggression, and
• Underlying medical conditions including
OVERVIEW pain, endocrinopathies, neurologic, and disruption of human–animal bond.
• Aggression directed toward household sensory decline. • May be normal canine Safety Recommendations
members or people with an established behavior; can be strongly influenced by • Owners must ensure safety by identifying and
relationship with the dog, often in situations previous experience (e.g., socialization, early avoiding situations that may evoke fearful or
when they are handling or attempting to development, unpleasant outcomes including aggressive response; identification and avoidance
interact with the dog, or involving access to previous aggressive encounters, punishment), of triggers is essential to ensure safety, for pet
certain resources. • Variety of motivations and other behavioral disorders such as fear, welfare, and to provide environment in which
including fear, protective, conflict, and anxiety, and impulsivity. • Owner’s inability pet can learn and desired outcomes be achieved,
possessiveness. • Usually within range of to read early signs of fear or conflict. prior to implementing behavior modification.
normal behavior, but may be excessive, • Owner’s failure to create or maintain • Safety measures include training to wear a
abnormal, or related to underlying medical predictable pattern of positive interactions. basket muzzle, use of head collars or harnesses
conditions. with leashes attached, and use of confinement
SYSTEMS AFFECTED training and barriers (e.g., safe haven, gates,
Behavioral closed doors) to keep dog from triggers and
triggers from dog. • Owners should be advised
INCIDENCE/PREVALENCE DIAGNOSIS of their liability for bites. • Treatment more
• Approximately 7%. • Represents 20–44% DIFFERENTIAL DIAGNOSIS likely to be successful if aggression‐provoking
of behavioral referral caseloads may be skewed • Fear/defensive aggression. • Territorial stimuli can be effectively prevented prior to
as many cases unreported. • Bites from larger aggression. • Possessive aggression. behavior modification. • Common triggers
dogs may require medical attention, therefore • Protective aggression. • Conflict‐related include handling or moving dog when on
more likely documented. aggression. • Generalized anxiety disorder. furniture or resting, use of physical punishment,
SIGNALMENT • Pain‐related aggression. • Irritable touching painful areas, and removing valued
Breed Predilections
aggression. items; this can be managed by keeping dog
• Behavior is a result of interplay between CBC/BIOCHEMISTRY/URINALYSIS away from areas/furniture, when using physical
ontogeny and phylogeny. • Environmental To rule out underlying medical conditions punishment, using pain control and taking dog
stimuli may play a more critical role in and as baseline prior to drug use. to veterinarian for uncomfortable procedures,
aggression. • May be increased occurrence in and not to give (or confine when giving) valued
OTHER LABORATORY TESTS items. • If safety cannot be ensured, dogs should
related dogs. • May be genetic factors As needed to rule out underlying medical
associated with impulse dyscontrol in English be removed from household and euthanasia
conditions; thyroid screening. considered if prognosis poor for safe rehoming.
springer spaniel and English cocker spaniel;
more common in conformation lineage than IMAGING Behavior Therapy
field lineage in English springer spaniels. • In As needed to rule out underlying medical • Structured interaction programs (such as
other breeds, dogs bred for show may be conditions (e.g., pain); MRI if CNS disease “Learn to earn” or “Say please by sitting”)
associated with less aggression. suspected. where dog is consistently taught to perform a
Mean Age and Range DIAGNOSTIC PROCEDURES desired behavior (e.g., sit) before receiving
• Usually manifested by social maturity N/A anything it values (e.g., attention, petting,
(12–36 months of age). • Genetic concerns feeding, toys) give dog control of its resources
and poorer prognosis if signs arise before for being calm, provide structure and predict
12 weeks. ability in all interactions, teach impulse control,
and train dog using positive interactions (e.g.,
Predominant Sex TREATMENT good things happen by sitting calmly). • Use
May be overrepresented in males (castrated CLIENT EDUCATION positive reinforcement to teach alternative
and intact). desirable behaviors that are incompatible (e.g.,
General Comments
SIGNS • Treatment requires multifaceted approach,
response substitution) with those that have
• Barking, growling, lip‐lifting, snarling, including immediate management to ensure resulted in aggression. • Teach each behavior
snapping, lunging, biting, directed toward safety and prevent recurrence, behavior in neutral situations using most motivating
familiar people. • Subtle communication modification, and medication (where rewards (e.g., food, toys, play, attention),
signals may include blocking access to indicated). • Realistic expectation is for including sit and relax on verbal cue; down‐
resources, hard stare, taller stance, tail elevated, managing triggers, most often for rest of dog’s settle; go to bed or crate; focus on owner (e.g.,
ears perked forward, and approaching or life, and gradually improving, not resolving, watch/look), and hand targeting (e.g., touch
direct contact. • May be accompanied by the problem. • Successful treatment requires nose to owner’s hand). Private sessions with
fearful/submissive body postures/facial owner understanding of canine social force‐free trainer often recommended to
expressions (e.g., crouching, backing away, ears behavior and communication, identification achieve foundation basics before any exposure.
back, tail tucked, looking away, lip‐licking). • Behavior modification—desensitization is
of all aggression‐eliciting stimuli, willingness
• May be more frequent when handled or and ability to follow safety and management process by which dogs are exposed to triggers
approached when resting, avoiding, or hiding recommendations, and effective implemen under their threshold; rewards should be given
(e.g., under furniture) or grabbing (e.g., tation of reward‐based behavior modification. when calm (e.g., food, toys, verbal praise, or
collar). • Protective or possessive aggression • Educate owners that use of physical or
physical attention); counter‐conditioning is
arises in vicinity of highly valued objects/space verbal punishment, confrontation, or process in which positive associations paired
or people. • Fear aggression can be defensive establishing dominance such as with alpha with exposure to stimulus, (e.g., most valued
A Aggression Toward Familiar People—Dogs (continued)
treats); operant counter‐conditioning or effects, cardiac conduction disturbances if PREVENTION/AVOIDANCE

response substitution is process in which predisposed, agitation. Safety and management recommendations are
acceptable alternative behaviors that are For Situational or Adjunctive Use lifelong.
incompatible with undesirable behavior are POSSIBLE COMPLICATIONS
reinforced. • Reinforce your dog for being Alpha‐2 Agonists
• Clonidine 0.01–0.05 mg/kg PO PRN Injuries to humans.
calm as family members approach or beyond
threshold distance when in a location or in 1.5–2 hours before eliciting trigger, up to EXPECTED COURSE AND PROGNOSIS
possession of an item that might trigger q8–12h. • Side effects—transient hyperglycemia, • Lifelong management is necessary.
aggression; always use nonconfrontational anticholinergic, hypotension, collapse, • Prognosis for improvement determined by
techniques; start handling in nonpainful/ bradycardia, agitation. severity of aggression; motivation; whether
sensitive areas. • Start by staying below Serotonin 2a Antagonist/Reuptake triggers can be identified, avoided, and safely
threshold that would result in fear and/or managed; owner compliance; and level that
Inhibitors might be achieved with behavior modification
aggression, then gradually (baby steps) increase • Trazodone 2–5 mg/kg PO PRN prior to
stimulus intensity by decreasing distance, and medication. • Prognosis more favorable if
eliciting trigger, up to q8h—may titrate up to aggression occurs at low intensity and in
increasing distractions, or moving to more 8–10 mg/kg if no adverse effects. Use cautiously
challenging environments. • Progress is slow predictable situations.
at higher doses and when combining with other
(typically months); however, immediate safety drugs that increase serotonin due to risk of
and welfare can be achieved if triggers can be serotonin syndrome. • Side effects—sedation,
identified and prevented or avoided; owners anorexia, ataxia, GIT effects, cardiac
should be counselled on reading and conduction disturbances, agitation. MISCELLANEOUS
monitoring body language to identify thresholds
and avoid setbacks. • Owners must always be Benzodiazepines ASSOCIATED CONDITIONS
vigilant for stimuli that might incite fear or • Might be used to reduce anxiety prior to Other fear‐ or anxiety‐related conditions;
aggression. • Discuss whether referral to eliciting triggers. • Side effects—sedation, possessive and redirected aggression,
veterinary behavior specialist is recommended lethargy, ataxia, paradoxical excitement, may impulsivity, reactivity.
for counseling on risk assessment, prognosis, disinhibit aggression. ZOONOTIC POTENTIAL
behavioral management, behavior modification, CONTRAINDICATIONS Human injury/bite wounds.
and medication. Corticosteroids may contribute to polypha PREGNANCY/FERTILITY/BREEDING
SURGICAL CONSIDERATIONS gia, increased food guarding, and irritability. Do not breed dogs that exhibit aggressive
Aggression may be lower in neutered animals, PRECAUTIONS behavior.
but opposite has also been reported. Use caution, as any psychotropic medication SEE ALSO
may cause undesirable changes in behavior, • Aggression, Food and Resource Guarding—
including increased irritability or aggression. Dogs. • Aggression, Overview—Dogs.
POSSIBLE INTERACTIONS • Fears, Phobias, and Anxieties—Dogs.
MEDICATIONS Do not combine selective serotonin reuptake ABBREVIATIONS
DRUG(S) OF CHOICE inhibitors (SSRIs), tricyclic antidepressants • GIT = gastrointestinal tract. • MAO =
• No medications licensed for treatment of (TCAs), or monoamine oxidase (MAO) monoamine oxidase. • SSRI = selective
canine aggression; owners must give informed inhibitors (e.g., amitraz, selegiline), and use serotonin reuptake inhibitor. • TCA =
consent that use is off‐label and be advised of cautiously or avoid with opioids, tramadol, or tricyclic antidepressant.
potential side effects and risks. • Medications other medications that increase serotonin—
can result in serotonin syndrome. Suggested Reading
are likely indicated for moderately intense Herron ME, Shofer SS, Reisner IR. Survey of the
fear and anxiety, impulsivity, and reactivity. ALTERNATIVE DRUGS use and outcome of confrontational and non‐
• Ensure that owners understand risks in Natural products—dog‐appeasing confrontational training methods in client‐
owning an aggressive dog, that medication pheromones, supplements containing alpha‐ owned dogs showing undesired behaviors. Appl
will not ensure safety, and that they must casozepine or l‐theanine, or a calming Anim Behav Sci 2009, 177:47–54.
follow safety procedures. • Proper diagnosis probiotic might be considered for mild to Horwitz D, ed. Blackwell’s 5 Minute Consult
with behavioral modification plan, together moderate anxiety or used adjunctively. Clinical Companion: Canine and Feline
with appropriate selection of behavioral Behavior, 2nd ed. Hoboken, NJ: Wiley‐
drugs, leads to most successful outcome. Blackwell, 2018, pp. 45–57.
Selective Serotonin Reuptake Inhibitors Sueda KL, Malamed R. Aggression toward
• Fluoxetine 0.5–2 mg/kg PO q24h. FOLLOW‐UP people—a guide for practitioners. Vet Clin
• Paroxetine 0.5–1 mg/kg PO q24h. N Am 2014, 14:599–628.
• Sertraline 1–3 mg/kg PO q24h. • Side
PATIENT MONITORING Authors Wailani Sung and Jeannine Berger
• Clients will need ongoing assistance and
effects—sedation, irritability, gastrointestinal Consulting Editor Gary M. Landsberg
tract (GIT) effects, agitation; decreased should receive at least one follow‐up within Acknowledgment The authors and editors
appetite is common and usually transient. first 1–3 weeks after the consultation. acknowledge the prior contributions of
Provisions for further follow‐up should be Meredith E. Stepita and Laurie Bergman.
Tricyclic Antidepressants made at that time. • Drugs should only be
• Clomipramine 1–3 mg/kg q12h (label‐ prescribed under supervision and monitoring
restricted for aggression). • Side effects— of veterinarian.
sedation, GIT effects, anticholinergic Client Education Handout
available online
Aggression Toward Humans—Cats A
CAUSES & RISK FACTORS DIET

• Play motivated—lacking in opportunities Potential anxiolytic effects of “calming” diets
for normal play: solitary cat, insufficient and/ (see Supplements).
BASICS or inappropriate toys; history of owner using CLIENT EDUCATION
DEFINITION hands/feet to play with kitten and/or playing • Play motivated—normal play behavior and
Human‐directed aggression in cats. roughly with kitten. importance of opportunities for appropriate play.
• Fear—poor socialization with humans and/
PATHOPHYSIOLOGY • Fear—avoidance of fear‐inducing
or feral living, aversive event associated with a situations: ongoing exposure may worsen
• Most common causes for human‐directed
person, or people in general. signs, cause severe stress, and compromise
aggression in cats include play, fear/pain‐
• Pain related—medical/physical condition welfare.
related, redirected, maternal, and petting
such as abscess, especially in indoor/outdoor cat. • Redirected—addressing primary stimuli,
intolerance.
• Redirected—occurs during interference in, such as outside cats.
• Context contributes greatly when making
or interruption of, situations that have caused • Maternal—normal maternal and kitten‐
correct diagnosis. For example, play aggression
cat to become aggressively aroused, such as protective behavior; same as for fear‐
is likely to be seen in young, solitary cat,
cat fight (between familiar household cats), motivated aggression.
while pain‐related/fear aggression is common
presence of a cat outside, or noise. • Petting intolerance—normal feline
behavior seen in clinic setting.
• Maternal—recent birth of litter. grooming patterns; observation of cat’s
SYSTEMS AFFECTED • Petting intolerance—etiology unknown. warnings so that behavior does not escalate.
• Behavioral. Cats tend to groom each other on head/neck,
• Gastrointestinal—decreased appetite if fear so human petting of cat in other locations Behavior Modification Exercises
and/or pain related. may contribute to aggressive reaction. Desensitization and Counter‐Conditioning
• Hemic/lymphatic/immune—chronic stress (DS&CC)
effects on immune function. • Desensitization—exposing cat to fear‐
• Ophthalmic—dilated pupils in response to inducing stimulus (scary person) at a low level
autonomic nervous system stimulation. so cat does not react fearfully or aggressively.
• Skin/exocrine—may show displacement
DIAGNOSIS
Over time, intensity of stimulus is increased
behaviors such as overgrooming. DIFFERENTIAL DIAGNOSIS (i.e., distance between cat and stimulus is
GENETICS See Causes & Risk Factors. decreased) without causing fearful responses.
No known genetic basis. CBC/BIOCHEMISTRY/URINALYSIS • Operant conditioning (response substitution)—
• To rule out contributing medical conditions rewarding cat with special treat, toy,
and screening prior to drug use. grooming, petting, for relaxation.
Aggression is second to inappropriate elimin
• Urinalysis if concurrent inappropriate Classical Conditioning (CC)
ation for feline cases seen by veterinary
behavior specialists. elimination or marking. Classical counter‐conditioning conditioning—
OTHER LABORATORY TESTS pairing threatening stimulus (e.g., a person)
GEOGRAPHIC DISTRIBUTION
Middle age/senior cats—thyroid profile. with tasty treat, toy, petting; example: scary
None
person = tuna fish.
SIGNALMENT IMAGING
• Cats of any age, sex/neuter status, breed can
If indicated based on clinical examination
be affected. and/or suspected pain.
• Play‐motivated aggression more likely in DIAGNOSTIC PROCEDURES
juvenile, solitary cat. Thorough behavioral history, including MEDICATIONS
description of cat’s postures during aggression and Short‐term use of medication may be
SIGNS necessary to decrease overall levels of anxiety
• Play motivated—cat approaches its “victim,”
injuries inflicted, context, presence of outside
cats, early historical information, litter box use, and reactivity in more severe cases.
crouches in wait, stalks and chases; tail is
twitching and ears are forward. Typically will food consumption, and hiding behaviors. DRUG(S) OF CHOICE
attack moving target. PATHOLOGIC FINDINGS Azapirones
• Fear/pain related—ears back, body and tail N/A • Buspirone 0.5–1.0 mg/kg PO q12h.
lowered, piloerection, pupils dilated; may hiss • Most useful for fearful and withdrawn cats;
and growl. Avoidance of person(s) who elicit decreases
aggression. Attacks if approached and/or anxiety and may increase “self‐confidence.”
cornered. Extreme cases: expression of anal • Anecdotal reports of “increase in affection,”
glands, urination, and/or defecation. Hiding
TREATMENT therefore might be useful in severe cases of
behavior. APPROPRIATE HEALTH CARE petting intolerance.
• Redirected—cat highly aroused by stimulus Only if health/medical issue diagnosed. • Response noted in 1–2 weeks.
and seeks out alternate target. Aggression can NURSING CARE Selective Serotonin Reuptake Inhibitors
be very severe given cat’s level of arousal. Only if health/medical issue diagnosed.
• Maternal—usually predictable and self‐
(SSRIs)
ACTIVITY • Fluoxetine, paroxetine, sertraline 0.5–
limiting. Queen will act to protect her kittens.
• Petting intolerance—cat signals its • Play motivated—cat should be provided 1.5 mg/kg PO q24h.
with increased opportunity for appropriate • SSRIs must be given daily; may take 4–8
“displeasure” by twitching its tail and skin
when being petted in an undesired location play, either in the form of toys, human weeks to reach peak effects.
and/or for too long. Ears usually back; interaction, or additional housemate. Tricyclic Antidepressants (TCAs)
mydriasis; may hiss and growl before turning • Redirected—cat should be denied access to • Amitriptyline 0.5–2.0 mg/kg PO q12–24h.
to bite person. windows where outside cats can be seen. • Clomipramine 0.25–1.0 mg/kg PO q24h.
A Aggression Toward Humans—Cats (continued)
• TCAs must be given daily; may take 4–8 ALTERNATIVE DRUG(S)

weeks to reach peak effects. Pheromones
Benzodiazepines • Used alone or concurrently with drugs. MISCELLANEOUS
• Alprazolam 0.125–0.25 mg/cat PO • F3 facial pheromone (Feliway®) diffuser,
q8–24h. spray, and wipes. ASSOCIATED CONDITIONS
• Diazepam 0.1–1.0 mg/kg PO q12–24h • Maternal pheromone—Feliway MultiCat N/A
(rarely used due to potential hepatopathies). (Friends) diffuser for feline social conflict. AGE‐RELATED FACTORS
• Can be given “as needed” for specific • Maternal pheromone collar (NurtureCALM Play motivated—typically seen in young,
encounters with people inducing fear 24/7). solitary cat in household.
response and during DS&CC and CC Supplements ZOONOTIC POTENTIAL
sessions. Used alone or concurrently with drugs: People injured during aggressive attack should
• Can be used in conjunction with
L‐theanine (Anxitane®); alpha‐casozepine seek prompt medical attention; infection by
azapirones, SSRIs, and TCAs. (Zylkene®); combination products also Bartonella henselae can result from cat scratch
CONTRAINDICATIONS/PRECAUTIONS/ containing thiamine, whey protein, and or bite.
POSSIBLE INTERACTIONS calming plant extracts (Solliquin®); or diets
• None of drugs listed are approved for use supplemented with alpha‐casozepine and
Avoid medications in breeding/nursing cats.
in cats. l‐tryptophan (Multifunction Urinary + Calm
• All medications to be administered orally, as Diet, Royal Canin®). SYNONYMS
have not been shown to reach therapeutic N/A
levels by transdermal dosing. SEE ALSO
• Azapirones—side effects uncommon, but • Aggression, Overview—Cats.
occasional excitement noted; should not be FOLLOW‐UP • Fears, Phobias, and Anxieties—Cats.
given in combination with monoamine
PATIENT MONITORING ABBREVIATIONS
oxidase (MAO) inhibitor; avoid use in the
• Weekly follow‐up recommended in early • ALT = alanine aminotransferase.
aggressor cat as may increase any “bully”
stages of treatment. • AST = aspartate aminotransferase.
behavior.
• For cats on medication, follow‐up blood • CC = classical conditioning.
• Neither SSRIs nor TCAs should be given
testing recommended every 6–12 months. • DS & CC = desensitization and counter‐
with each other, nor in combination with
conditioning.
MAOIs. PREVENTION/AVOIDANCE • MAO = monoamine oxidase.
• SSRIs—side effects include mild sedation • Play motivated—provide opportunities for
• SSRI = selective serotonin reuptake inhibitor.
and decreased appetite, constipation, and appropriate play. • TCA = tricyclic antidepressant.
urinary retention; competitive inhibition of • Fear—avoidance of fear‐inciting stimuli;
cytochrome P450 liver enzymes; when early socialization to people and events may Suggested Reading
administered concurrently with medication help prevent some occurrences of fear‐related Bradshaw J, Ellis S. The Trainable Cat: A
utilizing P450 enzymes, elevated plasma levels responses to people. Practical Guide to Making Life Happier for
of medications may increase. • Pain—treat underlying conditions. You and Your Cat. New York: Basic Books,
• TCAs—side effects include sedation, • Redirected—address possible arousing 2016.
constipation, diarrhea, urinary retention, stimuli, indoors and outdoors. Horwitz D, ed. Blackwell’s 5 Minute Consult
appetite changes, ataxia, decreased tear • Maternal—as for fear. Clinical Companion: Canine and Feline
production, mydriasis, cardiac arrhythmias, • Petting intolerance—limit amount of time Behavior, 2nd ed. Hoboken, NJ: Wiley‐
tachycardia, and changes in blood pressure. petting cat; DS&CC to petting. Blackwell, 2018, pp. 143–250.
• Benzodiazepines—side effects include Landsberg GM, Hunthausen W, Ackerman L.
POSSIBLE COMPLICATIONS Behavior Problems of the Dog and Cat, 3rd
sedation, ataxia, muscle relaxation, increased
Potential human injury, especially if cat is ed. St. Louis, MO: Saunders Elsevier, 2013,
appetite, paradoxical excitation, and increased
approached, cornered, and/or highly aroused. pp. 327–343.
friendliness; idiopathic hepatic necrosis has
been reported in cats following treatment EXPECTED COURSE AND PROGNOSIS Overall K. Manual of Clinical Behavioral
with diazepam. • Progress occurs slowly; relearning is a Medicine for Dogs and Cats. St. Louis,
• Specific recommendations for the use of process and each case is individual. MO: Mosby, 2013, pp. 390–426.
diazepam—baseline physical exam, CBC, and • If medications are indicated, begin at low Seksel K. Behavior problems. In: Little SE,
blood chemistries to confirm good health; dose and titrate up as necessary. ed., The Cat: Clinical Medicine and
repeat the blood chemistries at 3–5 days; if • To discontinue medication, wait until new Management. St. Louis, MO: Saunders,
elevated alanine aminotransferase (ALT) or behavior is stable (8–12 weeks) and wean off 2012, pp. 219–224.
aspartate aminotransferase (AST), discontinue slowly, usually over weeks. Author Terry Marie Curtis
medication. • If aggressive behavior recurs, return to Consulting Editor Gary M. Landsberg
lowest effective dose.
Aggression, Food and Resource Guarding—Dogs A
OTHER LABORATORY TESTS an alternative behavior, (e.g., drop, touch)

As needed to rule out underlying medical (see training below).
conditions, particularly if signs of polyphagia; • If the dog is in possession of an object that
BASICS thyroid screen. must be removed for safety, offer a reward
OVERVIEW IMAGING (e.g., treat, toy, walk) of higher value or use a
• Aggression displayed while guarding food As needed to rule out underlying medical stimulus (e.g., doorbell) that will move the
(e.g., in food bowl, dog “chews”), scavenged conditions, (e.g., pain); MRI if CNS disease dog away.
items, objects (e.g., toys, stolen objects), • If safety cannot be ensured, the dog should
suspected.
resting locations (e.g., bed, couch), or people. be removed from the household.
Usually within the range of normal behavior, DIAGNOSTIC PROCEDURES
Gastrointestinal diagnostics. BEHAVIOR THERAPY
but may be excessive or abnormal due to early • Structured interaction programs where the
experience, learning, genetic factors, or dog is taught to consistently perform a
underlying medical conditions. desired behavior (e.g., sit) before receiving
SYSTEM AFFECTED anything it values (e.g., attention, petting,
Behavioral. TREATMENT treats, going for a walk) give the dog control
GENERAL COMMENTS of its resources for being calm, provide
SIGNALMENT
• Treatment consists of a multifaceted
structure and predictability in all interactions,
No breed or sex predilections.
approach including management to ensure teach impulse control, and train the dog
SIGNS using positive interactions (e.g., good things
safety and prevent recurrence, behavior
• Barking, growling, lip-lifting, snarling, happen by sitting calmly).
modification, and medication (if indicated).
snapping, lunging, biting, directed toward • Provide sufficient outlets for play, chew, and
• A realistic expectation is for successful
other dogs or people. feeding, such as in food-filled toys in
management, not full resolution. In most
• Subtle communication signals may include locations and at times where the dog can be
cases, owners will need to manage triggers for
blocking access to resources, hard stare, taller left alone or physically confined, (e.g., to a
the rest of the dog’s life.
stance, tail elevated, and ears perked forward room, behind a barrier, or in a safe haven
• Successful treatment depends on the owner’s
when in possession of valued resource. (pen, crate)) until the dog finishes with the
understanding of canine social behavior and
• May be accompanied by fearful/submissive resource, will walk away, or can be cued away
communication, identifying and preventing
body postures/facial expressions (e.g., and rewarded.
all aggression-eliciting stimuli (e.g., situations,
crouching, backing away, ears back, tail • Training—focus on teaching behaviors in
people, resources), willingness and ability to
tucked, looking away, lip licking). neutral situations using positive reinforcement
follow safety recommendations, and effective
• Can be motivated by fear—defensive or (e.g., food, toys, play, petting) that can be
implementation of reward-based behavior
offensive. used to:
modification.
• Most common near valued resources (e.g., ◦◦ Keep the dog away from resources, (e.g.,
• Owners must be educated about the risks of
food), stolen items (e.g., tissues, owner leave it, go to bed or crate, or watch).
using physical punishment and training
clothing), scavenged items (e.g., garbage), and ◦◦ Move the dog away from resources, (e.g.,
techniques that use “dominating,” such as
lasting items (e.g., chews). touch (hand target), find it).
alpha rolls, corrections with choke chains or
CAUSES & RISK FACTORS ◦◦ Release the object (e.g., drop).
prong collars, verbal punishment, and of
• Underlying medical conditions, especially • Private sessions with a force-free trainer
physically taking away resources that can lead
pain, endocrinopathies, gastrointestinal to increased aggression, anxiety, and resource may provide the best guidance for successful
disease, or those causing changes in appetite. guarding, and disruption of the human– training.
• May be a normal canine behavior, • Behavior modification—desensitization
animal bond.
influenced by previous negative experience (DS) is the process by which dogs are exposed
SAFETY RECOMMENDATIONS to their triggers under their threshold (e.g.,
(e.g., lack of socialization, physically
• Prevention/avoidance is essential to ensure distance, low-value resource). Food, toys,
removing resources, punishment or confron
safety, address the pet’s welfare, and prevent verbal praise, or attention/petting can be used
tation) or other behavioral disorders, such
further repetition and potential intensification as rewards for calm responses. Counter-
as anxiety.
of the problem. conditioning (CC) is the process in which
• Owner’s inability to read and recognize
• Safety measures include training dogs to favored rewards are paired with the stimulus
signs of fear or conflict.
wear a basket muzzle, placing head collars or to change the emotional response to one that
harnesses with leashes attached, and the use is positive.
of pet gates and confinement training to • Gradually (baby steps) increase stimulus
prevent access to resources that might be intensity, staying below the threshold that
DIAGNOSIS guarded. would result in fear and/or aggression, (e.g.,
• Confine the dog away from potential decreasing distance, increasing resource value,
victims and items and/or keep people away changing environments).
• Fear aggression.
from the dog when it is in possession of • The owner can toss treats when walking by
• Social status aggression.
resources that might be guarded; alternately, the food bowl at sufficient distance that the
• Conflict-related aggression.
the dog must be under direct physical control, pet associates approach with a positive outcome
• Generalized anxiety disorder.
(e.g., with leash attached), of a responsible adult. in association with the food bowl and toys.
• Pain-related aggression.
• Identify and prevent or avoid any situation • Progress is slow (typically months).
• Irritable aggression.
that might trigger aggression. Never forcibly Carefully monitor body language to avoid
CBC/BIOCHEMISTRY/URINALYSIS remove objects in the dog’s possession. Wait setbacks.
To rule out underlying contributing medical until the dog is finished with the resource and • Owners must be vigilant to prevent approach
conditions. will walk away, or cue and reward the dog for in situations where dog might guard.
A Aggression, Food and Resource Guarding—Dogs (continued)
• Discuss referral to a veterinary behavior psychotropic drugs, steroids) may increase

specialist where recommended for assessment resource guarding.
and counseling. • Corticosteroids can be contraindicated
in food‐aggressive dogs; could cause or MISCELLANEOUS
contribute to polyphagia, resource guarding, ASSOCIATED CONDITIONS
and irritability. Other fear- or anxiety-related conditions.
MEDICATIONS ZOONOTIC POTENTIAL
Human injury and bite wounds.
DRUG(S) OF CHOICE
• Medications are generally not indicated for PREGNANCY/FERTILITY/BREEDING
resource guarding. FOLLOW-UP Do not breed dogs that exhibit aggressive
• May be indicated for moderate to marked PATIENT MONITORING behavior.
fear or anxiety, or when behavior is abnormal In most cases, follow-up should be within the SEE ALSO
in intensity, reactivity, or impulsivity. first 1–3 weeks after consultation. Provisions • Aggression to Unfamiliar People and
• Owners must receive informed consent of for further follow-up should be made at that Unfamiliar Dogs—Dogs.
potential risks and side effects, that the use of time. • Aggression toward Familiar People—Dogs.
a medication is off-label, and that medication PREVENTION/AVOIDANCE • Aggression, Overview—Dogs.
does not insure safety. Owner should receive counseling from first
• For ongoing medication, a selective ABBREVIATIONS
visit on socialization, making positive • CC = counter-conditioning.
serotonin reuptake inhibitor (SSRI; e.g., associations with handling, reward-based
fluoxetine, paroxetine, sertraline) or • DS = desensitization.
training to cues (including touch and drop), • SSRI = selective serotonin reuptake
clomipramine might be indicated. and never forcing a pet to relinquish
• For situational or as needed use, trazodone, inhibitor.
resources.
clonidine, or benzodiazepines might be Suggested Reading
considered alone or in conjunction with an POSSIBLE COMPLICATIONS Horwitz D, ed. Blackwell’s 5 Minute Consult
ongoing medication. Injuries to dogs and humans. Clinical Companion: Canine and Feline
• For doses, side effects, precautions, and EXPECTED COURSE AND PROGNOSIS Behavior, 2nd ed. Hoboken, NJ: Wiley-
contraindications, see Aggression toward • Resolution may not be achievable and Blackwell, 2018, pp. 100–109.
Familiar People—Dogs. lifelong management is usually necessary. Authors Jeannine Berger and Wailani Sung
CONTRAINDICATIONS/POSSIBLE • Prognosis for improvement depends on Consulting Editor Gary M. Landsberg
severity of aggression, number and type of Acknowledgment The authors and editors
INTERACTIONS
resources guarded, and whether they can be acknowledge the prior contribution of
• Use caution, as any psychotropic medic
effectively identified and prevented. Meredith E. Stepita and Laurie Bergman.
ation might cause undesirable changes in
behavior, including increased irritability and • Prognosis is highly dependent on owner
aggression. Drugs that increase appetite (e.g., compliance.
Aggression, Intercat Aggression A
growling, yowling, spitting, hissing, swatting, • Changes in social group such as addition of
lunging, chasing/stalking, and/or biting other “new” cat. • Scratching and biting during
cats, dilated pupils, may be accompanied by first introduction. • Access to outdoors
BASICS body language of fear (e.g., classic Halloween and/or intrusion of unfamiliar cats onto
DEFINITION cat stance: piloerection, back arched, tail up) territory. • Crowding or lack of adequate
Intercat aggression—offensive or defensive or more offensive body language (tense social space and access to resources.
aggression between cats consisting of staring, muscles, tail head elevated but rest of tail
displacing, vocalizing (growling, yowling, down, back straight or slightly slanted toward
shrieking), spitting, hissing, swatting, lunging, head, ears forward or to the side), excessive
chasing/stalking, and/or biting other cats. facial marking, and perhaps urine marking.
DIAGNOSIS
PATHOPHYSIOLOGY Victim (Usually Defensive)
• Covert—avoidance of aggressor, hiding, DIFFERENTIAL DIAGNOSIS
• May be normal behavior or abnormal.
• May be caused by underlying medical change in grooming and eating habits, hyper- Behavioral Differentials
disease (e.g., CNS) or concurrent medical vigilance, dilated pupils. • Overt—hissing, • Fear-related aggression—cat may hiss, spit,
disease that may lower the threshold for swatting, running, vocalizing (including arch the back, display piloerection, and
irritable responses (e.g., pain, hyperthyroid). growling), Halloween cat stance, may escalate attempt to flee unless escape is thwarted;
• May be multiple motivations including to defensive attack if cornered. pupil dilation will accompany a fear response.
predatory/play, disputes over territory, sexual, Elimination Outside of Litter Box • Status-related aggression—may occur with
fear, anxiety, and redirected, fear, anxiety, • Aggressors may block access to litter box change or instability of social hierarchy and
non-recognition, and redirected. area, forcing victims to choose alternative control of access to resources; it is undecided
locations; secondary substrate and/or location if cats have dominance hierarchies or if
SYSTEMS AFFECTED
preferences and aversions can develop. • Both conflict is better explained by territorial
• Behavioral. • Skin/exocrine—secondary to
victims and aggressors may urine mark. defense. • Territorial aggression—in response
traumatic injury. • Immune—chronic stress
• Extremely fearful cats may urinate or to threat to territory; boundaries marked with
may alter the immune response. • Secondary
defecate in midst of aggressive events. urine, feces, or scent glands. • Redirected
infection (cat bite abscesses) is not uncommon.
aggression—exposure to agitating stimuli
• Nervous. Physical Examination (cats in yard, visitors, noises, scents, etc.),
GENETICS • Normal, except injury from fights or if with aggression directed toward target other
None. However, friendliness may be mostly underlying medical issues. • Stress may affect than stimulus. • Failure of recognition—
related to paternal effects. eating and self-grooming (increased or aggression between feline housemates after
decreased). returning from separation (e.g., veterinary
Unknown CAUSES visit, grooming); most likely due to change in
• Lack of appropriate socialization to other odor, visual cues, or stress of returning cat.
SIGNALMENT • Maternal aggression—aggression during
cats prior to 7 weeks of age. • May be
Breed Predilections component of normal social behavior. • Social periparturient period; females guard kittens
None and environmental instability such as addition and nesting sites. • Intermale aggression—
of new cat, loss of resident cat, odor stimuli between males in response to territorial
Mean Age and Range
(return of cat from veterinarian or giving one disputes, hierarchical status, or mates; may be
• Can occur at any age due to changes in social
cat a bath), aging or illness of one or both cats, more pronounced at social maturity. • Sexual
environment or be redirected. • Previously
cats reaching social maturity. • Household aggression—male typical behavior of chasing,
stable relationships can deteriorate as cats reach
change, e.g., moving, changing furniture or pouncing, biting on nape of neck, and
social maturity (2–4 years of age).
resting areas. • Genetically unrelated cats and mounting. • Predatory/play-related aggression—
Sex cats that have recently moved in together are predatory components of play directed
• Intact males more likely to initiate intercat more likely to show aggressive behaviors toward another cat; recipient often older cat
aggression (related to territory, and/or toward each other. • Resident cats commonly that is not interested in playing.
proximity to females). • Females will defend need prolonged exposure to new cats before Medical Differentials
their young from unfamiliar individuals. accepting them into group. • Resource • Any illness causing malaise, pain, or
• Male kittens more likely to initiate intercat limitation, e.g., vertical and/or horizontal increased irritability. • Endocrine—e.g.,
aggression related to predatory components space, hiding/resting areas, food, water, and hyperthyroidism. • Neurologic—e.g.,
of play. litter boxes in multicat households. • Exposure neoplasia, seizures, cognitive decline.
SIGNS to arousing stimuli (cats in yard, visitors, • Infectious—e.g., toxoplasmosis, feline
noises, scents, etc.) can cause redirected immunodeficiency virus (FIV), feline
Historical Findings
aggression, after which aggression might leukemia virus (FeLV). • Iatrogenic—
• May arise spontaneously and vary in
persist. • Medical problems including CNS medications that increase irritability or
frequency and intensity. • Owners most likely
disorders, hyperthyroidism, or any disorder disinhibit aggression (e.g., mirtazapine,
to seek behavioral intervention if there are
that causes pain and/or increased irritability. benzodiazepines, buspirone). • Toxins—lead,
physical injuries, the welfare of the aggressor
and/or victim is compromised, or fighting RISK FACTORS illicit substances.
becomes sufficiently distressing. • Human • Singleton and/or bottle-raised kittens. CBC/BIOCHEMISTRY/URINALYSIS
attempts to interrupt fighting may trigger • Lack of socialization exposure and To rule out medical causes and as baseline if
human-directed aggression/injury. experience with conspecifics during socializ- drug therapy indicated.
ation period (2–7 weeks) and beyond. • Male
Aggressor (Usually Offensive) intact cats. • Postpartum females with kittens. OTHER LABORATORY TESTS
• Covert signs—staring, displacing other cats, • FeLV/FIV. • Total thyroxine (T4) in cats
• Separating and returning housemate (e.g.,
stiff body language/movements while >6 years.
following veterinary visit, groomer).
approaching other cat. • Overt signs—
A Aggression, Intercat Aggression (continued)
IMAGING room together without having aggressive controlled visual introduction, across glass or
As indicated based on history and physical events. Cats should stay at a distance that screen door, in their kennels, or on leash and
signs. allows for calm participation. • Engage cats harness, insuring they are at a distance that
DIAGNOSTIC PROCEDURES in daily sessions of pleasurable activities (e.g., prevents overt/covert aggression. Feed cats or
• Detailed behavioral and medical history.
play, training, eating delectable food treats) engage in play for classical counter-
• Identify if there is a clear aggressor and/or
at distances that do not incite aggression. conditioning. • Over many sessions gradually
victim and if aggression is overt or covert. Gradually move fun sessions closer to each reduce distance between cats, being careful
• If multiple cats, determine which cats spend
other, making sure to stay at a distance that to stay far enough apart during each session
time together and mutually groom, and does not trigger overt/covert aggression. that no overt or covert behavioral signs of
• Teach cats a “come and/or go to place” cue aggression and/or fear are seen. Start and
which avoid each other. • Identify preferred
core areas of each cat for feeding, play, and using positive reinforcement at times, in end all sessions on successful note. • Teach
resting, and locations of any house soiling or situations, and with sufficient rewards that each cat a “come and/or go to place” cue
marking. • Identify number, location, types cats are most able to learn. • Interrupt or using operant counter-conditioning and
of litter boxes, and their management. redirect cats by cueing to come or go to their positive reinforcement at times when cats are
• Videos, photographs, and/or drawn floor
place, or by luring one or both cats to their not stressed. Practice several times daily so
plans can provide spatial details and infor- safe zones with food, treats, wand toys, tossed each cat learns to respond reliably. • When
mation regarding body language during social toys, or laser pointers before aggression starts ready to allow cats more freedom with each
interactions. • Note any other changes in or as initial signs are seen (e.g., staring, tail other, follow instructions for less severe
demeanor, routine, eating, and grooming. twitching, pupil dilation). • Aversives and/or intercat aggression (above).
punishers can increase aggressive behavior SURGICAL CONSIDERATIONS
PATHOLOGIC FINDINGS and increase negative associations with other
None unless concurrent medical diseases. Neutering reduces roaming, intercat
cats, so must be avoided. • Goal of manage aggression, and urine spraying in approxi-
ment and safety is to prevent aggressive mately 90% of intact males. Neutering/
events. In an emergency, use of laundry spaying reduces mounting and sexual
basket or blanket placed between or over cats behavior.
TREATMENT can stop aggression, and direct cat to its safe
area until calm, but should not be considered
APPROPRIATE HEALTH CARE as a standalone treatment. • Bell the
Treat as outpatient. aggressor (using quick release or safety collar)
NURSING CARE so both owners and victim can quickly MEDICATIONS
Supportive care if any injuries. identify his or her location. • Increase DRUG(S) OF CHOICE
number of resources and locations (e.g., As all medications are extra-label, insure
ACTIVITY food, water, scratching, perching, bedding,
• May need to be restricted if confinement client is informed, and review target desirable
play and feeding toys) throughout the outcomes and potential adverse effects.
required to prevent perpetuation of aggression residence, including each cat’s core area.
and negative emotional responses. Efficacy of multimodal environmental For Aggressor and/or Victim
• Provide sufficient alternate outlets for each enrichment should not be underestimated. Selective Serotonin Reuptake Inhibitors
cat during confinement and during release. • Increase litter boxes to number of cats plus (SSRIs)
CLIENT EDUCATION one divided among multiple locations, so • Fluoxetine or paroxetine 0.5–1 mg/kg PO
For chronic, severe cases or for aggression that that one cat cannot keep another from q24h. • Drugs of choice for aggression,
does not respond to treatment, may require accessing boxes; locations with more than anxiety, and/or urine marking; may decrease
permanent separation, either by rehoming one one exit/entry are ideal. • Increase number of impulsivity. • Side effects may include
of the cats or by confining them in separate hiding and resting areas, especially by gastrointestinal upset, decreased appetite,
parts of the home. increasing vertical space (e.g., shelves, sedation, urinary retention, constipation,
Cases with Low Frequency of Intense, window sills). • No new cats should be lowered seizure threshold, and increased
added to the house. agitation/irritability.
Injurious Aggressive Outbursts
• Separate cats when they cannot be super- Cases Where Cats Cannot be in Same Tricyclic Antidepressants (TCAs)
vised (create “safe zones”). • Either keep Room without Immediately Becoming • Clomipramine 0.25–0.5 mg/kg PO
separate in same areas each day in effort to Agitated q24h—serotonin selective tricyclic, for
form separate core territories for each cat, or • Separate cats completely when anxiety and aggression. • Side effects include
“time share” space between cats. • Confine unsupervised. • Meet each cat’s needs for gastrointestinal upset, sedation, urinary
newly introduced cat or aggressor to smaller, play, litter boxes, food, water, perching, retention, constipation, and lowered seizure
less familiar area. • For multiple cats, resting, and attention. • Large wire dog threshold. Do not use in patients with
separate by stability of relationship between kennel or vertically oriented wire cat cage arrhythmias or cardiomyopathies.
cats. Any despotic/bully cats should be (with shelving) may be better tolerated than Pheromones
confined alone. • Consider “artificial smaller cat kennels and can be used for • Feliway® Multicat/Friends (Ceva)—
allomarking” to form communal scent controlled exposure. • Cats may be taught synthetic feline mammary gland pheromone
between cats that are fighting; a towel to tolerate harnesses and leashes so that they that may be helpful for reducing intercat
(facecloth) may be rubbed (cephalocaudally) can be used during training and controlled social conflicts when combined with a
to obtain scent of one cat and then rubbed reintroduction. This is especially valuable for multimodal plan. • Feliway Classic (Ceva)—
onto other cat, and vice versa. • Towels the aggressor. • Set up desensitization and synthetic feline facial pheromone that may be
should be left in environment to allow for counter-conditioning sessions daily; initially helpful in reducing stress and associated
habituation to each other’s scent, especially if utilize physical and visual barriers (e.g., marking behavior.
cats are kept separated. • Reward cats with opposite sides of solid door). • Proceed to
food, play, and/or attention for being in same
(continued) Aggression, Intercat Aggression A
For Victim (Anxitane, Virbac), or with alpha-casozepine

Azapirone (Zylkene®, Vetoquinol), Royal Canin
• Buspirone 0.5–1 mg/kg PO q8–24h— Veterinary Diet Calm® (contains alpha-
reserved for victims to increase social casezopine, l-tryptophan, and nicotinamide), MISCELLANEOUS
confidence. • Side effects rare; may include or Hill’s Prescription Diet® Multicare Feline ASSOCIATED CONDITIONS
decreased sociability and increased agitation/ Urinary Stress (contains l-tryptophan and • Urine marking/spraying. • House soiling.
irritability; victim may be more confident and milk protein hydrolysate). • Excessive grooming. • Fearful/anxiety-
fight back. related behavior. • Human-directed or
Benzodiazepines interspecies aggression.
• Lorazepam 0.125–0.25 mg/CAT PO up to AGE-RELATED FACTORS
q12–24h or oxazepam 0.2–0.5 mg/kg PO FOLLOW-UP Predatory/play-related aggression more
q12–24h for anxious or fearfully aggressive common in young active and playful cats
PATIENT MONITORING
cats and as an appetite stimulant, helping housed indoors with more sedentary or aged
• Monitor patients 2 weeks after treatment
to facilitate classical counter-conditioning; individuals.
initiation and monthly for first few months;
may be used as needed, with peak effects ZOONOTIC POTENTIAL
follow-up visit should be scheduled 4–8
seen within 1 hour. • Side effects may Human intervention may lead to bite or
weeks into treatment if drugs dispensed to
include increased appetite, ataxia, inhibited scratch injuries.
assess response and adjust dose if necessary.
learning, and disinhibition of aggression.
• Benzodiazepines may rarely cause cases of PREGNANCY/FERTILITY/BREEDING
• Note: controlled substance; dependence
fatal hepatopathies; patients should be Most behavioral medications are contra
can develop; should be gradually weaned if
rechecked immediately if any adverse events indicated in breeding animals.
used consistently for longer than 2 weeks.
occur, including anorexia. • Medication
CONTRAINDICATIONS should be used for at least 4–6 weeks after SYNONYMS
• Benzodiazepines should be used cautiously resolution of signs, then gradually weaned by Feline intraspecies aggression.
or avoided in cats with hepatopathies. • SSRIs reducing dosage no faster than 25% per day SEE ALSO
and TCAs may produce anticholinergic side on weekly basis. • Some patients require • Aggression, Overview—Cats.
effects. • SSRIs and TCAs should be used long-term medication; recheck laboratory • Kitten Behavior Problems.
with caution in patients with cardiac work every 6 months to 1 year, depending on
abnormalities, seizures, and liver disease. ABBREVIATIONS
health and age.
• FeLV = feline leukemia virus.
PRECAUTIONS PREVENTION/AVOIDANCE • FIC/FLUTD = feline idiopathic cystitis/
• Any behavioral drug may produce para- • Proper socialization through 2–7 weeks of feline lower urinary tract disease.
doxical reactions, including fear, anxiety, age and ongoing. • Gradual introduction more • FIV = feline immunodeficiency virus.
hyperexcitability, and/or aggression. closely resembles natural process through • MAOI = monoamine oxidase inhibitor.
• Medications that alter serotonin levels which new cats enter existing group at the • SSRI = selective serotonin reuptake
have the potential to produce serotonin periphery and may be accepted over time. inhibitor.
syndrome. • Negative initial encounter often associated • T4 = thyroxine.
POSSIBLE INTERACTIONS with future intercat aggression. • Related and • TCA = tricyclic antidepressant.
• Avoid concurrent use of SSRIs and TCAs;
familiar cats less likely to have intense intercat
INTERNET RESOURCES
avoid using monoamine oxidase inhibitors aggression. • In stable multicat households,
• https://indoorpet.osu.edu/cats • https://
(MAOIs, such as selegiline) with SSRIs and avoid adding additional cats. • Avoid reintro-
catvets.com
TCAs; use SSRIs and TCAs cautiously or duction aggression by avoiding separating cats
when possible. Suggested Reading
avoid with buspirone, tramadol, and
Heath S. Feline aggression. In: Horwitz DF,
tryptophan due to possible serotonin POSSIBLE COMPLICATIONS
Mills D, eds. BSAVA Manual of Canine and
syndrome. • Caution with concurrent Abrupt withdrawal of behavioral medic-
Feline Behavioural Medicine, 2nd ed.
medications considered substrates of ations may result in aggression and rebound
Gloucester: BSAVA, 2009, pp. 223–235.
cytochrome P450. anxiety.
Landsberg G, Hunthausen W, Ackerman L.
ALTERNATIVE DRUG(S) EXPECTED COURSE AND PROGNOSIS Feline aggression. In: Behavior Problems of
• Amitriptyline (TCA) 0.5–1 mg/kg PO • Prognosis for most cases is fair; complicated the Dog and Cat, 3rd ed. Philadelphia, PA:
q12–24h—for anxious cats, especially if by prolonged duration, high intensity, under- Elsevier Saunders, 2013, pp. 327–343.
comorbid recurrent feline idiopathic cystitis/ lying medical conditions, and incomplete Pachel CL. Intercat aggression: restoring harmony
feline lower urinary tract disease (FIC/ owner compliance. In one study 62% were in the home. A guide for practitioners. Vet Clin
FLUTD); not selective for serotonin reuptake considered cured and 37% not cured North Am 2014, 44:565–579.
inhibition and likely less effective for (rehomed, euthanized, or permanently Authors E’Lise Christensen Bell and Kenneth
aggressor. Side effects include sedation, separated). • Recent and mild cases may have M. Martin
decreased grooming, and increased weight. better long-term outcomes. Consulting Editor Gary M. Landsberg
• Dietary supplementation with l-theanine
A Aggression, Overview—Cats
perceived need to defend multiple resources stiffening of shoulders/legs, crouching, dilation
(e.g., people, food, resting areas, feeding areas, of pupils, hissing, spitting, growling, piloerec-
elimination sites, etc.). • Territorial behaviors tion, staring, chasing, stalking, pawing, lunging.
BASICS include marking with urine and/or feces, • Cardiovascular—signs associated with
DEFINITION bunting (rubbing of cheeks on surfaces to sympathetic activation and hypothalamic‐pitui-
• Aggression is a behavioral strategy used to deposit pheromones), and scratching (also tary‐adrenal (HPA) activation. • Endocrine/
manage aversive situations. • May be normal and deposits pheromones and leaves visual mark) metabolic—long‐term aggression associated
appropriate in certain contexts. • May be that may be associated with aggression. • In with fear/stress/anxiety, symptoms associated
abnormal with deleterious effects on cat’s physical severe cases, aggressor may seek out the other with long‐term activation of HPA system.
and emotional well‐being. • Aggressive— individual and attack. • Body posture with • Gastrointestinal (GI)—with chronic HPA
describes both mood and temperament traits territorial aggression is assertive and confident. stimulation: may see cat more prone to
relating to propensity to show aggression when Pain Aggression (toward People anorexia and GI ulcers; with acute fear
environmental circumstances dictate. aggression: evacuation of bowel and possible
and Animals) diarrhea; inflammatory bowel disease (IBD)
Play Aggression (toward People) Cats in pain may show aggression (hiss, possible in chronic stress. • Hemic/lymphatic/
• Typically refers to cat who scratches and growl, scratch, bite) when physically handled immune—decreased immune response with
bites owners during play. • Not true or immediately prior to or after activity such chronic HPA stimulation; stress leukogram.
aggression, but overzealous play without as jumping on or off a piece of furniture. • Both victim and aggressor may suffer injuries;
proper impulse control due to lack of training
Maternal Aggression with chronic activation of HPA, muscle wasting
or proper intraspecific social feedback. • Cat’s
Female cat may show aggressive behavior may occur. • Nervous—increased reactivity up
intent is not to harm the person. • Behavior
toward individuals approaching her kittens. to 72 hours following aggressive event; may see
encouraged and rewarded by owners through
Impulse Control Aggression increase in aggression with decreased provoca-
rough play with kitten; when larger and
Cats who show intense aggressive responses to tion as synapses in amygdala become sensitized;
stronger, becomes perceived as aggression
mild stimuli without much or any warning in some animals may be associated with
rather than overzealous play.
may have impulse control disorder arising decreased serotonin, causing aggressive
Predatory Aggression (toward People or outbursts; may see ritualized motor patterns,
from dysfunctional serotonin neural circuits.
Other Animals) shaking, or trembling. • Ophthalmic—dilated
• Cats have innate drive to “hunt” or show Frustration‐Induced Aggression (to pupils with sympathetic stimulation. • Renal/
predation, which includes stalk, hide, and People and Other Animals) urologic—may see spraying or small amounts
pounce. • Predatory behavior is not a direct Some cats with very outgoing, social personali- of urine on horizontal surfaces; stress may be
function of hunger. • Typically stimulated by ties may exhibit aggression if restricted life contributor to feline interstitial cystitis.
fast movements and can progress to cat indoors does not meet their behavioral needs. • Respiratory—tachypnea in acute cases or
hiding and waiting for animal or person to Contact‐Induced/Petting Aggression when stressed. • Skin/exocrine—damage due
walk by. • Play is way for young cats to to fights or to excessive grooming associated
(toward People) with fear/anxiety/distress.
perfect predation skills; play aggression and
• Cats may show early signs of aversion during
predatory aggression may overlap. SIGNALMENT
petting and handling with ears going back and
Redirected Aggression (toward People tail swishing. • If physical contact continues, • Preliminary evidence that behavioral traits
or Other Animals) they may bite. • Owners often miss early in cats vary by breed and sex. • Males more
• Cats who see, hear, or smell a trigger and warning signs. • When cats groom one another, likely to show aggression toward other cats,
direct aggressive behavior toward the closest they typically limit grooming to the head while females more likely to show aggression
bystander. • In some cases, one person or region. • Some cats appear to be particularly toward owners. • Abyssinian, Russian blue,
animal in the home becomes designated sensitive to being stroked along the dorsum. Somali, Siamese, and chinchilla breeds showed
victim, and cat may bypass a nearby more aggression. • Maine Coon, ragdoll, and
Intercat Aggression within Home Scottish folds showed least aggressiveness.
individual and attack preferred target. • Cats • After introducing new cat to home, 50% of
may remain aroused for 24–72 hours after cat owners report fighting (scratching and SIGNS
triggering event. • Common triggers inciting biting). • Number of cats, sex, and age are not • May appear at social maturity (2–4 years of
redirected aggression are seeing another cat or significant factors in predicting which cats will age) except for play‐related and should occur
wildlife outside or loud noises. show aggression toward each other. • Any of in specific social contexts/interactions. If
Fear/Defensive Aggression (toward the above categories of aggression are all onset occurs in older cat, medical causes
possibilities for fights between or among cats. should be ruled out first. • General com-
People or Other Animals)
• Fear/anxiety is most common cause of ments—most owners able to detect overt
• Cat will show body postures indicative of
intraspecific aggression. • Learning—conse- signs of aggression (biting, hissing, growling),
fear/anxiety and may use aggression as strategy
quences/outcome (reinforcement, punish- but may miss more subtle signs of aggression
to manage that aversive situation. • Typical
ment) further compound the problem. that typically occur between cats (staring) and
behaviors include combination of any of the
resulting anxious behaviors that can result in
following: hissing, spitting, piloerection, PATHOPHYSIOLOGY aggression (meatloaf position, averting gaze,
arched back, turning away, running away, Behavior problems are typically multifactorial in etc.). Videotapes of intercat interactions allow
cowering, rolling on back, and pawing cause. Figure 1 illustrates some of the common clinician to assess behavior.
(defensive) if cornered. • With learning and components that need to be evaluated to
repetition, may display more offensive signs. accurately diagnose and treat aggression cases. CAUSES
• Underlying medical issues can cause
Territorial Aggression (toward People or SYSTEMS AFFECTED aggression. • Temperament/behavior
Other Animals) • Behavioral—vary with type of aggression, influenced by genetics, rearing, socialization,
• Some cats, particularly males, show territorial occur alone or in combination: tail swishing/ environment in which cat lives, and types of
behavior in domestic home settings due to twitching, ears turned sideways or flattened, interactions cat has with people.
(continued) Aggression, Overview—Cats A
Learning redirected or so they can avoid cat. • After • Repeat physical exams in older patients
aggressive outburst, keep aggressor isolated in semiannually, as painful conditions may
Communication a room for at least 24 hours (as long as cat exacerbate aggression.
remains aroused after attack). • Pheromones. EXPECTED COURSE AND PROGNOSIS
Social interactions
• Medications. • Depends on type of aggression and compli-
Genetics
ance of clients with suggested behavior plan.
Environment
AGGRESSION
• Most cases need combination of behavioral
modification, environmental modification,
MEDICATIONS training, and, when necessary, medication.
• Some types of aggression can resolve or
Physiology
DRUG(S) OF CHOICE
improve within a few weeks, whereas others
• Selective serotonin reuptake inhibitors
Learning may take several months or longer. • Some
(SSRIs)—fluoxetine or paroxetine 0.5 mg/kg
forms of aggression have poor prognosis.
PO q24h. • Tricyclic antidepressants (TCAs)—
clomipramine 0.25–1.0 mg/kg PO q24h.
Figure 1.
• Buspirone at 0.5–1.0 mg/kg q8–24h,
benzodiazepines such as oxazepam at 0.2–
0.5 mg/kg q12–24h, or lorazepam 0.125– MISCELLANEOUS
0.25 mg/cat might reduce fear and build AGE‐RELATED FACTORS
confidence and support counter‐conditioning • Older cats—cognitive decline, CNS disease,
DIAGNOSIS in fearful cat that avoids or retreats. arthritis, meningioma, other medical conditions.
DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS • Age 2–4 years—social maturity, when cats
• CNS diseases (e.g., infections, toxins, • Cats with renal or hepatic disease. may start to show certain kinds of aggression.
tumors, partial seizures, focal seizures). • Caution with TCAs and SSRIs in diabetics.
• Hyperthyroid. • Hepatic encephalopathy. SEE ALSO
• TCAs in patients with cardiac • Aggression, Intercat Aggression.
• Any condition causing pain (e.g., arthritis, abnormalities.
pancreatitis, dental disease, anal sacculitis, • Aggression Toward Humans—Cats.
diabetic neuropathy). • Lead poisoning. POSSIBLE INTERACTIONS ABBREVIATIONS
• TCAs and SSRIs should not be used • FCV = feline calicivirus. • FeLV = feline
CBC/CHEMISTRY/URINALYSIS together. • Mirtazapine should be used
Physical examination, baseline blood, and leukemia virus. • FIV = feline immunodefi-
cautiously in combination with TCA or SSRI. ciency virus. • GI = gastrointestinal. • HPA =
urine screening followed by additional • Practitioner should evaluate all drugs and
diagnostics as indicated based on history, hypothalamic‐pituitary‐adrenal. • IBD =
natural supplements administered to verify inflammatory bowel disease. • SAMe =
examination, and laboratory results. safety in combination. S‐adenosyl‐L‐methionine‐tosylate disulfate.
OTHER LABORATORY TESTS ALTERNATIVE DRUG(S) • SSRI = selective serotonin reuptake
• Discuss Bartonella testing in any cat that • Amitriptyline 0.5–1.0 mg/kg PO q12–24h. inhibitor. • TCA = tricyclic antidepressant.
bites or scratches people. • Thyroid levels. • S‐adenosyl‐L‐methionine‐tosylate disulfate Suggested Reading
• Urinalysis ± culture if house soiling. (SAMe) 100 mg PO q24h. • Alpha‐casozepine Bain M. Feline aggression toward family
• Feline serology—feline calicivirus (FCV), 75 mg (15 mg/kg or greater) PO q24h. members: a guide for practitioners. Vet Clin
feline leukemia virus (FeLV), female immuno- • l‐theanine 25 mg PO q24h. • Cat‐appeasing North Am Small Anim Pract 2014,
deficiency virus (FIV). pheromone (Feliway® Multicat or Friends). 44:581–594.
• F3 cheek gland pheromone (Feliway). Crowell‐Davis SL, Murray T, Dantas L.
• Calming and stress diets containing alpha‐ Veterinary Psychopharmacology, 2nd ed.
casozepine and l‐tryptophan. Hoboken, NJ: Wiley, 2018.
TREATMENT Levine ED, Perry P, Scarlett J, et al. Intercat
• Never use physical correction/punishment; aggression in households following the
may escalate aggression. • Never try to introduction of a new cat. Appl Anim
physically handle or manipulate a cat in an FOLLOW‐UP Behav Sci 2004, 90:325–336.
aggressive state. • Avoid known triggers. Pachel C. Intercat aggression: restoring
• Identify triggers and desensitize and PATIENT MONITORING harmony in the home: a guide for practi-
counter‐condition to triggers. • Implement • Call owners once every 1–2 weeks for first tioners. Vet Clin North Am Small Anim
safety measures (nail caps, wearing long 2 months after treatment plan has been Pract 2014, 44:565–579.
pants/long sleeves, keep flattened cardboard recommended; determine implementation of Author Leslie Sinn
boxes around home to place between target safety recommendations and behavioral plan. Consulting Editor Gary M. Landsberg
and cat, redirect behavior in early arousal • If medication dispensed, dose should be Acknowledgment The author and editors
phase). • Behavior modifications to redirect reevaluated every 3–4 weeks. • Frequency of acknowledge the prior contribution of Emily
cat and reduce arousal (specific plans follow‐up will be dictated by severity of case D. Levine.
dependent upon specifics of each case). and owner compliance. • CBC, chemistry, T4
• Train cat to commands such as “sit,” “go to prior to medication; recheck liver and kidney
place,” etc. • Environmental enrichment and values 2–3 weeks after starting medication; Client Education Handout
meeting behavioral needs. • Teach owners to recheck bloodwork annually in young healthy available online
identify early signs of arousal so cat can be patients, semiannually in older patients.
A Aggression, Overview—Dogs
one type of impulsive human-directed Breed Predispositions
aggression, colloquially called “rage,” directed Any breed or breed mix.
toward familiar persons and triggered by Mean Age and Range
BASICS controlling gestures. Any age, although some forms of aggression
DEFINITION • Aggression generally has a learned may arise more commonly at sexual or social
• Action by one dog directed against another component, whereby dogs learn to use maturity, while medical causes increasingly
organism with the result of limiting, depriving, aggression to manage distance from fearful more likely in adult- or senior-onset aggression.
or harming. Aggression refers to any behavior stimuli or control resources, as this behavior
along an aggression continuum, from a stare is often effective as a distance-increasing Predominant Sex
to immobility (freeze), growl, snarl, lunge, air technique. • Either sex.
snap, single bite, multiple bite, multiple • Males—intact or castrated, most commonly
SYSTEMS AFFECTED implicated in cases of human-directed
attacks, and chase and attack. • Behavior.
• Numerous functional types have been “dominance”-type aggression. Intact males
• Other, if there is an underlying medical overrepresented in dog-bite fatalities, but
posited. Here, aggression is classified on the etiology.
basis of (1) affective aggression, (2) predatory covariables, such as owner management, are
aggression, and (3) play-related aggression. GENETICS present.
Affective states, such as fear and arousal, and • In some breeding programs, aggressive • Females—spayed most commonly implicated
motivational factors, such as hunger and tendencies and bite styles have been selected in aggression to other female dogs in the home.
sexual drive, influence the probability of overt for (or against). In some studies, spayed females less likely than
aggression, such as biting. Affective aggression • Behavioral genetics is an active area of males to display human-directed aggression.
may be human-directed or dog-directed. research, with several genes identified that SIGNS
Within these contexts, there may be may be associated with fear and aggression in
dogs. General Comments
additional specificity, such as human-directed • Any dog can display aggression. Many factors,
aggression toward unfamiliar persons, or • One study in the United States linked
English springer spaniels that display human- including temperament, experience, and
human-directed aggression toward familiar situational factors, influence propensity to bite.
persons. Often dogs display aggression in a directed dominance aggression to one
breeding sire, implicating a heritable component. • Dogs may display behavioral signals as
single context. warnings, including immobility, growls, snarls,
• Human-directed aggression toward familiar • One study of human-directed dominance
aggression among English cocker spaniels or air snaps, which may provide time to avoid
persons in response to controlling gestures overt aggression. These signs should not be
was historically called dominance aggression, reported that males were more aggressive than
females, and dogs with solid coat color were punished, as this might decrease the probability
although newer terminology, such as conflict of warning signs without affecting the
aggression, may be used to avoid erroneous more aggressive than those with parti coat
color. underlying risk, or may further intensify the
semantic assumptions inherent in the term aggressive (defensive) response. Instead, the
“dominance.” INCIDENCE/PREVALENCE animal should be safely removed from the
• Human- or animal-directed aggression, • Reported problem by approximately 30% situation and the underlying triggers for the
generally toward unfamiliar individuals and of owners. affective state addressed.
specific to home location, is called territorial • Most common diagnostic category seen by
aggression. Location is commonly at door of board-certified veterinary behaviorists in Historical Findings
entry, but may also involve defense of special North America. • Variable.
favored locations such as beds. • According to Centers for Disease Control • Basis for risk analysis and details of treat-
• Predatory aggression refers to behaviors and Prevention, about 4.7 million people ment program. Important questions: Who/
associated with chasing and hunting prey. It is bitten by dogs each year in United States, what was the target? Who was present to
often considered nonaffective and may be although this number considered an under- manage the dog? How severe were the
socially facilitated by other dogs. Predatory estimation as majority of dog bites not resulting injuries? What are the circumstances
behaviors may be triggered by movement or reported. (including location, time) in which aggression
high-pitched sounds, and may be redirected • In United States, estimated that one in five occurred? Are there any reliable triggers for
to humans or objects. of those bitten require medical attention for aggressive behavior? Abnormalities in mentation
• Play-related aggression involves aggressive dog bite–related injuries. or awareness might indicate a medical cause.
gestures, such as growling and biting, in the • Among children and adults, males more Physical Examination Findings
context of play and is commonly displayed likely than females to be bitten. • Usually unremarkable.
toward other dogs or humans. It is often • Based on emergency room data in United • Use extreme care when handling aggressive
initiated by signs of play, such as the play States, rate of dog bite–related injuries highest dogs.
bow. for children aged 5–9 years. • A comfortable, well-fitting basket muzzle
• In all cases, medical factors that might • In majority of cases, people are bitten by recommended prior to examination of any
contribute to aggression (including pain) dogs that are known to them; this is not the dog with history of human-directed aggression.
must be evaluated. case for dog injury–related fatalities. Desensitize and countercondition to muzzle
PATHOPHYSIOLOGY GEOGRAPHIC DISTRIBUTION application and use. Basket-style muzzles allow
• Affective aggression involves arousal of the Worldwide dogs to pant.
sympathetic nervous system. Some pathologic • Abnormalities on physical or neurologic
SIGNALMENT examination may suggest organic disease
conditions are associated with an increase in
aggression because of CNS effects such as Species process (e.g., neurologic, pain, blindness).
pain or irritability. Dog Dogs can display aggression during preictal,
• Abnormalities in the CNS serotonin neuro- ictal, or postictal periods. Dogs with underlying
transmitter system have been implicated in
(continued) Aggression, Overview—Dogs A
pain typically display defensive (body- • Others as indicated by history and physical • The dog should calmly be removed from
protective) aggression. exam. aggression-provoking situations.
• Safe, nonconfrontational techniques that
CAUSES IMAGING
• Part of normal range of behavior; strongly • May be indicated to identify sources of pain
manage resources and use positive reinforce-
influenced by individual temperament, or disease. ment to teach the dog appropriate responses
experience, early socialization (before 12 • MRI or CT—particularly if cerebral
should be employed.
weeks), and other variables. disease/neoplasia suspected. • Confrontational management techniques,
• Harsh handling and confrontational
such as roll-overs, or even verbal discipline
DIAGNOSTIC PROCEDURES increase the probability of a defensive
responses can escalate aggression and should • Collection of thorough behavioral history
be avoided. aggressive response, may lead to human
and evaluation of medical concerns. injury, and should be strictly avoided.
• May be manifestation of organic condition, • Postmortem fluorescent antibody test • Management (“dominance”) techniques
such as hepatic encephalopathy or pain. indicated for any aggressive dog for which
• In all cases, evaluate medical causes of
including punishment are associated with
rabies is differential diagnosis. defensive fear responses by the dog and an
aggression.
PATHOLOGIC FINDINGS increased risk of human-directed aggression.
RISK FACTORS None These should be avoided and replaced with
• Inadequate socialization during canine positive management techniques.
critical period (3–12 weeks). • The client should be advised to consider
• Traumatic/fearful/negative experience(s). personal and legal liability risks of keeping the
• Predisposing environmental conditions— dog. Human injury, bite-related lawsuits, and
lack of training, inadequate restraint, harsh TREATMENT homeowner’s insurance claims can result from
handling. APPROPRIATE HEALTH CARE canine aggression. Such risk assessment may
• Inability of owner to safely confine or help the client objectively evaluate the situation.
• Manage any underlying medical
manage the dog in order to prevent future conditions. • Euthanasia should be considered if safe
incidents. Helpful devices include barrier • Management success—combination of management cannot be employed, or when
fence, muzzle, collar or head halter, leash. multiple modalities: safe environmental the risk of injury is high.
• Previous aggression/bite history (number of
control, behavior modification to teach SURGICAL CONSIDERATIONS
incidents, number of bites per incident, animals appropriate behavior, and pharma-
target, severity of injury); legal citation for Castration of males may reduce the incidence
cotherapy. of intermale aggression.
biting. • Consult veterinarian with experience and
• Unpredictability of aggressive behaviors,
training in aggression management.
lack of warning signals. • Euthanasia should be discussed or
• Presence of children, elderly people, or
recommended when risk of injury is high.
other humans or animals at high risk living in Note recommendation in medical record. MEDICATIONS
or visiting household. • Rehoming aggressive dogs may put those DRUG(S) OF CHOICE
involved at liability risk. • None approved by FDA for treatment of
NURSING CARE aggression.
A boarding facility able to safely manage the • No drug will eliminate probability of
DIAGNOSIS dog might be used until a safe management aggression.
DIFFERENTIAL DIAGNOSIS plan can be implemented, or until an outcome • Use drugs only when safe management plan
• Thorough medical evaluation should be decision can be made. has been implemented.
conducted on all cases of aggression. • Inform client of extra-label nature of
ACTIVITY medication and risk involved; document in
• Identify pathologic conditions associated Since frustration and arousal may increase
with aggression before making purely medical record; obtain signed informed
incidence of aggression, appropriate and safe consent.
behavioral diagnosis. exercise regime should be incorporated into
• Rule out developmental abnormalities • Drugs that increase serotonin may be
treatment program. helpful to reduce anxiety, arousal, and
(e.g., hepatic shunts), metabolic disorders
(e.g., hepatic encephalopathy), endocrino- DIET impulsivity.
pathies (e.g., hypothyroidism, hyperadreno- There is minimal evidence that a low-protein • Treatment duration—minimum 4 months,
corticism), dermatopathy, neurologic diet may reduce territorial aggression in dogs, maximum lifetime.
conditions (intracranial neoplasm, seizures), an effect that might be enhanced with trypto- • See Table 1 for drugs used to facilitate
toxins, inflammatory diseases, cognitive phan supplementation. management of aggression in combination
dysfunction, acute or chronic pain, and CLIENT EDUCATION with safe management plan.
iatrogenic causes, such as glucocorticoid • Safe practices should dictate all decisions. These CONTRAINDICATIONS
administration. practices include safe confinement, physical • Fluoxetine should be used cautiously in
CBC/BIOCHEMISTRY/URINALYSIS barriers, head halters, leash control, muzzle use, cases of seizures.
• Usually no significant findings unless
and supervision by a competent adult. • Clomipramine contraindicated in cases of
underlying medical etiology. • Situations that have led to aggression cardiac conduction disturbances or seizures;
• Indicated to evaluate dog as candidate for
in the past should be listed and a specific in one open trial, clomipramine was no more
behavioral medications. plan developed to avoid these situations effective than control in cases of human-
and associated locations in the future, directed aggression.
OTHER LABORATORY TESTS and a long-term management plan developed.
• Thyroid testing.
A Aggression, Overview—Dogs (continued)
Table 1
Drugs and dosages used to manage canine aggression.
Drug Drug Class Oral Dosage in Dogs Frequency Side Effects—Usually Transient
Fluoxetine SSRI 1.0–2.0 mg/kg q24h Decreased appetite, sleepiness
Paroxetine SSRI 1.0–2.0 mg/kg q24h Constipation
Sertraline SSRI 2.0–4.0 mg/kg q24h Sleepiness
Clomipramine TCA 1.0–3.0 mg/kg q12h Sleepiness, vomiting
PRECAUTIONS • Reduce risk of aggression in young dogs SEE ALSO

Benzodiazepines (e.g., diazepam) may (3–12 weeks) with positive socialization • Aggression—Between Dogs in the
contribute to behavioral disinhibition. program; avoid intimidation techniques and Household.
Aggression may increase when dogs lose their negative, fear-inducing situations. • Aggression, Food and Resource
fear of the repercussions of biting. POSSIBLE COMPLICATIONS Guarding—Dogs.
• Aggression to Unfamiliar People and
POSSIBLE INTERACTIONS • Injury to humans or animals.
Do not use selective serotonin reuptake • Liability to client, veterinarian. Unfamiliar Dogs—Dogs.
inhibitors (SSRIs) or tricyclic antidepressants • In cases of dog-directed aggression, • Aggression Toward Children—Dogs.
(TCAs) with monoamine oxidase inhibitors, although not the intended target, humans • Aggression Toward Familiar People—Dogs.
including amitraz and selegiline, or with each who interfere are often seriously injured, ABBREVIATIONS
other because of risk of serotonin syndrome. either by accident or by redirected aggression; • SSRI = selective serotonin reuptake inhibitor.
Caution when combining SSRI or TCA with owners should not reach for fighting • TCA = tricyclic antidepressant.
any drug that might increase serotonin, dogs—pull apart with leashes. INTERNET RESOURCES
including trazodone. • Aggressive dogs are at risk for relinquish-
• https://www.avma.org/resources-tools/
ALTERNATIVE DRUG(S) ment or euthanasia. pet-owners/dog-bite-prevention
• Trazodone (4–10 mg/kg PO q12h or PRN) EXPECTED COURSE AND • https://www.cdph.ca.gov/Programs/CID/
may be used with drugs listed in Table 1 to PROGNOSIS DCDC/CDPH%20Document%20Library/
reduce anxiety and arousal. • Aggressive dogs weighing over 18.5 kg are DontLettheDogsBiteActivityBook.pdf
• Clonidine (0.01–0.05 mg/kg PO q12h or at increased risk for behavioral euthanasia. Suggested Reading
PRN) may be used with drugs listed in • Aggressive dogs may be successfully Casey RA, Loftus B, Bolster C, et al. Human
Table 1 to reduce anxiety and arousal. managed, but should not be considered directed aggression in domestic dogs (Canis
• Natural products that may aid in reducing “cured.” familiaris): occurrence in different contexts
anxiety—l-tryptophan (10 mg/kg PO bid); • Prognosis is case dependent due to risk and risk factors. Appl Anim Behav Sci
alpha-casozepine (15 mg/kg or higher daily) factors and management features of each 2014, 152:52–63.
alone or in diet combined with l-tryptophan; situation. deKeuster T, Jung H. Aggression toward
l-theanine alone (2.5–5 mg/kg bid) or in familiar people and animals. In: Horwitz DF,
combination with products containing whey Mills D, eds. BSAVA Manual of Canine and
protein, Phellodendron amurense, and Feline Behavioural Medicine, 2nd ed.
Magnolia officinalis; “calming” probiotic Gloucester: BSAVA, 2009, pp. 182–210.
supplement; or dog-appeasing pheromone. MISCELLANEOUS
Landsberg G. Canine aggression. In: Landsberg
AGE-RELATED FACTORS G, Hunthausen W, Ackerman L, eds.
Onset of aggression in mature dogs suggests Behavior Problems of the Dog and Cat, 3rd
medical cause; carefully evaluate sensory ed. New York: Saunders/Elsevier, 2013, pp.
FOLLOW-UP acuity, sources of pain, endocrinopathy, 197–326.
cognitive function. Pike A. Managing canine aggression in the
PATIENT MONITORING home. Vet Clin North Am Small Anim
Weekly to biweekly contact recommended in ZOONOTIC POTENTIAL
• Dog bites are significant public health risk. Pract 2018, 48:387–402.
initial phases to guide clients with behavior Authors Margaret E. Gruen and Barbara L.
• Rabies is potential cause of aggression.
modification plans and medication manage- Sherman
ment. PREGNANCY/FERTILITY/BREEDING Consulting Editor Gary M. Landsberg
PREVENTION/AVOIDANCE TCAs and trazodone are contraindicated in
• To prevent aggressive incidents, avoid all
breeding males and pregnant females.
situations that have led to aggression in the SYNONYMS Client Education Handout
past, using safe confinement, gates, halters, Biting available online
collars, leashes, muzzles.
Alkaline Hyperphosphatasemia in Dogs A
Physical Examination Findings • Hyperbilirubinemia in EHBO, end-stage

• Highly variable depending on cause; often chronic hepatopathies, acute hepatic
normal. • Hepatomegaly or microhepatica. toxicities, infections. • Hypercholesterolemia
BASICS • Jaundice. • Abdominal pain. • Musculo with many causes of cholestasis,
DEFINITION skeletal—pendulous abdomen, muscle atrophy, endocrinopathies. • Urinalysis—proteinuria
Increase in serum alkaline phosphatase (ALP) lameness, difficulty walking, palpable bony with hyperadrenocorticism, other liver
activity above reference interval. swelling. • Dermatologic—alopecia, cutaneous disorders; dilute urine, bacteriuria, pyuria
hyperpigmentation, comedones, thin skin, with endocrinopathies; glucosuria with
PATHOPHYSIOLOGY pyoderma, calcinosis cutis. diabetes mellitus, copper-associated hepatopathy;
• ALPs are heterogeneous group of isoen-
CAUSES ammonium biurate crystalluria with
zymes that catalyze hydrolysis of organic
• Age and breed (see Signalment). • Drug portosystemic vascular anomaly (PSVA;
phosphate esters in extracellular space.
induced. • Bone-related disorders—neopla- young dogs). • Conditions with often sole
• Membrane-bound enzymes present in liver,
sia, osteomyelitis, hyperparathyroidism increase in serum ALP include idiopathic
bone, placenta, intestine, and kidney. • Total
(primary or secondary), healing fractures. vacuolar hepatopathy, hepatic nodular hyper-
serum ALP attributed to liver (L-ALP), bone
• Chronic stress, acute-phase response plasia, drug-induction breed-related disorders,
(B-ALP), and glucocorticoid-induced (G-ALP)
(endogenous cortisol). • Endocrinopathies some hepatic neoplasias, sudden acquired
isoenzymes; proportion of each isoenzyme
(hyperadrenocorticism, diabetes mellitus, retinal degeneration (SARDS).
changes with age in normal dogs. • Serum
hypothyroidism). • Primary hepatobiliary • Hyperphosphatemia, hypercalcemia (young
ALP activity increases with cholestatic,
disorders. • Extrahepatic disorders—extrahe- growing dogs, usually mild). • Hyperglycemia—
necroinflammatory, and neoplastic injury;
patic biliary obstruction (EHBO), pancreatic/ mild with hyperadrenocorticism.
many hepatic and nonhepatic causes; affected
intestinal/other inflammation, neoplasia. • Azotemia—prerenal or renal with
dogs often asymptomatic. • Anticonvulsants
• Infection—Leptospirosis, sepsis, viral. pancreatitis, pyelonephritis, Leptospirosis.
(phenobarbital, primidone, phenytoin) and
steroids can induce L-ALP synthesis; steroids, • Systemic inflammation/infection causing OTHER LABORATORY TESTS
inflammation, and chronic disease can induce ischemic injury/cholestasis. • Hepatic or • Serum bile acids; redundant test if
G-ALP synthesis. • ALP has high sensitivity nonhepatic neoplasia (e.g., benign or hepatic hyperbilirubinemia. • Testing for
but poor specificity for hepatobiliary disease; malignant mammary tumors). endocrine disorders—hypothyroidism or
reflects common induction of enzyme synthesis RISK FACTORS hyperadrenocorticism based on clinical
due to nonhepatic causes, i.e., “reactive hepato- • Age (young). • Breed—Siberian husky, signs, physical exam findings, and
pathy.” • Increased ALP activity with Scottish terrier. • Breed association to associated laboratory abnormalities.
concurrent increase in GGT activity increases conditions causing alkaline hyperphosphata- • Infectious disease testing—leptospirosis
specificity for hepatobiliary disease. semia (e.g., Shetland sheepdog predisposition PCR, microagglutination test (MAT),
to gallbladder mucocele). immunoglobulin (Ig) M; urine, bile
SYSTEMS AFFECTED
cultures; tick-borne disease screening.
• Multiple organ systems can influence ALP
• Blood pressure measurement. • Urine
synthesis. • Increased ALP activity does not
protein qualitative; quantitative with
cause direct damage to other organ systems.
protein; creatinine if inactive sediment and
GENETICS DIAGNOSIS culture negative.
• Benign familial alkaline hyperphosphata-
LABORATORY FINDINGS IMAGING
semia in Siberian huskies—presumed
Drugs That May Alter Laboratory Results • Radiographs—for liver most useful for
autosomal. • Vacuolar hepatopathy of
Corticosteroids, certain anticonvulsants. hepatomegaly, microhepatica; nonhepatic
Scottish terriers—breed relationship.
findings may also be identified (pancreatitis,
INCIDENCE/PREVALENCE Disorders That May Alter Laboratory ascites, cystoliths, pyometra, pleural effusion).
Increased ALP activity is common Results • Sonographic evaluation for hepatic
biochemical abnormality in dogs. • Severe hemolysis (>500 hemolysis index) parenchymal abnormalities (hyper- or
SIGNALMENT can falsely elevate ALP. • Lipemia and icterus hypoechoic nodules, heterogeneity, hyper- or
• Any age, breed, or sex. • Young dogs, have no significant effect on ALP. hypoechoic hepatic echogenicity; changes in
<1 year of age—increased B-ALP activity. CBC/BIOCHEMISTRY/URINALYSIS echodensity, echotexture; microhepatica,
• Siberian huskies and Scottish terriers. • Thrombocytosis possible with hyperadreno hepatomegaly, hepatic masses), biliary tract
• Older dogs—conditions causing increased corticism and pancreatic, gastrointestinal (gallbladder mucocele, gallbladder wall
L-ALP, G-ALP, and/or B-ALP activity. disease. • Thrombocytopenia possible with abnormalities, cholelithiasis, choledochitis,
leptospirosis, hepatic failure, neoplasia. biliary tract neoplasia), pancreas, adrenal
SIGNS enlargement, neoplasia. • Abdominal CT ±
• Leukocytosis or leukopenia with left shift,
General Comments monocytosis with sepsis, systemic angiography may be useful if suspicion of
• Many dogs with increased ALP activity are inflammation. • Stress leukogram with pancreatitis, gallbladder disease, or hepatic
asymptomatic. • Dogs with hepatic or hyperadrenocorticism. • Concurrent elevation vascular disorders.
nonhepatic disorders causing increased ALP of other liver enzyme activities including DIAGNOSTIC PROCEDURES
may be asymptomatic or have clinical signs alanine aminotransferase (ALT), aspartate • Hepatic fine-needle aspirate (FNA) for
related to underlying disorder. • Dogs with aminotransferase (AST), and/or gamma cytology; caution as cytologic and histologic
drug-induced elevations of ALP may have glutamyltransferase (GGT), depending on agreement may be as low as 30%; cytology is
clinical signs related to drug side effects. underlying cause. • ± markers of hepatic not diagnostic for many hepatobiliary
Historical Findings synthetic dysfunction (hypoalbuminemia, conditions. • FNA of liver tends to agree
• Dependent on cause. • Medication history hypoglycemia, hypocholesterolemia, with histology in cases of vacuolar hepato-
important, including exposure to topical/ decreased blood urea nitrogen [BUN]); pathy, hepatic lipidosis, and some neoplasias
ocular medications used by humans. many primary hepatic disorders. (e.g., lymphoma). • If primary hepatobiliary
A Alkaline Hyperphosphatasemia in Dogs (continued)
disease suspected after elimination of other SYNONYMS

causes, hepatic biopsy may be warranted; • Elevated ALP. • Serum alkaline phosphatase
biopsy at least three liver lobes; laparoscopic (SAP).
or wedge samples preferred; Tru-Cut® needle MEDICATIONS
SEE ALSO
biopsy may be too small, use 14–16G needle. DRUG(S) OF CHOICE • Bile Duct Obstruction (Extrahepatic).
PATHOLOGIC FINDINGS • Specific for underlying cause. • Certain • Cholangitis/Cholangiohepatitis Syndrome.
Variable depending on cause; see specific drugs/supplements have general hepatobiliary • Cholecystitis and Choledochitis.
chapters for pathologic findings. protective effects; see Hepatosupportive • Cholelithiasis.
Therapies. • Copper Associated Hepatology.
CONTRAINDICATIONS • Glycogen-Type Vacuolar Hepatopathy
Depending on cause, drugs requiring hepatic • Hepatic Failure, Acute.
metabolism or capable of causing hepatotoxicity • Hepatic Nodular Hyperplasia and Dysplastic
TREATMENT should be limited or avoided when possible. Hyperplasia.
APPROPRIATE HEALTH CARE • Hepatitis, Chronic.
PRECAUTIONS
• Dictated by underlying disorder. • Hyperadrenocorticism (Cushing’s Syndrome)—
Drugs known to induce elevation of ALP may
• Asymptomatic dogs often do not require Dogs.
confuse monitoring of underlying condition.
any specific treatment. • Leptospirosis.
• Pancreatitis—Dogs.
NURSING CARE
Variable as above. ABBREVIATIONS
• ALP = alkaline phosphatase.
ACTIVITY FOLLOW-UP • ALT = alanine aminotransferase.
Alteration of activity typically unnecessary.
PATIENT MONITORING • AST = aspartate aminotransferase.
DIET • Dependent on the underlying cause. • B-ALP = bone isoform.
• Dietary alteration unnecessary in most • Suspected benign causes of ALP elevation • BUN = blood urea nitrogen.
cases. • Dietary fat restriction in some cases can be monitored for elevations in other serum • G-ALP = glucocorticoid isoform.
(pancreatitis, hypertriglyceridemia, obesity, liver enzyme activities, further elevation in • EHBO = extrahepatic biliary obstruction.
chronic EHBO). • Commercial liver diets ALP, and/or synthetic hepatic function tests. • FNA = fine-needle aspirate.
rarely indicated (see Portosystemic Vascular • GGT = gamma glutamyltransferase.
Anomaly, Congenital; Hepatic Encephalopathy). EXPECTED COURSE AND PROGNOSIS • Ig = immunoglobulin.
• Dependent on underlying cause.
CLIENT EDUCATION • L-ALP = liver isoform.
• Increased ALP activity for which underlying
• Dictated by underlying disorder. • Clients • MAT = microagglutination test.
cause cannot be found after complete diagnostic • PSVA = portosystemic vascular anomaly.
with asymptomatic dogs should be counseled evaluation may be benign.
on potential for subsequent development of • SAP = serum alkaline phosphatase.
endocrine disease, neoplasia (Scottish • SARDS = sudden acquired retinal
terriers), other causes. • Liver biopsy degeneration.
necessary for definitive diagnosis if other Suggested Reading
underlying causes are ruled out and/or if ALP MISCELLANEOUS Cortright CC, Center SA, Randolph JF, et al.
value continues to elevate; rarely pursued ASSOCIATED CONDITIONS Clinical features of progressive vacuolar
initially in asymptomatic dogs without other Elevation of other serum liver enzymes, hepatopathy in Scottish Terriers with and
underlying disorder. hyperbilirubinemia, alterations in hepatic without hepatocellular carcinoma: 114 cases
SURGICAL CONSIDERATIONS synthetic function tests. (1980–2013). J Vet Intern Med 2014,
• Refractory hypotension is common peri-
245:797–788.
AGE-RELATED FACTORS Lidbury JA, Steiner JM. Diagnostic
and postoperative complication in dogs with Young dogs (see Signalment).
obstructive cholestasis (see EHBO). • Dogs evaluation of the liver. In: Washabau RJ,
with end-stage hepatic disease (cirrhosis) may ZOONOTIC POTENTIAL Day MJ, eds., Canine and Feline
have alterations of coagulation and/or higher Leptospirosis has high zoonotic potential; see Gastroenterology. St. Louis, MO: Elsevier,
anesthetic risk. Leptospirosis. 2013, pp. 863–875.
PREGNANCY/FERTILITY/BREEDING Author Sara A. Wennogle
Placental ALP can increase in late-term Consulting Editor Kate Holan
pregnant cats; not reported in dogs.
Alkalosis, Metabolic A
decrease in plasma albumin concentration; deprivation; postobstructive diuresis;

plasma albumin is a weak acid. • Compensatory polyuric renal failure. • Hypokalemia.
metabolic alkalosis occurs in response to RISK FACTORS
BASICS respiratory acidosis; this is associated with low • Administration of loop or thiazide diuretics.
DEFINITION pH and increased PCO2. • Vomiting. • Stomach drainage. • Diseases
A process in the body that leads to an increase SYSTEMS AFFECTED associated with hypoalbuminemia (e.g.,
in pH above the reference interval. An increase • Nervous—muscle twitching and seizures protein-losing nephropathy, liver failure).
in blood pH is specifically termed alkalemia. occur rarely in dogs. Metabolic alkalosis and
Associated with an increase in plasma associated hypokalemia may precipitate hepatic
–
bicarbonate concentration (HCO3 ; dogs, encephalopathy in patients with liver failure.
>24 mEq/L; cats, >22 mEq/L) and base • Urinary—kidneys rapidly and effectively
excess (BE; >4 mmol/L) with a compensatory excrete excessive alkali. In patients with DIAGNOSIS
increase in carbon dioxide tension (PCO2). Cl– deficiency and volume depletion, kidneys DIFFERENTIAL DIAGNOSIS
–
PATHOPHYSIOLOGY cannot excrete excess alkali. Therefore, High plasma HCO3 and hypochloremia may
• Metabolic alkalosis may develop from either metabolic alkalosis is maintained. In these also occur in animals compensating for chronic
a gain of bicarbonate or a loss of acid: patients, Cl– administration is required for respiratory acidosis, in which PCO2 is high
–
◦ Bicarbonate gain subsequent to: contraction renal compensation to occur. Volume and pH is low despite high HCO3 and low
alkalosis due to free water deficit; iatrogenic expansion will hasten compensation. Patients Cl concentration; blood gas determination is
–
administration of alkalinizing therapy (e.g., with mineralocorticoid excess have excessive required to differentiate.
–
NaHCO3 ); metabolism of organic ions Cl– loss. Therefore, Cl– administration does LABORATORY FINDINGS
(lactate, citrate, acetate, and ketones); not lead to hyperchloremia and correction of
hypokalemia; and renal ammoniagenesis. metabolic alkalosis (so-called chloride-resist- Drugs That May Alter Laboratory Results
◦ Acid loss subsequent to: gastric or renal acid ant metabolic alkalosis). • Respiratory—low None
loss (loop or thiazide diuretic); mineralocorti- [H+] (increased pH) decreases alveolar Disorders That May Alter Laboratory
coid excess; presence of nonreabsorbable ventilation. Hypoventilation increases PCO2 Results
anions; decreased weak acids (hypoalbumine- and helps offset the effects of high plasma • Too much heparin (>10% of sample)
– –
mia, hypophosphatemia). ◦ Renal HCO3 HCO3 on pH. In dogs, for each 1 mEq/L –
decreases pH, PCO2, and HCO3 . • Blood
–
excretion very efficient in eliminating an increase in plasma HCO3 there is an expected samples stored at room temperature for more
–
excess HCO3 load, but hindered by decreased increase of approximately 0.7 mmHg in than 15 minutes have low pH because of
effective circulating volume; hypokalemia, PCO2. Limited data available for cats, but increased PCO2. • Exposure to room air
hypochloremia, and hyperaldosteronism; degree of respiratory compensation appears to decreases PCO2. • Venous samples may have
metabolic alkalosis persists only if renal be similar. pH 0.5–1 unit lower and PCO2 5–10 mmHg
–
excretion of HCO3 is impaired, which SIGNALMENT higher than arterial sample.
primarily occurs from continued high rate of Any breed, age, or sex of dog and cat.
alkali administration, or some stimulus for Valid if Run in Human Laboratory?
kidneys to retain Na+ in presence of a relative SIGNS Yes
Cl– deficit. • Hypochloremic (corrected) Historical Findings CBC/BIOCHEMISTRY/URINALYSIS
metabolic alkalosis results from loss of fluid • Administration of loop diuretics • High total CO2 (total CO2 in samples
rich in Cl– and hydrogen ion (H+), primarily (e.g., furosemide) or thiazides. • Vomiting. handled aerobically closely approximates
–
from alimentary tract or kidneys; loss of Cl– HCO3 ). • Low blood ionized calcium
and H+ associated with increase in plasma concentration. • Serum electrolyte
– • Signs related to underlying disease or
HCO3 concentration; with Cl– loss and abnormalities vary with underlying cause.
accompanying potassium depletion
volume depletion, kidneys reabsorb Na+ with • Hypochloremia—consider hypochloremic
– (e.g., weakness, cardiac arrhythmias, ileus).
HCO3 instead of Cl–, perpetuating metabolic metabolic alkalosis, the most common reason
• Muscle twitching caused by low ionized
alkalosis. Hypochloremic alkalosis divided for metabolic alkalosis in dogs and cats, which
calcium concentration. • Dehydration in
into chloride-responsive and chloride-resistant: usually results from diuretic administration or
volume-depleted patients. • Muscle twitching
◦ Chloride-responsive results primarily from vomiting of stomach contents. • High Na+ but
and seizures in patients with neurologic
loss of Cl– rich fluid and characterized by normal Cl– concentration—consider chloride-
involvement (rare).
decreased extracellular fluid volume, hypo- resistant metabolic alkalosis (e.g., hyperadreno-
chloremia, and low urinary Cl– concentration; CAUSES corticism or primary hyperaldosteronism) or
this type of alkalosis responds to • Chloride-responsive—gastrointestinal losses administration of alkali. • Hypoalbuminemia—
administration of chloride salt. ◦ Chloride- (e.g., gastric vomiting, nasogastric tube consider hypoalbuminemic metabolic alkalosis
resistant characterized by excessive mineralo- suctioning); renal losses (diuretic therapy); (e.g., liver failure, protein-losing enteropathy,
corticoid leading to increased effective and rapid correction of chronic hypercapnia and protein-losing nephropathy). In vitro,
circulating volume and is not responsive to (respiratory acidosis). • Chloride-resistant— a 1 g/dL decrease in albumin concentration is
chloride salt. • Hypokalemia may contribute hyperadrenocorticism and primary hyperaldo- associated with an increase in pH of 0.093 in
to metabolic alkalosis by shifting H+ intra- steronism. • Oral administration of cats and 0.047 in dogs. • Hypokalemia—likely
cellularly; stimulating apical H+/K+ ATPase alkalinizing agents—sodium bicarbonate or results from intracellular potassium shifting
in collecting duct; stimulating renal other organic anions with Na+ (e.g., lactate, due to metabolic alkalosis or underlying
ammoniagenesis; impairing Cl– reabsorption acetate, gluconate); administration of problem (e.g., vomiting of stomach contents or
in distal nephron; and reducing glomerular cation-exchange resin with nonabsorbable loop diuretic administration). • Urinary
filtration rate (GFR), which decreases filtered alkali (e.g., phosphorus binders). Cl– concentrations—chloride-responsive
–
load of HCO3 and, in presence of volume • Hypoalbuminemia—liver disease, protein- metabolic alkalosis characterized by urine
depletion, impairs renal excretion of excess losing nephropathy, protein-losing enteropathy. Cl– concentrations <10 mEq/L, whereas
–
HCO3 . • Hypoalbuminemic alkalosis is due to • Free water deficit—diabetes insipidus; water
A Alkalosis, Metabolic (continued)
chloride-resistant metabolic alkalosis associated failure), oral administration of compounds SYNONYMS

with urine Cl– concentrations >20 mEq/L. containing Cl– without Na+ is recommended • Nonrespiratory alkalosis. • Chloride-
OTHER LABORATORY TESTS to correct alkalosis; if diuresis needed due to responsive metabolic alkalosis—metabolic
–
Blood gas analysis reveals high HCO3 , PCO2, volume overload, carbonic anhydrase alkalosis that responds to Cl– administration.
pH, and BE. Unlike HCO3-, BE is inde- inhibitor (e.g., acetazolamide) or potassium- • Chloride-resistant alkalosis—metabolic
pendent of changes in metabolic acid-base sparing diuretic (e.g., spironolactone, alkalosis secondary to increased mineralo
status, and is thus more reliable measure of amiloride) can be used to correct alkalosis. corticoid activity that does not respond to
metabolic acid-base changes. • H2-blocking agents such as famotidine Cl– administration. • Hypochloremic
decrease gastric acid secretion and may be alkalosis—metabolic alkalosis caused by low
IMAGING considered as adjunctive therapy if gastric Cl– concentration. • Hypoalbuminemic
None losses are ongoing. • Antiemetics may help alkalosis—metabolic alkalosis caused by low
DIAGNOSTIC PROCEDURES prevent further gastric acid loss. albumin concentration. • Concentration
• Blood pressure—combination of hyperten- Hypoalbuminemic Alkalosis alkalosis—metabolic alkalosis resulting from
sion, hypernatremia, and hypokalemia with • Treatment for hypoalbuminemic alkalosis decreased free water in plasma. • Contraction
metabolic alkalosis may indicate presence of should be directed at underlying cause and alkalosis—metabolic alkalosis formerly
hyperaldosteronism. • Diagnostic testing for decreased colloid oncotic pressure. • Enteral attributed to volume contraction, but now
hyperadrenocorticism or primary hyperaldo- nutrition will facilitate endogenous albumin known to be caused by Cl– depletion; volume
steronism (e.g., plasma renin activity and production. • Consider species-specific depletion is common but not essential feature.
aldosterone concentration). plasma or albumin (e.g., canine albumin) SEE ALSO
therapy. • Hypochloremia.
CONTRAINDICATIONS • Hypokalemia.
• Avoid chloride-free fluids—they may ABBREVIATIONS
TREATMENT correct volume depletion, but will not correct • BE = base excess.
• Acid-base disturbances are secondary hypochloremic alkalosis. • Avoid using salts • GFR = glomerular filtration rate.
phenomena; diagnosis and treatment of of potassium without Cl– (e.g., potassium • H+ = hydrogen ion.
–
underlying disease process are essential to phosphate)—potassium will be excreted in • HCO3 = bicarbonate.
successful resolution of acid-base disorders. urine and will correct neither alkalosis nor • PCO2 = carbon dioxide tension.
• Severe alkalemia is uncommon, but may be potassium deficit. Suggested Reading
life-threatening. Patients with chronic
PRECAUTIONS de Morais HA. Chloride ion in small animal
respiratory disease and respiratory alkalosis
Do not use distal-acting, potassium-sparing practice: the forgotten ion. J Vet Emerg Crit
are at risk of developing severe alkalemia if
diuretics (e.g., spironolactone) in volume- Care 1992, 2:11–24.
they start vomiting or receive diuretics.
depleted patients. de Morais HA, Constable PD. Strong ion
• Discontinue drugs that may cause
POSSIBLE INTERACTIONS approach to acid-base disorders. In:
metabolic alkalosis. • Chloride-responsive—
None DiBartola SP, ed., Fluid, Electrolyte and
fluid of choice for patients with volume
Acid-Base Disorders, 4th ed. St. Louis, MO:
depletion is 0.9% saline or balanced isotonic ALTERNATIVE DRUG(S) Saunders, 2012, pp, pp. 316–330.
replacement fluid supplemented with KCl; None de Morais HA, Leisewitz AL. Mixed acid-base
patients with hypokalemia may require large
disorders. In: DiBartola SP, ed., Fluid,
amounts of KCl (see Hypokalemia).
Electrolyte and Acid-Base Disorders, 4th ed.
• Chloride-resistant metabolic alkalosis can
St. Louis, MO: Saunders, 2012, pp. 302–315.
only be corrected by resolution of underlying
FOLLOW-UP DiBartola SP. Metabolic acid-base disorders.
disease; metabolic alkalosis usually mild in
In: DiBartola SP, ed., Fluid, Electrolyte and
these patients. • If metabolic alkalosis PATIENT MONITORING Acid-Base Disorders, 4th ed. St. Louis, MO:
associated with hypokalemia and total body Acid-base status—frequency dictated by Saunders, 2012, pp. 271–280.
potassium deficits, correcting deficit with KCl underlying disease and patient response to Hopper K. Traditional acid-base analysis. In:
is particularly effective way to reverse treatment. Silverstein DC, Hopper K, eds. Small
alkalosis.
POSSIBLE COMPLICATIONS Animal Critical Care Medicine, 2nd ed. St.
NURSING CARE • Hypokalemia. • Neurologic signs. Louis, MO: Elsevier, 2015, pp. 289–299.
Supportive care to maintain normal hydration, Robinson EP, Hardy RM. Clinical signs,
plasma volume, and adequate nutrition. diagnosis, and treatment of alkalemia in
dogs: 20 cases (1982–1984). J Am Vet Med
Assoc 1988, 192:943–949.
MISCELLANEOUS Authors Helio S. Autran de Morais and
ASSOCIATED CONDITIONS Stephen P. DiBartola
MEDICATIONS Consulting Editor J.D. Foster
• Hypokalemia. • Hypochloremia.
DRUG(S) OF CHOICE Acknowledgment The authors and editors
AGE-RELATED FACTORS acknowledge the prior contribution of Lee E.
Hypochloremic Alkalosis None
• If chloride-responsive alkalosis occurs Palmer.
during edematous state (e.g., congestive heart PREGNANCY/FERTILITY/BREEDING
N/A
Alopecia—Cats A
• Alopecia universalis (normal in sphynx

cats):
◦◦ Hereditary, complete absence of primary
BASICS DIAGNOSIS hairs; decreased secondary hairs.
DEFINITION DIFFERENTIAL DIAGNOSIS ◦◦ Sebaceous and apocrine ducts open onto
Common problem, seen as abnormal lack of skin surface; oily feel to skin.
Infectious
hair coat. ◦◦ Wrinkled foreheads; gold eyes; no
• Dermatophytosis.
whiskers; downy fur on paws, tip of tail,
PATHOPHYSIOLOGY • Parasites
and scrotum.
Specific and unique for each cause. ◦◦ Mites—Demodex gatoi, cheyletiella,
◦◦ Comedones with or without secondary
SYSTEMS AFFECTED notoedres are often pruritic and scaly;
folliculitis.
• Endocrine/metabolic.
Demodex cati cause hair loss with minimal
• Feline hypotrichosis:
• Hemic/lymphatic/immune.
inflammatory change in many cases.
◦◦ Siamese and Devon Rex cats (autosomal
◦◦ Fleas can cause alopecia if patient is
• Skin/exocrine. recessive alopecia).
hypersensitive and pruritic; severe on caudal
SIGNALMENT ◦◦ Poorly developed primary telogen hair
dorsum, abdomen, and around ears.
• Age, breed, or sex predilections specific to follicles.
◦◦ Tick attachment sites can cause alopecic
each condition. ◦◦ Born with normal coat, which becomes
granuloma.
• Neoplastic- and paraneoplastic-associated thin and sparse as young adult.
• Bacterial:
alopecias generally recognized in older cats. ◦◦ Alopecia secondary to deep bacterial Environmental
SIGNS infection. • Solar damage—skin can be damaged
Depends on specific diagnosis. Knowing ◦◦ Superficial bacterial infections secondary with prolonged sun exposure; most
whether cat is pruritic is a very important part to underlying cause. common in outdoor light-colored cats.
of workup for alopecia. • Viral: Areas with thin hair most affected: ears,
◦◦ Herpesvirus can cause neuralgia, pruritus, eyes, and nose; early signs alopecia, scaling,
CAUSES alopecia, and ulcerated eosinophilic skin and erythema; can transform to squamous
• Infectious—dermatophytosis, parasitic lesions, most commonly on the face. cell carcinoma.
(mites, fleas), superficial and deep ◦◦ FIV- and FeLV-associated giant cell • Burns/frostbite—burns are location
bacterial infections, viral: herpesvirus, dermatosis. dependent’ sometimes have a drip-like
papillomaviral plaques, feline immuno- ◦◦ Papillomaviral plaques in older cats may pattern if caused by hot liquid; affect pressure
deficiency virus (FIV)– and feline leukemia transform to squamous cell carcinoma. points if due to heating pad. Third-degree
virus (FeLV)–associated giant cell burns will have permanent scars. Frostbite
dermatosis. Hypersensitivities
commonly affects ear tips and causes alopecia
• Hypersensitivity—atopy/allergy, oral • Food, flea bites, or environmental allergens
and necrosis.
medication reaction, topical medication (atopy)—ears, face, and abdomen are most
• Scarring is loss of hair follicles and usually
reaction. affected.
pigment from area of skin.
• Disorders of hair follicle cycling—telogen • Oral medication reactions—severe facial
effluvium, Cushing’s (iatrogenic and hyper- pruritus caused by methimazole: symptoms Ischemic
adrenocorticism), hypothyroidism resolve when medication discontinued. • Post matting/traction—caused by loss of
(iatrogenic). • Topical parasite preventives—rare cause of blood supply to hair follicle due to tight
• Congenital—hair follicle dystrophy, alopecia at site of application; usually temporary. prolonged matting or pulling of hair; usually
alopecia universalis (normal in sphynx cats), hair regrows with time.
Disorders of Hair Follicle Cycling
feline hypotrichosis (Siamese and Rex cats), • Post traumatic—rare, alopecia with little
• Telogen effluvium:
pinnal hypotrichosis. inflammation can be seen with injuries where
◦◦ Caused by severe stressful situation or
• Environmental—solar damage, burns, nerve or blood supply interrupted to the skin.
hormonal change such as anesthesia/
frostbite, scarring. surgery, parturition, severe illness, drugs. Autoimmune
• Ischemic—post matting alopecia, post ◦◦ Sudden onset of large symmetric areas of • Alopecia areata—rare, alopecia with little
traumatic. hair thinning or alopecia. outward inflammation, most common on
• Autoimmune—alopecia areata, pemphigus ◦◦ Hair regrows over weeks. face and head.
foliaceus. • Cushing’s syndrome: • Pemphigus foliaceus—crusting and alopecia
• Neoplastic—epitheliotropic lymphoma, ◦◦ Long-term (months) corticosteroid on ears, sometimes nose, feet, and other areas;
mastocytosis, squamous cell carcinoma administration, oral or injectable. pruritus variable.
in situ. ◦◦ Megestrol acetate administration. Neoplastic
• Manifestation of internal disease— ◦◦ Hyperadrenocorticism from adrenal • Epitheliotropic lymphoma—scaly alopecia,
sebaceous adenitis (thymoma-associated tumor or pituitary tumor. eventually plaques and nodules.
exfoliative dermatitis), paraneoplastic ◦◦ Causes symmetric alopecic and atrophic/ • Squamous cell carcinoma in situ—papillo-
alopecia, mural lymphocytic folliculitis, thin skin, sometimes skin fragility/tearing, maviral plaques: in older cats, scaly, crusty,
hyperthyroidism, hyperadrenocorticism, ear tips droop. often pigmented, multifocal, sometimes
diabetes. • Hypothyroidism—iatrogenic is most pruritic.
• Psychogenic—compulsive disorder. common cause, due to treatment of hyper- Manifestation of Internal Disease
RISK FACTORS thyroidism. • Thymoma-associated exfoliative dermatitis:
FeLV/FIV—reported risk for demodicosis Congenital ◦◦ Nonpruritic dramatic scaling dermatitis
(not all cases associated with viral • Hair follicle dystrophy/sebaceous gland that starts on head and neck.
infection). dystrophy can cause thin hair diffusely or ◦◦ Surgical removal of thymoma resolves
waxy accumulations on the hairs. dermatitis over 4–5 months.
A Alopecia—Cats (continued)
• Paraneoplastic alopecia: EXPECTED COURSE AND PROGNOSIS

◦◦ Most cases associated with pancreatic Determined by specific diagnosis.
adenocarcinomas, bile duct carcinomas.
◦◦ Nonpruritic alopecia has acute onset, TREATMENT
progresses rapidly; bilaterally symmetric, • See specific chapters for full list of
ventrally distributed (also located along medications, doses, and other therapies.
bridge of nose and periocular); hair epilates • If pet is compliant, shampoo and topical MISCELLANEOUS
easily; dry fissuring footpads; skin often therapy may relieve secondary problems such ZOONOTIC POTENTIAL
thin and hypotonic; rapid weight loss. as hyperkeratosis, crusting, or secondary • Dermatophytosis—can cause skin lesions in
• Mural lymphocytic folliculitis—sometimes bacterial infections. humans.
paraneoplastic: alopecia of face, eyelids, • Cheyletiellosis—can cause irritation in
muzzle; skin has thick, waxy feel; histologic humans.
lymphocytic invasion of follicular outer root SEE ALSO
sheath and epidermis. MEDICATIONS • Cheyletiellosis.
• Hyperthyroidism—alopecia due to
DRUG(S) OF CHOICE • Demodicosis.
self-barbering; can see weight loss as well. • Dermatophytosis.
• Hyperadrenocorticism—symmetric, • Demodicosis—fluralaner topically as per
label every 3 months; lime sulfur dips at • Diabetes Mellitus Without Complication—
nonpruritic; older cat if natural, any age if Cats.
iatrogenic; can have severe skin fragility. weekly intervals for six dips; other mites and
fleas also respond to appropriate topical or • Feline Paraneoplastic Alopecia.
• Diabetes—unkempt and unhealthy coat,
oral treatments. • Flea Bite Hypersensitivity and Flea Control.
skin infections. • Hyperadrenocorticism (Cushing’s Syndrome)—
• Allergic dermatitis—antihistamines only
Psychogenic rarely helpful; novel restricted-ingredient diet; Cats.
Although anxiety may make overgrooming corticosteroids; cyclosporine (5–7 mg/kg/day • Hyperthyroidism.
worse from any underlying condition, a pure initially); allergen-specific immunotherapy; • Lymphoma, Cutaneous Epitheliotropic.
compulsive disorder is very rare; all other ectoparasite control. • Pemphigus.
causes of alopecia must be ruled out prior to • Hyperthyroidism—methimazole, • Sebaceous Adenitis, Granulomatous.
considering. thyroidectomy, or radioactive iodine • Squamous Cell Carcinoma, Skin.
CBC/BIOCHEMISTRY/URINALYSIS therapy. • Thymoma.
Abnormalities may be noted with diabetes • Diabetes mellitus—regulation of glucose ABBREVIATIONS
mellitus, hyperadrenocorticism, and levels (insulin, weight loss, diet). • FeLV = feline leukemia virus.
hyperthyroidism. • Hyperadrenocorticism—discontinue • FIV = feline immunodeficiency virus.
glucocorticoids if iatrogenic; if natural,
OTHER LABORATORY TESTS Suggested Reading
• FeLV and FIV—risk factors for demodico-
trilostane, mitotane, and surgery are options.
Backel K, Cain C. Skin as a marker of general
• Paraneoplastic alopecia—surgical excision
sis and other infections. feline health: cutaneous manifestations of
• Thyroid hormones—document hyperthy-
of neoplasia; but neoplasia often fatal.
infectious disease. J Feline Med Surg, 2017,
• Epitheliotropic lymphoma—corticoster-
roidism/hypothyroidism. 19(11):1149–1165.
oids, lomustine.
IMAGING Diesel A. Cutaneous hypersensitivity derma-
• Sebaceous adenitis—surgical removal of
• Abdominal ultrasound—assess adrenals in toses in the feline patient: a review of allergic
thymoma, corticosteroids, cyclosporine.
hyperadrenocorticism and look for neoplasia skin disease in cats. Vet Sci, 2017, 4(2):25.
• Squamous cell carcinoma in situ—surgical
in animals with paraneoplastic syndrome. Mecklenburg L, Linek M, Tobin DJ. Hair
excision, retinoids (topical and oral), topical
• Chest radiographs/ultrasound to rule out Loss Disorders in Domestic Animals.
imiquimod cream.
thymoma. Chichester: Wiley, 2009.
• CT scan—look for pituitary or other
PRECAUTIONS Vogelnest LJ. Skin as a marker of general
neoplasia tumors in animals with hyperadreno- Toxicity with griseofulvin and itraconazole feline health: cutaneous manifestations of
corticism. (see Dermatophytosis). systemic disease. J Feline Med Surg, 2017,
19(9):948–960.
DIAGNOSTIC PROCEDURES Author Melissa N.C. Eisenschenk
• Skin scrapes. Consulting Editor Alexander H. Werner
• Dermatophyte culture. Resnick
• Parasite treatment trials, since negative skin FOLLOW-UP Acknowledgment The author and editors
scrapes do not rule out all parasites. PATIENT MONITORING acknowledge the prior contribution of Karen
• Skin biopsy. Determined by specific diagnosis. Helton Rhodes.
• Shirts/collar to prove self-trauma if pruritus
is questioned. PREVENTION/AVOIDANCE
• Food elimination trials if parasites and
Determined by specific diagnosis.
dermatophytes are ruled out. POSSIBLE COMPLICATIONS available online
• Intradermal allergy testing. Determined by specific diagnosis.
Alopecia—Dogs A
RISK FACTORS • Epitheliotropic lymphoma—diffuse,

Chronic corticosteroid use causes hair cycle generalized truncal alopecia with scaling and
arrest with other signs of iatrogenic Cushing’s. intense erythema; later nodule and plaque
BASICS formation.
DEFINITION • Pemphigus foliaceus—hair loss associated
• Common disorder. with scale and crust formation.
• Characterized by complete or partial loss of • Sebaceous adenitis—hair straightening,
hair in areas where it is normally present.
DIAGNOSIS thinning, with dry hyperkeratosis; standard
• May be associated with multiple causes, be DIFFERENTIAL DIAGNOSIS poodles and crosses, Havanese, other breeds.
the primary problem, or be secondary to an • Allergic dermatitis with secondary
Multifocal Alopecia
underlying cause. • Demodicosis—partial to complete alopecia
infections and self-trauma due to pruritus.
PATHOPHYSIOLOGY with erythema, comedones, and mild scaling; Specific Locations
• Multiple causes. lesions may become inflamed and crusted. • Pinnal alopecia/pattern baldness—
• Represents removal of hair or disruption in • Dermatophytosis—partial to complete miniaturization of hairs and progressive
the growth of the hair from hypersensitivity, alopecia with scaling, with or without alopecia; dachshund, greyhound, American
infection, genetic abnormality, trauma, erythema, not usually ring-like. water spaniel, Portuguese water spaniel,
immunologic attack, mechanical “plugging,” • Staphylococcal folliculitis—circular patterns Boston terrier, Manchester terrier, whippet,
endocrine abnormalities, neoplasia, drug of alopecia with epidermal collarettes, erythema, Italian greyhound, Chihuahua.
reaction, and/or blockage of receptor sites for crusting, and hyperpigmented macules. • Pinnal alopecia with crusting or necrosis—
stimulation of hair growth cycle. • Injection/topical medication reactions— consider vasculitis, which can have many
inflammation with alopecia and/or cutaneous triggers.
SYSTEMS AFFECTED
atrophy from scarring. • Traction alopecia—hair loss secondary to
• Endocrine/metabolic.
• Rabies vaccine vasculitis—well-demarcated having barrettes or rubber bands applied to
• Hemic/lymphatic/immune.
patch of alopecia observed 1–3 months post the hair, or prolonged tight matting of the
• Skin/exocrine.
vaccination. Small-breed dogs more predisposed. hair.
SIGNALMENT • Alopecia areata—noninflammatory areas of • Post-clipping alopecia—failure to regrow
Age, breed, and sex predilections are specific complete alopecia. after clipping associated with slow or arrested
to each cause listed. • Sebaceous adenitis of short-coated breeds— hair cycle.
SIGNS annular to polycyclic areas of alopecia and • Melanoderma (alopecia of Yorkshire
• May be acute in onset or slowly progressive. scaling. terriers)—symmetric alopecia of pinnae,
• Multifocal patches of alopecia are associated Symmetric Alopecia bridge of nose, tail, and feet.
with folliculitis caused by demodicosis, • Seasonal/cyclic/canine flank alopecia—
• Hyperadrenocorticism—truncal alopecia
dermatophytosis, or, most commonly, associated with atrophic skin, comedones, serpiginous flank alopecia with hyperpig-
staphylococcus infection. and pyoderma, as well as other systemic signs. mentation; boxer, English bulldog, Airedale
• Large, more diffuse areas of alopecia may • Hypothyroidism—thinning of truncal
terrier.
indicate follicular dysplasia or metabolic • Black hair follicular dysplasia—alopecia of
haircoat; generalized alopecia is uncommon
component. presentation; alopecic “rat” tail. black-haired areas only.
• Pattern and degree of hair loss, along with • Dermatomyositis—alopecia of face, tip of
• Noninflammatory alopecia (alopecia
presence of pruritus, are important for X)—symmetric truncal alopecia associated ears, tail, and digits; associated with scale
establishing differential diagnoses. with hyperpigmentation; alopecia often starts crusting and scarring.
CAUSES along collar area of neck; Pomeranian, chow Breed-Related Alopecia
• Infectious—dermatophytosis, parasitic chow, Akita, Samoyed, Keeshonden, Alaskan • Alopecic breeds—Chinese crested, Mexican
(mites, fleas), superficial and deep bacterial Malamute, and Siberian husky. hairless, Inca hairless, Peruvian Inca orchid,
infections. • Hyperestrogenism (females)—symmetric American hairless terrier (often associated
• Hypersensitivity/reaction—atopy/allergy, alopecia of flanks and perineal and inguinal with comedones, folliculitis, and furunculosis).
oral medication reaction, topical medication regions with enlarged vulva and mammary • Congenital hypotrichosis—cocker spaniel,
reaction. glands; may also be associated with exogenous Belgian shepherd, poodle, whippet, beagle,
• Disorders of hair follicle cycling—telogen hormone exposure. French bulldog, Yorkshire terrier, Labrador
effluvium, Cushing’s (iatrogenic and hyper- • Male feminization from Sertoli cell tumor— retriever, bichon frise, Lhasa apso, basset hound.
adrenocorticism), hypothyroidism alopecia of perineum and genital region with • Color dilution alopecia—blue or fawn
(iatrogenic), alopecia X, seasonal flank gynecomastia. Doberman pinscher, silver Labrador, cream
alopecia. • Seasonal/cyclic/flank alopecia—common, chow chow, blond Irish setter, blue pit bull
• Congenital—hair follicle dystrophy. serpiginous flank alopecia with hyperpig- terrier, other breeds with dilute coat colors.
• Environmental—solar damage, burns, mentation; boxer, English bulldog, Airedale • Melanoderma with alopecia—Yorkshire
frostbite, scarring. terrier. terrier.
• Ischemic—post-matting alopecia, barrette • Color mutant/dilution alopecia—brittle or • Seasonal/cyclic/canine flank alopecia—
or rubber band too tight, dermatomyositis, coarse hair, thinning of blue or fawn-colored serpiginous flank alopecia with hyperpig-
post vaccine, vasculitis. hair coat, and secondary folliculitis; other mentation; boxer, English bulldog, Airedale
• Autoimmune—alopecia areata, pemphigus colors of hair normal. terrier.
foliaceus, sebaceous adenitis, vasculitis. • Follicular dysplasia—slowly progressive • Pinnal alopecia/pattern baldness—
• Neoplastic—epitheliotropic lymphoma. alopecia affecting one color of hair. miniaturization of hairs and progressive
• Manifestation of internal disease—hypo- • Anagen defluxion and telogen defluxion— alopecia; dachshund, greyhound, American
thyroidism, hyperadrenocorticism. acute onset of alopecia due to stressful event. water spaniel, Portuguese water spaniel, Boston
A Alopecia—Dogs (continued)
terrier, Manchester terrier, whippet, Italian • Dermatophytosis—terbinafine, ketoconazole, SEE ALSO

greyhound, Chihuahua. fluconazole, itraconazole, lime sulfur dips, • Demodicosis.
• Noninflammatory alopecia (alopecia griseofulvin. • Dermatophytosis.
X)—symmetric truncal alopecia associated • Staphylococcal folliculitis—investigate and • Flea Bite Hypersensitivity and Flea
with hyperpigmentation; alopecia often starts treat underlying cause, shampoo and antibiotic Control.
along collar area of neck; Pomeranian, chow therapy. • Hyperadrenocorticism (Cushing’s
chow, Akita, Samoyed, keeshond, Alaskan • Sebaceous adenitis—topical therapy, Syndrome)—Dogs.
Malamute, Siberian husky. essential fatty acid supplementation, • Hypothyroidism.
CBC/BIOCHEMISTRY/URINALYSIS cyclosporine. • Lymphoma, Cutaneous Epitheliotropic.
Rule out metabolic causes such as hyperadreno- • Iatrogenic Cushing’s—stop all glucocorti- • Pemphigus.
corticism. coids. • Sebaceous Adenitis, Granulomatous.
• Natural hyperadrenocorticism—trilostane, • Sertoli Cell Tumor.
OTHER LABORATORY TESTS mitotane, surgical removal of tumor.
• Thyroid panel—do not rely on low T4 ABBREVIATIONS
• Hypothyroidism—levothyroxine supple-
(total thyroxine) alone); diagnose hypo- • ACTH = adrenocorticotropic hormone.
mentation. • HDDST = high-dose dexamethasone-
thyroidism. • Follicular dysplasia—control concurrent
• Adrenocorticotropic hormone (ACTH)- suppression test.
allergies and infections. • LDDST = low-dose dexamethasone-
response test, low-dose dexamethasone- • Alopecia X and seasonal flank alopecia—
suppression test (LDDST), and high-dose suppression test.
sometimes responds to melatonin. • T4 = Total thyroxine.
dexamethasone-suppression test (HDDST)— • Ischemic lesions—consider pentoxifylline.
evaluate for hyperadrenocorticism. Suggested Reading
• Sex hormone profiles (questionable CONTRAINDICATIONS Behrend EN, Kooistra HS, Nelson R, et al.
validity, often not useful for diagnosis or N/A Diagnosis of spontaneous canine
therapy). POSSIBLE INTERACTIONS hyperadrenocorticism: 2012 ACVIM
IMAGING None consensus statement (small animal). J Vet
Ultrasonography—evaluate adrenal glands for ALTERNATIVE DRUG(S) Intern Med, 2013 27(6):1292–1304.
evidence of hyperadrenocorticism. None Mecklenburg L, Linek M, Tobin DJ. Hair
Loss Disorders in Domestic Animals.
DIAGNOSTIC PROCEDURES Chichester: Wiley, 2009.
• Cytology. Moriello KA, Coyner K, Paterson S, Mignon
• Skin scraping. B. Diagnosis and treatment of dermatophytosis
• Fungal culture. FOLLOW-UP in dogs and cats: clinical consensus
• Skin biopsy—very useful to evaluate status guidelines of the World Association for
of follicle/hair growth as well as epidermal PATIENT MONITORING
Determined by cause. Veterinary Dermatology. Vet Dermatol,
changes associated with specific conditions. 2017, 28(3):266–e68.
POSSIBLE COMPLICATIONS Morris DO. Ischemic dermatopathies. Vet
N/A Clin North Am Small Anim Pract, 2013,
43(1):99–111.
TREATMENT Vandenabeele S, Declercq J, De Cock H,
• Treatments depend on the underlying
Daminet S. Canine recurrent flank alopecia:
causes of alopecia; see specific chapters for MISCELLANEOUS a synthesis of theory and practice. Vlaams
each condition. Diergeneeskd Tijdschr, 2014,
ASSOCIATED CONDITIONS 83(6):275–283.
• Bathing can be useful as adjunctive therapy
N/A Author Melissa N.C. Eisenschenk
for many conditions.
AGE-RELATED FACTORS Consulting Editor Alexander H. Werner
N/A Resnick
Acknowledgment The author and editor
ZOONOTIC POTENTIAL acknowledge the prior contribution of Karen
MEDICATIONS Dermatophytosis can cause skin lesions in Helton Rhodes.
humans.
DRUG(S) OF CHOICE
• Demodicosis or other external parasites — PREGNANCY/FERTILITY/BREEDING
Avoid retinoids and griseofulvin in pregnant Client Education Handout
isoxazoline antiparasitics as per label. available online
animals.
Alopecia, Noninflammatory—Dogs A
lack of normal shed. • Males with hyper- diffuse pattern of alopecia. • Sebaceous
estrogenism may attract other male dogs. adenitis—inflammatory cause of alopecia
Physical Examination Findings more common in specific breeds (Samoyed,
BASICS Akita). • Hypothyroidism and
• Alopecia—usually diffuse and bilaterally
DEFINITION symmetric truncal alopecia sparing the head hyperadrenocorticism—may cause very
• Uncommon alopecic disorders that are and distal extremities; uncommon with similar pattern of diffuse alopecia associated
associated with abnormal hair follicle cycling. hyperandrogenism. • Hair coat—may be dry with lack of hair follicle cycling. • Follicular
• Both endocrine and nonendocrine diseases or bleached. • Secondary seborrhea, pruritus, dysplasia including color dilution alopecia
can be associated with alopecia. • Definitive pyoderma, comedones, ceruminous otitis and black hair follicular dysplasia—alopecia
diagnosis often requires ruling out the more externa, and hyperpigmentation—variable. should be color restricted. • Patterned
common endocrine alopecias. • Enlargement of nipples, mammary glands,
alopecia of various breeds (dachshund,
vulva, prepuce—may be associated with Boston terrier, greyhound, water spaniel, and
PATHOPHYSIOLOGY
hyperestrogenism. • Macular melanosis and others)—breed-specific alopecia of unknown
• Many factors affect the hair cycle, both
linear preputial dermatitis—may be associ- cause. • Seasonal/cyclic/canine flank alopecia—
hormonal and nonhormonal. • Increased
ated with hyperestrogenism. • Abnormal- alopecia of flank and dorsum, often serpiginous
sex hormones can affect the hair cycle.
sized or different-sized testicles—may be patterns with hyperpigmentation, more often
Estrogen is a known inhibitor of anagen,
associated with hyperestrogenism or in short-coated breeds (boxer, English
the growth phase of the hair follicle. • The
hyperandrogenism. • Testicles may also bulldog, Airedale) and may recur seasonally.
mechanism by which alopecia X influences
appear normal in size. • Tail gland • Postclipping alopecia—hair fails to regrow
the hair cycle is not known. • Exposure to
hyperplasia and perianal gland hyperplasia— following clipping; however, hair regrowth
human exogenous hormone replacement
usually associated with hyperandrogenism. occurs within one year. • Telogen
therapy.
• Systemic signs (polyuria/polydipsia [PU/
defluxion—alopecia occurs 1–2 months
SYSTEMS AFFECTED following illness or severe stressful episode
PD]/polyphagia) are usually not present.
• Behavioral. • Endocrine/metabolic. • Hemic/ and usually more sudden in onset, with
lymphatic/immune. • Skin/exocrine. CAUSES relative ease of epilation.
GENETICS Hyperestrogenism—Females CBC/BIOCHEMISTRY/URINALYSIS
Breed predispositions exist for alopecia X; Estrogen excess associated with cystic ovaries, • Usually unremarkable. • Anemia,
however, the mode of inheritance is unknown. ovarian tumors (rare), exogenous estrogen hypercholesterolemia associated with severe
supplementation, or exposure to human hypothyroidism. • Anemia and/or bone
topical hormone replacement. marrow hypoplasia or aplasia can be
• Hyperestrogenism and hyperandrogenism
are uncommon to rare causes of alopecia. Hyperestrogenism—Males associated with hyperestrogenism.
• Alopecia X is relatively common in • Estrogen excess due to Sertoli cell tumor OTHER LABORATORY TESTS
predisposed breeds. (most common), seminoma, or interstitial cell • Serum sex hormone concentrations—often
tumor (rare), or exposure to human topical normal, treat according to suspected
hormone replacement. • Associated with diagnosis based on clinical signs and ruling
None
male pseudohermaphrodism in miniature out other disorders. • Serum estradiol
SIGNALMENT schnauzers. concentrations—sometimes elevated in male
Species Hyperandrogenism—Males dogs with testicular tumors or female dogs
Dogs Androgen-producing testicular tumors with cystic ovaries; however, normal fluctuation
(especially interstitial cell tumors). of estradiol occurs throughout the day, making
Breed Predilections
interpretation of estradiol concentrations
• Hyperestrogenism and hyperandrogenism— Alopecia X difficult. • Adrenal sex hormone panel not
no breed predilections. • Alopecia X— Hairs fail to cycle, but underlying endocrine useful for diagnosis of alopecia X.
miniature poodle and plush-coated breeds cause has not been identified.
such as Pomeranian, chow chow, Akita, IMAGING
RISK FACTORS Radiography, ultrasonography, and
Samoyed, keeshond, Alaskan Malamute, and
• Intact male and female dogs at increased
Siberian husky; recently described in laparoscopy—identify cystic ovaries, ovarian
risk for developing testicular tumors and tumors, testicular tumors (scrotal or
Schipperke breed.
ovarian cysts/tumors, respectively. abdominal), adrenal tumors, sublumbar
Mean Age and Range • Cryptorchid males at increased risk for lymphadenopathy, and possible thoracic
• Hyperestrogenism and hyperandrogenism— developing testicular tumors. • Exogenous metastases of malignant tumors.
middle-aged to old intact dogs. • Alopecia estrogen supplementation. • Exposure to
X—1–5 years of age; however, older dogs human exogenous hormone replacement DIAGNOSTIC PROCEDURES
may develop the condition. therapy. • No known risk factors for alopecia • Preputial cytology—may demonstrate
X other than breed predisposition. cornification of cells in males with hyper
Predominant Sex
estrogenism (similar to bitch in estrus).
• Hyperandrogenism, primarily intact males.
• Skin biopsy.
• Hyperestrogenism, primarily intact females
or males. • Alopecia X, neutered or intact PATHOLOGIC FINDINGS
dogs of either sex. DIAGNOSIS Histologic changes associated with endocrine
dermatoses (telogen hairs, follicular keratoses,
SIGNS DIFFERENTIAL DIAGNOSIS hyperkeratosis, excess trichilemmal keratini-
Historical Findings • Inflammatory causes of alopecia zation [flame follicles], thin epidermis, and
• Overall change in hair coat—dry or (pyoderma, demodicosis, and dermato thin dermis) may also be seen with
bleached because hairs not being replaced; phytosis)—usually cause patchy rather than noninflammatory alopecias including
A Alopecia, Noninflammatory—Dogs (continued)
hyperestrogenism and alopecia X. Histopathology 4 treatments. Hair regrowth can take up to treatment. Therefore, if hair regrowth
will help rule out inflammatory causes of 6 months. Effective in approximately occurs, discontinue treatment to preserve
alopecia (pyoderma, demodicosis, 40–50% of cases. treatment for future recurrence of
dermatophytosis, sebaceous adenitis) and some CONTRAINDICATIONS alopecia. Risk of treatment should be
of the other differentials listed above. None weighed with the fact that this is a
cosmetic disease.
PRECAUTIONS
• Melatonin at high doses can cause insulin
resistance. Use caution in treating dogs with
TREATMENT diabetes mellitus. • Medroxyprogesterone
DIET acetate can cause mammary nodules and MISCELLANEOUS
None cystic endometrial hyperplasia with long-term ASSOCIATED CONDITIONS
use. Diabetes mellitus has been reported in a • Pyoderma, seborrhea, comedones may be
CLIENT EDUCATION few dogs.
Alopecia X is a cosmetic condition resulting in associated with alopecia. • Behavioral changes
coat loss only and there is no definitive cure for POSSIBLE INTERACTIONS associated with hyperestrogenism or hyper-
the hair loss. The risk of treatment should be None androgenism.
emphasized. Hair regrowth will only occur in a ALTERNATIVE DRUG(S) AGE-RELATED FACTORS
portion of dogs regardless of treatment chosen, • Mitotane—15–25 mg/kg once daily as None
and hair loss may recur months to years later in induction for 5–7 days, followed by twice ZOONOTIC POTENTIAL
spite of continued treatment. weekly maintenance; hair regrowth occurs None
SURGICAL CONSIDERATIONS in portion of dogs treated and can take up
to 3 months to become evident. Use of this PREGNANCY/FERTILITY/BREEDING
Hyperestrogenism/Hyperandrogenism drug can result in an Addisonian crisis and N/A—neutering usually recommended for
• Castration—scrotal testicular tumors. other side effects, as for treatment of managing these conditions.
• Exploratory laparotomy—diagnosis and Cushing’s syndrome. • Trilostane—dosages SYNONYMS
surgical removal (ovariohysterectomy and as described for treatment of Cushing’s Alopecia X—growth hormone-responsive
castration) for ovarian cysts and tumors and syndrome; hair regrowth occurs in a portion alopecia, castration-responsive alopecia,
abdominal testicular tumors. of dogs treated and can take up to 3 months adrenal hyperplasia-like syndrome, adrenal
Alopecia X to become evident. Use of this drug can sex hormone imbalance of plush-coated
• Neuter intact animals—a certain number result in an Addisonian crisis and other side breeds, among others.
will regrow hair following neutering; hair effects, as for treatment of Cushing’s ABBREVIATIONS
regrowth may take up to 3 months to become syndrome. • ACTH = adrenocorticotropic hormone.
evident. • Microneedling technique may • PU/PD = polyuria/polydipsia.
induce hair regrowth.
INTERNET RESOURCES
https://vetmed.tennessee.edu/vmc/
FOLLOW-UP SmallAnimalHospital/Dermatology
PATIENT MONITORING Suggested Reading
MEDICATIONS • Medroxyprogesterone acetate—complete Frank LA. Endocrine and metabolic diseases.
DRUG(S) OF CHOICE physical examination and chemistry panel In: Miller WH, Griffin CE, Campbell KL,
General Treatments regularly. • Mitotane—electrolytes and eds., Muller and Kirk’s Small Animal
• Topical antiseborrheic shampoos—for
cortisol with adrenocorticotropic hormone Dermatology, 7th ed. Philadelphia, PA:
comedones and seborrhea associated with (ACTH) stimulation testing regularly. W.B. Saunders, 2013, pp. 501–553.
• Trilostane—electrolytes and cortisol with Frank LA. Alopecia X in a Pomeranian.
alopecia. • Antibiotics and topical antimicrobial
shampoos—for secondary skin infections ACTH stimulation testing regularly. Clinicians Brief, 2017, Nov:26–30.
associated with alopecia. PREVENTION/AVOIDANCE Stroll S, Dietlin C, Nett-Mettler CS.
None Microneedling as a successful treatment for
Alopecia X alopecia X in two Pomeranian siblings. Vet
• Melatonin—implants (8 mg or 18 mg every POSSIBLE COMPLICATIONS Dermatol 2015, 26:387–390.
4–6 months) or oral (3 mg q12h for small None Author Linda A. Frank
breeds and 6–12 mg q12h for large breeds); EXPECTED COURSE AND PROGNOSIS Consulting Editor Alexander H. Werner
evidence of hair regrowth may take up to 3 • Estrogen- and androgen-secreting Resnick
months. Effective in approximately 40% of tumors—resolution of signs should occur
cases. Because this treatment is benign, it is within 3–6 months after castration or
considered the treatment of choice following ovariohysterectomy. • Alopecia X—hair Client Education Handout
neutering. Once hair regrowth has occurred, regrowth will occur in only a portion of available online
discontinue treatment. • Medroxyprogesterone dogs regardless of treatment chosen and
acetate—5–10 mg/kg SC q4 weeks for hair loss may recur in spite of continued
Ameloblastoma A
• Squamous cell carcinoma may be histopathological margin on local

misdiagnosed as ameloblastoma. recurrence. J Vet Dent 2017,
34(4):241–247.
BASICS Author Nick Dervisis
OVERVIEW Consulting Editor Timothy M. Fan
• Common oral tumor of odontogenic (tooth
structure) ectoderm origin.
TREATMENT
• Surgical excision such as hemi- or total
• Biologically these tumors are benign
mandibulectomy or maxillectomy with
histologically, but possess locally invasive
>1–2 cm margins is recommended as a
properties.
curative treatment option. Always submit
• Tumors may arise anywhere within the
resected tissue for histopathology, in order to
dental arcade.
confirm the original diagnosis, and evaluate
• Several histologic subtypes exist with
soft tissue and bone margins.
similar invasive behavior.
• Radiation therapy may provide long-term
SIGNALMENT control in large tumors, or when owners
• Middle-aged and old dogs. decline surgery.
• Rare in cats. • Intralesional chemotherapy with bleomycin
SIGNS has been reported, but results are generally
• Dogs may present with a smooth, firm, inferior to those of surgery or radiation.
gingival mass that is usually nonulcerated.
• May be incidental finding during dental
prophylaxis/procedures. If involving rostral
dental arcade, incisor teeth can be displaced MEDICATIONS
and enveloped by proliferative tissue.
DRUG(S) OF CHOICE
CAUSES & RISK FACTORS N/A
N/A
INTERACTIONS
N/A
DIAGNOSIS
• Epulis.
• Gingival hyperplasia.
FOLLOW-UP
Careful oral examination at 1, 3, 6, 9, and
• Squamous cell carcinoma.
12 months after definitive treatment is
• Amelanotic melanoma.
recommended to monitor for local
• Plasma cell tumor.
recurrence.
• Other tumors related to the odontogenic
apparatus.
Unaffected
MISCELLANEOUS
N/A Suggested Reading
Amory JT, Reetz JA, Sanchez MD, et al.
IMAGING Computed tomographic characteristics of
• Dental radiographs may show bone odontogenic neoplasms in dogs. Vet Radiol
lysis deep to the superficial mass. Not Ultrasound 2014, 55(2):147–158.
particularly useful for diagnostic or treatment Fiani N, Verstraete FJ, Kass PH, Cox DP.
planning. Clinicopathologic characterization of
• Regional and distant metastasis has not odontogenic tumors and focal fibrous
been described. hyperplasia in dogs: 152 cases (1995–2005).
• CT is ideal for planning surgery or J Am Vet Med Assoc 2011,
radiation therapy, especially in large or caudal 238(4):495–500.
tumors. Goldschmidt SL, Bell CM, Hetzel S, Soukup
DIAGNOSTIC PROCEDURES J. Clinical characterization of canine
• Deep tissue biopsies are necessary and acanthomatous ameloblastoma (CAA) in
recommended for definitive diagnosis. 263 dogs and the influence of postsurgical
A Amphetamine and ADD/ADHD Medication Toxicosis
• Gastrointestinal (GI)—anorexia, vomiting, • 5-fluorouracil.
diarrhea. • Ma huang, guarana, or ephedra.
BASICS INCIDENCE/PREVALENCE CBC/BIOCHEMISTRY/URINALYSIS

N/A • CBC—generally normal with mild to
DEFINITION moderate intoxications; disseminated
Acute neurologic, neuromuscular, and cardiac SIGNALMENT
intravascular coagulopathy secondary to
toxicosis as the result of excessive consumption Species severe hyperthermia (rare).
of amphetamine or a derivative. May be due Dogs and cats, although more prevalent in dogs. • Chemistry—generally normal with mild to
to ingestion of prescription medications or moderate intoxications.
Breed Predilections
illegal drugs. • Azotemia—prerenal: secondary to
N/A
PATHOPHYSIOLOGY dehydration; renal: secondary to
Mean Age and Range rhabdomyolysis and myoglobinuria (rare).
• Amphetamine and its derivatives belong to the
N/A • Elevated liver enzymes—secondary to
CNS stimulant class phenylethylamines. Various
substitutions of the basic phenylethylamine Predominant Sex seizures and/or hyperthermia (rare).
structure account for many pharmaceutical N/A • Hypoglycemia.
and illicit compounds found today. • Urinalysis—evidence of myoglobinuria,
SIGNS
• Amphetamine is a sympathomimetic that is urine specific gravity (high: prerenal azotemia;
structurally related to norepinephrine. Historical Findings isosthenuria: renal failure).
• Central action—stimulates cortical centers • Abnormal behavior—usually hyperactivity,
anxiety or pacing, anorexia, fast heart rate, OTHER LABORATORY TESTS
including cerebral cortex, medullary respiratory • Electrolytes—imbalances secondary to GI
center, and reticular activating systems. panting; observed or evidence of exposure by
owner/caretaker. effects.
• Peripheral action—directly stimulates alpha • Acid-base status—acidosis may occur.
and beta receptors and stimulates release of • Onset of signs typically begins within 30
minutes to 6 hours post ingestion; depends • Over-the-counter urine drug screens—
norepinephrine from stores in adrenergic watch for false positive or negative; consult
nerve terminals. on product formulation.
user handbook for further information.
• Amphetamine may slow catecholamine Physical Examination Findings • Amphetamines are present in blood, urine,
metabolism by inhibition of monoamine • Nervous—hyperactivity, agitation, and saliva; consult with local veterinary
oxidase. restlessness, head bobbing, pacing, circling, diagnostic lab or human hospital for
• Several different product formulations, vocalization, disorientation, hyperesthesia, availability and proper sample submission.
including immediate and extended release ataxia, lethargy or depression (less common).
and topical patch. • Cardiovascular—tachycardia or bradycardia IMAGING
• Amphetamines are well absorbed orally; (less common, may be reflexive), hypertension. N/A
peak plasma levels are generally reached in • Neuromuscular—muscle fasciculation or DIAGNOSTIC PROCEDURES
1–3 hours; this may be delayed with extended tremors, seizures. • ECG for presence of any tachyarrhythmia
release formulations. • Gastrointestinal—vomiting, diarrhea, or less commonly bradyarrhythmia.
• Metabolism is minimal. anorexia, excessive salivation. • Blood pressure—identification of
• The half-life, which varies from 7 to 34 • Respiratory—tachypnea. hypertension.
hours, and rate of excretion of unchanged • Ophthalmic—mydriasis with possibly poor
PATHOLOGIC FINDINGS
amphetamine in the urine are both dependent to unresponsive pupillary light response. On necropsy presence of amphetamines may
upon urine pH, with shorter half-lives • Other—hyperthermia.
be found in gastric contents, urine, plasma,
associated with more acidic urine.
CAUSES liver, kidney, or muscle.
• Clinical signs may be seen at doses below
Accidental ingestion or administration,
1 mg/kg.
malicious poisoning.
• Oral lethal dose in dogs for most
amphetamines ranges from 10 mg/kg to RISK FACTORS
23 mg/kg and for methamphetamine sulfate Households with children or adults currently TREATMENT
it is 9–11 mg/kg. Oral lethal dose for taking prescription or illicit amphetamine or
derivative. APPROPRIATE HEALTH CARE
amphetamine sulfate is 20–27 mg/kg.
Majority of cases require emergency inpatient
• Amphetamine and its derivatives are used
intensive care management.
in humans to treat attention deficit disorder
(ADD)/attention deficit hyperactivity NURSING CARE
disorder (ADHD), narcolepsy, and obesity. • Intravenous fluid therapy to correct
• Illicit use of amphetamines in humans is
DIAGNOSIS dehydration and electrolyte imbalances as
also prevalent. DIFFERENTIAL DIAGNOSIS well as support renal function and promote
• Strychnine. excretion of amphetamines; use blood
SYSTEMS AFFECTED
• Organochlorine insecticides. pressure to help guide fluid rate.
• Cardiovascular—stimulation most
• Methylxanthine. • Cool intravenous fluids, fans, cool water
common: tachycardia and hypertension.
• 4-aminopyridine. baths for hyperthermia.
• Nervous—stimulation most common,
• Metaldehyde.
depression uncommon. ACTIVITY
• Phenylpropanolamine.
• Neuromuscular—stimulation: muscle Minimize activity and stimuli.
• Albuterol.
tremors and seizures. DIET
• Nicotine.
• Respiratory—stimulation, tachypnea. Withhold food if moderately to severely
• Tremorgenic mycotoxins.
• Ophthalmic—mydriasis. affected. Bland diet for few days post
• Hypernatremia.
• Pseudoephedrine, phenylephrine. exposure if significant GI signs were noted.
(continued) Amphetamine and ADD/ADHD Medication Toxicosis A
CLIENT EDUCATION PRECAUTIONS SYNONYMS

In case of exposure, owner should contact N/A • Common brand names of prescription
local veterinarian or veterinary poison center POSSIBLE INTERACTIONS amphetamine drugs and their active
immediately. • Amphetamines inhibit metabolism of
ingredient—Adderall® (amphetamine and
SURGICAL CONSIDERATIONS adrenergic blockers (doxazosin, phenoxy dextroamphetamine); Ritalin®, Metadate®,
N/A benzamine, prazosin, terazosin), and Concerta® (methylphenidate); Daytrana®
phenobarbital, and phenytoin. (methylphenidate transdermal patch);
• Amphetamines potentiate metabolism of
Focalin® (dexmethylphenidate); Vyvanse®
coumarin anticoagulants, monoamine oxidase (lisdexamfetamine); Cylert® (pemoline);
inhibitors, opioid analgesics, and tricyclic Adipex-P® (phentermine); Dexedrine®
MEDICATIONS antidepressants. (dextroamphetamine).
• Illicit drug street names—ice, glass,
DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) crank, speed, uppers, ecstasy, meth, and
Decontamination Phenobarbital, pentobarbital, and propofol many others.
• Induce emesis—if recent exposure and pet for CNS stimulatory signs.
is not already symptomatic. SEE ALSO
• Antidepressant Toxicosis—SSRIs and
• Apomorphine—0.04 mg/kg IV, subcon-
junctival. SNRIs.
• Antidepressant Toxicosis—Tricyclics.
• Hydrogen peroxide 3%—2.2 mL/kg,
maximum dose 45 mL. FOLLOW-UP • Pseudoephedrine/Phenylephrine Toxicosis.
• Gastric lavage if extremely large ingestion PATIENT MONITORING ABBREVIATIONS
or patient is already symptomatic. • Monitor in hospital until resolution of • ADD = attention deficit disorder.
• Activated charcoal with cathartic. clinical signs. • ADHD = attention deficit hyperactivity
CNS Signs of Stimulation • If severely affected, monitor liver and disorder.
kidney values every 24 hours for 72 hours or • DIC = disseminated intravascular
• Acepromazine 0.05–1.0 mg/kg IV/IM, start
low and titrate to effect. until resolution. coagulation.
• GI = gastrointestinal.
• Chlorpromazine 0.5 mg/kg IV, titrate up as PREVENTION/AVOIDANCE
needed. All medications and illicit drugs should be INTERNET RESOURCES
• Cyproheptadine (serotonin antagonist)— kept out of pets’ reach at all times. • https://www.aspcapro.org/animal-health/
dogs, 1.1 mg/kg orally or rectally, may be POSSIBLE COMPLICATIONS toxicology-poison-control
repeated q8h as needed for signs consistent • http://www.petpoisonhelpline.com
Acute renal failure secondary to myoglobinuria
with serotonin syndrome; cats, 2–4 mg/cat, or disseminated intravascular coagulation Suggested Reading
may repeat q12h as needed for signs (DIC; rare). Stern LA, Schell M. Management of attention-
consistent with serotonin syndrome. deficit disorder and attention-deficit/
• Methocarbamol (for muscle tremors)— EXPECTED COURSE
hyperactivity disorder drug intoxication in
50–220 mg/kg IV, titrate to effect; do not AND PROGNOSIS dogs and cats. Vet Clin North Am Small
exceed 330 mg/kg/day. • Expected course of clinical signs is 12–72 Anim Pract 2012, 42(2):279–287.
Cardiovascular Signs hours, depending on dose, product formulation, Teitler JB. Evaluation of a human on-site
• Tachyarrhythmia—beta blockers such as
effectiveness of decontamination and urine multi drug test for emergency use
propranolol 0.02–0.04 mg/kg IV or esmolol treatment, and rate of elimination. with dogs. J Am Anim Hosp Assoc 2009,
or metoprolol; caution using propranolol in • Prognosis—most patients do well with prompt 45(2):59–66.
significantly hypertensive patient. and appropriate veterinary care. Seizures or severe Volmer PA. Human drugs of abuse. In:
• Ventricular premature contractions—
hyperthermia may be poor prognostic indicator. Bonagua JD, Twedt DC, eds., Current
lidocaine: dogs at 2–4 mg/kg IV (to maxi- Veterinary Therapy XIV. St. Louis, MO:
mum of 8 mg/kg over 10-minute period); Elsevier, 2009, pp. 144–145.
cats: start with 0.1–0.4 mg/kg and increase Volmer PA. “Recreational” drugs. In: Peterson
cautiously to 0.25–0.75 mg/kg IV slowly if no MISCELLANEOUS ME, Talcott PA, eds., Small Animal Toxicology,
response; cats are reportedly very sensitive to 3rd ed. St. Louis, MO: Elsevier, 2013, pp.
lidocaine, so monitor carefully if used. ASSOCIATED CONDITIONS 309–334.
N/A Wismer T. Amphetamines. In: Osweiler GD,
Promote Elimination
Ascorbic acid or ammonium chloride—for AGE-RELATED FACTORS Hovda LR, Brutlag AG, Lee JL, eds.
urinary acidification to promote elimination; N/A Blackwell’s Five-Minute Veterinary Consult
however, only use if can measure acid-base status. ZOONOTIC POTENTIAL Clinical Companion Small Animal
Pets exposed to human waste products from Toxicology. Ames, IA: Wiley-Blackwell,
CONTRAINDICATIONS 2011, pp. 125–130.
• While diazepam has been successfully used those taking amphetamines or derivatives
could become symptomatic. Author Kirsten E. Waratuke
to treat amphetamine exposures, there is Consulting Editor Lynn R. Hovda
evidence that benzodiazepines may intensify PREGNANCY/FERTILITY/BREEDING
neurologic signs. Amphetamines are a known teratogen in
• Urinary acidification if unable to monitor humans. They have been found to cross the
acid-base status or if myoglobinuria is present. placenta in animals and may also be found
• Inducing emesis in symptomatic patient. in milk.
A Amyloidosis
SIGNALMENT immune‐mediated diseases (SPAID, systemic
Species lupus erythematosus, juvenile polyarteritis of
Dog and cat. beagle); amyloid deposits can be found in up
BASICS to 35% of feline immunodeficiency virus
Breed Predilections (FIV)‐positive cats. • Neoplasia (lymphoma,
DEFINITION
• Dog—Chinese Shar-Pei, beagle, English plasmacytoma, multiple myeloma, mammary
Group of conditions of diverse causes in
foxhound, Walker hound, collies. • Cat— tumors, testicular tumors). • Familial—
which extracellular deposition of insoluble
Abyssinian, Siamese, oriental shorthair. Chinese Shar-Pei, English foxhound, and
fibrillar proteins (amyloid) in various organs
and tissues compromises normal function. Mean Age and Range beagle dogs; Abyssinian, Siamese, and
• Cats—mean age at diagnosis 7 years; range oriental shorthair cats. • Other—cyclic
PATHOPHYSIOLOGY
1–17 years; Abyssinian cats with familial renal hematopoiesis in gray collies.
• Patients usually affected by reactive (secondary)
amyloidosis usually die by 5 years of age;
amyloidosis; tissue deposits contain amyloid A
Siamese cats with familial amyloidosis of liver
protein (AA), fragment of acute‐phase reactant
and thyroid gland usually develop signs of
protein called serum amyloid A protein (SAA).
liver disease when 1–4 years old. • Dogs—
• Macrophage‐derived cytokines, e.g., IL‐1 and
mean age at diagnosis 9 years; range 1–15
DIAGNOSIS
IL‐6, stimulate hepatocytes to synthesize SAA. DIFFERENTIAL DIAGNOSIS
years; Chinese Shar-Pei affected younger, with
• Cellular and extracellular components • Depends on organ affected. • Renal
median age at diagnosis of 5 years, range
involved in formation and deposition of AA. (glomerular) amyloidosis—immune‐complex
3.6–17 years. • Prevalence increases with age.
• Specific pathophysiology varies among glomerulonephritis (GN; e.g., membrano-
different species and breeds; reactive Predominant Sex
proliferative GN [MPGN], membranous GN
amyloidosis occurs as familial disease in None
[MGN]), non‐immune‐complex GN,
Chinese Shar-Pei dog and Abyssinian cat. SIGNS glomerulosclerosis, focal segmental
• Chinese Shar-Pei dog—mutation involving glomerulosclerosis, other glomerulopathies.
overexpression of HAS2 results in General Comments
Clinical signs depend on organs affected; • Renal (medullary) amyloidosis—other
overproduction of hyaluronic acid, which acts causes of medullary renal disease (e.g.,
as danger signal activating inflammasome usually caused by kidney involvement.
pyelonephritis, chronic interstitial nephritis).
pathway and IL‐1 production; this mutation Historical Findings • Hepatic amyloidosis—other causes of
linked to increased likelihood of developing • No clear history of predisposing disorder in hepatic dysfunction (e.g., infectious,
shar‐pei autoinflammatory disease (SPAID), most cases. • Anorexia, lethargy, polyuria/ inflammatory, portosystemic shunt,
and also responsible for breed’s meat‐mouth polydipsia, weight loss, vomiting. • Owners neoplasia); in animals with hepatic fracture
phenotype; amyloid deposition occurs in may appreciate ascites and peripheral edema and hemoabdomen, consider other causes of
medulla of all dogs, with majority of dogs also in animals with glomerular amyloidosis. hemoabdomen (e.g., hemangiosarcoma,
having glomerular involvement. • Non‐shar‐ • Chinese Shar-Pei dogs may have history of hematoma).
pei dogs—amyloid deposits found more previous episodic joint swelling and high
commonly in glomeruli than medulla. fever that resolves spontaneously within few CBC/BIOCHEMISTRY/URINALYSIS
• Abyssinian cat—amyloid deposits usually days (SPAID). • Siamese and oriental • CBC—nonregenerative anemia found in
found in medulla, but may occur in glomeruli. shorthair cats may present with acute collapse some dogs and cats. • Chemistry profile—
• Siamese and oriental shorthair cats with and hemoabdomen due to spontaneous changes reflect distribution of amyloid
familial amyloidosis—amyloid deposition hepatic fracture. deposition; with renal medullary amyloidosis,
occurs in liver. • Pancreatic islet amyloid azotemia, hyperphosphatemia, metabolic
Physical Examination Findings acidosis may be seen; hypoalbuminemia
polypeptide, or amylin, deposits in pancreas of
• Related to primary inflammatory or common with glomerular amyloidosis;
old cats; amylin secreted with insulin by
neoplastic disease process. • Animals with renal hyperglobulinemia may be seen due to
pancreatic beta cells; chronic increased stimulus
disease may have muscle wasting, abnormal underlying inflammatory condition resulting
for secretion of amylin by beta cells (e.g., states
renal palpation, uremic ulceration, hypertensive in reactive amyloidosis. • Urinalysis—
of insulin resistance) leads to pancreatic islet
fundic lesions. • Fluid retention may be present isosthenuria, proteinuria, cylindruria
cell amyloidosis.
(ascites, peripheral edema). • Chinese Shar-Pei common with renal amyloidosis; proteinuria
SYSTEMS AFFECTED dogs may have evidence of SPAID if present may be mild or absent in patients without
• Renal/urologic—predilection for renal AA during active flare‐up (joint effusion and pain, glomerular amyloidosis; isosthenuria may not
deposition. • Liver, spleen, adrenal glands, fever). • Signs of thromboembolic disease may be present in patients without medullary
pancreas, tracheobronchial tree, gastrointestinal be present in up to 40% of dogs with renal involvement.
tract also may be affected. amyloidosis (dyspnea with pulmonary embolism,
caudal paresis with aortic embolism). • Siamese OTHER LABORATORY TESTS
GENETICS • Urine protein–creatinine ratio (UPC) should
• Familial amyloidosis occurs in Chinese and oriental shorthair cats with hepatic
dysfunction may have jaundice; pallor and be performed for quantification of proteinuria.
Shar-Pei, English foxhound, and beagle dogs, • Urine sodium dodecyl sulfate–polyacrylamide
and in Abyssinian, oriental shorthair, and abdominal fluid wave may be present with
hepatic fracture and hemoabdomen. gel electrophoresis (SDS‐PAGE)—can
Siamese cats. • A genetic mutation that differentiate between high and low molecular
increases likelihood of SPAID in shar‐pei dogs CAUSES weight proteinuria; high molecular weight
has been identified; chronic inflammatory • Neoplasia and chronic infectious and proteinuria expected with glomerular disease.
episodes in SPAID result in renal amyloid noninfectious inflammatory conditions can
deposition. be found in 30–50% of dogs with reactive IMAGING
INCIDENCE/PREVALENCE amyloidosis. • Chronic inflammation— Abdominal Radiographic Findings
Uncommon, occurs mostly in dogs; rare in systemic mycoses, chronic bacterial infections, Kidneys—usually small in affected cats; small,
cats, except Abyssinian, Siamese, and oriental parasitic infections (dirofilariasis, leishmaniasis, normal size, or large in affected dogs.
shorthair. hepatozoonosis), inflammatory and
(continued) Amyloidosis A
Abdominal Ultrasonographic Findings therapy (heparin, low molecular weight EXPECTED COURSE AND PROGNOSIS
• Renal size, shape, and architecture variable; heparin, or factor Xa inhibitors). • Disease is progressive and usually advanced at
kidneys usually hyperechoic and small in Management of Renal Insufficiency time of diagnosis. In one study, median survival
affected cats; may be small, normal size, or large time for all dogs with renal amyloidosis 5 days
in affected dogs. • Echogenic effusion may be and Hypertension (range: 0–443 days), shorter in Chinese
present in cats with hepatic amyloidosis, due to • As indicated by IRIS guidelines for stage of
Shar-Pei dogs (2 days, range: 0–368 days).
hepatic fracture and hemoabdomen. renal disease. • Amlodipine (0.3–0.8 mg/kg • Serum creatinine concentration has signifi-
PO SID) as first‐line therapy for management cant negative association with survival. • Cats
DIAGNOSTIC PROCEDURES of hypertension.
Renal biopsy—histopathology required for with renal insufficiency because of amyloidosis
definitive diagnosis, and to rule out other Management of Amyloid Deposition usually survive <1 year; cats with systemic
causes of GN; ultrasound‐guided sampling • Dimethylsulfoxide (DMSO; dogs—90% amyloidosis (i.e., liver, vascular) have grave
preferred over surgical methods; samples DMSO diluted 1 : 4 with sterile water prognosis due to complications such as hepatic
should be assessed under dissecting microscope subcutaneously at dosage of 90 mg/kg 3 times fracture and pulmonary hemorrhage.
to ensure glomeruli present; risk factors for per week) may help patients by solubilizing
hemorrhage include body weight <5 kg, amyloid fibrils, reducing serum concentration
serum creatinine >5 mg/dL. of SAA, and reducing interstitial inflammation
and fibrosis in affected kidneys, though benefit MISCELLANEOUS
PATHOLOGIC FINDINGS of DMSO is controversial. • Colchicine
• Amyloid deposits appear homogeneous and (dogs—0.01–0.04 mg/kg PO q24h) impairs ASSOCIATED CONDITIONS
eosinophilic when stained by hematoxylin and release of SAA from hepatocytes, and used for • Shar‐pei autoinflammatory disease.
eosin and viewed by conventional light micro- amyloidosis in humans with familial • Juvenile polyarteritis in beagles.
scopy. • Demonstrate green birefringence after Mediterranean fever (familial amyloidosis SEE ALSO
Congo red staining when viewed under similar in pathology to SPAID); no evidence • Chronic Kidney Disease.
polarized light; AA amyloid loses Congo red for benefit once patient develops renal • Glomerulonephritis.
affinity after permanganate oxidation. amyloidosis and dysfunction; colchicine used • Proteinuria.
• Ultrastructurally, fibrils are 9–11 nm in particularly in shar‐pei dogs with episodic
diameter, nonbranching, haphazardly arranged. ABBREVIATIONS
fever or polyarthritis before development of
• AA = amyloid A protein. • BUN = blood urea
renal failure.
nitrogen. • DMSO = dimethylsulfoxide.
PRECAUTIONS • FIV = feline immunodeficiency virus.
• Dose reduction of drugs may be needed in • GN = glomerulonephritis.
TREATMENT patients with renal insufficiency. • Use of • MGN = membranous GN.
APPROPRIATE HEALTH CARE nonsteroidal anti‐inflammatory drugs • MPGN = membranoproliferative GN.
• Identify underlying inflammatory and (NSAIDs) should be avoided in patients with • NSAID = nonsteroidal anti‐inflammatory
neoplastic processes and treat if possible. renal insufficiency; SPAID flare‐ups usually drug. • SAA = serum amyloid A protein.
• Animals symptomatic from uremia or resolve on their own, do not require NSAIDs. • SDS‐PAGE = sodium dodecyl sulfate–
clinically dehydrated may require hospitalization. • Animals with glomerular disease are prone polyacrylamide gel electrophoresis.
• Stable, euhydrated animals can be managed to overhydration due to abnormal renal • SPAID = shar‐pei autoinflammatory disease.
as outpatients with standard therapy for sodium handling; fluid therapy should be • UPC = urine protein–creatinine ratio.
proteinuria. used judiciously, only to correct dehydration;
even patients with mild hypoalbuminemia
Suggested Reading
DIET Bartges J, Wall J. Amyloidosis. In Bartges J,
can become significantly overhydrated from
• Low‐protein, low‐phosphorous renal diets Polzin DJ. Nephrology and Urology of
inappropriate fluid therapy.
recommended for animals with proteinuria Small Animals. Oxford: Wiley‐Blackwell,
and/or renal dysfunction. • Esophageal 2011, pp. 547–554.
feeding tube placement should be considered Olsson M, Meadows JRS, Truvé K, et al. A
for enteral hydration and nutritional support. novel unstable duplication upstream of
CLIENT EDUCATION FOLLOW‐UP HAS2 predisposes to a breed‐defining skin
• Discuss progression of disease and potential PATIENT MONITORING phenotype and a periodic fever syndrome in
for underlying primary disease process. BUN, creatinine, albumin, electrolyte Chinese Shar‐Pei dogs. PLoS Genet 2011,
• Discuss familial predisposition in suscep- concentrations, 3-day pooled UPC, and 7:e1001332.
tible breeds. blood pressure 1 month following medication Segev G, Cowgill LD, Jessen S et al. Renal
changes, and every 3-4 months in stable amyloidosis in dogs: a retrospective study of
patients. 91 cases with comparison of the disease
between Shar‐Pei and non‐Shar‐Pei dogs.
PREVENTION/AVOIDANCE J Vet Intern Med 2012, 26:259–268.
MEDICATIONS Do not breed affected animals. Author Nahvid M. Etedali
DRUG(S) OF CHOICE POSSIBLE COMPLICATIONS Consulting Editor J.D. Foster
• Renal insufficiency and progressive chronic Acknowledgment The author and book
Management of Proteinuria
kidney disease. • Nephrotic syndrome and editors acknowledge the prior contributions
• Animals with proteinuria should be
fluid overload. • Thromboembolic disease of Helio S. Autran de Morais and Stephen
treated with standard therapy for proteinuria
occurs in up to 40% of dogs, but uncommon P. DiBartola.
(see Glomerulonephritis and Proteinuria).
• Patients with evidence of active thrombo- in cats. • Hepatic rupture causing hemoabdo-
embolic disease require antiplatelet drugs men (hepatic amyloidosis). • Otic and airway
(clopidogrel or aspirin) and/or anticoagulant hemorrhage (vascular amyloidosis) reported.
available online
A Anaerobic Infections
• Necrosis due to trauma or hypoperfusion. • Amoxicillin with clavulanate (22–30 mg/kg
• Neoplasia. PO q12h)—antibiotic of choice; clavulanate
CBC/BIOCHEMISTRY/URINALYSIS improves activity against Bacteroides.
BASICS Injectable potentiated beta-lactams include
• Neutrophilic leukocytosis, monocytosis.
OVERVIEW • Biochemical abnormalities depend on
ampicillin/sulbactam, ticarcillin/clavulanate,
• Anaerobic bacteria require low oxygen specific organ involvement. and piperacillin/tazobactam.
tension to live, and constitute a large portion • Cefoxitin (30 mg/kg IV/IM q6–8h)—
• Sepsis suggested by leukocytosis/leukopenia,
of the normal flora. hypoglycemia, hypoalbuminemia. reliable activity against anaerobes.
• May be Gram-positive or Gram-negative • Clindamycin (11–33 mg/kg PO q12–24h;
cocci or rods, and individual organisms vary OTHER LABORATORY TESTS 10 mg/kg IV q12h)—useful for respiratory
in potential to withstand oxygen exposure. • Anaerobic bacterial culture often unrewarding tract infections.
• Most common genera—Bacteroides, because of fastidious growth requirements • Chloramphenicol (25–50 mg/kg PO q8h,
Fusobacterium, Actinomyces, Propionibacterium, and errors in sample handling. dogs only)—good tissue penetration but
Peptostreptococcus (enteric Streptococcus), ◦◦ Appropriate media and containers should bacteriostatic; concern for human exposure.
Porphyromonas, and Clostridium. be available prior to sample collection. • Metronidazole (10 mg/kg IV/PO q12h)—
• Most anaerobic infections are polymicrobial ◦◦ Samples should not be refrigerated. useful against all clinically significant
and can contain anaerobes admixed with ◦◦ Suitable samples for culture include fluid anaerobes except Actinomyces.
facultative anaerobes or aerobic bacteria or tissue. • Cefovecin (8 mg/kg SC)—infections
(especially E. coli). IMAGING originating from the periodontal cavity, skin,
• Injurious toxins and enzymes elaborated by As indicated for individual patient; gas may or urinary tract.
the organisms may allow extension of be apparent radiographically. • Imipenem—significant activity against
infection into adjacent, healthy tissue. serious, resistant infections, not first-line
DIAGNOSTIC PROCEDURES choice.
SIGNALMENT • Cytologic inspection of fluid or tissue • Quinolones—newer third-generation
Dog and cat. reveals degenerate neutrophils with morpho- quinolones (e.g., pradofloxacin) have
SIGNS logically diverse intracellular and extracellular some activity against anaerobes; others
bacteria; presence of large filamentous ineffective.
General Comments bacteria is suggestive.
• Depend on body system involved. • Gram staining should be performed on CONTRAINDICATIONS/POSSIBLE
• Areas associated with mucous membranes sample. INTERACTIONS
are more commonly associated with anaerobic N/A
infection.
• It is possible to overlook anaerobes in an
infectious process, leading to confusion in
interpreting culture results and selection of TREATMENT
antimicrobials. • Wound drainage/debridement should be FOLLOW-UP
established as soon as possible—including PATIENT MONITORING
placement of drains or thoracostomy tubes, as Varies with the circumstances of each
• Foul odor associated with wound or
indicated. patient.
exudative discharge.
◦◦ Combine with systemic antimicrobial
• Gas in the tissue or exudates. POSSIBLE COMPLICATIONS
therapy.
• Discolored tissue. Localized infection may progress to systemic
◦◦ Devitalized tissue should be aggressively
• Ascites (peritonitis), pleural effusion infection if not appropriately identified and
debrided.
(pyothorax), or signs of pyometra (vaginal treated.
◦◦ Improves local blood flow and increases
discharge, palpable structure in caudal
tissue oxygen tension. EXPECTED COURSE AND PROGNOSIS
abdomen).
• Exploratory surgery indicated when anaerobic Dependent upon identification and
• Dental disease.
organisms complicate osteomyelitis or intraab- resolution of the underlying cause; long-term
• Wounds or deep abscesses that do not heal
dominal disease (e.g., pyometra, peritonitis). antibiotic therapy may be required.
as anticipated.
• Usually caused by normal flora; break in
protective barriers allows bacterial invasion.
• Predisposing factors—immunosuppression, MEDICATIONS MISCELLANEOUS
bite wounds, dental disease, open fractures, DRUG(S) OF CHOICE ASSOCIATED CONDITIONS
abdominal surgery, migrating foreign bodies. • Antimicrobial therapy alone is unlikely to See Causes & Risk Factors.
be successful without debridement or
drainage. Suggested Reading
◦◦ Antibiotic selection—largely empiric
Greene CE, Jang SS. Anaerobic infections. In:
(difficult to isolate anaerobes). Greene CE, ed., Infectious Diseases of the
DIAGNOSIS ◦◦ Because most anaerobic infections are
Dog and Cat, 4th ed. St. Louis, MO:
DIFFERENTIAL DIAGNOSIS polymicrobial, therapy targeted against Saunders Elsevier, 2011, pp. 411–416.
• Infection with aerobic or fungal organ- both anaerobes and aerobic organisms is Author Sharon Fooshee Grace
isms—culture recommended. indicated. Consulting Editor Amie Koenig
Anal Sac Disorders A
• Compulsive disorder (anal licking). • Colitis

or other intestinal disorder. • Keratinization
disorder. • Anal sac neoplasia (adenocarcinoma,
BASICS squamous cell carcinoma, melanoma). • Perianal MEDICATIONS
OVERVIEW adenoma, adenocarcinoma. • Perianal fistulae. DRUG(S) OF CHOICE
• Anal sacs are reservoirs for secretions CBC/BIOCHEMISTRY/URINALYSIS Infection
normally evacuated by compression during Use of appropriate oral antibiotics: cephalexin
defecation. • Normal gland secretions vary Impaction/Infection
Usually normal. (dog, 22–30 mg/kg q12h), amoxicillin
widely in consistency and color. • Disorders trihydrate–clavulanate potassium (dog,
include impaction, infection/sacculitis, and Neoplasia 13.75 mg/kg q12h; cat, 62.5 mg/cat q12h),
neoplasia. • Treatment options include Hypercalcemia—anal sac adenocarcinoma. clindamycin (dog, 11–22 mg/kg q24h; cat,
manual expression, flushing, antibiotics, and 11–30 mg/kg q24h), trimethoprim–sul-
surgical excision. famethoxasole (dog, 15 mg/kg q12h);
None unless indicated by an underlying cause.
SIGNALMENT metronidazole (dog, 15–25 mg/kg q12–24h);
IMAGING
Impaction/Infection enrofloxacin (dog, 10–20 mg/kg q24h),
None unless indicated by an underlying cause.
• Dogs and cats (rarely)—no age or sex orbifloxacin (dog/cat, 5 mg/kg q24h).
predisposition. • Breeds predisposed CONTRAINDICATIONS/POSSIBLE
• Digital palpation of anal sacs—should not be
(impaction)—smaller breeds (miniature/toy INTERACTIONS
palpable externally. • Expression of anal sac
poodle, Chihuahua, American cocker and Trimethoprim–sulfamethoxasole—
contents—varies widely in gross appearance and
English springer spaniel). Dobermans highly susceptible to type III
microscopic characteristics. • Cytology (normal
Neoplasia dogs/cats)—one study reports Gram-positive hypersensitivity reactions.
• Adenocarcinoma—English cocker spaniel cocci/rods, Gram-negative cocci/rods, yeast,
most commonly reported. nondegenerate neutrophils without phagocytosis,
SIGNS mononuclear cells, and corneocytes; erythrocytes
uncommonly found in dogs, rare in cats. Another
Impaction/Infection study had similar findings but with intracellular FOLLOW-UP
• Anal/perianal pruritus—often manifested bacteria in clinically normal dog anal sacs. Impaction/Infection
by “scooting.” • Hesitancy to defecate. • Reassess patients weekly initially, then as
• Tenesmus. • Tail chasing. • Foul-smelling, Impaction/Infection
• Cytology—no statistically significant necessary to monitor healing. • Manually
nonfeces anal discharge. • Refusal to sit and/ express anal sac contents and/or flush contents
or lift tail. • Cats—excessive licking of the difference in bacterial counts or inflammatory
cells found between normal dogs and those with until sacs empty without intervention.
ventral abdomen and tail head. • Abscess— • Trimethoprim–sulfamethoxasole—monitor
often unilateral; localized pain and discharge. clinical signs of anal sac disease. • Bacterial
culture and susceptibility—Bacillus, Escherichia tear production, liver function; affects thyroid
Neoplasia coli, Micrococcus, Proteus mirabilis, Streptococcus serum values.
• Mass or swelling in perianal region. spp., others possible.
• Tenesmus, constipation, polyuria/polydipsia
(due to hypercalcemia with adenocarcinoma). Neoplasia
• L4-Cd myelopathy reported in one cat • Surgical excision with histopathology.
(adenocarcinoma). MISCELLANEOUS
CAUSES & RISK FACTORS SEE ALSO
• Adenocarcinoma, Anal Sac
Impaction/Infection • Perianal Fistula
• Predisposing factors—changes in muscle TREATMENT
tone, fecal form (soft stool/diarrhea), secretion Suggested Reading
Impaction/Infection Helton Rhodes KA, Werner A. Blackwell’s
character/volume leading to decreased/lack of • Gentle manual expression and/or flushing of
expression; intestinal disease, obesity, endocrine Five-Minute Veterinary Consult: Clinical
contents. Sedation may be necessary to flush Companion: Small Animal Dermatology, 3rd
disease. • Infection/abscess—chronic or severely impacted or painful anal sacs.
recurrent impactions. ed. Hoboken, NJ: Wiley-Blackwell, 2018.
• Feeding high-fiber diets may help natural James DJ, Griffin CE, Polissar NL, Neradilek
expression of anal sacs. • Identification of MB. Comparison of anal sac cytological
underlying causes of predisposing disease. findings and behaviour in clinically normal
• Chronic disease—anal sac excision. dogs and those affected with anal sac
• Infection—infusion of antibiotic and/or
DIAGNOSIS corticosteroid medications directly into the anal
disease. Vet Derm 2010, 22:80–87.
Author Heather D. Edginton
DIFFERENTIAL DIAGNOSIS sacs, drainage of abscesses, use of appropriate Consulting Editor Alexander H. Werner
Impaction/Infection/Neoplasia oral antibiotics and/or antiyeast medication. Resnick
• Hypersensitivity (flea, atopy, food). Neoplasia Acknowledgment The author acknowledges
• Tapeworm infestation. • Tail fold bacterial • Surgical excision and staging; combine with the prior contribution of Alexander H.
folliculitis. • Malassezia dermatitis. chemotherapy. Werner Resnick.
A Anaphylaxis
SIGNALMENT
Species
BASICS Dog and cat. DIAGNOSIS
DEFINITION Breed Predilections DIFFERENTIAL DIAGNOSIS
• Acute manifestation of a type I hyper • Dogs—numerous breeds documented as • Other types of shock.
sensitivity reaction mediated through the having a predilection for developing atopy. • Asthma.
introduction of an antigen into a host having • Cats—no breeds documented as having • Depends on the major organ system
antigen-specific antibodies of the predilection for atopy. involved or if reaction is localized; diagnosis
immunoglobulin (Ig) E subclass. Mean Age and Range can be made largely based on history and
• Binding of antigen to mast cells sensitized • Dogs—age of clinical onset ranges from clinical signs.
with IgE results in the release of preformed 3 months to several years; most affected CBC/BIOCHEMISTRY/URINALYSIS
and newly synthesized chemical mediators. animals 1–3 years old. Because of the acute onset of disease, no tests
• Anaphylactic reactions may be localized • Cats—age of clinical onset ranges from reliably predict individual susceptibility.
(atopy) or systemic (anaphylactic shock). 6 months to 2 years.
• Anaphylaxis not mediated by IgE is OTHER LABORATORY TESTS
Predominant Sex • In heartworm-endemic areas, a positive
designated an anaphylactoid (nonimmunologic)
• Dogs—atopy more common in females, heartworm test may indicate a worm embolus
reaction and will not be discussed; however,
no predilection for acute anaphylaxis. as a cause for anaphylaxis.
the treatment is the same for either reaction.
• Cats—no reported sex predilection. • If ascites is present, abdominocentesis may
PATHOPHYSIOLOGY reveal hemoperitoneum.
• First exposure of the patient to a particular
SIGNS
• Intradermal skin testing to identify allergens.
antigen (allergen) causes a humoral response General Comments
• Radioallergosorbent test to quantify the
and results in production of IgE, which binds • Initial clinical signs vary depending on the
concentration of serum IgE specific for a
to the surface of mast cells. The patient is then route of exposure to the inciting antigen particular antigen.
considered to be sensitized to that antigen. (allergen).
• Second exposure to the antigen results in • Shock—a severe anaphylactic reaction IMAGING
cross-linking of two or more IgE molecules attributable to cardiovascular collapse and • Radiographic findings—if hemoperitoneum
on the cell surface, resulting in mast cell impaired oxygen delivery. is present, ascites may be apparent in abdominal
degranulation and activation. Release of mast • May be localized to the site of exposure, but radiographs.
cell granules initiates an anaphylactic reaction. may progress to a systemic reaction. • Ultrasonographic findings—may show
• Major mast cell–derived mediators include presence of edema in the gall bladder wall
Historical Findings (“halo sign”) or peritoneal effusion.
histamine, eosinophilic chemotactic factor,
• Onset of signs usually within minutes,
arachidonic acid and metabolites (e.g., DIAGNOSTIC PROCEDURES
history of exposure to insects or medications.
prostaglandins, leukotrienes, and thromboxanes), Limited, because a severely allergic animal can
• Dogs—pruritus, urticaria, vomiting,
platelet-activating factor, and proteases. develop an anaphylactic reaction when
defecation, urination, collapse if severe.
Release of these mediators causes an exposed to even small quantities of antigen.
• Cats—intense pruritus about the head,
inflammatory response characterized by
dyspnea, salivation, vomiting, collapse if PATHOLOGIC FINDINGS
increased vascular permeability, smooth
severe. • Lesions vary, depending on severity of
muscle contraction, inflammatory cell influx,
and tissue damage. Physical Examination Findings reaction, from localized cutaneous edema to
• Clinical manifestations depend on the route • Localized cutaneous edema and erythemia severe pulmonary edema (in cats) and visceral
of antigen exposure, the dose of antigen, and at the site of exposure, macropapular rash. pooling of blood (in dogs).
the level and specificity of the IgE response. • Dyspnea, cyanosis, respiratory wheezes. • Other nonspecific findings vary and are
• Tachycardia, hypotension (poor pulses), characteristic of shock.
SYSTEMS AFFECTED • Nonspecific characteristics of localized
• Gastrointestinal—salivation, vomiting, and
pale or muddy mucous membranes in
animals with shock. reactions include edema, vasculitis, and
diarrhea. thromboembolism.
• Conjunctivitis, lacrimation.
• Cardiovascular—hypotension, cardiac
• Painful abdomen, hepatomegaly (dogs).
arrhythmias, shock.
• Hyperexcitability possible in early stages,
• Respiratory—dyspnea, cyanosis/hypoxemia.
• Skin/exocrine—pruritus, urticaria, and edema.
altered mentation from hypoperfusion in
• Hepatobiliary (dogs)—portal hypertension,
systemic anaphylaxis.
TREATMENT
vasoconstriction, ascites. CAUSES
Virtually any agent; those commonly APPROPRIATE HEALTH CARE
GENETICS In an acutely affected animal, the reaction is
Familial basis reported for type I hypersensi reported include venoms (bees, wasps and
hornets, fire ants, etc.), blood-based products considered a medical emergency requiring
tivity reaction in dogs. hospitalization and intensive care.
(including antivenom and other animal-
INCIDENCE/PREVALENCE derived products), vaccines, medications, NURSING CARE
• Localized type I hypersensitivity reactions and foods. Elimination of inciting antigen, if possible.
not uncommon.
• Systemic type I hypersensitivity reactions rare.
RISK FACTORS Systemic Anaphylaxis
Previous exposure (sensitization) increases • Goal—emergency life support through the
GEOGRAPHIC DISTRIBUTION the chance of the animal developing a maintenance of an open airway, treating
None reaction. circulatory collapse, and reestablishing
physiologic parameters.
(continued) Anaphylaxis A
• Administer fluids (isotonic crystalloids and/ • Bronchodilators—aminophylline (10 mg/ PREVENTION/AVOIDANCE

or colloids) intravenously to counteract kg IM or slowly IV) in severely dyspneic If inciting antigen (allergen) can be identified,
hypotension; in severely affected animals, patients; albuterol inhalers (90 μg/actuation, eliminate or reduce exposure.
pressor agents (e.g., pinephrine) may be via inhalation). POSSIBLE COMPLICATIONS
necessary to support blood pressure. • Oxygen should be administered to
None
• In coagulopathic animals, transfusion with hypoxemic patients, either by mask or a
fresh frozen plasma or red blood cell– cage with an elevated oxygen content EXPECTED COURSE
containing products may be indicated. (targeting a 40% fraction of inspired AND PROGNOSIS
Localized Anaphylaxis oxygen [FiO2]). • If localized reaction is treated early, prognosis
• Norepinephrine (0.5–3 μg/kg/min IV). is good.
Goal—limit the reaction and prevent
progression to a systemic reaction. Localized Anaphylaxis • Some patients with systemic anaphylaxis
• Antihistamines—diphenhydramine that respond initially can have a recurrence of
ACTIVITY shock, usually within 12 hours of initial
N/A hydrochloride (0.5–1.0 mg/kg IV/IM/PO);
famotidine (0.5–1.0 mg/kg IV); ranitidine presentation.
DIET (0.5–2.5 mg/kg IV). • If the animal is in shock on presentation,
If a food-based allergen is suspected • Prednisolone (1–2 mg/kg PO). prognosis is guarded.
(uncommon), avoid foods associated with • If shock develops, initiate treatment for a
hypersensitivity reaction. systemic anaphylaxis.
CLIENT EDUCATION CONTRAINDICATIONS
• Discuss the unpredictable nature of the None
disease.
MISCELLANEOUS
• Discuss the need to recognize that the PRECAUTIONS ASSOCIATED CONDITIONS
animal has an allergic condition that may Localized reaction can develop into systemic None
require immediate medical care. reaction.
AGE-RELATED FACTORS
SURGICAL CONSIDERATIONS POSSIBLE INTERACTIONS None
None N/A
ZOONOTIC POTENTIAL
ALTERNATIVE DRUG(S) None
N/A
N/A
MEDICATIONS SEE ALSO
DRUG(S) OF CHOICE Shock, hypovolemic.
FOLLOW-UP ABBREVIATIONS
Systemic Anaphylaxis
• Epinephrine hydrochloride (5–10 μg/kg
PATIENT MONITORING • FiO2 = fraction of inspired oxygen.
• Closely monitor hospitalized patients for • Ig = immunoglobulin.
[0.005–0.01 mg/kg] IV/IM).
• Corticosteroids—dexamethasone sodium
24–48 hours. Suggested Reading
• In patients with systemic anaphylaxis,
phosphate (0.1–0.5 mg/kg IV), methylpredni- Shmuel DL, Cortes Y. Anaphylaxis in dogs
solone sodium succinate (30 mg/kg IV). monitoring should focus on normalization and cats. J Vet Emerg Crit Care 2013,
• Isotonic crystalloid fluids (20–30 mL/kg IV
and monitoring of blood pressure, heart rate 23(4):377–394.
over 15–20 minutes, followed by reassessment and rhythm, urine output, coagulation status, Author Paul W. Snyder
and additional boluses if necessary, targeting a and oxygenation. Consulting Editor Melinda S. Camus
maximum of 90 mL/kg in dogs and 60 mL/kg • If patients have continued fluid loss (e.g.,
in cats) to treat hypotension and relative due to diarrhea or vomiting), fluid admini-
hypovolemia. stration rates should be adjusted accordingly. Client Education Handout
• Atropine (0.02–0.04 mg/kg IV) to treat available online
symptomatic bradycardia.
A Anemia of Chronic Kidney Disease
• High blood urea nitrogen • Dosage—0.8–1.0 μg/kg SC once weekly
(BUN) : creatinine ratio may predict until PCV reaches low end of target, then
concurrent GI bleeding. decrease to q2-4 weeks as needed to maintain
BASICS target; check PCV first to avoid overtreatment.
OVERVIEW • Serum iron—normal or variably low. • If PCV exceeds target, discontinue until
• Progressive decrease in packed cell volume • Transferrin saturation—normal or variably upper target range is achieved, then increase
(PCV), red blood cell (RBC) count, and low (<20%). dosing interval.
hemoglobin, and hypoplasia of erythroid • Feline leukemia virus (FeLV), feline • Iron dextran (5–10 mg/kg IM) should be
elements of bone marrow are predictable immunodeficiency virus (FIV), mycoplasma, administered as needed to normalize serum
features of chronic kidney disease (CKD). or rickettsial testing to exclude infection- iron and transferrin saturation before initiating
• Anemia is normocytic, normochromic, induced myelodyscrasia. and during EPO treatment; injectable iron
nonregenerative, and proportional to stage of • Serum EPO—inappropriately normal or more effective than oral preparations.
CKD; underlying cause of anemia is low. • r-HuEPO—original synthetic erythropoiesis-
multifactorial. stimulating protein, replica of human EPO
• Gastrointestinal (GI) blood loss, reduced IMAGING (Epogen® and Procrit®); higher potential for
RBC survival, deficiencies in iron and/or • Small, irregular kidneys with loss or anti-r-HuEPO antibody production and pure
folate, cytokines, and inflammatory mediators disruption of renal architecture often seen. red cell aplasia (PRCA); use no longer
may be involved; however, primary cause of • Less commonly enlarged, polycystic, recommended,
anemia in CKD is inadequate production of hydronephrotic, infiltrative.
Anabolic Steroids
erythropoietin (EPO) by the kidneys. DIAGNOSTIC PROCEDURES Not indicated.
• EPO is hormone that regulates bone Bone marrow cytology—erythroid hypo-
marrow RBC generation and is produced in plasia; myeloid : erythroid ratio normal or
peritubular interstitial cells in response to high; stainable iron normal or low.
decreased tissue oxygen.
SIGNALMENT FOLLOW-UP
Any patient with advanced CKD—juvenile PATIENT MONITORING
or acquired. • PCV and blood pressure.
TREATMENT
SIGNS • Stabilize azotemia in patients with uremic • Iron and transferrin saturation—at 1, 3,
• Anemia contributes to anorexia, weight crisis. and 6 months, then semiannually.
loss, fatigue, lethargy, depression, weakness, • Ensure adequate nutrition. • Discontinue EPO if patient develops
and behavior changes characterizing CKD. • Stabilize any metabolic derangement (e.g., evidence of polycythemia, local or systemic
• Pallor. acidosis) that could contribute to shortened sensitivity, PRCA, or refractory hypertension.
• Tachypnea. RBC lifespan. POSSIBLE COMPLICATIONS
• Tachycardia. • Minimize micronutrient deficiencies that
• Systolic murmur. EPO Related
could reduce RBC production. • Development of polycythemia, seizures,
CAUSES & RISK FACTORS • Identify and manage GI bleeding.
hypertension, iron depletion, injection pain,
• All inherited, congenital, and acquired • Parenteral iron supplementation if needed.
and mucocutaneous reactions.
forms of CKD. • Correct systemic hypertension.
• Development of PRCA during epoetin alfa
• Exacerbated by iron deficiency, inflammatory treatment suggests formation of anti-r-
or neoplastic disease, GI bleeding, hemolysis, HuEPO antibodies, which neutralize r-HuEPO
and myeloproliferative disorders. and native EPO, causing severe anemia in
20–30% of animals; often reversible with
MEDICATIONS cessation of treatment.
DRUG(S) OF CHOICE • Development of anti-r-HuEPO antibodies
Blood Transfusion occurs in <10% of patients receiving
DIAGNOSIS • Short-term, rapid correction needed if darbepoetin alfa.
• Signs associated with production of
DIFFERENTIAL DIAGNOSIS hypoxic distress (typically PCV ≤15%)—give
• Anemia of chronic infectious, inflammatory, compatible packed RBCs. anti-r-HuEPO antibodies include decreasing
or neoplastic disease; myeloproliferative • May transfuse intermittently for prolonged PCV, erythroid hypoplasia, reticulocyte count
disease; chronic blood loss; aplastic anemia; management, although compatibility issues nearing zero, and myeloid : erythroid ratio ≥8.
are likely to occur. • EPO replacements should be used cautiously
endocrine disease; drug reaction; chronic
immune-mediated, toxic, viral, rickettsial, or • Preferred treatment is EPO support for or withheld if hypertension or iron deficiency
parasitic anemia; hemodilution. progressive or symptomatic anemia. develops; treatment can be reinstituted once
• Regenerative anemia excludes diagnosis of
hypertension or iron deficiency is corrected.
EPO Replacement
anemia of CKD. • Darbepoetin alfa (Aranesp®)—an analogue Transfusion Related
• Incompatibility reaction.
CBC/BIOCHEMISTRY/URINALYSIS of recombinant human EPO (r-HuEPO)
with prolonged half-life and sustained effects; • Circulatory or iron overload.
• Normocytic, normochromic, hypoprolif-
very effective with less tendency for antibody • Systemic hypertension.
erative anemia.
induction; should be used preferentially to • Transmissible infection.
• Reticulocytes—low corrected indices and
absolute counts (≤10,000/μL). epoetin alfa. EXPECTED COURSE AND PROGNOSIS
• Typically, IRIS stage 3 or greater CKD. • Target PCV—dogs, 30–35%; cats, 30%. • Correction of anemia increases appetite,
activity, and quality of life.
(continued) Anemia of Chronic Kidney Disease A
• Use of EPO replacement agents requires • FIV = feline immunodeficiency virus. Cowgill LD, James KM, Lew JK, et al. Use of
careful assessment of risks and benefits. • GI = gastrointestinal. recombinant human erythropoietin for
• Short-term prognosis depends on severity • PCV = packed cell volume. management of anemia in dogs and cats
of CKD. • PRCA = pure red cell aplasia. with renal failure. J Am Vet Med Assoc
• Long-term prognosis is guarded to poor • RBC = red blood cell. 1998, 212:521–528.
because of underlying CKD. • r-HuEPO = recombinant human Fiocchi EH, Cowgill LD, Brown DC, et al.
erythropoietin. The use of Darbepoetin to stimulate
Suggested Reading erythropoiesis in the treatment of anemia of
Chalhoub S, Langston C, Eatroff A. Anemia of chronic kidney disease in dogs. J Vet Intern
renal disease: what it is, what to do, and what’s Med 2017, 31:476–485.
MISCELLANEOUS new. J Feline Med Surg 2011, 13:629–640. Authors Sheri Ross and Cedric P. Dufayet
Chalhoub S, Langston C, Farrely J. The use Consulting Editor J.D. Foster
ABBREVIATIONS
of Darbepoetin to stimulate erythropoiesis Acknowledgment The authors and book
• BUN = blood urea nitrogen.
in anemia of chronic kidney disease. J Vet editors acknowledge the prior contribution of
• CKD = chronic kidney disease.
Intern Med 2012; 26:363–369. Ilaria Lippi.
• EPO = erythropoietin.
A Anemia, Aplastic
Other Drugs
• Antibiotics to treat secondary infections if
fever and neutropenia present. • Whole or
BASICS DIAGNOSIS component blood transfusion if indicated.
OVERVIEW DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS/POSSIBLE
• A disorder of hematopoietic precursor cells Causes of pancytopenia with normal to INTERACTIONS
characterized by replacement of normal bone increased bone marrow cellularity (e.g., N/A
marrow with adipose tissue. There is decreased myelodysplastic syndromes, leukemias,
production of granulocytes, erythrocytes, and myelofibrosis).
platelets, resulting in pancytopenia in the CBC/BIOCHEMISTRY/URINALYSIS
peripheral blood. The disease is sometimes • Leukopenia characterized by neutropenia
also referred to as aplastic pancytopenia. • In with or without lymphopenia. • Normocytic,
FOLLOW-UP
the acute form, neutropenia and thrombo normochromic, nonregenerative anemia. PATIENT MONITORING
cytopenia predominate because of the shorter • Thrombocytopenia. • Daily physical examination. • CBC every
life spans of these cells; in the chronic form, 3–5 days. • Repeat bone marrow evaluation
nonregenerative anemia also occurs. In both OTHER LABORATORY TESTS
if necessary.
forms, the bone marrow exhibits variable • Immunologic tests for infectious
degrees of panhypoplasia. • Precipitating diseases, e.g., serologic titers, ELISA, PREVENTION/AVOIDANCE
causes can include infectious diseases, drug or immunofluorescent antibody (IFA). • Castration of cryptorchid males (to prevent
toxin exposure, and starvation; immune- • PCR for infectious agents. • Positive development of Sertoli or interstitial cell
mediated mechanisms are often suspected. tests for antierythrocyte antibodies tumors). • Vaccination for infectious diseases.
• Hemic/lymphatic/immune systems (Coombs’ test) and/or antinuclear antibody • Frequent monitoring of CBC in cancer
affected. (ANA) may indicate immune-mediated patients receiving chemotherapy or radiation.
mechanisms. POSSIBLE COMPLICATIONS
SIGNALMENT
IMAGING • Sepsis. • Hemorrhage.
Dogs and cats, no apparent breed or sex
predilection. In one study, the mean age of N/A EXPECTED COURSE AND PROGNOSIS
nine affected dogs was 3 years. DIAGNOSTIC PROCEDURES • Guarded to poor. • Recovery of hemato-
• Bone marrow aspiration—frequently an poiesis may take weeks to months, if it occurs
SIGNS inadequate or fatty sample is obtained at all. • Spontaneous recovery occasionally
• Acute form—fever, petechial because of decreased hematopoietic tissue occurs, especially in younger animals.
hemorrhages, epistaxis, hematuria, melena; and replacement by adipocytes. • Bone
i.e., signs due to neutropenia and thrombo- marrow core biopsy—permits an evaluation
cytopenia. • Chronic form—pale mucous of architecture and reveals hypoplasia
membranes, weakness, lethargy; i.e., signs of cell lines and replacement by adipose
due to anemia, in addition to signs observed MISCELLANEOUS
tissue.
in acute forms. SEE ALSO
CAUSES & RISK FACTORS Pancytopenia.
Often not identified. ABBREVIATIONS
Infectious Agents TREATMENT • ANA = antinuclear antibody.
• Feline leukemia virus (FeLV), feline Supportive treatment, antibiotics, blood • FeLV = feline leukemia virus.
immunodeficiency virus (FIV). • Canine and component therapy, as dictated by clinical • FIV = feline immunodeficiency virus.
feline parvovirus. • Rickettsial organisms condition and results of infectious disease • IFA = immunofluorescent antibody (test).
(e.g., Ehrlichia spp.) testing. • NSAID = nonsteroidal anti-inflammatory
drug.
Drugs and Chemicals • rhG-CSF = recombinant human granulocyte
• Estrogen (exogenous administration, Sertoli colony-stimulating factor.
and interstitial cell tumors). • Methimazole
(cats). • Chemotherapeutic drugs, including MEDICATIONS Suggested Reading
Brazzell JL, Weiss DJ. A retrospective study of
azathioprine, cyclophosphamide, cytosine DRUG(S) OF CHOICE aplastic pancytopenia in the dog: 9 cases
arabinoside, doxorubicin, vinblastine, and • Cyclosporine A—10–25 mg/kg PO q12h (1996–2003). Vet Clin Path 2006,
hydroxyurea. • Antibiotics, including (dogs), 4–5 mg/kg PO q12h (cats). 35:413–417.
trimethoprim–sulfadiazine, cephalosporins, • Mycophenolate mofetil—10 mg/kg PO/IV Weiss DJ. Aplastic anemia. In: Weiss DJ,
and chloramphenicol. • Griseofulvin. q12h. • Recombinant hematopoietic growth Wardrop KJ, eds., Schalm’s Veterinary
• Nonsteroidal anti-inflammatory drugs factors, e.g., recombinant human granulocyte Hematology, 6th ed. Ames, IA: Blackwell,
(NSAIDs), including phenylbutazone and colony-stimulating factor (rhG-CSF) 5 μg/ 2010, pp. 256–260.
meclofenamic acid. • Fenbendazole, kg/day SC. • Androgen and corticosteroid Author R. Darren Wood
albendazole. • Captopril. • Quinidine. administration have been largely unsuccessful. Consulting Editor Melinda S. Camus
• Thiacetarsamide. • Ionizing radiation.
• Mycotoxins (cats).
Anemia, Heinz Body A
CBC/BIOCHEMISTRY/URINALYSIS Alternative Drug(s)

• Diagnosis of Heinz body anemia requires Use of dietary antioxidants (e.g., bioflavo-
regenerative anemia, evidence of hemolytic noids) is controversial, but may help prevent
BASICS process, presence of Heinz bodies in peripheral further formation of Heinz bodies.
OVERVIEW blood, and elimination of other causes of CONTRAINDICATIONS/POSSIBLE
• Heinz bodies occur in red blood cells (RBCs) hemolysis or blood loss. • Regenerative
anemia; severity depends on dose and INTERACTIONS
following damage from chemical or dietary Administration of methylene blue to treat
oxidants, can cause hemolytic anemia. • When duration of oxidant exposure. • Hb
concentration and mean corpuscular methemoglobinemia may exacerbate Heinz
oxidants overwhelm protective reductive body formation.
pathways in RBCs, denaturation of hemoglobin hemoglobin concentration (MCHC) may be
(Hb) causes precipitation and attachment to falsely increased due to Heinz body
cell membrane. • RBCs with Heinz bodies are interference with measurement. • Heinz
removed by splenic macrophages, and bodies on routinely stained blood smear
occasionally undergo intravascular lysis, appear as small, nonstaining to pale red,
forming ghost cells. • The spleen may round inclusions that may protrude from FOLLOW-UP
occasionally remove Heinz bodies, resulting in RBC surface. • Single, small (<0.5 μm) PATIENT MONITORING
spherocytes. • Cats more susceptible to Heinz Heinz bodies may be found in cats without Serial CBCs and review of blood smears to
body formation because have less reductive anemia, but large or multiple Heinz bodies in assess RBC regeneration and disappearance of
enzymatic capacity and closed splenic anemic cat suggest hemolytic anemia. • Dogs Heinz bodies.
circulation, preventing macrophages from may have concurrent eccentrocytosis.
removing Heinz bodies. • Healthy cats may • Hyperbilirubinemia, bilirubinuria, hemo-
Counsel clients about identifying and
have low numbers of Heinz bodies without globinemia, and hemoglobinuria possible
preventing exposure to oxidant compounds.
anemia. • Heinz bodies reported in patients with intravascular hemolysis.
with hyperthyroidism, lymphoma, and diabetes POSSIBLE COMPLICATIONS
mellitus. • Heinz bodies may be accompanied Without proper treatment and removal of
• New methylene blue stains Heinz bodies
by methemoglobinemia (Hb containing Fe3+) oxidant, condition can be fatal.
blue, making them easy to identify and quantify
and/or eccentrocytes (indicating oxidative on a blood smear. • Measure methemoglobin EXPECTED COURSE AND PROGNOSIS
damage to RBC membranes). or perform spot test if blood is dark or chocolate- Prognosis is good with removal of oxidant
SIGNALMENT colored. • Serum zinc concentration. and supportive care once hemolytic crisis
No species, sex, breed, or age disposition. is over.
IMAGING
SIGNS Abdominal radiographs may reveal metallic
foreign bodies contributing to zinc toxicity.
Historical Findings
• Oxidant exposure. • Sudden onset of DIAGNOSTIC PROCEDURES
weakness, lethargy, or anorexia secondary to N/A MISCELLANEOUS
anemia. • Signs related to underlying disease SEE ALSO
if present. • Acetaminophen (APAP) Toxicosis.
Physical Examination Findings • Methemoglobinemia.
• Pale, occasionally icteric mucous membranes, • Zinc Toxicosis.
dark or chocolate-colored if methemoglobine- TREATMENT
• Immediate identification and removal of ABBREVIATIONS
mia. • Tachypnea, tachycardia. • Hb = hemoglobin.
oxidant may be sufficient, though often takes
CAUSES & RISK FACTORS several days after exposure for severity of • MCHC = mean corpuscular hemoglobin
• Dietary—onions (raw, cooked, dehydrated, anemia to reach nadir. • Treatment depends concentration.
powdered), garlic, propylene glycol (cats). on severity and may include IV fluids, RBC • RBC = red blood cell.
• Drugs—acetaminophen, phenacetin (cats), transfusions, oxygen, and restricted activity. Suggested Reading
phenazopyridine (cats), methylene blue, • Endoscopy or surgery to remove metallic Andrews D. Disorders of red blood cells.
vitamin K1 or K3 (dogs), DL-methionine items in gastrointestinal tract. In: Handbook of Small Animal Practice,
(cats), benzocaine, phenylhydrazine (dogs), 5th ed. St. Louis, MO: Saunders, 2008,
propofol (cats). • Miscellaneous—zinc (bolts, pp. 632–635.
pennies minted after 1982, dermatologic or Desnoyers M. Anemias associated with
sun creams), naphthalene (mothballs), skunk oxidative injury. In: Schalm’s Veterinary
musk. MEDICATIONS Hematology, 6th ed. Ames, IA: Blackwell,
2010, pp. 239–245.
DRUG(S) OF CHOICE
Author Melinda S. Camus
• Acetaminophen toxicity in cats—
Consulting Editor Melinda S. Camus
N-acetylcysteine (Mucomyst®) 140 mg/kg PO/
Acknowledgment The author and book
IV, followed by seven additional treatments of
DIAGNOSIS 70 mg/kg PO/IV q8h). • Ascorbic acid
editors acknowledge the prior contribution
of Jennifer S. Thomas.
DIFFERENTIAL DIAGNOSIS (vitamin C) 30 mg/kg PO q6-12h, to reduce
Immune-mediated or hemoparasitic hemolysis. methemoglobin concentrations.
A Anemia, Immune-Mediated
Mean Age and Range Cats
• Dogs—mean age 5–6 years (range: 1–13 • Toxicity (acetaminophen, zinc, onions,
years). • Cats—mean age 2 years (range: garlic). • Severe hypophosphatemia.
BASICS 0.5–9 years). • Congenital feline porphyria. • Increased
DEFINITION Predominant Sex osmotic fragility (Abyssinian, Somali).
Accelerated removal or hemolysis of red blood • Female dogs at higher risk. • Male cats CBC/BIOCHEMISTRY/URINALYSIS
cells (RBCs) due to a type II hypersensitivity overrepresented. • CBC—anemia, normal to high mean
reaction. cell volume (MCV), spherocytosis,
SIGNS
PATHOPHYSIOLOGY polychromasia, ghost cells, leukocytosis with
• Antibodies form against endogenous RBC Historical Findings neutrophilia and left shift, monocytosis;
antigens (primary/nonassociative immune- • Lethargy/weakness/collapse. • Anorexia. anemia nonregenerative in 30% of dogs and
mediated hemolytic anemia [IMHA]), or • Dyspnea, tachypnea. • Vomiting and/or 50% of cats. • Serum biochemistry—
RBC membrane antigens, or antigens diarrhea. • Pigmenturia. • Pica (cats). hyperbilirubinemia, high alanine
altered by infectious organisms, drugs, or Physical Examination Findings aminotransferase (ALT). • Urinalysis—
neoplasia (secondary/associative IMHA). • Pale mucous membranes, tachycardia, hemoglobinuria, bilirubinuria.
• Immunoglobulin deposited on RBC tachypnea. • Splenomegaly/hepatomegaly. OTHER LABORATORY TESTS
membrane, causing either direct intra • Icterus and pigmenturia (hemoglobin or • Positive saline agglutination test. • Direct
vascular hemolysis or accelerated bilirubin). • Fever/lymphadenopathy. antiglobulin (Coombs’) test—positive
extravascular removal by monocyte/ • Systolic heart murmur. • Petechiae, in up to 75% of animals with IMHA.
macrophage system. • Intravascular ecchymoses, or melena (if concurrent • Reticulocytosis if regenerative.
hemolysis occurs when adsorbed antibodies thrombocytopenia or DIC). • Other findings • Thrombocytopenia—60% of dogs.
(especially immunoglobulin [Ig] M) activate possible (e.g., joint pain) when IMHA is • Prolonged activated partial thromboplastin
complement. • Extravascular removal of component of systemic lupus erythematosus time (APTT), ± prolonged prothrombin time
RBCs occurs when RBCs coated with (SLE). • Necrosis of extremities and ear tips (PT), increased fibrin degradation products
antibodies (especially IgG) are engulfed by in cold-type IMHA (rare). (FDP) and d-dimer, decreased antithrombin
splenic macrophages. • RBC agglutination CAUSES & RISK FACTORS in animals with DIC. • Blood smear—
occurs when IgM or high titers of IgG evidence of hematologic parasites.
causes RBC bridging. • Nonregenerative Primary IMHA • Infectious disease testing—especially
IMHA caused by immune-mediated Poorly characterized immune dysregulation. Babesia spp. (serology, PCR), Mycoplasma
destruction of RBC precursors in bone Secondary IMHA hemofelis (PCR), other vector-borne
marrow. • Infectious causes—hemotrophic pathogens.
SYSTEMS AFFECTED Mycoplasma spp., Ehrlichia spp., Anaplasma IMAGING
• Hemic/lymphatic/immune—destruction of phagocytophilum, Anaplasma platys, Babesia Abdominal radiography, ultrasonography—
RBCs, release of proinflammatory mediators, spp., Leishmaniasis, Dirofilaria immitis, hepatomegaly/splenomegaly, neoplasia.
disseminated intravascular coagulation (DIC). feline leukemia virus (FeLV), feline immuno-
• Cardiovascular—signs of anemia, thrombo deficiency virus (FIV), chronic bacterial DIAGNOSTIC PROCEDURES
embolism. • Hepatobiliary—hyperbiliru- infection. • Neoplasia—lymphoma, Bone marrow aspirate to identify nonregen-
binemia, icterus, bilirubinuria; centrilobular lymphoid leukemia, hemangiosarcoma, erative (RBC precursor-directed) IMHA or
necrosis. • Respiratory—tachypnea hemophagic histiocytic sarcoma. • Drugs— myelofibrosis in chronic cases.
(secondary to anemia or inflammation), penicillins, cephalosporins, propylthiouracil, PATHOLOGIC FINDINGS
hypoxemia (pulmonary thromboembolism methimazole, sulfonamides. • SLE. • Hepatosplenomegaly, centrilobular hepatic
[PTE]). • Integument—rare: cold-type IMHA • Neonatal isoerythrolysis. • Dog erythrocyte necrosis. • Splenic and hepatic extramedullary
causes necrosis of extremities and ear tips. antigen (DEA) incompatible blood transfusion. hematopoiesis. • PTE and DIC.
• Vaccination, surgery, hormonal changes, or
GENETICS other stressful events hypothesized as
Cocker spaniels are at increased risk. potential triggers.
Most common hemolytic anemia of dogs, TREATMENT
relatively rare in cats. APPROPRIATE HEALTH CARE
GEOGRAPHIC DISTRIBUTION • Inpatient intensive care during acute
Secondary IMHA may have higher prevalence
DIAGNOSIS hemolytic crisis and if complications
where associated infectious diseases endemic; DIFFERENTIAL DIAGNOSIS such as DIC, PTE, thrombocytopenia,
incidence may vary seasonally. Dogs gastrointestinal (GI) bleeding, or need
• Toxicity (zinc, onions, garlic, naphthalene,
for multiple transfusions occur.
SIGNALMENT • Outpatient when PCV stable, hemolysis
skunk musk). • Snake/spider envenomation
Species controlled, and clinical signs of anemia
(coral snakes, recluse spiders). • Severe
Dog and cat. hypophosphatemia. • Anemia due to resolved.
Breed Predilections hemorrhage, hemoperitoneum. NURSING CARE
• Cocker spaniel, English springer • Microangiopathic anemia due to splenic • Fluid therapy as needed. • Packed RBCs
spaniel, Old English sheepdog, Doberman neoplasia or torsion. • Pyruvate kinase or (or whole blood), fresh frozen plasma (FFP) if
pinscher, collie, bichon frise, miniature phosphofructokinase deficiency. coagulopathic. • Oxygen therapy as needed.
pinscher, Finnish spitz. • Domestic • Monitor for complications.
shorthair cats.
(continued) Anemia, Immune-Mediated A
ACTIVITY cause bone marrow suppression, secondary ZOONOTIC POTENTIAL

Cage rest. infection, pancreatitis (azathioprine), GI upset None
(cyclosporine, azathioprine, mycophenolate SYNONYMS
DIET
mofetil), gingival hyperplasia, papillomatosis • Autoimmune hemolytic anemia.
N/A
(cyclosporine), infertility. • Immune-mediated anemia.
CLIENT EDUCATION ALTERNATIVE DRUG(S)
• IMHA can be fatal and difficult to SEE ALSO
• Chlorambucil—for cats, 0.1–0.2 mg/kg
treat, with guarded prognosis. • Lifelong • Anemia, Regenerative.
PO q24h initially, then q48h. • Human IV • Cold Agglutinin Disease.
maintenance therapy may be needed; immunoglobulin (hIVIG; 0.5–1 g/kg IV) in
side effects may be severe. • Disease may dogs not responding to other therapies. ABBREVIATIONS
recur. • ALT = alanine aminotransferase.
SURGICAL CONSIDERATIONS • APTT = activated partial thromboplastin
Splenectomy can be considered if medical time.
management fails. • DEA = dog erythrocyte antigen.
FOLLOW-UP • DIC = disseminated intravascular
PATIENT MONITORING coagulation.
• Monitor heart rate, respiratory rate, body • FDP = fibrin degradation products.
temperature frequently. • Monitor for • FeLV = feline leukemia virus.
MEDICATIONS adverse reactions to treatment. • If PTE • FFP = fresh frozen plasma.
DRUG(S) OF CHOICE suspected, CT angiography indicated for • FIV = feline immunodeficiency virus.
• Corticosteroids—prednisone 2–3 mg/kg/ diagnosis; oxygenation can be assessed with • GI = gastrointestinal.
day PO; dexamethasone sodium phosphate pulse oximetry or arterial blood gas analysis. • hIVIG = human IV immunoglobulin.
(0.2–0.4 mg/kg IV q24h) can be used in • Initially, check packed cell volume (PCV) • Ig = immunoglobulin.
patients unable to take oral medication. daily until stable, then every 1–2 weeks for 2 • IMHA = immune-mediated hemolytic
• Adjunctive immunosuppressants (if poor months; if still stable, recheck monthly for 6 anemia.
response to corticosteroids or to avoid side months, then 2–4 times/year. • CBC and • MCV = mean cell volume.
effects of prednisone)—cyclosporine 5 mg/kg reticulocyte count at least monthly; if • PCV = packed cell volume.
PO q12h, cats: 0.5–3 mg/kg PO q12h; neutrophil count falls <3,000 cells/μL, • PT = prothrombin time.
mycophenolate mofetil 8–12 mg/kg PO/IV discontinue cytotoxic drugs until count • PTE = pulmonary thromboembolism.
q12h; azathioprine 2 mg/kg PO q24h, can recovers; reinstitute at lower dosage. • RBC = red blood cell.
decrease to 0.5–1.0 mg/kg PO q48h after 3 • SLE = systemic lupus erythematosus.
weeks or if bone marrow suppression occurs, Consider need for vaccination on case-by-case Suggested Reading
monitor for side effects; do not use in cats. basis in dogs with IMHA; measurement of titers Garden OA, Kidd L, Mexas AM, et al.
• Once PCV above 30%, decrease prednisone prior to elective vaccinations may be indicated. ACVIM consensus statement on the
dosage to 1 mg/kg PO q12h; then taper by diagnosis of immune-mediated hemolytic
maximum rate of 25–50% per month over POSSIBLE COMPLICATIONS
anemia in dogs and cats. J Vet Intern Med
3–6-month period, depending upon PCV • Pulmonary/multiorgan thromboembolism.
2019, 33(2):313–334.
and severity of side effects; additional • DIC. • Centrilobular hepatic necrosis and
Kohn B, Weingart C, Eckmann V, et al.
immunosuppressant drugs may be tapered as renal tubular necrosis secondary to hypoxia.
Primary immune-mediated hemolytic
well. • For prevention of thromboembolism • Infection secondary to immunosuppressive
anemia in 19 cats: diagnosis, therapy, and
consider unfractionated heparin 150–300 U/ therapy. • GI ulceration due to high-dose
outcome (1998–2004). J Vet Intern Med
kg SC q6–8h (dose adjusted based on APTT glucocorticoids. • Iatrogenic
2006, 20:159–166.
prolongation or measurement of anti-Xa hyperadrenocorticism.
Swann JW, Garden OA, Fellman CL, et al.
activity) and/or clopidogrel 1–2 mg/kg PO EXPECTED COURSE AND PROGNOSIS ACVIM consensus statement on the
q24h; low molecular weight heparins • Mortality—30–70% (dog), 24% (cat). treatment of immune-mediated hemolytic
(enoxaparin 0.8 mg/kg SC q6–8h or dalteparin • Hyperbilirubinemia >5 mg/dL, autoagglu- anemia in dogs. J Vet Intern Med 2019,
150 U/kg SC q8h) or rivaroxaban (0.5– tination, intravascular hemolysis, severe 33(3):1141–1172.
1.0 mg/kg PO q24h) may be considered in thrombocytopenia, hypoalbuminemia Author Bridget C. Garner
lieu of unfractionated heparin. • Address associated with poorer prognosis. • Response Consulting Editor Melinda S. Camus
underlying cause (secondary IMHA). to treatment may take weeks to months; Acknowledgment The author and book
• Therapeutic plasma exchange/plasmapheresis nonregenerative IMHA may have more editors acknowledge the prior contribution of
may be useful adjunctive therapy. gradual onset than typical IMHA and be J. Catharine R. Scott-Moncrieff.
slower to respond to treatment. Most
CONTRAINDICATIONS
patients receive immunosuppressive
Anticoagulant medications should be used Client Education Handout
therapy for 4–8 months.
cautiously in patients with thrombocytopenia available online
(<40,000 platelets/μL).
PRECAUTIONS
• Prednisone/prednisolone can cause signs of
MISCELLANEOUS
hyperadrenocorticism and may increase risk of
PTE, pancreatitis, diabetes mellitus, secondary ASSOCIATED CONDITIONS
infection, gastric ulcers (consider gastric See above.
protectants). • Immunosuppressive drugs can
A Anemia, Iron-Deficiency
• Reticulocyte indices reticulocyte corpuscular making oral therapy of little value until
hemoglobin concentration mean (CHCMr), partial iron repletion has occurred.
reticulocyte hemoglobin content (CHr), • Oral iron supplementation should continue
BASICS hypochromic reticulocyte RBCs (%HYPOr), 1–2 months, or until resolved.
OVERVIEW and %LowCHr are sensitive for detecting • Ferrous sulfate powder—place in food or
Caused by chronic external blood loss or iron-limited erythropoiesis, but not specific. drinking water, 100–300 mg PO q24h.
iron-limited erythropoiesis. • Lab tests indicating iron-limited erythro- • Ferrous gluconate—325 mg PO q24h.
poiesis do not differentiate true from CONTRAINDICATIONS/POSSIBLE
SIGNALMENT
functional iron deficiency. Clinical findings of
• Fairly common in adult dogs, rare in adult INTERACTIONS
inflammatory disease are required to differentiate
cats. • Oral iron is associated with unexplained
iron-limited erythropoiesis. Inflammatory
• Transient neonatal iron-deficiency anemia death in kittens and should be avoided.
disease and true iron deficiency may also
may occur at 5–10 weeks of age in kittens. • Kittens undergo spontaneous iron
occur concurrently.
SIGNS • Thrombocytosis due to chronic blood loss.
replection beginning at 5–6 weeks of age.
• Signs of anemia (e.g., lethargy, weakness, • Hypoproteinemia—from blood loss.
tachypnea, pale mucous membranes).
• Cardiovascular—bounding pulses,
• Hypoferremia (serum iron <70 μg/dL) and
tachycardia, systolic heart murmur.
transferrin saturation <15% support diagnosis. FOLLOW-UP
• Gastrointestinal—intermittent melena or
• Serum iron values may be normal during • Monitor CBC every 1–4 weeks, more
hematochezia, diarrhea.
iron repletion if blood loss is intermittent. frequently as needed.
• Integumentary—heavy hematophagous
• Fecal exam for hookworms. • Effective treatment associated with an
parasite burden (e.g., fleas), wounds.
• Fecal examination for occult blood or increase in MCV and reticulocyte volume.
CAUSES & RISK FACTORS melena. • Erythrocyte histogram—effective treatment
• Chronic external blood loss. reduces microcytic subpopulation over time
IMAGING
• Gastrointestinal—hookworms, lymphoma (2–3 months).
Abdominal radiography, ultrasonography—
or other neoplasia, ulceration (related to
abnormalities in gastrointestinal tract causing
medications, [e.g., non-steroidal anti-
blood loss.
inflammatories] or disease [e.g., renal disease]).
• Less common—severe flea infestation, DIAGNOSTIC PROCEDURES
urinary tract hemorrhage. • Bone marrow aspirate, staining with Prussian
• Iatrogenic—blood donor overuse, excessive blue (dogs only) to indicate body iron stores. MISCELLANEOUS
diagnostic blood sampling. • Gastrointestinal endoscopy to identify sites ABBREVIATIONS
• Inappropriate home-cooked diet (low of gastrointestinal blood loss. • CHCMr = mean reticulocyte corpuscular
dietary iron). hemoglobin concentration.
• CHr = reticulocyte hemoglobin content.
• HYPOr = hypochromic reticulocyte
RBCs.
DIAGNOSIS TREATMENT • MCHC = mean cell hemoglobin
• Identify/correct cause of blood loss, treat concentration.
DIFFERENTIAL DIAGNOSIS underlying disease. • MCV = mean cell volume.
• Any cause of anemia, especially • Administer iron until hematologic features • MCVr = mean reticulocyte volume.
hemorrhage. of iron deficiency resolve. • PCV = packed cell volume.
• Microcytic anemia in portosystemic shunt • If severe anemia (i.e., PCV <15%), • RBC = red blood cell.
disease may or may not be due to iron deficiency. transfusion may be required, using whole • RDW = red cell distribution width.
• Anemia of inflammatory disease—iron- blood (10–30 mL/kg IV) or packed RBC Suggested Reading
limited erythropoiesis. (10 mL/kg IV). Fry MM, Kirk CA. Reticulocyte indices in a
CBC/BIOCHEMISTRY/URINALYSIS canine model of nutritional iron deficiency.
• Packed cell volume (PCV) variably Vet Clin Pathol 2006, 35:172–181.
decreased; may be within reference interval. Radakovich LB, Santangelo KS, Olver CS.
• Regenerative or nonregenerative anemia. Reticulocyte hemoglobin content (CHr)
• Microcytosis—low normal or low mean cell MEDICATIONS does not differentiate true from functional
volume (MCV), low mean reticulocyte DRUG(S) OF CHOICE iron deficiency in dogs. Vet Clin Pathol
volume (MCVr), anisocytosis, widened 2015, 44:511–518.
Parenteral Iron Supplementation Schaefer DM, Stokol T. The utility of
erythrocyte histogram, or increased red cell
• Iron therapy should begin with injectable iron. reticulocyte indices in distinguishing iron
distribution width (RDW). Decreased mean
• Iron dextran—10–20 mg/kg IM (dog), deficiency anemia from anemia of inflam-
cell hemoglobin concentration (MCHC) not
sensitive or specific. 50 mg IM (cat), followed by oral supple- matory disease, portosystemic shunting, and
• Red blood cell (RBC) morphology—
mentation. breed-associated microcytosis in dogs. Vet
microcytosis, hypochromia, keratocyte Oral Iron Supplementation—Dogs Only Clin Pathol 2015, 44:109–119.
(indicating oxidative damage), and schistocyte • Animals with severe iron deficiency may Authors Glade Weiser and Melinda S. Camus
formation. have impaired intestinal iron absorption, Consulting Editor Melinda S. Camus
Anemia, Nonregenerative A
• Signs reflecting primary condition—oral

ulcerations (CKD), cachexia, organomegaly,
GI or nervous system abnormalities (cobalamin
BASICS malabsorption, lead poisoning), symmetric DIAGNOSIS
DEFINITION alopecia (hypothyroidism, hyperestrogenism). DIFFERENTIAL DIAGNOSIS
Low red blood cell (RBC) mass due to low Regenerative anemia can initially appear
CAUSES
erythroid production, without evidence of nonregenerative (especially in cats); exacerba-
polychromasia or reticulocytosis in peripheral Nonregenerative Anemia without Other tion of chronic condition may produce
blood. Anemia with reticulocyte counts <80 × Cytopenias appearance of acute onset.
103/μL (dog) or 60 × 103/μL (cat) considered • Anemia of inflammatory disease (AID)—
nonregenerative. Caused by altered erythro- most common cause of mild nonregenerative CBC/BIOCHEMISTRY/URINALYSIS
poiesis or bone marrow injury. anemia (also anemia of chronic disease). CBC and Blood Smear
PATHOPHYSIOLOGY • CKD—decreased EPO production by • Packed cell volume (PCV), hematocrit
• Alterations in erythropoiesis include kidneys; uremic toxins shorten RBC lifespan (HCT), RBC count, and hemoglobin
deficient erythropoietin (EPO) production, and impair bone marrow response to EPO. concentration low.
nutritional deficiency, cytokine-mediated iron • Chronic liver disease—shortened RBC • Anemia usually normocytic, normochromic,
sequestration, disturbed metabolism in or survival due to changes in RBC membrane with normal mean cell volume (MCV) and
destruction of RBC precursors (e.g., immune- lipids; functional iron deficiency due to mean corpuscular hemoglobin concentration
mediated). decreased transferrin synthesis and impaired (MCHC); occasionally severe vitamin B12
• Bone marrow injury usually caused by mobilization of hepatic iron. deficiency; characteristic large erythrocytes
toxins, infection, or infiltrative processes. • Hypothyroidism, hypoadrenocorticism— can be masked by presence of misshapen and/
• Anemia of inflammatory disease results thyroid hormones and cortisol stimulate or small RBCs, giving normal MCV but
from increased hepcidin production and erythropoiesis. widened red cell distribution.
release of cytokines from white blood cells • Immune-mediated destruction of precursors— • Macrocytosis (high MCV)—without
(WBCs) leading to iron sequestration and spectrum from nonregenerative IMHA to polychromasia suggests nuclear maturation
decreased iron absorption. Low serum iron pure red cell aplasia. defect; seen in cats with FeLV.
and transferrin, increased ferritin, decreased • Microcytosis suggests maturation complete;
Nutritional or Mineral Deficiency/Toxicity
EPO production, shortened RBC lifespan iron deficiency most common cause; in late
• Iron deficiency—usually due to chronic
result in anemia. stages concurrent hypochromasia common
external blood loss. in dogs.
SYSTEMS AFFECTED • Copper deficiency—secondary to chelation
• Characteristic RBC morphologies—
• Cardiovascular—shock from decreased therapy. schistocytes ± hypochromic RBCs common
systemic oxygen delivery. • Cobalamin (vitamin B12) and/or folate
with iron deficiency; acanthocytes with liver
• Hemic/lymph/immune. deficiency—rare; can be caused by dietary disease; target cells with iron deficiency, liver
• Hepatobiliary—from hypoxic injury. insufficiency, malabsorption, congenital disease, hypothyroidism.
defects in cobalamin absorption. • Inflammatory leukogram supports AID.
SIGNALMENT
• Disruption of precursor metabolism—
• Nonregenerative immune-mediated • Thrombocytosis common in iron deficiency.
chronic lead toxicity and possibly high • High number of nucleated red blood cells
hemolytic anemia (IMHA)—middle-aged
concentrations of aluminum, arsenic, and (NRBCs) without polychromasia or
female dogs and male cats <3 years old.
cadmium inhibit heme synthesis; cadmium disproportionate to degree of anemia and
• Congenital cobalamin malabsorption
and lead cause renal toxicity, impaired EPO polychromasia seen with lead toxicity,
reported in Komondor, beagle, giant
production. extramedullary hematopoiesis (EMH), heat
schnauzer, Australian shepherd, border collie,
shar-pei. Nonregenerative Anemia with Other stroke, bone marrow injury.
Cytopenias • RBC or WBC precursors in peripheral
SIGNS
• Toxicities—drugs or chemicals, hormones blood without orderly progression to more
General Comments (e.g., estrogen). mature forms suggest myelodysplasia or
Usually secondary; signs associated with • Infections—feline leukemia virus (FeLV), myeloproliferative disease.
primary disease often precede signs of feline immunodeficiency virus (FIV), • Cobalamin malabsorption characterized by
anemia. ehrlichiosis, babesiosis, Cytauxzoon felis, normocytic anemia, neutropenia, hypersegmented
Historical Findings parvovirus (occasionally just erythroid line neutrophils; megaloblastic changes possible
• Lethargy, exercise intolerance, inappetence, affected). in marrow.
pica. • Infiltrative processes—myelodysplasia, • RBC inclusions may be visible on blood smear
• Other findings reflect primary condition— myeloproliferative and lymphoproliferative with some infectious diseases (e.g., C. felis).
polyuria/polydipsia (chronic kidney disease diseases, histiocytic sarcoma, metastatic Serum Biochemistry and Urinalysis
[CKD]), old paint exposure (lead poisoning), neoplasia, myelofibrosis, osteosclerosis. • CKD—azotemia with isosthenuria, possible
estrogen therapy or feminization in male proteinuria, hypokalemia.
RISK FACTORS
dogs, failure to thrive (hereditary cobalamin • Liver disease—elevated alanine aminotrans-
• CKD.
malabsorption). ferase (ALT) ± alkaline phosphatase (ALP)
• Inflammatory or chronic disease.
Physical Examination Findings • Multicat household/cattery (infectious activities, elevated total bilirubin, bile acids,
• Pallor, heart murmur (due to anemia), disease risk). ammonia concentrations, hypoglycemia,
tachycardia, tachypnea, shock. • Daily exposure to toxins (e.g., old homes with hypoalbuminemia.
• Digital rectal examination may reveal lead paint, environmental pollution). • Hypothyroidism—hypercholesterolemia
melena if gastrointestinal (GI) blood loss. (>500 mg/dL).
A Anemia, Nonregenerative (continued)
• Hypoadrenocorticism—hyponatremia,
hyperkalemia, lymphocytosis, eosinophilia.
OTHER LABORATORY TESTS TREATMENT MISCELLANEOUS
• Reticulocyte count. • Anemia usually resolves with resolution of
• Spherocytosis, autoagglutination, or PREGNANCY/FERTILITY/BREEDING
underlying disease. Pregnant animals have mildly low PCV.
positive Coombs’ test supports immune- • Conditions associated with severe anemia
mediated destruction of erythroid precursors. or pancytopenia often carry guarded to poor SEE ALSO
• Serum iron profile—with iron deficiency prognosis and may involve long-term • Anemia, Immune-Mediated.
both serum iron and ferritin low, while total treatment with incomplete resolution. • Anemia, Iron-Deficiency.
iron-binding capacity varies; with AID, serum • Mild to moderate anemia (PCV >20%) • Blood Transfusion Reactions.
iron low but serum ferritin high. generally requires no immediate supportive • Shock, Hypovolemic.
• Serum lead—indicated when NRBCs intervention. ABBREVIATIONS
present; >30 μL/dL (0.3 ppm) strongly • Patients with severe anemia (PCV <12–15%) • ACTH = adrenocorticotropic hormone.
supports lead intoxication. require transfusion for stabilization (e.g., • AID = anemia of inflammatory disease.
• Serologic testing—FeLV, FIV in cats; 6–10 mL/kg packed RBCs or 10–20 mL/kg • ALP = alkaline phosphatase.
Ehrlichia canis, Anaplasma phagocytophilia in whole blood). • ALT = alanine aminotransferase.
dogs, particularly if anemia with thrombo- • Determine blood type prior to transfusion • CKD = chronic kidney disease.
cytopenia. (imperative for cats, ideal for dogs). • EMH = extramedullary hematopoiesis.
• Endocrine testing—adrenocorticotropic • If blood volume and tissue perfusion • EPO = erythropoietin.
hormone (ACTH) stimulation test or compromised by concurrent blood loss or • FeLV = feline leukemia virus.
thyroid function testing to rule out shock, administer isotonic crystalloid solution • FIV = feline immunodeficiency virus.
hypoadrenocorticism or hypothyroidism, (10–20 mL/kg IV, repeat as necessary) or • GI = gastrointestinal.
respectively. isotonic colloid solution (2–5 mL/kg IV, to • HCT = hematocrit.
• Serum cobalamin, homocysteine, methyl- total 20 mL/kg/24h). See Shock, Hypovolemic. • IMHA = immune-mediated hemolytic
malonic acid ± urine methylmalonic acid • With chronic anemia, animals may be anemia.
concentrations—to diagnose hereditary hypervolemic, and volume overload may be a • MCHC = mean corpuscular hemoglobin
cobalamin malabsorption. concern during blood and fluid therapy. concentration.
DIAGNOSTIC PROCEDURES • MCV = mean cell volume.
Cytologic Examination of Bone Marrow • NRBC = nucleated red blood cell.
• PCV = packed cell volume.
and Core Biopsy
• RBC = red blood cell.
• Cytologic examination of bone marrow
aspirate indicated in all patients unless
MEDICATIONS • WBC = white blood cell.
primary cause apparent, and bone marrow DRUG(S) OF CHOICE Suggested Reading
core biopsy useful in evaluation of bone • EPO or darbopoetin in patients with Hohenhaus, AE, Winzelberg SE.
marrow architecture and overall cellularity. anemia of CKD. Nonregenerative anemia. In: Ettinger SJ,
• Erythroid hypoplasia or aplasia confirms • Iron supplementation in patients with iron Feldman EC, eds., Textbook of Veterinary
pure red cell aplasia; erythroid hyperplasia deficiency anemia. Internal Medicine: Diseases of the Dog and
suggests IMHA; increased erythrophagia or • Immunosuppressive drugs. Cat, 8th ed. St. Louis, MO: Elsevier
incomplete maturation sequence suggests • May supplement with cobalamin (vitamin Saunders, 2017, pp. 838–843.
immune-mediated or toxic injury to specific B12) at rate of 100–200 mg PO q24h (dogs) Rebar AH, MacWilliams PS, Feldman BF,
maturation stage, or incomplete recovery or 50–100 mg PO q24h (cats); parenteral et al. Erythrocytes: overview, morphology,
from previous injury. cyanocobalamin administration (50 μg/kg quantity. In: A Guide to Hematology in
• Expanded erythron and high numbers of SC/IM weekly to monthly) needed in dogs Dogs and Cats, Jackson, WY: Teton
metarubricytes suggest iron deficiency; with inherited cobalamin malabsorption. NewMedia. http://www.ivis.org/advances/
absence of iron stores supportive in dogs, but PRECAUTIONS Rebar/Chap4/chapter.asp?LA=1
not cats. Monitor for transfusion reactions. Author Joyce S. Knoll
• Disorderly maturation and atypical cellular Consulting Editor Melinda S. Camus
morphology suggest myelodysplastic syndrome.
• Hypercellular marrow with increased blast
cells consistent with hematopoietic neoplasia;
immunophenotyping can identify affected FOLLOW-UP
cell line.
• Hypocellular sample can suggest aplastic PATIENT MONITORING
marrow or myelofibrosis. • With severe anemia—serial physical
examinations, PCV/CBC, blood smear
Abdominal Radiographs, Ultrasound examination every 1–2 days.
As part of evaluation for underlying causes • Stable animals with chronic or slowly
such as neoplasia, CKD, or GI blood loss. improving disease course—reevaluate every
1–2 weeks.
Anemia, Nuclear Maturation Defects (Anemia, Megaloblastic) A
• Differentiation based on distinctive CBC • In animals with hypocobalaminemia,

and bone marrow findings. supplement with vitamin B12 (0.25–1 mg
• In cats, FeLV infection is primary cyanocobalamin SC weekly to monthly or
BASICS differential. hydroxycobalamin IM every few months;
OVERVIEW CBC/BIOCHEMISTRY/URINALYSIS oral may be effective in some patients—
• Nonregenerative anemia characterized by • Classically, anemia macrocytic and
dogs, 250–1000 μg/day PO; cats,
impaired DNA synthesis in red blood cell normochromic, but often normocytic. 250 μg/day PO).
(RBC) precursors (nuclear : cytoplasmic • Large, fully hemoglobinized RBC; few to CONTRAINDICATIONS/POSSIBLE
asynchrony). many nucleated RBC precursors, no INTERACTIONS
• Affected RBC precursors fail to divide polychromasia. Avoid drugs known to cause megaloblastic
normally and thus are larger than corresponding • In dogs, mild to moderate anemia; may anemia in patients whose condition results
normal precursors; their nuclei are deficient see neutropenia with hypersegmented from other causes.
in chromatin with open and stippled neutrophils.
appearance; these giant precursors with • In cats, mild to marked anemia.
atypical nuclei are known as megaloblasts. • In cats with FeLV, anemia may occur with
Hemoglobin content in these precursors is myelodysplastic syndrome or leukemia.
normal. • In dogs with inherited cobalamin
• Asynchronous changes most prominent in malabsorption, can see proteinuria and FOLLOW-UP
RBC precursors, but white blood cell (WBC) variable biochemistry derangements. • Monitor response to treatment by CBC
and platelet precursors similarly affected. (weekly to every few months).
OTHER LABORATORY TESTS • Closely monitor FeLV-positive cats for
SIGNALMENT • FeLV in blood and bone marrow. disease progression.
• Cats—often associated with feline leukemia • Genetic tests for dogs with inherited • Prognosis depends on underlying cause;
virus (FeLV) infection. cobalamin malabsorption (available at in FeLV-positive cats, prognosis poor; with
• Dogs—usually acquired, but may be University of Pennsylvania, PennGen). drug-induced anemia, prognosis good if
inherited. • Serum cobalamin. drug discontinued; inherited cobalamin
• Breed predilection for inherited cobalamin • Methylmalonic acid (MMA) in serum or malabsorption has good prognosis, with
malabsorption—giant schnauzers, Australian urine (increase caused by inhibited cobalamin- lifelong cobalamin supplementation.
shepherds, Komondorok, and beagles— dependent enzyme).
present as young as 8–12 weeks; border
collies as young adults. IMAGING
• Familial macrocytosis and megaloblastic N/A
change in toy/miniature poodles. DIAGNOSTIC PROCEDURES
SIGNS
MISCELLANEOUS
Bone Marrow Biopsy
• In dogs, anemia often not symptomatic. • In dogs, usually hyperplastic; may be SEE ALSO
For cobalamin deficiency, clinical signs hypocellular with hemosiderosis. • Anemia, Nonregenerative.
include gastrointestinal signs and failure to • In cats, may be hypo- or hyperplastic. • Feline Leukemia Virus (FeLV) Infection.
thrive. Affected poodles usually not anemic. • Maturation arrest with nuclear : cytoplasmic ABBREVIATIONS
• In cats, anemia may be mild to marked, if asynchrony possible in all cell lines. • FeLV = feline leukemia virus.
FeLV positive. • Megaloblastic RBC precursors. • FIV = feline immunodeficiency virus.
CAUSES & RISK FACTORS • Macrophage hyperplasia with phagocytosis • MMA = methylmalonic acid.
• Infectious—FeLV most common cause in of nucleated RBCs. • RBC = red blood cell.
cats. Feline immunodeficiency virus (FIV) • WBC = white blood cell.
infrequently reported as causative agent. Suggested Reading
• Nutritional—folic acid and cobalamin Harvey JW. Veterinary Hematology: A
deficiencies, primarily in dogs with inherited Diagnostic Guide and Color Atlas. Beijing:
cobalamin malabsorption (uncommon with TREATMENT Elsevier, 2012, pp. 273–275.
other causes of cobalamin deficiency). • Anemia often mild and does not need
Rebar AH, MacWilliams PS, Feldman BF,
• Toxic—many drugs such as immuno specific therapy. FeLV-positive cats may
et al. A Guide to Hematology in Dogs and
modulators, chemotherapeutic agents, require blood transfusion for stabilization.
Cats. Jackson, WY: Teton NewMedia, 2002,
anticonvulsants, antibiotics. • Target underlying cause and address
pp. 57–58.
• Congenital—toy/miniature poodles. concurrent signs.
Weiss, DJ. Congenital dyserythropoiesis. In:
Weiss DJ, Wardrop KJ, eds., Schalm’s
Veterinary Hematology, 6th ed. Ames, IA:
Wiley-Blackwell, 2010, pp. 196–198.
Author Lisa S. Kelly
DIAGNOSIS MEDICATIONS Consulting Editor Melinda S. Camus
DIFFERENTIAL DIAGNOSIS DRUG(S) OF CHOICE Acknowledgment The author and book
• In dogs, all other mild to moderate • In animals with drug toxicity, discontinue editors acknowledge the prior contribution of
nonregenerative anemias, including anemia of offending drug. Alan H. Rebar.
inflammatory disease and lead poisoning.
A Anemia, Regenerative
SIGNS
• Pallor.
• Weakness, exercise intolerance, collapse.
BASICS • Anorexia. DIAGNOSIS
DEFINITION • Possible heart murmur, tachycardia, DIFFERENTIAL DIAGNOSIS
Decreased circulating red blood cell (RBC) bounding pulses (unless hemorrhage is Differentiated from nonregenerative anemia
mass (indicated by low packed cell volume present). by a reticulocyte count above the regenerative
[PCV] or hematocrit [HCT], hemoglobin, • Possible jaundice and hemoglobinuria. threshold for that species, generally above
and total RBC count) accompanied by • Petechiae, epistaxis, melena suggest blood 80 × 103/μL in dogs and 60 × 103/μL in cats.
appropriate, compensatory increase in RBC loss due to vasculitis or thrombopathia.
LABORATORY FINDINGS
production by the bone marrow. • Hematomas or cavity bleeds suggest
coagulation factor inhibition or deficiency. Disorders That May Alter Laboratory
PATHOPHYSIOLOGY • Clinical signs depend on degree of anemia Results
• Caused by blood loss or hemolysis.
and rapidity of onset. • Lipemia can cause mild in vitro hemolysis,
• Hemolysis—caused by intrinsic RBC
• Rapid loss of 15–25% blood volume or without appreciable anemia, and may falsely
defects (e.g., congenital RBC membrane acute hemolysis results in shock. elevate mean corpuscular hemoglobin
defects or enzyme deficiencies) or extrinsic • With chronic anemia, compensatory concentration (MCHC).
factors (e.g., RBC parasites, oxidative injury, increases in heart rate, and eventually heart • Autoagglutination may falsely decrease
hemolysins, osmotic changes, immune- size, occur; hemoglobin can drop to as low as
mediated RBC destruction, hemophagocytic RBC count and increase MCV.
50% of minimum normal value without overt • Exercise and excitement can increase RBC
neoplasia, heat stroke, and severe hypophos- signs of shock or decreased oxygen delivery.
phatemia). count, PCV, and reticulocyte count through
CAUSES splenic contraction, masking severity of anemia.
SYSTEMS AFFECTED • Immune-mediated (IMHA). Valid If Run in Human Laboratory?
• Cardiovascular—murmurs with marked
• RBC toxins—snake venom and bee stings • Dogs—yes.
anemia; tachycardia. may cause RBC hemolysis; oxidants can cause • Cats—yes, if hematology instrument uses
• Hemic/lymph/immune—erythroid
Heinz body formation. species-specific parameters; instruments
hyperplasia in bone marrow; splenic • Erythrocyte parasites—cats: Mycoplasma designed for analysis of human specimens
extramedullary hematopoiesis (EMH). spp., Cytauxzoon felis (may be nonregenerative); may undercount small feline RBCs and be
• Hepatic—decreased oxygen delivery causes
dogs: Mycoplasma haemocanis, Babesia spp. unable to distinguish between erythrocytes
centrilobular degeneration of liver. • Mechanical RBC fragmentation—caused and platelets.
• Renal—severe intravascular hemolysis rarely
by vasculitis, thromboembolic disease, or
leads to pigmentary nephropathy and acute disease of any vascular organ; rare cause of CBC/BIOCHEMISTRY/URINALYSIS
renal failure. significant anemia unless accompanied by • PCV, RBC count, and hemoglobin are
• Musculoskeletal—progressive osteoclerosis below the reference interval.
hemorrhage.
seen in pyruvate kinase (PK)-deficient dogs. • Inherited RBC abnormalities: • Total protein is often low with blood loss
SIGNALMENT ∘∘ PK deficiency. anemia and may be the only sign with acute
• PK deficiency—basenji, beagle, cairn ∘∘ Phosphofructokinase (PFK) deficiency. blood loss due to splenic contraction, which
terrier, Chihuahua, dachshund, Labrador ∘∘ Increased RBC osmotic fragility (unknown elevates the circulating RBC count.
retriever, labradoodle, miniature poodle, pug, RBC defect), leads to recurrent severe anemia • RBC indices vary depending on the cause of
West Highland white terrier, and American and splenomegaly. anemia and degree of regenerative response:
Eskimo; Somali, Abyssinian, domestic ∘∘ Feline congenital porphyria—enzyme ∘∘ Mean cell volume (MCV) is normal to
shorthair cats. deficiency in heme synthetic pathway leads to high with regeneration, but low with iron
• PFK deficiency—Australian labradoodle, accumulation of heme precursors, hemolytic deficiency.
English springer spaniel, American cocker anemia, and brown-red discoloration of teeth ∘∘ MCHC is normal to low in most
spaniel, cockapoo, English cocker spaniel, and bones; Siamese tend to have severe patients, low with iron deficiency, and
whippet, wachtelhund, and mixed breed dogs hemolytic anemia, while domestic shorthair artificially high with hemolysis.
with spaniel parentage. cats have less severe autosomal dominant trait • Specific RBC morphologies may suggest
• Marked RBC osmotic fragility—English that causes mild anemia. the cause of hemolysis:
springer spaniel; Abyssinian, Somali, Siamese, • Hypophosphatemia—severe hypophospha ∘∘ Marked spherocytosis suggests immune-
and domestic shorthair cats. temia impairs adenosine triphosphate (ATP) mediated disease in dogs.
• Feline congenital porphyria—Siamese and production, leading to increased erythrocyte ∘∘ Heinz bodies or eccentrocytes suggest
domestic shorthair cats. fragility and hemolysis; seen with refeeding oxidant injury.
• Heritable coagulopathies (e.g., factor VIII syndrome and insulin administration. ∘∘ Numerous schistocytes suggest
or IX deficiency), von Willebrand disease. • Blood loss: microangiopathy.
• Immune-mediated hemolytic anemia ∘∘ Trauma. ∘∘ RBC parasites may be found on or within
(IMHA)—middle-aged female dogs, especially ∘∘ Bleeding neoplasms. RBC.
American cocker spaniels, English springer ∘∘ Coagulopathies (e.g., warfarin toxicity, • Agglutinated RBCs indicate anemia is
spaniels, Irish setters, Old English sheepdogs, hemophilia, thrombocytopenia). immune mediated; distinguish autoaggluti
poodles, and Shetland sheepdogs. ∘∘ Blood-feeding parasites. nation from rouleaux by saline agglutination
• Hemophagocytic histiocytic sarcoma— ∘∘ Gastrointestinal ulcers. test (see Appendix X).
Bernese mountain dog, Rottweiler, golden • Hemolysis is often accompanied by an
retriever, and flat-coated retriever. inflammatory leukogram.
(continued) Anemia, Regenerative A
• Animals with IMHA often have a • RBC replacement (packed RBCs or whole • During and following transfusion, monitor
concurrent thrombocytopenia, while iron blood) indicated with severe anemia (PCV for transfusion reactions (see Blood Transfusion
deficiency is often accompanied by thrombo- <15%) or rapid drops (>15%) in HCT. Reactions).
cytosis. Initial dosage depends on product selected;
• Hyperbilirubinemia and bilirubinuria 1 mL/kg of packed RBCs will raise the HCT
accompany marked hemolysis; hemoglobin- by approximately 1%; 3 mL/kg of whole
emia and hemoglobinuria can be seen blood will raise the PCV by approximately
following intravascular hemolysis. 1%, both depending on the PCV of the MISCELLANEOUS
OTHER LABORATORY TESTS donor product. SEE ALSO
• In cases of hemorrhage or coagulopathy, • Anemia, Heinz Body.
• Reticulocytosis may be absent in the first
3–5 days after onset of blood loss or hemolysis. fresh whole blood will also provide volume • Anemia, Immune-Mediated.
• Direct antiglobulin test (Coombs’ test) is
expansion and coagulation factor replacement, • Anemia, Iron-Deficiency.
indicated when IMHA is suspected, in the compared to packed RBCs. • Babesiosis.
absence of agglutination; a positive test is • Determine blood type prior to transfusion, • Bartonellosis.
confirmatory. especially in cats (who have preexisting • Blood Transfusion Reactions.
• The rapid osmotic fragility test detects
autoantibodies to opposite blood types). • Cytauxzoonosis.
erythrocyte membrane defects and can help Cross-match against donor blood if blood • Phosphofructokinase Deficiency.
to discriminate hemolytic from nonhemolytic typing reagents not available, or if patient • Pyruvate Kinase Deficiency.
conditions. requires second transfusion more than 4 days • Von Willebrand Disease.
• Coagulation testing may be indicated in
after first transfusion. • Zinc Toxicosis.
cases of blood loss. • Animals with chronic blood loss or
ABBREVIATIONS
• PCR is more sensitive for diagnosis of
hemolytic anemias are generally normovolemic
• ATP = adenosine triphosphate.
Babesia and hemotropic Mycoplasma than with increased cardiac output, therefore
• EMH = extramedullary hematopoiesis.
microscopic blood smear exam; can attention should be paid to transfusion
• HCT = hematocrit.
differentiate between species. volumes and rates.
• IMHA = immune-mediated hemolytic
• PCR for PK deficiency. anemia.
• PCR for PFK deficiency. • MCHC = mean corpuscular hemoglobin
DIAGNOSTIC PROCEDURES concentration.
Fine-needle aspiration and cytologic exam of MEDICATIONS • MCV = mean cell volume.
abnormal spleen, lung, or lymph nodes may • PCV = packed cell volume.
DRUG(S) OF CHOICE
help to diagnose hemophagocytic histiocytic • PFK = phosphofructokinase.
• Iron may benefit animals with chronic
sarcoma. • PK = pyruvate kinase.
blood-loss anemia (see Anemia, Iron-
Deficiency). • RBC = red blood cell.
• Hemolytic anemias—varies with cause of Suggested Reading
hemolysis. Piek C. Immune-mediated haemolytic
anemia and other regenerative anemias.
TREATMENT In: Ettinger SJ, Feldman EC, eds.,
• Emergency if anemia is severe or has Textbook of Veterinary Internal Medicine:
developed rapidly. Diseases of the Dog and Cat, 8th ed. St.
• Massive hemorrhage leads to hypovolemic
FOLLOW-UP Louis, MO: Elsevier Saunders, 2017,
shock and decreased oxygen delivery to PATIENT MONITORING pp. 829–837.
tissues; acute hemolysis also leads to decreased • Initially, monitor PCV and morphologic Rebar AH, MacWilliams PS, Feldman BF,
oxygen content in the blood. features of RBCs on a blood smear every 24 et al. Erythrocytes: overview, morphology,
• In cases of massive hemorrhage, crystalloid hours to evaluate effectiveness of treatment quantity. In: A Guide to Hematology in
fluids can rapidly correct hypovolemia and and bone marrow responsiveness; polychrom- Dogs and Cats, Jackson, WY: Teton
restore circulation, but RBC replacement asia may be seen as regenerative response NewMedia. http://www.ivis.org/advances/
(and resolving the source of hemorrhage) is starts. Rebar/Chap4/chapter.asp?LA=1
necessary for definitive therapy. • As regeneration becomes apparent, recheck Author Joyce S. Knoll
every 3–5 days. Consulting Editor Melinda S. Camus
A Anisocoria
SIGNALMENT • Distinguish between neurologic and ocular
• Dog and cat. causes.
• All ages affected.
BASICS CBC/BIOCHEMISTRY/URINALYSIS
• No gender predisposition.
N/A
DEFINITION SIGNS
Asymmetric pupils. Unequal pupil size. OTHER LABORATORY TESTS
N/A
PATHOPHYSIOLOGY CAUSES
• Disruption of sympathetic (causing miosis) IMAGING
Neurologic • See Table 1.
or parasympathetic (causing mydriasis)
See Table 1. • Ultrasound—use to identify ocular,
innervation to the eye.
• Ocular disease—numerous causes. Ocular retrobulbar, or jugular groove lesions.
See Table 2. • MRI—use to identify CNS lesions.
SYSTEMS AFFECTED • CT—use to identify tympanic bulla lesions.
• Nervous. RISK FACTORS
• Ophthalmic. N/A DIAGNOSTIC PROCEDURES
• See Table 1.
GENETICS • Cerebral spinal fluid (CSF) tap—evaluate
None for CNS inflammation/infection.
INCIDENCE/PREVALENCE • ERG—evaluate retinal function.
DIAGNOSIS • Pharmacologic testing—see Figure 1;
Common
DIFFERENTIAL DIAGNOSIS postganglionic lesions cause denervation
GEOGRAPHIC DISTRIBUTION • Must determine which pupil is abnormal— supersensitivity, resulting in more rapid
None see Figure 1 and Tables 1 and 2. constriction or dilation with application of
Table 1
Neurologic lesions causing anisocoria.
Sign Pupillary Light Lesion Localization Differential List Diagnostic Test

Reflex (PLR)
Mydriasis—inability to No direct, present Ipsilateral optic nerve/chiasm Neuritis, neoplasia MRI/CSF tap/ERG
constrict the pupil indirect Encephalitis, neoplasia, trauma, MRI/CSF tap
retrobulbar mass Ultrasound orbit
Miosis—inability to Present Brainstem Encephalitis, neoplasia, trauma MRI/CSF tap
dilate the pupil C1-T2 myelopathy or C6-T3 Trauma, myelitis, neoplasia, intervertebral MRI/myelogram/CT
brachial plexus disc herniation (IVDH; rare) MRI/ultrasound
Vagosympathetic trunk Jugular venipuncture, trauma MRI/CT
Tympanic bulla Otitis media, neoplasia, trauma MRI
Trigeminal nerve Neuritis, neoplasia
Table 2
Ocular diseases causing anisocoria.
Lesion Associated Signs Causes

Anterior uveitis Miosis, aqueous flare, corneal edema, conjunctival hyperemia Infectious/inflammatory disease, trauma, neoplasia
Glaucoma Mydriasis Primary glaucoma, secondary glaucoma
Sluggish/absent PLR, increased intraocular pressure, corneal edema
Neoplasm Miosis/mydriasis, iris color change Lymphoma, melanoma
Posterior synechia Variable pupil shape, sluggish/absent PLR, anterior uveitis Secondary to anterior uveitis
Iris atrophy Variable pupil shape, iridal thinning, sluggish PLR Old age change
Iris hypoplasia Sluggish/absent PLR, irregular pupil margin, other ocular abnormalities Congenital
Pharmacologic Mydriasis Atropine
blockade Absent direct/consensual PLR
Normal vision
Spastic pupil syndrome Miosis, normal vision Feline leukemia virus
(continued) Anisocoria A
Anisocoria
Miotic pupil in the dark Pupils dilated and equal in dark
Intact direct and indirect PLR Incomplete or absent PLR
PARASYMPATHETIC
SYMPATHETIC DYSFUNCTION DYSFUNCTION
1% hydroxyamphetamine
1% phenylephrine
0.5% 0.2%
Dilation physostigmine pilocarpine
No dilation
Delayed No Rapid No Rapid No
No dilation Dilation constriction constriction constriction constriction Constriction constriction
Normal eye
or pre Post
ganglionic Normal Preganglionic Iris atrophy Normal
Post ganglionic
lesion ganglionic
lesion Evaluate for
Normal Evaluate for lesion of the
Lesion in brainstem iris,
the iris or or
Abnormal eye oculomotor
Evaluate for oculomotor oculomotor nerve or
central nerve nerve brainstem
(spinal cord Evaluate disease
or brain), Evaluate central,
tympanic
brachial brachial plexus,
bulla or
plexus or vagosympathetic
trigeminal
vago- trunk, bulla and
nerve
sympathetic trigeminal nerve
trunk lesion
Figure 1.
pharmacologic agents. Differentiation of SEE ALSO

pre- or postganglionic lesions can be • Anterior Uveitis—Cats.
difficult if based solely on pharmacologic • Anterior Uveitis—Dogs.
testing. FOLLOW-UP • Glaucoma.
PATHOLOGIC FINDINGS PATIENT MONITORING • Horner’s Syndrome.
Dependent on underlying diagnosis. N/A • Iris Atrophy.
• Optic Neuritis and Papilledema.
N/A ABBREVIATIONS
POSSIBLE COMPLICATIONS • CSF = cerebrospinal fluid.
N/A • IVDH = intervertebral disc herniation.
TREATMENT • PLR = pupillary light reflex.
Dependent on underlying disease. EXPECTED COURSE AND PROGNOSIS
Depends on underlying disease. Suggested Reading
Cottrill NB. Differential diagnosis of
anisocoria. In: Bonagura J, Twedt D, eds.,
Kirk’s Current Veterinary Therapy, 14th ed.
St. Louis, MO: Saunders, 2009, pp.
MEDICATIONS MISCELLANEOUS 1168–1174.
DRUG(S) OF CHOICE ASSOCIATED CONDITIONS Lorenz MD, Kornegay JN. Blindness, anisocoria
Dependent on underlying disease. N/A and abnormal eye movements. In: Lorenz
MD, Kornegay, JN, eds., Handbook of
CONTRAINDICATIONS AGE-RELATED FACTORS Veterinary Neurology, 4th ed. St. Louis,
N/A N/A MO: Saunders, 2004, pp. 283–295.
PRECAUTIONS ZOONOTIC POTENTIAL Author Heidi L. Barnes Heller
N/A N/A Consulting Editor Kathern E. Myrna
POSSIBLE INTERACTIONS PREGNANCY/FERTILITY/BREEDING
N/A N/A
ALTERNATIVE DRUG(S) SYNONYMS available online
N/A None
A Anorexia
SYSTEMS AFFECTED • Animals lacking a sense of smell (anosmia)
All body systems. often show a lack of interest in food.
BASICS GENETICS CBC/BIOCHEMISTRY/URINALYSIS
N/A • Abnormalities vary with different
DEFINITION underlying diseases. • May be normal.
Anorexia is the lack or loss of appetite for INCIDENCE/PREVALENCE
food. Hyporexia is a reduction in appetite, Unknown OTHER LABORATORY TESTS
while dysrexia is a change in appetite or lack • Additional diagnostic tests may be necessary
of consistent appetite. Anorexia results in N/A to investigate specific diseases suggested by
decreased food intake, which then leads to history, physical examination, and preliminary
SIGNALMENT tests. • Heartworm serology, tick serology,
weight loss, dehydration, nutritional
deficiencies, and/or sarcopenia. Species retrovirus serology, thyroid level, and histologic/
Dog and cat. cytologic examination of tissue/cell samples
PATHOPHYSIOLOGY may be required to make a definitive diagnosis.
• The control of appetite is a complex Breed Predilections • A baseline cortisol or an adrenocorticotropic
interaction between the central nervous system, N/A hormone (ACTH) stimulation test to rule out
the environment, and the gastrointestinal (GI) Mean Age and Range hypoadrenocorticism is warranted even when
tract. • The hypothalamus and brainstem N/A there are no significant laboratory changes.
contain feeding‐regulatory neurons that act as
input stations for sensory and metabolic signals. Predominant Sex IMAGING
These cell populations project to several brain N/A • Thoracic and abdominal imaging
regions and interconnect extensively. • Sensory SIGNS (radiographs and ultrasound) studies are often
signals that affect appetite include the odor, included in the minimum database to detect
Historical Findings anatomic or functional abnormalities.
taste, texture, and temperature of food, as well
• Refusal to eat is a common presenting • Videofluoroscopy and endoscopy may be
as gastric and duodenal distention. • Metabolic
complaint and causes owners significant indicated to specifically evaluate pharyngeal,
signals for hunger and satiety include a variety
distress. • Weight loss may be reported. esophageal, and GI function and appearance.
of peptides and hormones released during the
fasting and fed states, as well as plasma Physical Examination Findings DIAGNOSTIC PROCEDURES
concentrations of glucose, amino acids, and • Findings vary depending on the underlying • Perform a nutritional assessment; collect a
fatty acids. • Insulin, glucagon, somatostatin, cause. • Low body condition score and thorough dietary history, evaluate food intake,
cholecystokinin, peptide tyrosine tyrosine muscle wasting may be evident depending and obtain body and muscle condition scores.
(PYY), and pancreatic peptide decrease hunger upon the duration of decreased food intake. • Elicit a thorough history regarding the
centrally. • Leptin, produced primarily by • Pseudoanorectic patients commonly display patient’s environment, changes in routine,
adipocytes, acts on specific hypothalamic halitosis, excessive drooling, difficulty with people, or other pets, to help identify
receptors to increase metabolism and decrease prehension or mastication, and odynophagia potential sources of psychologic stress.
appetite. • Neuropeptide Y, released from the (painful swallowing). • Observe the patient’s interest in food and
GI tract after food restriction, induces hunger CAUSES ability to prehend, masticate, and swallow
and decreases energy expenditure. • Ghrelin, food. • Complete a thorough physical
produced by the stomach, is a prokinetic and Anorexia/Hyporexia/Dysrexia examination including ophthalmic,
increases appetite; it decreases leptin and • Possible manifestations of a myriad of systemic oropharyngeal, neurologic, orthopedic,
increases neuropeptide Y production. disorders. • Psychological—food aversion, stress, thoracic, abdominal, and rectal exam to
• Serotonin is an important central mediator alterations in routine or environment. • Pain. determine the presence of disease.
and acts via a serotonergic tract that passes near • Toxicities and drug adverse effects. • GI and
pancreatic diseases. • Acid‐base disorders. PATHOLOGIC FINDINGS
the ventromedial hypothalamic nuclei (satiety
• Organ failure—e.g., cardiac, renal, hepatic. Dependent on underlying disease.
center). • Dopaminergic tracts in the hypo-
thalamus help regulate food intake and are • Endocrine and metabolic diseases. • Neoplasia.
closely associated with the lateral hypothalamic • Infectious diseases. • Immune‐mediated
nuclei (feeding center). • Environmental diseases. • Respiratory diseases. • Musculo
factors including the location and timing of skeletal diseases. • Neurologic diseases. TREATMENT
meals, as well as learned behaviors and circadian • Miscellaneous (e.g., motion sickness, high
environmental temperature). APPROPRIATE HEALTH CARE
rhythms, modulate appetite. • Brain lesions • Assisted feeding (enteral and/or parenteral
that affect the hypothalamus can decrease or Pseudoanorexia feeding) should be considered immediately
increase appetite; any disorder that decreases Any disease causing painful or dysfunctional for significantly malnourished patients (≥10%
cerebral arousal will potentially decrease food prehension, mastication, or swallowing. body weight loss, hypoalbuminemia, poor
intake. • Inflammatory and neoplastic diseases body condition score, evidence of muscle
RISK FACTORS
can cause hyporexia by the release of proinflamm- wasting, and/or chronic disease processes). In
N/A
atory cytokines. • The expected upregulation well‐conditioned patients with decreased
of dietary intake in response to increased energy appetite, assisted feeding should be considered
expenditure is frequently absent in patients if food consumption is less than the resting
with neoplastic and advanced cardiac diseases. energy requirement [RER = 70 x (body
• Exogenous and endogenous toxins (e.g., renal DIAGNOSIS weightkg 0.75)] for 3–5 days without trends
and liver failure) cause hyporexia. • Neoplasia, DIFFERENTIAL DIAGNOSIS toward improvement. • Force feeding should
metabolic disorders, pancreatitis, and primary • Pseudoanorexia is a term describing patients be avoided, particularly in cats, considering
GI diseases are associated with hyporexia. who are hungry but are unable to eat due to the association with conditioned food
• Fear, pain, and stress may decrease appetite. disorders causing dysfunction or pain of the aversions.
face, neck, oropharynx, and esophagus.
(continued) Anorexia A
NURSING CARE diazepam should be avoided in cats due to • Breakdown of the intestinal mucosal barrier
• Medications the patient is receiving should be possible idiosyncratic hepatotoxicosis. further compromises debilitated patients.
reviewed for possible side effects leading to • Cyproheptadine (0.2–0.4 mg/kg PO, 10–20
EXPECTED COURSE AND PROGNOSIS
reduced appetite. • Provide comfort and minutes prior to feeding), an antihistamine with Depends on the underlying cause(s).
nutrition to the patient while efforts are directed antiserotonergic properties, has been used as an
at identifying and correcting the underlying appetite stimulant with mixed success.
disease so that more specific treatment can be • Prokinetics such as metoclopramide (0.2–
provided. • Symptomatic therapy includes 0.4 mg/kg SC/PO q8–12h), ranitidine (2 mg/kg
correcting fluid deficits and electrolyte derange- SC/IV/PO q12h), or erythromycin (0.5–1 mg/ MISCELLANEOUS
ments, control of pain and/or nausea, reduction kg PO q8–12h) are useful if anorexia is associated ASSOCIATED CONDITIONS
in environmental stressors, and modification of with ileus. • Antiemetics are useful in decreasing N/A
the diet to improve palatability. nausea or vomiting, but are not appetite
stimulants. Ondansetron (0.5–1.0 mg/kg SC/ AGE‐RELATED FACTORS
ACTIVITY Nutritional support and glucose‐containing
N/A IV/PO q12h) and dolasetron (0.6–1.0 mg/kg
SC/IV/PO q24h) are potent antiemetics as 5‐ fluids may be necessary to treat or prevent
DIET HT3 antagonists. Maropitant is a substance P hypoglycemia in anorectic puppies and kittens.
• Palatability can be improved by adding analogue, which binds neurokinin‐1 receptors in ZOONOTIC POTENTIAL
flavored toppings such as low‐sodium broth, the chemoreceptor trigger zone (CRTZ) and N/A
increasing the moisture, fat, or protein vomiting center, inhibiting vomiting. Cerenia® is
content of the food, and warming the food to PREGNANCY/FERTILITY/BREEDING
maropitant, approved by the FDA for dogs and
body temperature. • When learned food N/A
cats as an antiemetic (dogs: 1 mg/kg SC/IV or
aversion is suspected, food should be removed 2 mg/kg PO q24h; cats: 1 mg/kg SC/IV/PO SYNONYMS
immediately at the first signs of aversion. q24h). • Omega‐3 fatty acids can reduce N/A
CLIENT EDUCATION inflammatory cytokines and have modest benefit SEE ALSO
Depends on specific diagnosis. for appetite. Weight Loss and Cachexia.
SURGICAL CONSIDERATIONS CONTRAINDICATIONS ABBREVIATIONS
N/A Avoid antiemetics and prokinetics if GI • 5‐HT = 5‐hydroxytryptamine (serotonin).
obstruction is present or suspected. • ACTH = adrenocorticotropic hormone.
PRECAUTIONS • CRTZ = chemoreceptor trigger zone.
N/A • GI = gastrointestinal. • MAOI = monoamine
MEDICATIONS oxidase inhibitor. • PYY = peptide tyrosine
POSSIBLE INTERACTIONS
tyrosine. • RER = resting energy requirement.
DRUG(S) OF CHOICE Mirtazapine should not be combined with
• SSRI = selective serotonin reuptake inhibitor.
• Pharmacologic interventions aimed at drugs that interact with or affect serotoninergic
• TCA = tricyclic antidepressant.
improving appetite should not replace diagnostic systems including monoamine oxidase
efforts to identify the specific cause(s) of inhibitors (MAOIs), tricyclic antidepressants INTERNET RESOURCES
decreased appetite. • Mirtazapine antagonizes (TCAs), and selective serotonin reuptake https://entyce.aratana.com/resources/clinical‐
inhibitory, presynaptic, α2‐adrenergic receptors, inhibitors (SSRIs). Ondansetron and dolasetron, references
facilitating release of norepinephrine and as well as metoclopramide, are 5‐HT3 Suggested Reading
serotonin (5‐HT). It is also a 5‐HT2 and 5‐HT3 antagonists, and care should be used with Forman MA. Anorexia. In: Ettinger SJ, Feldman
antagonist on the postsynaptic neuron. combining these drugs with mirtazapine. EC, Côté E, eds. Textbook of Veterinary
Stimulation of 5‐HT1 produces antidepressant ALTERNATIVE DRUG(S) Internal Medicine, 8th ed. St. Louis, MO:
effects, while inhibition of 5‐HT2 and 5‐HT3 N/A Elsevier Saunders, 2017, pp. 97–100.
produces anti‐emetic and appetite‐stimulating Quimby JM, Lunn KF. Mirtazapine as an
effects. Canine dosing is 0.5 mg/kg q24h. appetite stimulant and anti‐emetic in cats
Mirataz® is FDA approved for use in cats, with a with chronic kidney disease: a masked
recommended dose of a 1.5 in. strip applied to placebo‐controlled crossover clinical trial.
the inner pinna once daily for 14 days. FOLLOW‐UP Vet J 2013, 197(3):651–655.
Alternatively, 1.88 mg/cat PO q24–48h (for cats PATIENT MONITORING Schermerhorn T. Gastrointestinal endocrinol-
with chronic kidney disease) can be given to • Body weight, body and muscle condition ogy. In: Ettinger SJ, Feldman EC, Côté E,
stimulate appetite. • Capromorelin is a ghrelin score, and hydration assessment. • Monitor eds., Textbook of Veterinary Internal
receptor agonist that stimulates appetite centrally caloric intake to ensure return of appetite is Medicine, 8th ed. St. Louis, MO: Elsevier
in the hypothalamus. Entyce® is capromorelin, sufficient to meet nutritional needs. Saunders, 2017, pp. 1833–1838.
approved by the FDA for dogs as an appetite PREVENTION/AVOIDANCE Wofford JA, Zollers B, Rhodes L, et al.
stimulant. A trial in healthy laboratory beagles N/A Evaluation of the safety of daily administra-
demonstrated significant increases in food tion of capromorelin in cats. J Vet
consumption and weight compared to placebo, POSSIBLE COMPLICATIONS Pharmacol Ther 2018, 41(2):324–333.
and a clinical field trial in inappetent client‐ • Dehydration, malnutrition, cachexia, and Author Andrea Wang Munk
owned dogs demonstrated increases in appetite sarcopenia are sequelae of prolonged anorexia/ Consulting Editor Mark P. Rondeau
and body weight compared to placebo. Dosing hyporexia/dysrexia; these exacerbate the Acknowledgment The author and book
at 3 mg/kg PO q24h is safe for long‐term underlying disease. • A loss of more than editors acknowledge the prior contribution of
administration. Capromorelin is not approved 25–30% of body protein compromises the Kathryn E. Michel.
for cats, though a safety trial has been published immune system and muscle strength, and death
and clinical trials are underway. • Diazepam results from infection and/or cardiopulmonary
(0.1 mg/kg IV q24h) is a short‐acting appetite failure. • Hepatic lipidosis is a possible Client Education Handout
stimulant with sedative properties. Oral complication of anorexia, particularly in cats. available online
A Antebrachial Growth Deformities
• Congenital agenesis of the radius (cats and • Complete symmetric closure of distal physis—
rarely dogs)—occurs infrequently; results in may note straight limb with a widened radiocarpal
severely bowed antebrachium and carpal or radiohumeral joint space; may note caudal
BASICS subluxation. bow (recurvatum) to radius and ulna.
DEFINITION • Asymmetric closure of medial aspect of
Abnormally shaped antebrachium and distal SIGNALMENT distal radial physis—varus angular deformity;
part of the thoracic limb, and/or malalign- Species occasionally internal torsion and pronation.
ments of the elbow or antebrachiocarpal Dog and cat. • Closure of lateral aspect of distal radial
joints that result from maldevelopment of the physis—valgus angular deformity; external
Breed Predilections
radius or ulna in the growing animal. torsion and supination.
• Skye terrier—recessive inheritable form.
• Closure of proximal radial physis with
PATHOPHYSIOLOGY • Chondrodysplastic and toy breeds (especially
continued ulnar growth—malarticulation of the
• Antebrachium—predisposed to deformities basset hound, dachshund, Lhasa apso, Pekingese,
elbow joint; widened radiohumeral space; and
resulting from growth of one bone after Jack Russell terrier)—may be predisposed to
proximal subluxation of the humeroulnar joint
premature growth cessation or growth elbow malalignment and incongruity.
(increased humerus to anconeal process space).
retardation of the paired bone. • Giant breeds (e.g., Great Dane, wolfhound)—
• Decreased rate of elongation in one bone may be induced by rapid growth owing to CAUSES
behaves as a retarding strap; the growing excessive or unbalanced nutrition, OC, or HOD. • Trauma.
paired bone must twist and curve around the • Developmental basis.
Mean Age and Range
short bone or overgrow at the elbow or • Nutritional basis.
• Traumatic—any time during the active
carpus; causes joint malalignment. growth phase. RISK FACTORS
• Normal growth—bones elongate through the • Elbow malarticulations—during growth; • Thoracic limb trauma.
process of endochondral ossification, which may not be recognized until secondary • Excessive dietary supplementation.
occurs in the physis; physis closure occurs when arthritic changes become severe, occasionally
the germinal cell layer stops producing new at several years of age.
cartilage and the existing cartilage hypertro-
phies, ossifies, and is remodeled into bone. Predominant Sex
• Hereditary—may be a component of N/A
common elbow joint malalignment in many DIAGNOSIS
chondrodysplastic breeds (e.g., basset hound SIGNS DIFFERENTIAL DIAGNOSIS
and Lhasa apso). General Comments • Elbow dysplasia.
• Osteochondrosis (OC) or dietary oversupple- • Longer-limbed dogs—angular deformities • Fragmented medial coronoid process (FMCP).
mentation—possibly associated with retarda- generally more common. • Ununited anconeal process (UAP).
tion of endochondral ossification (retained • Shorter-limbed dogs—tend to develop • Panosteitis.
cartilaginous cores) in giant-breed dogs. more severe joint malalignments. • Flexor tendon contracture.
• Hypertrophic osteodystrophy (HOD)— • Age at time of premature closure—affects • HOD.
juvenile growth syndrome with physeal and relative degree of deformity and joint malarticula- CBC/BIOCHEMISTRY/URINALYSIS
periosteal inflammation that may impede growth. tion; dogs with more growth potential remaining N/A
• Trauma—most common cause; if germinal tend to develop more severe deformity.
cell layer of the physis is damaged, new OTHER LABORATORY TESTS
Historical Findings N/A
cartilage production and bone elongation are
• Traumatic—progressive limb angulation or
stopped. Commonly occurs with injury IMAGING
lameness noticed 3–4 weeks after injury;
(fractures or crushing injuries) involving the • Damage to growth potential of the
owner may not be aware of causative event.
distal ulnar or radial growth plates. physis—commonly cannot be seen at the
• Developmental elbow malalignments—
SYSTEMS AFFECTED insidious onset of lameness in one or both time of trauma; usually 2–4 weeks before
Musculoskeletal thoracic limbs; most apparent after exercise. radiographically apparent.
• Craniocaudal and mediolateral radiographic
GENETICS Physical Examination Findings views—include both entire elbow and carpal
• Skye terriers—reported as a recessive
Premature Distal Ulnar Closure joints; compare with normal contralateral limb.
inheritable trait. • Results in three deformities of the distal • Degree of angular deformities and relative
• Chondrodysplastic breeds (dogs)— shortening—determined by comparing relative
radius—lateral deviation (valgus), cranial
disturbed endochondral ossification results in bowing (procurvatum), and external torsion lengths of radius and ulna within the deformed
asynchronous growth of the paired bone resulting in supination of the manus. pair to the normal contralateral pair.
system, resulting in altered growth, angular • Relative shortening of limb length—if • Degree of torsional deformity—cross-
deformity, and possible elbow malalignment. unilateral can compare to the contralateral sectional imaging and creation of models
INCIDENCE/PREVALENCE normal limb. using stereolithography is most useful for full
• Traumatic—may occur in up to 10% of • Caudolateral subluxation of the radiocarpal appreciation of torsional deformity.
actively growing dogs that sustain injuries of joint and malarticulation of the elbow joint— • Elbow and carpal joints—evaluate for malalign-
the antebrachium; uncommon in cats. may occur; causes lameness and painful joint ment and degenerative change; presence of
• Elbow malalignment syndrome ± angular restriction. degenerative change is associated with less
deformity (chondrodysplastic dog breeds)— optimal outcome following surgical treatment.
Premature Radial Physeal Closure
fairly common and can be bilateral; clinical • Elbow joint—evaluate for associated UAP
• Affected limb—significantly shorter than
abnormality in affected individuals is variable. and FMCP.
the normal contralateral limb.
• Nutritionally induced—incidence decreasing DIAGNOSTIC PROCEDURES
• Severity of lameness—depends on degree of
as nutritional standards are improved. joint malarticulation. N/A
(continued) Antebrachial Growth Deformities A
PATHOLOGIC FINDINGS • Deformity (torsional and angular) correction— EXPECTED COURSE AND PROGNOSIS
Cartilage of abnormal growth plate often may be accomplished with a variety of osteotomy • Best results seen with early diagnosis and
replaced with bone. Angular deformity can techniques; may be stabilized with several surgical treatment—minimizes osteoarthritis.
occur due to retained cartilage core (OC) of different internal or external fixation devices. • Premature ulnar closure—easier to manage
the distal ulnar physis. • Joint malalignment (particularly elbow)— than premature closure of the radial growth
must correct to minimize arthritis develop- plates; prognosis dependent on severity of the
ment (primary cause of lameness); typically deformity, joint congruity, and presence of
performed via dynamic proximal ulnar degenerative joint disease; prognosis worsens
osteotomy (use triceps brachii muscle traction with increasing severity.
TREATMENT and joint pressure) or shortening longer bone • Limb lengthening by distraction osteogenesis—
(radial or ulnar ostectomy). requires extensive postoperative management
• Significant limb length discrepancies—dis- by the veterinarian and owner; high rate of
• Genetic predisposition—do not breed.
traction osteogenesis; osteotomy of the complications.
• Traumatic physeal damage—not seen at
shortened bone is progressively distracted at
time of injury; revealed 2–4 weeks later.
the rate of 1 mm/day with an external fixator
• In young (<6 months) animals, surgical
system to create new bone length.
treatment is generally recommended as soon
as possible following diagnosis; treatment MISCELLANEOUS
may require multiple surgical procedures.
ASSOCIATED CONDITIONS
NURSING CARE • OC.
N/A MEDICATIONS • HOD.
ACTIVITY • UAP.
DRUG(S) OF CHOICE
Exercise restriction—reduces joint malalign- Anti-inflammatory drugs—symptomatic AGE-RELATED FACTORS
ment damage; slows arthritic progression. treatment of osteoarthritis. The younger the patient at the time of
DIET traumatically induced physeal closure, the
CONTRAINDICATIONS
• Decrease nutritional supplementation in more severe the deformity and
Corticosteroids—do not use owing to
giant-breed dogs—slows rapid growth; may malarticulation.
potential systemic side effects and cartilage
reduce incidence. damage seen with long-term use. ZOONOTIC POTENTIAL
• Avoid excess weight—helps control arthritic N/A
pain resulting from joint malalignment and PRECAUTIONS
Nonsteroidal anti-inflammatory drugs PREGNANCY/FERTILITY/BREEDING
overuse.
(NSAIDs)—gastrointestinal irritation or N/A
CLIENT EDUCATION renal/hepatic toxicity may preclude use in SYNONYMS
• Discuss heritability in chondrodysplastic some patients. Radius curvus.
breeds.
• Explain that damage to physeal growth
POSSIBLE INTERACTIONS ABBREVIATIONS
potential is not apparent at time of trauma N/A • FMCP = fragmented medial coronoid
and that the diagnosis is often made 2–4 ALTERNATIVE DRUG(S) process.
weeks following an injury. N/A • HOD = hypertrophic osteodystrophy.
• Discuss the importance of joint malalign- • NSAID = nonsteroidal anti-inflammatory
ment and resultant osteoarthritis as primary drug.
causes of lameness. • OC = osteochondrosis.
• Emphasize that early surgical treatment • UAP = ununited anconeal process.
leads to a better prognosis. FOLLOW-UP Suggested Reading
• Depending on the patient’s age, treatment Fox DB. Radius and ulna. In Johnston SA,
PATIENT MONITORING
may involve multiple procedures. • Postoperative—depends on surgical treatment. Tobias KM, eds. Veterinary Surgery Small
SURGICAL CONSIDERATIONS • Periodic checkups—evaluate arthritic status Animal, 2nd ed. St. Louis, MO: Elsevier
• Premature closure of the distal ulnar physis in and anti-inflammatory therapy. Saunders, 2018, pp. 896–920.
a patient <5–6 months of age (significant Fox DB, Tomlinson JL. Principles of angular
amount of radial growth potential remaining)— limb deformity correction. In Johnston SA,
• Selective breeding of susceptible breeds.
treated with partial ulnar ostectomy; valgus Tobias KM, eds. Veterinary Surgery Small
• Avoid dietary oversupplementation in
deformities ≤25° may improve and may not Animal, 2nd ed. St. Louis, MO: Elsevier
rapidly growing giant-breed dogs.
require additional surgery; young patients and Saunders, 2018, pp. 762–774.
those with more severe deformities often require POSSIBLE COMPLICATIONS Author Spencer A. Johnston
a second definitive correction after maturity. Routinely seen with various osteotomy Consulting Editor Mathieu M. Glassman
• Radial or ulnar physeal closure in a mature fixation techniques (e.g., infection, nonunion
patient (limited or no growth potential) of osteotomy, fixator pin tract inflammation,
requires definitive deformity correction, joint undercorrection). Client Education Handout
realignment, or both. available online
A Anterior Uveitis—Cats
chamber. • Ciliary flush—injection of deep blepharospasm, as the latter is an active
perilimbal anterior ciliary vessels. • Deep process; minor conjunctival hyperemia may
corneal vascularization—circumcorneal be noted with Horner’s, but cornea and
BASICS distribution (brush border). • Miosis or anterior chamber are clear; clinical signs
DEFINITION resistance to pharmacologic dilation. • Iridal resolve with topical ophthalmic 1–10%
• Inflammation of the anterior uveal tissues, swelling—may be generalized or nodular. phenylephrine.
including iris (iritis), ciliary body (cyclitis), • Reduced intraocular pressure (IOP) CBC/BIOCHEMISTRY/URINALYSIS
or both (iridocyclitis). • May be associated consistent with anterior uveitis, but not • CBC—normal, or reflects underlying disease.
with concurrent posterior uveal and retinal uniform finding. • Posterior synechia— • Biochemistry—most common abnormality
inflammation (choroiditis; chorioretinitis). adhesions between posterior iris and anterior is elevated serum proteins (usually due to
• Unilateral or bilateral. lens surface. • Fibrin in anterior chamber. polyclonal gammopathy). • Urinalysis—
• Hypopyon or hyphema—accumulations of normal, or reflects underlying disease.
PATHOPHYSIOLOGY
white or red blood cells, respectively, in
• Increased permeability of the blood– OTHER LABORATORY TESTS
anterior chamber; usually settle in ventral
aqueous barrier due to infectious, immune- • Serum titers for FeLV, FIV, and FCoV;
aspect of chamber, but may be diffuse.
mediated, neoplastic, traumatic, or other FCoV titers not specific for feline infectious
• Chronic changes may include rubeosis iridis,
causes; plasma proteins and blood cells enter peritonitis (FIP), but very high titers may
iridal hyperpigmentation, secondary cataract,
aqueous humor. • Disruption of blood– increase the index of suspicion; reverse
lens luxation, pupillary seclusion, iris bombé,
aqueous barrier initiated and maintained by transcription polymerase chain reaction
secondary glaucoma, and phthisis bulbi.
chemical mediators. (RT-PCR) testing can help support diagnosis,
CAUSES but not definitive. • Toxoplasma gondii serum
SYSTEMS AFFECTED
• Infectious—mycotic (Blastomyces spp., immunoglobulin (Ig) M and IgG titers and/
• Ophthalmic. • Other systems if underlying
Cryptococcus neoformans, Coccidiodes immitis, or PCR performed on serum and/or aqueous
disease.
Histoplasma capsulatum); protozoal humor. • Bartonella spp. serology, PCR
INCIDENCE/PREVALENCE (Toxoplasma gondii, Leishmania infantum); (serum or aqueous humor).
• Relatively common. • True incidence/ bacterial (Bartonella spp., Mycobacterium
prevalence unknown. spp., or other bacteria); viral (feline immuno- IMAGING
deficiency virus [FIV], feline leukemia virus • Thoracic radiography—may show evidence
[FeLV], feline coronavirus [FCoV], feline of metastatic or infectious disease. • Ocular
Geographic location may affect incidence of
herpesvirus type 1 [FHV-1]); parasitic ultrasound—if opacity of ocular media
certain infections.
(ophthalmomyiasis, ocular nematodiasis). precludes direct examination; may reveal
SIGNALMENT • Idiopathic—lymphocytic-plasmacytic intraocular neoplasm or retinal detachment.
Species uveitis. • Immune-mediated—reaction to DIAGNOSTIC PROCEDURES
Cat lens proteins (due to cataract or lens trauma/ • Tonometry—low IOP consistent with
rupture). • Neoplastic—primary ocular uveitis; elevated IOP indicates glaucoma
Mean Age and Range
tumors, metastasis to uveal tract. • Metabolic— (primary or secondary to uveitis). • Ocular
• Mean age 7–9 years. • Any age may be
hyperlipidemia, hyperviscosity, systemic centesis—if retinal detachment is present,
affected.
hypertension. • Miscellaneous—trauma cytology of subretinal aspirate may reveal
Predominant Sex (blunt or penetrating), ulcerative keratitis, causative agents; anterior chamber centesis for
Males more commonly affected than females. corneal stromal abscess, toxemia. cytology, titers, or FCoV
SIGNS RISK FACTORS immunocytochemistry.
Historical Findings Immune suppression and geographic location PATHOLOGIC FINDINGS
• Cloudy eye—corneal edema, aqueous flare, may increase risk for certain infectious causes • Lymphoplasmacytic infiltrate of iris and
hypopyon. • Painful eye—blepharospasm, of uveitis. ciliary body (either diffuse or nodular) is most
photophobia, or rubbing eye; usually less common histopathologic finding.
severe than dogs. • Red eye—conjunctival • Histopathologic—may observe corneal
hyperemia and ciliary flush; usually less severe edema, peripheral corneal deep stromal
than dogs. • Vision loss—variable. vascularization, keratic precipitates, preiridal
DIAGNOSIS fibrovascular membrane, anterior or posterior
DIFFERENTIAL DIAGNOSIS synechia, entropion or ectropion uveae.
A thorough physical examination is crucial.
• Conjunctivitis—redness limited to Leukocyte accumulation in iris, ciliary body,
Ophthalmic Findings conjunctival hyperemia (no ciliary flush); sclera, choroid (lymphocytic, plasmacytic,
• Ocular discomfort—manifest by blepharo discharge thicker and more copious than suppurative, or granulomatous infiltrates,
spasm and photophobia. • Ocular uveitis; discomfort alleviated by topical depending on etiology), secondary cataract,
discharge—usually serous; sometimes mucoid anesthetic. • Glaucoma—elevated IOP, cyclitic membrane, vitreal traction bands, and
to mucopurulent. • Conjunctival hyperemia— dilated pupil, Haab’s striae, and buphthalmos. retinal detachment.
bulbar and palpebral conjunctiva affected. • Ulcerative keratitis—corneal fluorescein
• Corneal edema—diffuse; mild to severe. staining detects ulcers; corneal edema is either
• Keratic precipitates—multifocal aggregates localized to or most severe at site of ulcer;
of inflammatory cells adherent to corneal ocular discharge thicker and more copious
endothelium; most notable ventrally. than uveitis; discomfort alleviated by topical TREATMENT
• Aqueous flare—cloudiness of aqueous anesthetic. • Horner’s syndrome—miosis,
humor due to increased protein content and APPROPRIATE HEALTH CARE
enophthalmos, and nictitans protrusion are
cellular debris; visualized with a bright, Outpatient
similar, but Horner’s is nonpainful without
narrow beam of light shone through anterior ocular discharge; ptosis with Horner’s is not
(continued) Anterior Uveitis—Cats A
ACTIVITY Topical Mydriatic/Cycloplegic risk of idiopathic lymphocytic-plasmacytic

No changes. Atropine sulfate 1%—apply 1–4 times daily, uveitis and intraocular neoplasia.
DIET depending on severity of disease. Use lowest
frequency adequate to maintain dilated pupil; ZOONOTIC POTENTIAL
No changes. • None in most cases. • Some systemic
taper medication as condition resolves.
CLIENT EDUCATION Ointment in cats causes less salivation. infections causing uveitis may pose a risk to
• Systemic disease may cause ophthalmic signs; immunocompromised owners.
emphasize importance of appropriate diagnostic CONTRAINDICATIONS
• Avoid the use of miotic medications, PREGNANCY/FERTILITY/BREEDING
testing. • In addition to symptomatic treatment, Avoid systemic corticosteroids. Because of
treatment of underlying disease (when possible) including topical prostaglandins (e.g.,
latanoprost), in the presence of uveitis. systemic absorption, topical corticosteroids
is paramount. • Inform of potential may also pose a risk, especially with frequent
complications and emphasize compliance with • Topical and subconjunctival corticosteroids
are contraindicated with ulcerative keratitis. application.
treatment and follow-up recommendations to
reduce likelihood of complications. • Corticosteroids (especially systemic) SYNONYMS
should be avoided in cats with systemic Iridocyclitis
SURGICAL CONSIDERATIONS hypertension. • Avoid systemic nonsteroidal
• None in most cases. • Specific instances anti-inflammatory drugs (NSAIDs) in cats SEE ALSO
include removal of ruptured lenses and with renal disease and in combination with • Horner’s Syndrome.
surgical management of secondary glaucoma. corticosteroids. • Red Eye.
• Chronic uveitis leading to secondary ABBREVIATIONS
glaucoma commonly requires enucleation of PRECAUTIONS
Owing to concern for secondary glaucoma, • FCoV = Feline coronavirus.
the eye. • Enucleation is recommended in • FeLV = feline leukemia virus.
cats with uveitis related to diffuse iris topical atropine should be used judiciously
and IOP monitored periodically. • FHV-1 = feline herpesvirus type 1.
melanoma or other intraocular tumors. • FIP = feline infectious peritonitis.
POSSIBLE INTERACTIONS • FIV = feline immunodeficiency virus.
Systemic corticosteroids and NSAIDs should • Ig = immunoglobulin.
not be used concurrently. • IOP = intraocular pressure.
• NSAID = nonsteroidal anti-inflammatory
MEDICATIONS drug.
DRUG(S) OF CHOICE • RT-PCR = reverse transcription polymerase
chain reaction.
Corticosteroids
Topical
FOLLOW-UP Suggested Reading
• Prednisolone acetate 1% or dexamethasone PATIENT MONITORING Cullen C, Webb A. Ocular manifestations of
0.1%—apply 2–8 times daily, depending on Recheck in 3–7 days, depending on severity systemic diseases. Part 2: The cat. In: Gelatt
severity of disease; taper as condition resolves. of disease. IOP should be monitored to detect KN, ed., Veterinary Ophthalmology, 5th
• Stopping topical corticosteroids abruptly secondary glaucoma. Frequency of subse- ed. Ames, IA: Wiley-Blackwell, 2013,
may result in rebound ocular inflammation. quent rechecks dictated by severity of disease pp. 1978–2036.
Subconjunctival and response to treatment. Miller P. Diseases of the uvea. In: Maggs DJ,
• Often not required; indicated only in severe POSSIBLE COMPLICATIONS Miller PE, Ofri R, eds., Slatter’s
cases as one-time injection. • Triamcinolone • Secondary glaucoma—common Fundamentals of Veterinary Ophthalmology,
acetonide—4 mg by subconjunctival injection. complication of chronic uveitis in cats. 6th ed. St. Louis, MO: Elsevier Saunders,
• Methylprednisolone—4 mg by • Secondary cataract. • Lens luxation. 2018, pp. 254–276.
subconjunctival injection. • Retinal detachment. • Phthisis bulbi. Pickett JP. Anterior uvea and anterior
chamber. In: Martin C, Pickett J, Spiess B,
Systemic EXPECTED COURSE eds., Ophthalmic Disease in Veterinary
• Prednisone—1–3 mg/kg/day PO initially;
AND PROGNOSIS Medicine. Boca Raton, FL: CRC Press,
taper dose after 7–10 days. • Only if
• Guarded prognosis for affected eyes; 2018, pp. 411–474.
infectious causes of uveitis have been ruled
depends on underlying disease and response Stiles J. Feline ophthalmology. In: Gelatt KN,
out.
to treatment. • Cats with treatable underlying ed., Veterinary Ophthalmology, 5th ed.
Nonsteroidal Anti-inflammatory Drugs disease (e.g., toxoplasmosis) are more likely to Ames, IA: Wiley-Blackwell, 2013, pp.
(NSAIDs) have a favorable ophthalmic outcome than 1477–1559.
Topical those with idiopathic lymphoplasmacytic Author Ian P. Herring
• Flurbiprofen—apply 2–4 times daily, uveitis or untreatable underlying condition Consulting Editor Kathern E. Myrna
depending on severity of disease. (e.g., FIP, FIV).
• Diclofenac or ketorolac—apply 2–4
times daily, depending on severity of Client Education Handout
disease. available online
Systemic
• Meloxicam—0.3 mg/kg SC once. MISCELLANEOUS
• Robenacoxib—1 mg/kg PO once daily; AGE-RELATED FACTORS
limit duration of use to 3 days. • Younger cats more likely to be diagnosed
with infectious uveitis. • Older cats at higher
A Anterior Uveitis—Dogs
• Keratic precipitates—aggregates of flush); discharge usually thicker and more
inflammatory cells adherent to corneal copious; discomfort alleviated with topical
endothelium. • Aqueous flare—cloudiness of anesthetic. • Glaucoma—elevated IOP,
BASICS aqueous humor due to increased protein diffuse corneal edema, dilated pupil, Haab’s
DEFINITION content and cellular debris; best seen with a striae, buphthalmos. • Lens luxation—
• Inflammation of anterior uvea, including bright, narrow beam of light shone through corneal edema may be localized to site of
iris (iritis), ciliary body (cyclitis), or both anterior chamber. • Ciliary flush—injection lens contact with endothelium or diffuse as
(iridocyclitis). • May be associated with of deep perilimbal anterior ciliary vessels. a result of secondary uveitis and/or
posterior uveal and retinal inflammation • Deep corneal vascularization—circum glaucoma; breed associated. • Ulcerative
(choroiditis; chorioretinitis). • Unilateral or corneal distribution. • Miosis and/or keratitis—corneal fluorescein stain detects
bilateral. resistance to pharmacologic dilation. • Iridal ulcers; corneal edema localized to, or most
swelling. • Reduced intraocular pressure severe at, site of ulcer; discomfort alleviated
PATHOPHYSIOLOGY (IOP) is consistent with uveitis, but not a by topical anesthetic. • Corneal endothelial
• Increased permeability of blood–aqueous uniform finding. • Posterior synechia— dystrophy or degeneration—diffuse corneal
barrier due to infectious, immune-mediated, adhesions between posterior iris and anterior edema with normal IOP; conjunctival
traumatic, or other causes allows plasma lens surface. • Fibrin in anterior chamber. hyperemia and ocular discomfort generally
proteins and blood cells to enter aqueous • Hypopyon or hyphema—accumulation of absent. • Horner’s syndrome—miosis,
humor. • Disruption of blood–aqueous white or red blood cells, respectively, in enophthalmos, and nictitans protrusion in
barrier is initiated and maintained by anterior chamber; usually settles horizontally both conditions, but Horner’s is nonpainful
numerous mediators. in ventral aspect of chamber, but may be without ocular discharge; ptosis with Horner’s
SYSTEMS AFFECTED diffuse. • Chronic changes may include is distinguished from blepharospasm as the
• Ophthalmic. • Other systems if systemic rubeosis iridis, iridal hyperpigmentation, latter is an active process; minor conjunctival
disease. secondary cataract, lens luxation, pupillary hyperemia may be noted, but cornea and
INCIDENCE/PREVALENCE seclusion, iris bombé, secondary glaucoma, anterior chamber are clear; clinical signs of
• Relatively common. • True incidence/
and phthisis bulbi. Horner’s syndrome resolve with topical
prevalence unknown. ophthalmic 1–10% phenylephrine.
CAUSES
GEOGRAPHIC DISTRIBUTION • Infectious—fungal (Blastomyces dermatitidis, CBC/BIOCHEMISTRY/URINALYSIS
Geographic location may affect incidence of Cryptococcus neoformans, Coccidioides immitis, Normal, or reflect underlying disease.
certain infections. Histoplasma capsulatum, Candida spp., OTHER LABORATORY TESTS
Aspergillus spp., Encephalitozoon cuniculi), Serology for infectious diseases may be
SIGNALMENT protozoal (Toxoplasma gondii, Neospora indicated, especially in patients with signs of
Species caninum, Leishmania donovani), rickettsial systemic illness.
Dog (Ehrlichia canis, Rickettsia rickettsii), bacterial
(Leptospira spp., Bartonella spp., Brucella canis, IMAGING
Breed Predilections • Thoracic radiography and abdominal
Borrelia burgdorferi, and others), algal
• None for most causes. • Uveitis associated ultrasound may be warranted for systemic
(Prototheca spp.), viral (adenovirus, distemper,
with iridociliary cysts in golden retriever disease. • Ocular ultrasound is indicated if
rabies, herpes), parasitic (ocular filariasis,
(golden retriever pigmentary uveitis) and ocular media opacity precludes direct
ocular nematodiasis, ophthalmomyiasis).
Great Dane. • Increased incidence of examination.
• Immune-mediated—reaction to lens
uveodermatologic syndrome in Siberian
proteins (due to cataract or lens trauma), DIAGNOSTIC PROCEDURES
husky, Akita, Samoyed, and Shetland
uveodermatologic syndrome, postvaccinal • Tonometry—low IOP consistent with
sheepdog.
reaction to canine adenovirus vaccine, uveitis; elevated IOP indicates glaucoma
Mean Age and Range vasculitis. • Neoplastic—primary ocular (primary disease or secondary to uveitis).
• Any age. • Uveodermatologic syndrome— tumors (uveal melanoma, iridociliary adenoma/ • Ocular centesis—if retinal detachment is
mean 2.8 years. • Golden retriever pigmentary adenocarcinoma), metastasis to uveal tract present, cytology of subretinal aspirate may
uveitis—mean 8.6 years. (e.g., lymphosarcoma). • Metabolic— reveal causative agents; anterior chamber
SIGNS hyperlipidemia, hyperviscosity, systemic centesis unrewarding, except in cases of
hypertension. • Miscellaneous—idiopathic, lymphoma.
Historical Findings trauma, golden retriever pigmentary uveitis,
• Red eye (conjunctival hyperemia, ciliary PATHOLOGIC FINDINGS
ulcerative keratitis, corneal stromal abscess,
flush). • Cloudy eye (corneal edema, aqueous Histopathologic—may observe corneal
scleritis, lens instability/luxation.
flare, hypopyon). • Painful eye (blepharospasm, edema, peripheral corneal deep stromal
photophobia, or rubbing eye). • Vision RISK FACTORS vascularization, keratic precipitates, preiridal
loss—variable. Immune suppression and geographic location fibrovascular membrane, anterior or
may increase risk for infectious causes of posterior synechia, entropion or ectropion
Physical Examination Findings uveitis; consider breed predispositions. uveae. Leukocyte accumulation in iris,
Thorough physical examination is critical. ciliary body, sclera, choroid may be
Ophthalmic Findings lymphocytic, plasmacytic, suppurative, or
• Ocular discomfort—blepharospasm, granulomatous, depending on etiology.
photophobia, and rubbing eye. • Ocular Secondary cataract, cyclitic membrane,
discharge—usually serous; sometimes mucoid DIAGNOSIS vitreal traction bands, and retinal detach
to mucopurulent. • Conjunctival hyperemia— ment may be present.
bulbar and palpebral conjunctiva affected.
• Conjunctivitis—redness limited to
• Corneal edema—diffuse; mild to severe.
conjunctival hyperemia (i.e., no ciliary
(continued) Anterior Uveitis—Dogs A
Nonsteroidal Anti-inflammatory Drugs secondary cataract, secondary glaucoma, lens

(NSAIDs) luxation, retinal detachment, phthisis bulbi.
TREATMENT Topical EXPECTED COURSE AND PROGNOSIS
• Less effective than topical corticosteroids; Extremely variable; depends on underlying
APPROPRIATE HEALTH CARE can be combined with topical steroids. disease and response to treatment.
Outpatient • Flurbiprofen, diclofenac, ketorolac—apply
ACTIVITY 2–4 times daily, depending on severity of
• No changes in most cases. • Reduced disease.
exposure to bright light may alleviate Systemic
discomfort. • Do not use concurrently with systemic
MISCELLANEOUS
DIET corticosteroids; avoid in presence of hyphema. ZOONOTIC POTENTIAL
No changes. • Carprofen—2.2 mg/kg PO q12h or None in most cases. Some etiologies of
4.4 mg/kg PO q24h. • Meloxicam— systemic infection may pose a risk to
CLIENT EDUCATION 0.2 mg/kg on day 1, followed by 0.1 mg/kg immune-compromised owners.
• Systemic disease may cause ophthalmic
PO q24h. • Deracoxib—1–2 mg/kg PO PREGNANCY/FERTILITY/BREEDING
signs; emphasize importance of appropriate q24h. • Firocoxib—5 mg/kg PO q24h.
diagnostic testing. • In addition to sympto Avoid systemic corticosteroids. Because of
matic uveitis treatment, treatment of Topical Mydriatic/Cycloplegic possibility of systemic absorption, topical
underlying disease (when possible) is Atropine sulfate 1%—apply 1–4 times daily, corticosteroids may also pose risk, especially
paramount. • Inform of potential complications depending on severity of disease; use lowest with frequent application in small dogs.
and emphasize compliance with treatment frequency adequate to maintain dilated pupil SYNONYMS
and follow-up recommendations to reduce and ocular comfort; taper medication as Iridocyclitis
likelihood of complications. condition resolves.
SEE ALSO
SURGICAL CONSIDERATIONS CONTRAINDICATIONS Red Eye.
• None (most cases). • Specific instances • Avoid topical miotic medications (e.g.,
pilocarpine), including topical prostaglandins ABBREVIATIONS
include removal of ruptured lenses, removal
(e.g., latanoprost), in presence of uveitis. • IOP = intraocular pressure.
of cataracts causing uveitis (if prognosis is
• Avoid topical atropine in cases of uveitis • NSAID = nonsteroidal anti-inflammatory
otherwise favorable), surgical management of
with secondary glaucoma. • Topical and drug.
corneal disease causing uveitis, and surgical
management of secondary glaucoma. subconjunctival corticosteroids are contra Suggested Reading
indicated with ulcerative keratitis. • Avoid Cullen C, Webb A. Ocular manifestations of
systemic corticosteroids in dogs with systemic systemic diseases. Part 1: The dog. In:
infection. Gelatt KN, ed., Veterinary Ophthalmology,
PRECAUTIONS 5th ed. Ames, IA: Wiley-Blackwell, 2013,
MEDICATIONS Out of concern for secondary glaucoma, pp. 1897–1977.
topical atropine should be used judiciously Hendrix D. Diseases and surgery of the
DRUG(S) OF CHOICE canine anterior uvea. In: Gelatt KN, ed.,
and IOP should be monitored periodically.
Corticosteroids Veterinary Ophthalmology, 5th ed.
POSSIBLE INTERACTIONS Ames, IA: Wiley-Blackwell, 2013,
Topical Systemic corticosteroids and NSAIDs should
• Prednisolone acetate 1% or dexamethasone pp. 1146–1198.
not be used concurrently. Miller P. Diseases of the uvea. In: Maggs DJ,
0.1%—apply 2–8 times daily, depending on
severity of disease; taper as condition resolves. ALTERNATIVE DRUG(S) Miller PE, Ofri R, eds., Slatter’s
• Stopping topical corticosteroids abruptly N/A Fundamentals of Veterinary Ophthalmology,
may result in rebound ocular inflammation. 6th ed. St. Louis, MO: Elsevier Saunders,
2018, pp. 254–276.
Subconjunctival Pickett JP. Anterior uvea and anterior
• Often not required; indicated only in severe chamber. In: Martin C, Pickett J, Spiess B,
cases as one-time injection. • Triamcinolone
acetonide—4–6 mg, subconjunctival injection.
FOLLOW-UP eds., Ophthalmic Disease in Veterinary
Medicine. Boca Raton, FL: CRC Press,
• Methylprednisolone—3–10 mg, PATIENT MONITORING 2018, pp. 411–474.
subconjunctival injection. Recheck in 3–7 days, depending on severity Author Ian P. Herring
of disease. IOP should be monitored to detect
Systemic Consulting Editor Kathern E. Myrna
secondary glaucoma. Frequency of subsequent
• Prednisone—0.5–2.2 mg/kg/day PO
rechecks dictated by severity of disease and
initially; taper dose after 7–10 days. Long-term
response to treatment.
treatment with immunosuppressive medication Client Education Handout
may be warranted for immune-mediated uveitis. POSSIBLE COMPLICATIONS available online
• Use only if systemic infectious causes of • Many systemic complications, including
uveitis have been ruled out. death, may occur due to systemic etiology of
uveitis. • Ophthalmic complications include
A Antidepressant Toxicosis—SSRIs and SNRIs
• Ophthalmic—increased autonomic
function (mydriasis).
• Respiratory—increased bronchial smooth
BASICS muscle contraction (dyspnea). DIAGNOSIS
DEFINITION INCIDENCE/PREVALENCE DIFFERENTIAL DIAGNOSIS
• Toxicity secondary to the overdose of a Second most common human prescription • Toxicologic—TCAs, MAOIs, metaldehyde,
selective serotonin reuptake inhibitor (SSRI), medication toxicosis (after cardiac medicat- lead, ethylene glycol, hops, anticholinergics,
serotonin and norepinephrine reuptake ions). antihistamines.
inhibitor (SNRI), or coingestion of two types • Nontoxicologic—meningitis (e.g., rabies,
of serotonergic drugs. SIGNALMENT canine distemper), neoplasia, heat stroke,
• SSRIs include citalopram (Celexa®), Species malignant hyperthermia.
escitalopram (Lexapro®), fluoxetine (Prozac®), Dogs and cats. CBC/BIOCHEMISTRY/URINALYSIS
fluvoxamine (Luvox®), paroxetine (Paxil®), • CBC/biochemistry—no direct changes are
Mean Age and Range
sertraline (Zoloft®), vilazodone (Viibryd®), expected, but creatine kinase (CK) may be
Any age can be affected.
and vortioxetine (Brintellix®). SNRIs include elevated secondary to tremors.
desvenlafaxine (Pristiq®), duloxetine (Cymbalta®), SIGNS
• Urinalysis—myoglobinuria secondary to
levomilnacipran (Fetzima®), milnacipran Historical Findings rhabdomyolysis may be seen.
(Ixel®, Savella®), tofenacin (Elamol®, • Agitation or lethargy.
Tofacine®), and venlafaxine (Effexor®). OTHER LABORATORY TESTS
• Dilated pupils.
• Blood gas—metabolic acidosis may be
PATHOPHYSIOLOGY • Vomiting.
seen.
• SSRIs and SNRIs are antidepressants • Tremors.
• Testing for SSRIs/SNRIs can be performed,
that inhibit reuptake of serotonin, a neuro • Hypersalivation.
but the tests are not clinically useful.
transmitter involved in aggression, anxiety, • Diarrhea.
• Note: venlafaxine will give a false positive
appetite, depression, migraine, pain, and sleep. • Seizures.
for phencyclidine (PCP; angel dust) on many
Antidepressant effects are secondary to • Nystagmus.
urine drug screens.
inhibition of reuptake of serotonin into Physical Examination Findings
serotonergic neurons via binding to the DIAGNOSTIC PROCEDURES
• Agitation.
serotonin transporter, resulting in increased There are no diagnostic tests to confirm
• Ataxia.
synaptic availability of serotonin. SNRIs also serotonin syndrome.
• Mydriasis.
inhibit the reuptake of norepinephrine by the • Tremors.
same mechanism. • Vomiting.
• Excessive stimulation of serotonin receptors • Disorientation.
can occur by enhanced serotonin synthesis, • Hyperthermia.
increased presynaptic serotonin release,
TREATMENT
• Vocalization.
inhibition of serotonin uptake into the • Depression. APPROPRIATE HEALTH CARE
presynaptic neuron, inhibition of serotonin • Tachycardia. • Emesis (if asymptomatic and recent ingestion)
metabolism, or serotonin agonism. Ingesting • Hypotension. or gastric lavage (if large number of pills
too much of one medication or a combination • Diarrhea. ingested).
of medications that increase serotonin via • Blindness. • Activated charcoal with cathartic (if severe
different methods can lead to serotonin • Seizures. signs are expected, may need to repeat due to
syndrome. • Hypersalivation. long half-life).
• Serotonin syndrome is characterized in • Death. NURSING CARE
humans as a combination of symptoms that IV fluids to help maintain blood pressure and
include at least three of the following: CAUSES
• SSRI/SNRI overdose—accidental body temperature, and to protect kidneys
myoclonus, mental aberration, agitation, from myoglobinuria.
hyperreflexia, tremors, diarrhea, ataxia, or exposure, inappropriate administration, or
hyperthermia. therapeutic use. CLIENT EDUCATION
• Ingestion of an SSRI/SNRI along with If animal appears blind, sight should return.
• Toxic dosage varies widely among
commonly available SSRIs and SNRIs another class of medications that increases
and is not well defined in veterinary medicine. serotonin (tricyclic antidepressants [TCAs],
monoamine oxidase inhibitors [MAOIs],
SYSTEMS AFFECTED novel antidepressants, tramadol, fentanyl,
• Cardiovascular—decreased vascular tone meperidine, amphetamines, cocaine, MEDICATIONS
(hypotension), increased heart rate and stroke dextromethorphan, 5-hydroxytryptophan DRUG(S) OF CHOICE
volume (tachycardia). [5-HTP], buspirone, bupropion, • Agitation:
• Gastrointestinal—increased smooth muscle triptans, LSD). ◦◦ Phenothiazines (acepromazine 0.025–
contractility (vomiting, diarrhea). 0.05 mg/kg IV, titrate up as needed).
RISK FACTORS
• Nervous—stimulation (agitation, restlessness, ◦◦ Cyproheptadine (dog, 1.1 mg/kg; cat,
• Animals on a serotonergic drug.
seizures) and altered mental status (vocalization, 2–4 mg PO q4–6h or can be given rectally
• Underlying liver or kidney disease; cats are
disorientation). if vomiting).
attracted to venlafaxine and will eat multiple
• Neuromuscular—autonomic dysfunction ◦◦ Benzodiazepines (diazepam 0.5–2 mg/kg
capsules.
(hyperactivity) and neuromuscular IV; see Precautions).
hyperactivity (hyperreflexia, myoclonus, ◦◦ Tremors—methocarbamol (50–150 mg/kg
tremors). IV, titrate up as needed).
(continued) Antidepressant Toxicosis—SSRIs and SNRIs A
CONTRAINDICATIONS PREVENTION/AVOIDANCE ABBREVIATIONS

• High risk of serotonin syndrome—other • Keep medications out of the reach of • 5-HTP = 5-hydroxytryptophan.
SSRIs, SNRIs, MAOIs, TCAs, amphetamines, animals. • CK = creatine kinase.
5-HTP, clarithromycin, dextromethorphan, • Follow label directions when giving • DIC = disseminated intravascular
lithium, St. John’s wort. serotonergic drugs to animals. coagulation.
• Low risk of serotonin syndrome—tramadol, • MAOI = monoamine oxidase inhibitor.
fentanyl, amantadine, bupropion, carbamazepine, Renal failure secondary to myoglobinuria • PCP = phencyclidine (angel dust).
codeine. from rhabdomyolysis; disseminated intravas • SNRI = serotonin and norepinephrine
PRECAUTIONS cular coagulation (DIC) secondary to reuptake inhibitor.
• SSRI = selective serotonin reuptake
Benzodiazepines (e.g., diazepam) are reported hyperthermia.
by some sources to exacerbate serotonin inhibitor.
EXPECTED COURSE • TCA = tricyclic antidepressant.
syndrome and their use for SSRI/SNRI
toxicosis is not universally recommended. AND PROGNOSIS Suggested Reading
• Prognosis is good in most cases, with
POSSIBLE INTERACTIONS Pugh CM, Sweeney JT, Bloch CP, et al.
recovery in 12–24 hours. Selective serotonin reuptake inhibitor
• Decreased metabolism of SSRIs/SNRIs— • Patients that present in status epilepticus or
cimetidine, diuretics, quinidine, lithium. (SSRI) toxicosis in cats: 33 cases (2004–
with severe hyperthermia have a guarded 2010). J Vet Emerg Crit Care 2013,
• Increased levels of medications (decreased prognosis.
metabolism)—theophylline, coumadin, 23(5):565–570.
digoxin. Thomas DE, Lee JA, Hovda LR. Retrospective
evaluation of toxicosis from selective
serotonin reuptake inhibitor antidepres
sants: 313 dogs (2005–2010). J Vet Emerg
MISCELLANEOUS Crit Care 2012, 22(6):674–681.
Wismer TA. Antidepressant drug overdoses in
FOLLOW-UP AGE-RELATED FACTORS
dogs. Vet Med 2000, 95(7):520–525.
Young and elderly animals are more at risk for
PATIENT MONITORING Author Tina Wismer
developing serious toxicosis.
Blood pressure, heart rate, urine color—mon Consulting Editor Lynn R. Hovda
itor hourly, then less frequently as the animal PREGNANCY/FERTILITY/BREEDING
remains stable. SSRIs and SNRIs can cause increased litter
mortality and possible birth defects.
A Antidepressant Toxicosis—Tricyclic
Mean Age and Range exposure has occurred; not useful in
None determining degree of toxicity.
SIGNS • Serum TCA levels—can be used to
BASICS determine if exposure has occurred.
DEFINITION General Comments
• Signs can occur at therapeutic doses. IMAGING
• Toxicity secondary to the acute or chronic N/A
ingestion of a tricyclic antidepressant (TCA). • Signs of toxicosis can occur within
• TCA medications include amitriptyline, 30–60 minutes or be delayed by several DIAGNOSTIC PROCEDURES
amoxapine, clomipramine, desipramine, hours. • ECG to monitor for arrhythmias.
doxepin, imipramine, maprotiline (tetracyclic Historical Findings • Blood pressure monitoring.
antidepressant), nortriptyline, protriptyline, • Evidence of accidental consumption of the PATHOLOGIC FINDINGS
trimipramine, and many others. owner’s or another pet’s medication. No specific lesions expected.
PATHOPHYSIOLOGY • CNS depression (lethargy, ataxia).
• TCAs block the reuptake of norepine • Vocalization.
phrine, dopamine, and serotonin at the • Vomiting or hypersalivation.
neuronal membrane. They also have • Panting.
anticholinergic activity and are thought to • Agitation or restlessness. TREATMENT
have membrane-stabilizing effects on the • Tachypnea or dyspnea.
• Tremors. APPROPRIATE HEALTH CARE
myocardium (particularly inhibiting fast • Outpatient—not recommended for sympto-
sodium channels in the ventricular • Seizures.
matic patients, patients with cardiac disease,
myocardium). They can also have slight Physical Examination Findings or patients ingesting greater than a
alpha-adrenergic blocking activity and • CNS depression or stimulation. therapeutic dose of TCAs.
antihistaminic effects. • Tachycardia. • Inpatient—asymptomatic:
• TCAs are rapidly and well absorbed across • Ataxia. ◦◦ Decontamination with emesis (less than
the digestive tract. They can decrease GI • Mydriasis. 15 minutes of exposure time), gastric lavage
motility and delay gastric emptying, resulting • Hypothermia. in large exposures, and activated charcoal.
in delayed drug absorption. • Hypertension. ◦◦ Monitor at a clinic for a minimum of 6
• Lipophilic, protein bound, and well • Pallor. hours after exposure.
distributed across all tissues. • Cyanosis. • Inpatient—symptomatic: stabilize the
• They are metabolized by the liver and • Hyperthermia. cardiovascular (CV) system and CNS and
undergo enterohepatic recirculation. The • Arrhythmias. provide supportive care.
inactive metabolites are eliminated in the • Hypotension.
urine. • Urinary retention. NURSING CARE
• Constipation. • Fluid therapy—restore hydration due to
SYSTEMS AFFECTED
vomiting, regulate blood pressure when
• Nervous—increased dopamine, serotonin, CAUSES
hypotension is noted.
and norepinephrine levels in the CNS Accidental exposure, inappropriate
• Thermoregulation as needed.
contribute to CNS signs. administration, or therapeutic use.
• Enema with warm water if not defecating
• Cardiovascular—anticholinergic effects and
RISK FACTORS within 6–12 hours.
inhibition of norepinephrine reuptake • Concurrent use of other antipsychotic
contribute to tachycardia; alpha adrenergic ACTIVITY
medication.
blockade, cardiac membrane stabilization, N/A
• Preexisting cardiac disease.
and decreased cardiac contractility contribute DIET
to hypotension and arrhythmias. NPO if vomiting.
• Gastrointestinal (GI)—anticholinergic
effects may cause ileus and delayed gastric CLIENT EDUCATION
emptying. • With a prescribed TCA, instruct client to
• Ophthalmic—anticholinergic effects can DIAGNOSIS monitor for adverse or idiosyncratic effects,
cause pupillary dilation. and to stop the medication and contact the
DIFFERENTIAL DIAGNOSIS clinic if they occur.
• Renal/urologic—anticholinergic effects may • Toxicity caused by other antipsychotic
cause urinary retention. • Prevent exposure to nonprescribed
medication, stimulant substances (e.g., medication.
GENETICS amphetamines, cocaine, methylxanthines, or
Species and individual differences in pseudoephedrine), or substances capable of SURGICAL CONSIDERATIONS
absorption, metabolism, and elimination can causing cardiac arrhythmias (e.g., quinidine, N/A
be significant. propranolol, albuterol, digoxin).
• Nontoxicologic differentials include hyper
INCIDENCE/PREVALENCE kalemia, cardiac ischemia, cardiomyopathy, and
Incidence is unknown. other diseases of cardiac conduction.
SIGNALMENT CBC/BIOCHEMISTRY/URINALYSIS MEDICATIONS
Species Expected to be normal. DRUG(S) OF CHOICE
Dogs and cats. Decontamination
Breed Predilections • Blood gases—metabolic acidosis may be noted. • Emesis within 15 minutes of ingestion only
None • Over-the-counter (OTC) urine drug screen if asymptomatic; induce emesis with either
for TCAs—can be used to determine if hydrogen peroxide (dog, 1–2 mL/kg PO),
(continued) Antidepressant Toxicosis—Tricyclic A
apomorphine (dog, 0.03–0.05 mg/kg IV/IM, because of their potential to exacerbate

or 0.1 mg/kg SC, or 0.25 mg instilled in hypotension.
conjunctiva of eye), or dexmedetomidine • Do not induce emesis in a patient already
(cat, 7 μg/kg IM or 3.5 μg/kg IV). showing clinical signs. MISCELLANEOUS
• Gastric lavage under anesthesia may be ASSOCIATED CONDITIONS
PRECAUTIONS
considered with large exposures. N/A Serotonin syndrome may occur as a result of
• After emesis (or if >15 min of exposure), TCA ingestion.
administer activated charcoal (1–2 g/kg PO) POSSIBLE INTERACTIONS
• TCAs increase risk of hyperthermia, AGE-RELATED FACTORS
with a cathartic such as sorbitol (70% sorbitol
seizures, and death with use of monoamine None
at 3 mL/kg) or sodium sulfate (0.25 tsp/5 kg)
if no diarrhea. oxidase inhibitors (MAOIs). PREGNANCY/FERTILITY/BREEDING
• Repeat one-half dose of activated charcoal • Sympathomimetic and anticholinergic TCAs cross the placenta and can be found in
in 4–6 hours if patient is still symptomatic. medications increase the risk for arrhythmias breast milk; the significance of this is not
or cardiac effects from TCAs. known at this time.
Other • Levothyroxine increases the risk for
• Cyproheptadine—dogs, 1.1 mg/kg q8h PO SEE ALSO
arrhythmias when used with TCAs.
or rectally; cats, 2–4 mg/cat q12–24h PO or • Antidepressant Toxicosis—SSRIs and
rectally; used for treatment of serotonin ALTERNATIVE DRUG(S) SNRIs.
syndrome. N/A • Poisoning (Intoxication) Therapy.
• 20% intravenous lipid emulsion—prevents ABBREVIATIONS
lipophilic TCAs from reaching site of action by • CV = cardiovascular.
acting as sequestrant in expanded plasma lipid • GI = gastrointestinal.
phase; 1.5 mL/kg IV bolus followed by • MAOI = monoamine oxidase inhibitor.
0.25 mL/kg/min IV CRI for 1 hour. Can repeat FOLLOW-UP • OTC = over-the-counter.
bolus and CRI in 4–6 hours if serum is not PATIENT MONITORING • TCA = tricyclic antidepressant.
lipemic and a poor response to treatment is seen. • Acid-base status—monitor for acidosis and
• Sodium bicarbonate—used to maintain INTERNET RESOURCES
if implementing sodium bicarbonate therapy. • http://www.aspcapro.org/poison
blood pH at 7.55; if not monitoring acid-base • Blood pressure—monitor until asympto-
status, start with 2–3 mEq/kg IV over 15–30 • http://www.petpoisonhelpline.com
matic.
minutes in a symptomatic patient. • ECG—monitor until asymptomatic. Suggested Reading
• Diazepam—0.5–1 mg/kg IV, repeat if Gwaltney-Brant S. Antidepressants: tricyclic
necessary; for agitation or seizures. PREVENTION/AVOIDANCE antidepressants. In: Plumlee KH, ed.,
• Acepromazine—0.02 mg/kg IV, repeat Keep medications out of reach of pets. Clinical Veterinary Toxicology. St. Louis,
if necessary; for agitation or mild hyper- POSSIBLE COMPLICATIONS MO: Mosby, 2004, pp. 286–288.
tension. Pulmonary edema can occur secondary to Gwaltney-Brant S, Meadows I. Use of
• Phenobarbital—as needed for seizure control. aggressive fluid therapy. intravenous lipid emulsions in veterinary
CONTRAINDICATIONS EXPECTED COURSE AND PROGNOSIS clinical toxicology. Vet Clin North Am
• Atropine should not be used, because TCAs • Due to the variable half-lives of the Small Anim Pract 2018, 48:933–942.
have anticholinergic effects that are exacer different TCAs, signs can last 24 hours or Johnson LR. Tricyclic antidepressant
bated by atropine. longer. toxicosis. Vet Clin North Am Small Anim
• Trazodone should not be used, because it • Prognosis is generally good in patients Pract 1990, 20:393–403.
can result in serotonin syndrome when given exhibiting mild to moderate signs. Volmer PA. Recreational drugs: tricyclic
concurrently. • Prognosis is guarded in patients exhibiting antidepressants. In: Peterson ME, Talcott
• Magnesium sulfate should not be used as a severe signs such as seizures, arrhythmias, or PA, eds., Small Animal Toxicology, 3rd ed.
cathartic. Ileus or reduced GI motility will hypotension that are poorly responsive to St. Louis, MO: Elsevier Saunders, 2013, pp.
enhance absorption of magnesium and may therapy. 328–330.
result in magnesium toxicity. Wismer TA. Antidepressant drug overdoses in
• Beta blockers (e.g., propranolol, atenolol) dogs. Vet Med 2000, 95:520–525.
should not be used for tachycardia Author Cristine L. Hayes
Consulting Editor Lynn R. Hovda
A Aortic Stenosis
• Aortic stenosis reported as small contributor arteriosus (PDA) and SAS. • Volume
of feline congenital heart disease, about 6%; overload of PDA can cause relative aortic
approximately 2 out of 1,000 dogs and 0.2 per stenosis and be difficult to distinguish from
BASICS 1,000 cats evaluated at veterinary teaching PDA with mild SAS.
DEFINITION hospitals are diagnosed with aortic stenosis, CAUSES
• A narrowing of the left ventricular outflow SAS most often in dogs and supravalvular • Congenital heart disease. • Secondary to
tract (LVOT) that restricts blood flow leaving aortic stenosis most often in cats. valvular change, as with aortic valve
the ventricle; most commonly congenital, GEOGRAPHIC DISTRIBUTION endocarditis or calcification. • Component
often heritable. • Lesion is most commonly N/A of complex congenital heart disease, as with
subvalvular in dogs, but may be valvular or some cases of mitral valve dysplasia.
supravalvular (more often in cats). SIGNALMENT
• Subvalvular aortic stenosis (SAS) in dogs Species RISK FACTORS
is caused by fibrous tissue manifested as • Familial history of SAS. • SAS predisposes to
Dog and cat.
nodules, a ridge, a ring, or a tunnel‐like lesion. aortic valve endocarditis. • Aortic valve
Breed Predilections endocarditis predisposes to valvar aortic stenosis.
SAS may be associated with other defects,
• Newfoundland, bullmastiff, golden
including mitral valve dysplasia.
retriever, Rottweiler, bouvier des Flandres,
PATHOPHYSIOLOGY dogue de Bordeaux, German shepherd, and
• Restriction to outflow generates pressure boxer have highest incidence of SAS and
overload of left ventricle (LV). • Degree of familial component or heritability is reported. DIAGNOSIS
obstruction is related to severity of secondary • No breed predilection reported for cats. DIFFERENTIAL DIAGNOSIS
changes. • LV pressure overload causes • Systolic murmur must be differentiated
Mean Age and Range
thickened LV walls, resulting in diminished from other causes of similar murmurs.
• Clinical signs may be seen at any age.
blood supply relative to muscle demand and • Innocent or physiologic murmurs
• Although often inherited, SAS becomes
myocardial ischemia; this may result in commonly ausculted in athletic dogs, or with
identifiable during first few weeks to months
arrhythmogenesis and, if severe or infarction anemia, fever, stress, or excitement.
of life as subvalvular lesion progresses. • Full
occurs, mechanical dysfunction. • Restriction • Pulmonic stenosis and tetralogy of Fallot
phenotype is appreciated by 1 year of age.
to blood flow causes high‐velocity, turbulent cause similar murmur. • Weak pulses may
flow across valve, which may cause endothelial Predominant Sex also occur with conditions that reduce cardiac
damage, lead to aortic insufficiency (AI), and N/A output, such as heart failure, cardiomyopathy,
predispose to endocarditis. • SAS may lead to SIGNS and severe pulmonic stenosis. • Other
chamber enlargement, distortion of the mitral obstruction to flow may cause reduced pulse
valve annulus, and mitral regurgitation, with Historical Findings
quality, such as aortic thromboembolism, or
possible sequela of left‐sided congestive heart • Many dogs show no clinical signs and have
rarely aortic coarctation/tubular hypoplasia.
failure (CHF). • Sudden death is common no relevant historical findings. • Historical
with severe SAS and may be secondary to findings related to disease severity and may CBC/BIOCHEMISTRY/URINALYSIS
arrhythmias or infarction. include syncope, exercise intolerance, sudden Typically within normal limits.
death, and signs due to CHF such as respira- OTHER LABORATORY TESTS
SYSTEMS AFFECTED tory distress and/or coughing if severe.
• Cardiovascular—LV pressure overload
Genetic testing for mutation associated with
leading to arrhythmias, syncope, sudden death, Physical Examination Findings Newfoundland SAS is breeding tool to reduce
heart failure, endocarditis. • Respiratory— • Systolic left basilar ejection murmur; may frequency in this breed.
possible pulmonary edema with CHF. radiate to apex, right side of thorax, include IMAGING
• Multisystemic—possible due to low cardiac carotid arteries, and if very loud the cranium;
precordial thrill may be palpable; murmur Thoracic Radiography
output or endocarditis. • Mild disease may be radiographically silent.
intensity loosely correlated to severity; as
GENETICS disease worsens during early life, some may • LV hypertrophy may be subtle, as pressure
• SAS inherited in the Newfoundland, have absence of or quiet murmur that overload causes concentric hypertrophy. • Left
golden retriever, Rottweiler, bullmastiff, and develops to more characteristic finding by 1 heart enlargement. • Prominent aortic root and/
dogue de Bordeaux. • Mutation in phosphatidy- year. • Diastolic murmur may be present with or widened mediastinum. • Lung fields typically
linositol‐binding clathrin assembly protein significant AI; combination of this diastolic normal unless CHF with pulmonary venous
gene (PICALM) reported in Newfoundlands; murmur with systolic ejection murmur is distention and interstitial to alveolar infiltrates.
screening test is available. • Dominant to‐and‐fro murmur. • Arrhythmias may be Echocardiography
inheritance patterns proposed for ausculted. • Pulse deficits may be appreciated, • Findings variably present and associated with
Newfoundlands with incomplete penetrance often associated with ventricular arrhythmias. disease severity. • Ridge, ring, nodule, or
responsible for disease appearing to skip • Weak pulses may be appreciated that are tunnel‐like narrowing below aortic valve with
generations. • More than one gene or late or slow to rise with severe SAS (pulsus SAS. • Thickened LV free wall or interven
modifying genes may be involved. • Golden parvus et tardus). • Tachypnea, respiratory tricular septum. • Aortic valve thickening and
retrievers, Rottweilers, and bullmastiffs appear distress, and crackles may occur with CHF. increased echogenicity with valvar stenosis.
to inherit SAS in autosomal recessive pattern, • Mitral regurgitation and thickening of valve
but no associated mutation yet identified. General Comments
• Boxers have relatively small aorta compared leaflets possible. • Poststenotic aortic dilation.
INCIDENCE/PREVALENCE to other breeds, which can be difficult to • Hyperechoic myocardium associated with
• SAS is one of most common congenital heart distinguish from mild SAS. • Bull terriers ischemia. • AI with secondary LV chamber
defects of dogs; it is reported as second most overrepresented for combined mitral valve enlargement and volume overload if significant.
common, but difficulty in diagnosing mild dysplasia and SAS. • Newfoundland dogs • Left atrial enlargement may be seen with
disease may underestimate true prevalence. overrepresented for combined patent ductus significant mitral valve regurgitation. • Elevated
(continued) Aortic Stenosis A
LVOT flow velocity (>2.4 m/s), with acutely reduce pressure gradient and temporarily EXPECTED COURSE AND PROGNOSIS
acceleration proximal to stenosis and turbulent alleviate some clinical signs; however, effects not • Mildly affected dogs may have normal
flow distal to obstruction and valve. yet shown to be beneficial beyond those achieved lifespan and quality without therapy.
• Transvalvular pressure gradient estimated by with beta blockers. • Currently, data does not • Severely affected dogs have limited lifespans
LVOT flow velocity (4 × flow velocity2); support surgery or intervention, but this remains and typically succumb to sudden death or CHF;
estimated gradients of 25–49 mmHg area of continued research. in one study average lifespan for dogs with
considered mild, 50–79 mmHg moderate, and severe SAS on atenolol was about 4.5 years.
≥80 mmHg severe. • With myocardial failure,
estimated pressure gradient may be falsely low.
• Effective valve orifice, if calculated, is
reduced.
MEDICATIONS
DRUG(S) OF CHOICE MISCELLANEOUS
• Beta adrenergic blockers advocated with ASSOCIATED CONDITIONS
• ECG may show changes consistent with LV
moderate to severe SAS, particularly with Increased risk of infective endocarditis.
hypertrophy (tall R waves, widened QRS
ventricular arrhythmias, syncope, or ECG AGE‐RELATED FACTORS
complexes, left axis deviation); signs of
evidence of ischemia; may reduce myocardial SAS may not be immediately apparent at
myocardial ischemia (ST segment deviation or
oxygen demand, eliminate or protect against birth, but appears over first few weeks to
slurring); ventricular arrhythmias may occur
ventricular arrhythmias, and reduce heart months of life.
and contribute to syncope or sudden death.
rate; atenolol is most common (dogs,
• Holter monitoring may be used to quantify PREGNANCY/FERTILITY/BREEDING
0.5–1.5 mg/kg PO q12h; cats, 6.25 mg/cat
arrhythmia severity and therapeutic response. Contraindicated
PO q12–24h). • Therapy for ventricular
PATHOLOGIC FINDINGS arrhythmias, CHF, atrial fibrillation, or SYNONYMS
• Findings vary with severity, but typically endocarditis may be required. Subaortic stenosis, discrete subaortic stenosis.
include LV concentric or mixed (if significant
CONTRAINDICATIONS SEE ALSO
AI) hypertrophy. • Variable subvalvular lesion
• Beta blockers contraindicated in animals • Cardiomyopathy, Hypertrophic—Cats.
of dense fibrous tissue is seen. • Myocardial
with bronchoconstriction such as asthmatic • Cardiomyopathy, Hypertrophic—Dogs.
ischemia, necrosis, and replacement fibrosis
cats. • Starting beta blockers with CHF • Congestive Heart Failure, Left‐Sided.
may be evident. • Poststenotic dilation of aorta,
contraindicated and continued use in patients • Endocarditis, Infective.
associated valvular endothelial damage, and
that develop CHF is controversial.
sometimes left atrial enlargement are reported. ABBREVIATIONS
PRECAUTIONS • AI = aortic insufficiency. • CHF = congestive
• Beta blockers negatively impact cardiac heart failure. • LV = left ventricle. • LVOT = left
output and starting low doses with gradual up‐ ventricular outflow tract. • PDA = patent ductus
titration warranted. • Positive inotropes may arteriosus. • SAS = subvalvular aortic stenosis.
TREATMENT worsen fixed obstruction and are used with
APPROPRIATE HEALTH CARE caution when treating CHF. • Anesthetic drugs Suggested Reading
Therapy limited prior to onset of that cause hypotension, arrhythmias, or cardiac Caivano D, Dickson D, Martin M, et al. Murmur
complications and aimed at preventing depression should be avoided with severe SAS. intensity in adult dogs with pulmonic and
clinical signs. subaortic stenosis reflects disease severity. J
POSSIBLE INTERACTIONS Small Anim Pract 2018, 59(3):161–166.
NURSING CARE N/A Kienle RD, Thomas WP, Pion PD. The
Aimed at relieving symptoms and ALTERNATIVE DRUG(S) natural clinical history of canine congenital
complications such as arrhythmias, • Carvedilol (dogs, 0.5–1.5 mg/kg PO q12h). subaortic stenosis. J Vet Intern Med 1994,
syncope, and CHF. • Metoprolol tartrate (dogs, 0.5–1.5 mg/kg 8(6):423–431.
ACTIVITY PO q12h). Meurs KM, Lehmkuhl LB, Bonagura JD.
Restriction warranted with severe disease; Survival times in dogs with severe subvalvu-
exertion may increase incidence of arrhyth lar aortic stenosis treated with balloon
mias, syncope, and therefore risk of sudden valvuloplasty or atenolol. J Am Vet Med
death. Assoc 2005, 227(3):420–424.
FOLLOW‐UP Ontiveros ES, Fousse SL, Crofton AE, et al.
DIET Congenital cardiac outflow tract abnormali-
PATIENT MONITORING
Modest salt restriction with CHF. ties in dogs: prevalence and pattern of
• Monitor by ECG, Holter monitor, thoracic
CLIENT EDUCATION radiography, and echocardiography. inheritance from 2008 to 2017. Front Vet Sci
• SAS considered inherited disease; affected • Treatment of complications such as CHF 2019, 6(52), doi: 10.3389/fvets.2019.00052.
animals should not be bred. • Owners should and arrhythmias may necessitate additional Stern JA, White SN, Lehmkuhl LB, et al. A
be counseled on risk of endocarditis and monitoring for renal/electrolyte, blood single codon insertion in PICALM is
appropriate antibiotics for any wounds, pressure, and rhythm disturbances. associated with development of familial
infections, or surgical procedures. • Alert subvalvular aortic stenosis in Newfoundland
owners to risks of sudden death, CHF, and dogs. Hum Genet 2014, 133(9):1139–1148.
N/A
increased anesthetic risk. Author Joshua A. Stern
POSSIBLE COMPLICATIONS Consulting Editor Michael Aherne
Ventricular arrhythmias, syncope, myocardial
• No surgical or interventional technique has
infarction, sudden death, AI, mitral regurgi
been shown to extend life beyond medical
tation, endocarditis. Client Education Handout
therapy. • Balloon valvuloplasty or combined
available online
cutting and traditional balloon valvuloplasty may
A Aortic Thromboembolism
European study suggested cavalier King
Charles spaniels may be overrepresented.
BASICS Mean Age and Range DIAGNOSIS
Age range—1–20 years. Median age—
DEFINITION approximately 8–9 years (cats); 8–10 years DIFFERENTIAL DIAGNOSIS
A thrombus or blood clot that is dislodged (dogs). Hind limb paresis secondary to spinal
within the aorta, causing severe ischemia to neoplasia, trauma, myelitis, fibrocartilaginous
the tissues served by that segment of aorta. Predominant Sex infarction, or intervertebral disc protrusion.
Cats—males > females (2 : 1). Dogs—no sex These conditions resulting in spinal cord
PATHOPHYSIOLOGY predilection in United States; European study
• Aortic thromboembolism (ATE) is
injury present with signs of upper motor
suggested male predilection. neuron disease, whereas ATE patients present
commonly associated with myocardial disease
in cats, most commonly hypertrophic cardio- SIGNS with signs of lower motor neuron disease.
myopathy (HCM). It is theorized that abnormal Presence of 5 “Ps” is helpful to remember CBC/BIOCHEMISTRY/URINALYSIS
blood flow (stasis) and a hypercoagulable state classic clinical signs associated with ATE— • High creatine kinase due to muscle injury.
contribute to thrombus formation within the Pain, Paralysis or Paresis, Pulselessness, Pallor, • Higher blood lactate and lower blood
left atrium. The thrombus then embolizes and Poikilothermic (cold). glucose in affected limbs compared to normal
distally to the aorta. The most common site Historical Findings limbs.
of embolization is the caudal aortic • Acute onset paralysis and pain—most • High aspartate aminotransferase and
trifurcation (hind legs). Other less common common in cats. Vocalization and anxiety alanine aminotransferase due to muscle and
sites include the front legs, kidneys, also common. liver injury.
gastrointestinal tract, or cerebrum. • Lameness or gait abnormality, typically of • Stress hyperglycemia.
• ATE in dogs typically is associated with several weeks’ duration, more common in • High blood urea nitrogen and creatinine
neoplasia, sepsis, infectious endocarditis, dogs. due to low cardiac output and possible renal
Cushing’s disease, protein-losing nephropathy • Tachypnea or respiratory distress common emboli.
and enteropathy, or other hypercoagulable in cats. • Electrolyte derangements, due to low
states. However, in one recent retrospective • About 15% of cats may vomit prior to ATE. output and muscle damage, such as hypo
study, no concurrent condition was identified calcemia, hyponatremia, hyperphosphatemia,
in 58% of dogs. Physical Examination Findings and hyperkalemia, are not uncommon.
• Usually paraparesis or paralysis of rear legs • Nonspecific CBC and urinalysis changes.
SYSTEMS AFFECTED with signs of lower motor neuron injury. Less
• Cardiovascular—most affected cats have commonly, monoparesis of a front leg. In OTHER LABORATORY TESTS
advanced heart disease and left heart failure. dogs, majority are paretic and ambulatory. Routinely available coagulation profiles
• Nervous/musculoskeletal—severe ischemia • Absent or diminished femoral pulses. typically do not reveal significant
to muscles and nerves served by segment of • Pain upon palpation of legs. abnormalities because hypercoagulability
occluded aorta causes variable pain and • Gastrocnemius muscle often becomes firm results from hyperaggregable platelets. In
paresis. Gait abnormality or paralysis results several hours after embolization. dogs, thromboelastrography may suggest
in leg or legs involved. • Cyanotic or pale nail beds and foot pads. hypercoagulable state with clot strength
GENETICS • Tachypnea/dyspnea and hypothermia are (increased maximum amplitude) or shortened
HCM, a common associated disease, is likely common in cats. clotting time (decreased R).
heritable. Additionally, a family of domestic • Since commonly associated with heart IMAGING
shorthair cats with remodeled HCM who all disease in cats, cardiac murmur, arrhythmias,
Radiography
died of ATE has been reported. or gallop sound may be present.
• Cardiomegaly is common in cats.
INCIDENCE/PREVALENCE CAUSES • Pulmonary edema and/or pleural effusion
• In a recent observation study of over 1000 • Cardiomyopathy (all types). in approximately 50% of cats.
asymptomatic cats with HCM, nearly 12% • Hyperthyroidism. • Rarely, a mass is seen in the lungs, suggestive
developed ATE within 10 years after initial • Neoplasia. of neoplasia.
diagnosis. In two previous smaller case series • Sepsis (dogs).
Echocardiography
of cats with clinical and preclinical HCM, • Hyperadrenocorticism (dogs).
• In cats, changes consistent with
12–16% presented with signs of ATE; only • Protein-losing nephropathy and
cardiomyopathy. HCM is most common,
11–25% of cats had evidence of previously enteropathy (dogs). followed by restrictive or unclassified cardio-
known heart disease. myopathy, and then dilated cardiomyopathy.
• Rare in dogs.
RISK FACTORS
• In cats, cardiomyopathy, male sex, and • Most cases have severe left atrial enlarge
GEOGRAPHIC DISTRIBUTION gallop sound on exam are risk factors. ment (i.e., left atrial to aortic ratio of ≥2).
N/A Echocardiographic risk factors include Decreased left atrial function (fractional
SIGNALMENT enlarged left atrium, decreased left atrial shortening) and decreased left atrial appendage
function and left atrial appendage velocity, velocity (<0.2 m/s).
Species presence of spontaneous echocardiographic • Left atrial thrombus or spontaneous
Cat, rarely dog. contrast (smoke) or left atrial thrombus, and echocardiographic contrast (smoke) may be
Breed Predilections restrictive left ventricular filling pattern. seen.
Mixed-breed cats most commonly affected. • In dogs, hypercoagulable conditions, such Abdominal Ultrasonography
Abyssians, Birmans, and ragdolls over as neoplasia, sepsis, endocarditis, protein- • May be able to identify the thrombus and
represented in one study. In dogs, no breed losing nephropathies/enteropathies, and visualize lack of blood flow in the caudal aorta.
predilection identified in United States; hyperadrenocorticism are risk factors.
(continued) Aortic Thromboembolism A
• Typically unnecessary to reach a diagnosis initial episode will be on some type of anti- of 1 mg/kg q24h. Compared to aspirin,
in cats, but often needed to reach a diagnosis coagulant and heart failure medications that clopidogrel was superior in preventing
in dogs. may require frequent reevaluation and an reembolization, resulting in improved survival
DIAGNOSTIC PROCEDURES indoor lifestyle. times in cats that had survived an ATE. The
• Most cats that survive an initial episode will combination of unfractionated heparin and
ECG recover complete function to the legs; however, clopidogrel is commonly used for the manage-
• Sinus rhythm and sinus tachycardia most if ischemia is severe and prolonged, sloughing ment of ATE in cats.
common. Less common rhythms include of parts of the distal extremities or persistent
atrial fibrillation, ventricular arrhythmias, Other Options
neurologic deficits may result. In one study, • Aspirin is theoretically beneficial during
supraventricular arrhythmias, and sinus approximately 15% of cats had permanent
bradycardia. and after an ATE event due to its antiplatelet
neuromucscular abnormalities after surviving effects. The dose in cats is an 81 mg tablet
• Left ventricular enlargement pattern and the initial ATE.
left ventricular conduction disturbances (left PO q48–72h. Vomiting and diarrhea are not
• Prognosis in dogs is generally poor, but may uncommon. Some specialists advocate a mini
anterior fascicular block) are common. be better in dogs presenting with chronic (vs. dose of 5 mg/cat q72h. Antithrombotic dose
Doppler Blood Pressure acute) lameness and dogs treated appropriately recommendations for dogs range from 0.5 to
No or diminished audible blood flow in with warfarin. 2 mg/kg q24h. Always give aspirin with food.
affected limbs. SURGICAL CONSIDERATIONS • Warfarin, a vitamin K antagonist, is the
PATHOLOGIC FINDINGS • Surgical embolectomy typically not anticoagulant most widely used in humans
• Thrombus typically identified at caudal recommended, since patients are high risk and has been proposed for prevention of
aortic trifurcation. due to severe heart disease. reembolization in cats surviving an initial
• Occasionally, left atrial thrombus seen. • Rheolytic thrombectomy has been used episode. The initial dose is 0.25–0.5 mg/cat
• Emboli of kidneys, gastrointestinal tract, with limited success in a small number of cats PO q24h, or 0.05–0.2 mg/kg PO q24h in the
cerebrum, and other organs also may be seen. with ATE. dog. Overlap with heparin therapy for 3 days.
The dose is then adjusted to prolong the
prothrombin time (PT) approximately twice
its baseline value, or to attain an international
normalized ratio (INR) of 2 to 3. Long-term
MEDICATIONS management with warfarin can be challenging
TREATMENT
DRUG(S) OF CHOICE because of frequent monitoring and dose
APPROPRIATE HEALTH CARE Medical management focuses on (1) the adjustments in addition to bleeding complic
Initially, cats with ATE should be treated as thrombus, (2) analgesia, and (3) heart failure ations. In one study, dogs treated
inpatients, as many have concurrent treatments (if needed). appropriately with warfarin had a better
congestive heart failure (CHF) and require clinical outcome.
injectable drugs, in addition to being in Management of Thrombus • Low molecular weight heparin (LMWH)
considerable pain and distress. • Thrombolytic therapy (e.g., tissue has recently been proposed for the long-term
plasminogen activator [TPA]) is used prevention of feline ATE. LMWH has a more
NURSING CARE extensively in humans and infrequently in
• Fluid therapy is cautiously used, as most predictable relationship between dose and
animals. These drugs are expensive and carry response than warfarin and does not need
cats have advanced myocardial disease. If in a significant risk for bleeding complications;
CHF, IV fluids may not be necessary. monitoring or dose adjustments. It also has a
to date, improved treatment efficacy is lower risk of bleeding complications. The
• Supplemental oxygen or thoracocentesis unproven and thus they are rarely used in
may be beneficial if in CHF. main disadvantages are high drug cost and the
general practice. TPA is theorized to be more injectable route of administration. The two
• Initially, minimally handle affected legs. beneficial if given early, ideally within the first
However, as reperfusion occurs, physical LMWHs that have been used in feline ATE
few hours of the ATE. are dalteparin (100–150 units/kg SC q8–24h)
therapy (passive extension and flexion) may • Unfractionated heparin is the preferred
speed full recovery. and enoxaparin (1 mg/kg SC q12–24h). The
anticoagulant in general practice for initial best dose is unknown. LMWH is usually
• Do not perform venipuncture on affected management of feline ATE. Heparin has no
legs. started q24h due to cost. Some studies
effect on the established clot; however, it suggest q6h dosing is necessary for stable
• Animals may have difficulty posturing to prevents further activation of the coagulation
urinate and may need bladder expression to blood levels, but may increase bleeding risk.
cascade. In either cat or dog, use an initial LMWH can be used as an adjunctive anti-
prevent overdistention or urine scald. dose of 100–200 units/kg IV and then coagulant combined with clopidogrel.
ACTIVITY 200–300 units/kg SC q8h. Alternatively, • Rivaroxaban, a newer anticoagulant drug,
Restrict activity and stress. heparin can be continued as a constant rate is an inhibitor of activated clotting factor X
DIET infusion, at a dose of 25–35 units/kg/h. Some and prothrombinase activity that has shown
Initially, most cats are anorexic; tempt with advocate titrating the dose to prolong the promise for treatment and prevention of
any type of diet to keep them eating and activated partial thromboplastin time (APTT) arterial thromboembolism in both dogs and
avoid hepatic lipidosis. approximately twofold. cats. Rivaroxaban has a more predictable
• Clopidogrel is an antiplatelet aggregation anticoagulant effect than warfarin and does
CLIENT EDUCATION drug. A loading dose may be chosen for
• Short- and long-term prognosis is poor in
not require any monitoring or dose adjust
treatment of an acute ATE. The loading dose ments. The cat dose is 1.25 mg/cat PO q24h.
both dogs and cats. in the cat is 75 mg/cat PO once, and then a
• Many cats do not survive their initial
The dose recommended in dogs is 0.5–1 mg/
maintenance dose of 18.75 mg/cat (one- kg PO q24h. The main disadvantage of
episode of ATE; if they survive, the cat will fourth of a 75 mg tablet) PO q24h. The
often reembolize or die of CHF within a few rivaroxaban is its high cost at the time of this
loading dose in the dog is approximately writing. However, it has the advantage of a
months to one year. Most cats that survive an 10 mg/kg once, and then a maintenance dose shorter half-time than clopidogrel if there is a
A Aortic Thromboembolism (continued)
need to discontinue the medication because • Examine legs frequently to assess clinical
of a bleeding complication or need to response. Initially, APTT should be
perform an invasive procedure. A clinical trial performed once daily to titrate heparin dose.
is currently ongoing to compare rivaroxaban • If warfarin used, PT or INR is measured MISCELLANEOUS
and clopidogrel in cats that have survived an approximately 3 days after initiation of therapy ASSOCIATED CONDITIONS
ATE. and then weekly until desired anticoagulant See Causes & Risk Factors.
Analgesics effect reached. Thereafter, measure 3–4 times
AGE-RELATED FACTORS
• Buprenorphine in the cat is a useful and
yearly or when drug regimen is altered.
N/A
widely available drug for analgesia and PREVENTION/AVOIDANCE
ZOONOTIC POTENTIAL
sedation at a dose of 5–20 μg/kg IV, SC, Because of high rate of reembolization,
None
or in cheek pouch q6–8h. For stronger prevention with either clopidogrel, aspirin,
analgesia, use fentanyl or hydromorphone. warfarin, or LMWH is strongly PREGNANCY/FERTILITY/BREEDING
Butorphanol, while a good sedative, does recommended. N/A
not provide sufficient analgesia. POSSIBLE COMPLICATIONS SYNONYMS
• Acepromazine may be cautiously used for • Saddle thromboembolism.
• Bleeding with anticoagulant therapy.
its sedative and vasodilatory properties at a • Permanent neurologic deficits or muscular • Systemic thromboembolism.
dose of 0.01–0.02 mg SC q8–12h. However, abnormalities in hind limbs may arise with
vasodilatory effects are mixed and therefore SEE ALSO
prolonged ischemia. • Cardiomyopathy, Dilated—Cats.
results are often variable. • Recurrent CHF or sudden death. • Cardiomyopathy, Hypertrophic—Cats.
CONTRAINDICATIONS • Reperfusion injury and death usually • Cardiomyopathy, Restrictive—Cats.
N/A associated with hyperkalemic arrhythmias.
ABBREVIATIONS
PRECAUTIONS EXPECTED COURSE AND PROGNOSIS • APTT = activated partial thromboplastin
• Anticoagulant therapy with heparin, • Expected course is days to weeks for full time.
warfarin, or thrombolytics may cause recovery of function to legs. • ATE = aortic thromboembolism.
bleeding complications. • Prognosis, both short and long term, is • CHF = congestive heart failure.
• Avoid a nonselective beta blocker such as poor in cats. • HCM = hypertrophic cardiomyopathy.
propranolol as it may enhance peripheral • In two large studies, ~60% of cats were • INR = international normalized ratio.
vasoconstriction. euthanized or died during initial thrombo • LMWH = low molecular weight heparin.
embolic episode. Long-term prognosis varies • PT = prothrombin time.
POSSIBLE INTERACTIONS between 2 months and several years; however,
Warfarin may interact with other drugs, • TPA = tissue plasminogen activator.
average is a few months with treatment.
which may enhance its anticoagulant effects. Predictors of poorer prognosis include Suggested Reading
hypothermia (<99 °F) and CHF. One study Luis Fuentes V. Arterial thromboembolism:
ALTERNATIVE DRUG(S)
demonstrated median survival time of 77 risks, realities and a rational first-line
N/A
days in cats with CHF and 223 days in cats approach. J Feline Med Surg 2012,
without CHF. Predictors of better prognosis 14(7):459–470.
include normothermia, single leg affected, Winter RL, Sedacca CD, Adams A, Orton
and presence of motor function on initial EC. Aortic thrombosis in dogs: presenta-
exam. tion, therapy, and outcome in 26 cases. J
FOLLOW-UP Vet Cardiol 2012, 14:333–342.
• In dogs, the disease is rare and prognosis in
PATIENT MONITORING general is also poor. One study suggested a Author Teresa C. DeFrancesco
• ECG monitoring while cat in hospital is better prognosis if the dog had chronic Consulting Editor Michael Aherne
helpful to detect reperfusion injury and clinical signs and if treated with warfarin.
hyperkalemia-related ECG changes. Look for • Recurrence of ATE is common.
loss of P-waves and widening of QRS Client Education Handout
complexes. available online
• Monitoring electrolytes and renal
parameters periodically may be helpful to
optimize management of cardiac disease.
Apudoma A
OTHER LABORATORY TESTS used successfully in 2 dogs and 1 cat with

• Serum gastrin concentration—normal or gastrinoma.
high normal if gastrinoma. Antacid treatment CONTRAINDICATIONS/POSSIBLE
BASICS increases serum gastrin, resulting in false-
positive diagnosis of gastrinoma; withdrawal of INTERACTIONS
OVERVIEW
drugs for at least 7 days returns gastrin Because sucralfate may be less effective in an
• Tumors of endocrine cells that are
concentrations to baseline in dogs without alkaline environment and may reduce
capable of amine precursor uptake and
gastrinoma. • Induced gastrin secretion— absorption of other drugs, it should be given as
decarboxylation (APUD) and secretion of
increased gastrin concentration after IV calcium a suspension, 1–2 hours prior to antacid drugs.
peptide hormones. • APUD cells are
generally found in gastrointestinal tract and gluconate or secretin suggests gastrinoma; rarely
CNS. • Hypergastrinemia from gastrin- reported in veterinary medicine.
secreting tumors (gastrinomas) causes IMAGING
gastritis and duodenal hyperacidity, which Abdominal ultrasound may demonstrate
can cause gastric ulceration, gastric mucosal FOLLOW-UP
pancreatic mass or evidence of gastrointestinal
hypertrophy, esophageal dysfunction (chronic ulceration/thickened gastric wall; frequently, PATIENT MONITORING
reflux), and intestinal villous atrophy. the primary mass is too small to be detected. • Physical examination and clinical signs are
• Polypeptide-secreting tumors most useful measures of treatment effectiveness
(polypeptidomas) may not cause clinical DIAGNOSTIC PROCEDURES and disease progression. • Gastroscopy can
signs, but high concentration of pancreatic • CT or MRI to identify pancreatic masses monitor progression of gastritis, but is not
polypeptide may cause gastric hyperacidity and/or metastatic lesions. • Endoscopy with necessary. • Abdominal radiography or
and gastrointestinal ulceration. gastric and duodenal biopsy. • Aspirate any ultrasound may detect development of
detectable masses (rule out mast cell disease). abdominal masses. • Monitoring of CBC and
SIGNALMENT PATHOLOGIC FINDINGS serum protein levels may aid in assessing
• Gastrinoma—rare in dogs, very rare in cats; • Endoscopic biopsy—gastrointestinal gastrointestinal hemorrhage.
age range 3–12 years, mean 7.5 years (dogs). ulceration. • Histopathology of pancreatic
• Pancreatic polypeptidoma—extremely rare POTENTIAL COMPLICATIONS
tumors—islet cell tumor (not specific for Gastrointestinal perforations may occur with
in dogs. hormone type). • Immunocytochemical severe ulceration.
SIGNS staining can aid specific diagnosis. • Liver
and regional lymph node biopsies may reveal EXPECTED COURSE AND PROGNOSIS
• Vomiting. • Weight loss. • Anorexia. Survival time for gastrinoma ranges from
• Diarrhea. • Lethargy, depression. metastasis.
weeks to years.
• Melena. • Abdominal pain. • Hematemesis,
hematochezia. • Fever. • Polydipsia.
• Polypeptidomas may not cause any clinical
signs.
TREATMENT
CAUSES & RISK FACTORS • Most apudomas are malignant and have MISCELLANEOUS
Unknown metastasized by the time of diagnosis; SEE ALSO
long-term control is difficult. • Aggressive Gastroduodenal Ulceration/Erosion.
medical management can palliate signs for
months to years. • Surgical exploration and ABBREVIATIONS
excisional biopsy/surgical debulking of a • APUD = amine precursor uptake and
DIAGNOSIS pancreatic mass are important both decarboxylation.
diagnostically and therapeutically. • Medical • BUN = blood urea nitrogen.
DIFFERENTIAL DIAGNOSIS • NSAID = nonsteroidal anti-inflammatory
management for gastric hyperacidity.
• Conditions associated with hypergastrinemia, drug.
gastric hyperacidity, and gastrointestinal
ulceration: ◦ Uremia. ◦ Hepatic failure. Suggested Reading
◦ Drug-induced ulceration, e.g., nonsteroidal Hughes SM. Canine gastrinoma: a case study
anti-inflammatory drugs (NSAIDs) or and literature review of therapeutic options.
MEDICATIONS N Z Vet J 2006, 54(5):242–247.
steroids. ◦ Inflammatory gastritis. ◦ Stress-
induced ulceration. ◦ Mast cell disease. DRUG(S) OF CHOICE Lane M, Larson J, Hecht S, Tolbert MK.
• Omeprazole—proton pump inhibitor; potent Medical management of gastrinoma in a
CBC/BIOCHEMISTRY/URINALYSIS inhibitor of gastric acid secretion; preferred. cat. JFMS Open Rep 2016,
• Normal or reflective of chronic disease or • Histamine H2-receptor antagonists— 2(1):2055116916646389.
iron-deficiency anemia due to chronic cimetidine, ranitidine, famotidine; decrease acid Author Alyssa M. Sullivant
gastrointestinal bleeding. • Regenerative secretion by gastric parietal cells. • Sucralfate— Consulting Editor Patty A. Lathan
anemia. • Increased blood urea nitrogen adheres to ulcerated gastric mucosa and protects Acknowledgment The author and editor
(BUN). • Hypoproteinemia. • Electrolyte from acid; promotes healing by binding pepsin acknowledge the prior contribution of
abnormalities. and bile acids and stimulating local prosta Thomas K. Graves.
glandins. • Octreotide–somatostatin analog—
A Arteriovenous Fistula and Arteriovenous Malformation
• Acquired AVF typically results from local en bloc resection of an AVM is necessary
vascular damage via trauma, surgery, veni- for cure.
puncture, perivascular injection, or neoplasia. • Transcatheter therapies with coils,
BASICS devices, or glue are newer treatment
OVERVIEW options; potential advantages include less
• Abnormal, low-resistance connections invasive therapy and intravascular access to
between an artery and a vein (systemic or remote lesions. Coils or occlusive devices
portal) that bypass a capillary bed. DIAGNOSIS are often sufficient for treatment of AVF;
• Arteriovenous malformation (AVM)— AVMs have been terminated by glue
typically congenital, involving a vascular nidus, DIFFERENTIAL DIAGNOSIS embolization of the arterial nidus, and
or complex network of communicating vessels. • Peripheral lesions (limb, ear) may look like more recently by embolization or ligation
• Arteriovenous fistula (AVF)—often a mass. of the dominant outflow vein, which
acquired, direct, and singular connections. • Vascular aneurysm or pseudoaneurysm. appears to limit shunt flow.
• Large lesions cause marked drop in systemic • Atypical clinical findings, depending on • Lesions may recur. In some cases, staged
vascular resistance and compensatory increase in location, may suggest other disease processes; procedures or surgical removal of the affected
cardiac output; this may cause circulatory volume AVF/AVM may be a late diagnostic consid- limb or organ (e.g., amputation, liver
overload and congestive heart failure (CHF). eration. lobectomy) may be necessary.
• Variable location: CBC/BIOCHEMISTRY/URINALYSIS
◦◦ AVM most often reported in liver of dogs May reflect damage to systems in vicinity of
(termed arterioportal malformations/fistulas). lesion, i.e., hepatic, renal, or other organ
◦◦ AVF more often in limbs or at sites of dysfunction.
previous surgery/trauma.
OTHER LABORATORY TESTS MEDICATIONS
SIGNALMENT N/A DRUG(S) OF CHOICE
• Dog and cat (rare in both). • Depend on site of lesion and secondary
IMAGING
• No specific age, breed, or sex—AVMs clinical features.
typically in younger animals; 15% of hepatic Thoracic Radiography • Medical treatment for CHF or other organ
AVMs found in Labrador retrievers in a Cardiomegaly and pulmonary overcirculation dysfunction may be required before surgery.
recent multicenter study. with hemodynamically significant lesions.
Microhepatica and loss of abdominal detail in CONTRAINDICATIONS/POSSIBLE
SIGNS INTERACTIONS
hepatic AVMs.
Historical Findings Avoid excessive fluid administration; patients
Ultrasonography
• Depends on the lesion location (e.g., ascites are often volume overloaded and in a high
• Lesions appear as cavernous, often tortuous,
with hepatic AVM). cardiac output state.
vascular structures.
• Often prior trauma to affected area with AVF.
• May observe high-velocity, turbulent flow
• Warm, nonpainful swelling at site may be
on Doppler ultrasound.
noted.
• Hepatofugal flow in portal vein (away from the
• Shunt may cause local organ dysfunction.
liver) nearly always apparent in hepatic AVM.
Physical Examination Findings • Echocardiography may show four-chamber FOLLOW-UP
• Vary and depend on location. dilation and functional atrioventricular valve Postoperative reevaluation and imaging
• Signs of CHF (e.g., tachypnea, cough, regurgitation due to increased circulating needed to determine whether the lesion has
exercise intolerance) may develop with blood volume. recurred and if organ dysfunction has
chronic disease and high blood flow. resolved.
Cross-sectional Imaging
• Bounding pulses may be present due to
CT or MRI can aid in diagnosis, particularly
high ejection volume and rapid runoff
when contrast is timed to highlight vascular
through AVM/AVF.
anatomy.
• Continuous murmur (bruit) at the site.
• Cautious compression of the artery proximal Angiography MISCELLANEOUS
to the lesion abolishes the bruit. When blood Selective angiography is the optimal test and is
performed at time of intervention, if transcath- SEE ALSO
flow is high, this may also elicit an immediate
eter therapy is pursued; digital subtraction Congestive Heart Failure, Left-Sided.
reflex decrease in heart rate (Branham’s sign).
• Edema, ischemia, and congestion of organs angiography can improve visualization. ABBREVIATIONS
and tissues caused by high venous pressure in DIAGNOSTIC PROCEDURES • AVF = arteriovenous fistula.
proximity of lesion. N/A • AVM = arteriovenous malformation.
• If the lesion is on a limb, pitting edema, • CHF = congestive heart failure.
lameness, ulceration, scabbing, and gangrene Suggested Reading
may result. Weisse C, Berent A, eds. Veterinary Image-
• Lesions near vital organs may cause signs Guided Interventions. Ames, IA: Wiley-
associated with organ failure, e.g., ascites TREATMENT Blackwell, 2015.
(liver), seizures (brain), paresis (spinal cord). • Surgery can be difficult, labor-intensive, Author Brian A. Scansen
CAUSES & RISK FACTORS and may require blood transfusion. Ligation Consulting Editor Michael Aherne
• AVM is rare; frequently congenital. or division of an AVF is often curative;
Arteriovenous Malformation of the Liver A
cephalus; idiopathic epilepsy; metabolic Radiographic Contrast Angiography

disorders (e.g., hypoglycemia, hypokalemia, • Not indicated in most cases.
or hyperkalemia); HE (e.g., acquired liver • Venous portography—only confirms APSS.
BASIC disease or PSVA). • Hepatic arteriography—required to confirm
OVERVIEW • Abdominal effusion—pure transudate AV communication (celiac trunk or anterior
• Intrahepatic arteriovenous (AV) malfor (ascites; protein-losing nephropathy, mesenteric artery contrast injection).
mations (also referred to as AV fistulae) are protein-losing enteropathy, liver disease); Multisector CT
communications between proper hepatic modified transudate (congenital cardiac Noninvasive contrast imaging of hepatic
arteries and intrahepatic portal veins; this malformations, right-sided heart failure, vasculature; arterial and venous phases; three-
anatomic union results in hepatofugal (away pericardial tamponade, supradiaphragmatic dimensional reconstruction illustrates AV
from the liver) splanchnic circulation. vena caval obstruction, neoplasia, portal vein malformation, large liver lobe, atrophied liver.
• Blood flows directly from a hepatic artery thrombosis); hemorrhage.
into portal vasculature retrograde into the • Portal hypertension—chronic hepatic Echocardiography
vena cava through multiple acquired porto- disease, ductal plate malformations/ Rule out right-sided heart disease, pericardial
systemic shunts (APSS). congenital hepatic fibrosis, noncirrhotic or disease, and vena caval occlusion.
• Associated with ascites. idiopathic portal hypertension, cirrhosis, DIAGNOSTIC PROCEDURES
• Uncommon, usually congenital, but may be portal thrombi. • Multisector CT and exploratory laparotomy.
acquired (surgical injury, trauma, neoplasia). • Liver biopsy—collect samples from affected
SIGNALMENT • Erythrocyte microcytosis (APSS), target
and unaffected liver lobes; “normal” liver often
• Dogs, less common in cats. cells. demonstrates severe vascular arterialization
• Age-related presentation (congenital): <2 years. • Hypoalbuminemia with normal or low
(more severe than associated with PSVA).
• No sex or breed predilection. serum globulins; alkaline phosphatase (ALP)
SIGNS and alanine aminotransferase (ALT) activity
normal or moderately increased; variable low
General Comments blood urea nitrogen (BUN); hypocholestero
Vague or acute illness; present for signs caused lemia; anicteric. TREATMENT
by portal hypertension and APSS—ascites • Hyposthenuria or isosthenuria. APPROPRIATE HEALTH CARE
and hepatic encephalopathy (HE). • Ammonium biurate crystalluria. Inpatient—treat HE and ascites prior to
Historical Findings surgical approach or percutaneous selective
• Dogs may have a normal transition to acrylamide embolization.
• Coagulation tests—variable, may be
growth foods, unlike portosystemic vascular normal; low protein C activity reflects APSS. NURSING CARE
anomalies (PSVA) that demonstrate HE. • Total serum bile acids—preprandial values • Diet—restrict nitrogen intake to ameliorate
• May have an acute onset of ascites or HE. variable, postprandial values increased; classic HE and hyperammonemia; restrict sodium to
• Vague signs include lethargy, anorexia, shunting pattern. attenuate ascites formation.
vomiting, diarrhea, weight loss, polydipsia, • Plasma ammonia—usually increased, • HE—resolve endoparasitism, electrolyte
dementia, abdominal distention, and uroliths inferred by ammonium biurate crystalluria. and hydration disturbances, treat infections,
causing obstructive uropathy. • Peritoneal fluid—pure transudate (total initiate treatments to alter enteric uptake and
Physical Examination Findings protein <2.5 g/dL) or modified transudate. formation of HE toxins (see Hepatic
• Lethargic, poor body condition, ascites; Encephalopathy).
enlarged liver lobe containing the AV IMAGING • Ascites—mobilize by restricting activity and
malformation; rarely palpated on initial Radiography sodium intake and instituting dual diuretic
examination. • Abdominal effusion. therapy (furosemide and spironolactone);
• Rarely, bruit auscultated over AV • Microhepatia or normal-sized liver due to reserve therapeutic abdominocentesis for
malformation. enlarged lobe with AV malformation. tense ascites impairing ventilation, nutrition,
• Renomegaly. sleep, or recumbent posture (see Hypertension,
CAUSES & RISK FACTORS • Normal thorax. Portal; Portosystemic Shunting, Acquired;
• Usually congenital vascular malformations
Abdominal Ultrasonography and below).
(single or multiple vessels) reflecting failed
differentiation of common embryologic anlage. • Abdominal effusion. SURGICAL CONSIDERATIONS
• Rare—secondary to abdominal trauma, • Liver lobe with AV malformation—large • Resection of liver lobe containing AV
inflammation, neoplasia, surgical interventions, compared to most other liver lobes that are malformation is complicated by coexistence
or diagnostic procedures (e.g., liver biopsy). atrophied due to portal hypoperfusion. of additional hepatic vascular malformations;
• Portal hypertension—reflects arterialization • Tortuous anechoic tubules represent AV clinical cure possible but unlikely.
of valveless portal system—establishing structure with unidirectional pulsating or • Percutaneous selective acrylamide vascular
APSS. turbulent flow on color-flow Doppler. embolization; complicated by risk of thrombo-
• Hepatic artery and/or portal vein branches embolism of additional vasculature;
may appear tortuous. temporary improvement, but treatment may
• Hepatofugal portal flow (away from the be curative.
liver)—through APSS. • Multiple microscopic vascular malformations
DIAGNOSIS • Renomegaly. continue portal hypertension and APSS.
DIFFERENTIAL DIAGNOSIS • Urolithiasis—urinary bladder or renal pelvis. • Do not ligate APSS nor band the vena cava.
• CNS signs—infectious disorders (e.g., • Rule out portal thrombosis (luminal filling
distemper); toxicity (e.g., lead); hydro defect, abrupt blood flow termination).
A Arteriovenous Malformation of the Liver (continued)
interactions and may have a 24–48h delayed • Most patients require indefinite nutritional
onset of action; some clinicians recommend and medical management (HE, ascites)
chronic treatment to minimize GI bleeding because of coexisting microscopic vascular
MEDICATIONS and ulceration that may be chronic problems). malformations across the liver; APSS persists
DRUG(S) OF CHOICE • Gastroprotectant—sucralfate: 0.25–1.0 g/10 requiring continued management of HE.
kg PO q8–12h; titrate to effect, beware of
Hepatic Encephalopathy
drug interactions as sucralfate may bind other
See Hepatic Encephalopathy
medications, reducing bioavailability.
Ascites • Eliminate endoparasitism.
• Restrict sodium intake. MISCELLANEOUS
• Furosemide (0.5–2 mg/kg PO IM or IV
q12–24h)—combine with spironolactone. INTERACTIONS SEE ALSO
• Spironolactone (0.5–2 mg/kg PO q12h)— Avoid drugs dependent on hepatic biotrans • Ascites.
double initial dose as loading dose once. formation or first-pass hepatic extraction • Coagulopathy of Liver Disease.
• Chronic diuretic therapy—individualized (reduced by APSS) or that react with • Hepatic Encephalopathy.
to response, 4- to 7-day assessment intervals γ-aminobutyric acid (GABA)-benzodiazepine • Hypertension, Portal.
used to titrate dose to response, avoiding receptors because of propensity for HE. • Portosystemic Shunting, Acquired.
hydration, electrolyte, and HE complications. • Portosystemic Vascular Anomaly,
• Diuretic-resistant ascites—may require Congenital.
therapeutic abdominocentesis; to initiate ABBREVIATIONS
diuresis. • ALP = alkaline phosphatase.
• Vasopressin V2 receptor antagonists newly
FOLLOW-UP
• ALT = alanine aminotransferase.
available may control ascites accumulation. PATIENT MONITORING • APSS = acquired portosystemic shunt.
(See Portosystemic Shunting, Acquired.) Biochemistry—initially monthly until • AV = arteriovenous.
Bleeding Tendencies
stabilized after surgery or AV malformation • BUN = blood urea nitrogen.
See Coagulopathy of Liver Disease. embolization, thereafter quarterly; monitor • GABA = γ-aminobutyric acid.
for hypoalbuminemia, infection, optimization • HE = hepatic encephalopathy.
Gastrointestinal Hemorrhage of HE management, and control of ammo • PSVA = portosystemic vascular anomalies.
• Histamine type-2 receptor antagonists nium biurate crystalluria. Author Sharon A. Center
(famotidine 0.5–2.0 mg/kg PO, IV, or SC Consulting Editor Kate Holan
q12–24h); or HCl pump inhibitors EXPECTED COURSE AND PROGNOSIS
• Prognosis fair if patient survives surgical
(omeprazole 1.0 mg/kg/24h PO or
pantoprazole 1.0 mg/kg/24h IV; omeprazole resection of AV malformation or
may induce p450 cytochrome-associated drug embolization.
Arthritis (Osteoarthritis) A
to poorer vascularity of synovial membrane as • Joint instability.

well as lack of functionality of synovium due
to lack of motion in joint. CAUSES
BASICS • Osteophytes and enthesiophytes develop • Primary—no known cause.
around and within joint to increase load- • Secondary—results from initiating cause:
DEFINITION
bearing surface area. abnormal wear on normal cartilage (e.g., joint
Osteoarthritis (OA) or degenerative joint
• These changes reduce functionality and
instability, joint incongruity, trauma to
disease is a chronic and progressive disease
may eventually lead to ankylosis. cartilage or supporting soft tissues, obesity)
that leads to loss of articular cartilage and
or normal wear on abnormal cartilage
ultimately failure of the joint. OA is SYSTEMS AFFECTED (e.g., osteochondral defects).
characterized as a noninfectious disorder of Musculoskeletal—diarthrodial joints.
diarthrodial (synovial) joints, such that the RISK FACTORS
disease process involves the entire joint, not GENETICS • Working, athletic, and obese dogs place
just the articular cartilage. It is due to both • Primary OA rare, occurring more com- more stress on their joints.
primary (idiopathic) and secondary causes. monly in cats or in smaller (manus, pes) • Dogs with disorders that affect collagen or
joints of dogs. cartilage (Cushing’s disease, diabetes mellitus,
PATHOPHYSIOLOGY • Dogs—causes of secondary OA are varied, hypothyroidism, hyperlaxity, prolonged
• Ebb and flow characterization with periods of including hip and elbow dysplasia, osteo- steroid use).
calmness followed by periods of exacerbation chondritis dessicans (OCD), patellar
of clinical signs (flare-ups). luxations, congenital shoulder luxation,
• OA initiated by mechanical stress—traumatic Legg-Perthes, cranial cruciate ligament
injury, instability, abnormal conformation, rupture, intra-articular fractures, obesity, as
abnormal activity, etc. well as many other causes. DIAGNOSIS
• Inflammatory mediators and free radicals • Cats—causes of secondary OA are patellar DIFFERENTIAL DIAGNOSIS
such as metalloproteinases, serine proteases, luxation, hip dysplasia, obesity, and arthro- • Neoplastic (synovial sarcoma; rarely,
cysteine protease enzymes, and reactive pathy. chondrosarcoma; osteosarcoma).
oxygen species are released from damaged • Septic arthritis (caused by bacteria;
chondrocytes and synovium, resulting in INCIDENCE/PREVALENCE
spirochetes; L forms in cats; Mycoplasma;
breakdown of extracellular matrix of articular • Dog—very common; 20% of dogs older
Rickettsia; Ehrlichia; viruses such as feline
cartilage, causing collagen degradation and than 1 year have some degree of OA.
calicivirus; fungi and protozoa).
loss of collagen cross-linking. • Cat—90% of cats over 12 years of age had
• Immune-mediated arthritis (erosive vs.
• Collagen synthesis is altered, resulting in evidence of OA on radiographs.
nonerosive).
decreased collagen/proteoglycan interaction • Clinical problems are more prevalent in
• Other musculoskeletal conditions that
and reduced hydrophilic matrix properties. larger, overweight, and very active animals.
cause lameness.
• Extracellular matrix further compromised • Primary OA is rare.
• Neurologic conditions causing lameness or
by increased breakdown of proteoglycans decreased activity/weakness.
SIGNALMENT
along with manufacture of poorer-quality
proteoglycans. Species OTHER LABORATORY TESTS
• Nitric oxide released along with other free Dog and cat. • Coombs’ test, antinuclear antibody (ANA),
radicals, which mediates cartilage breakdown and rheumatoid factor may help to rule out
Mean Age and Range
and supports chronic inflammation. immune-mediated arthritis.
• Secondary OA due to congenital disorders
Chondrocyte apoptosis facilitated by • Serum titers for Borrelia, Ehrlichia, and
(OCD, hip dysplasia) seen in immature
cyclooxygenase-2 enzymes and oxidative stress. Rickettsia to evaluate for infectious arthritis.
animals; some present with OA signs when
• Synovitis is driving force of the inflamma- mature (hip and elbow dysplasia). IMAGING
tory cascade in OA, in addition to resulting in • Secondary to trauma—any age. • Radiographic changes—include joint capsular
decreased viscosity of synovial fluid, reducing distention, osteophytosis, enthesophytosis,
lubrication. SIGNS
soft-tissue thickening, and narrowed joint spaces.
• Poorer-quality synovial fluid reduces oxygen Historical Findings In severely affected patients: subchondral
and nutrient supply to chondrocytes as well as • Dogs—decreased activity level, unwilling to sclerosis and intra-articular calcified bodies
waste removal. perform certain tasks; intermittent lameness (joint mice).
• Subchondral bone becomes sclerotic, or stiff gait that slowly progresses; possible • Radiographic severity often does not
worsening loading qualities of bone and history of joint trauma, OCD, or develop- correlate with clinical severity.
overlying cartilage. mental disorders; may be exacerbated by • Stress radiography may identify underlying
• Pain of OA results from distention of the exercise, long periods of recumbency, and instability and accentuate joint incongruity
joint capsule and stimulation of pain cold weather. (e.g., distraction index, passive hip laxity of
receptors, inflammation of synovium, • Cats—overt lameness may not be seen. coxofemoral joint is predictive of hip OA).
increased mechanical loading of subchondral Reduction in activity, reluctance to jump, • Bone nuclear scintigraphy can assist in
bone, alteration of function of surrounding unkempt appearance, difficulty accessing localizing subtle OA.
tendons and ligaments, as well as develop- litter box, and increased irritability. • Arthroscopy can allow direct observation of
ment of periarticular fibrosis. cartilage and characterization by Modified
• The result of these processes is progressive Outerbridge Score.
• Stiff-legged or altered gait or nonuse of leg.
cartilage degradation ranging from fibrillation
• Decreased range of motion. DIAGNOSTIC PROCEDURES
to deep fissuring of cartilage. Full-thickness
• Crepitus. • Arthrocentesis and synovial fluid analysis—
cartilage loss can eventually occur.
• Joint swelling (effusion and/or thickening cell counts are normal or slightly increased
• Periarticular fibrosis occurs, resulting in a
of the joint capsule). (<2,000–5,000 cells/mL) predominantly
reduction of joint motion (and pain), leading
• Joint pain.
A Arthritis (Osteoarthritis) (continued)
mononuclear (macrophages) and occasional CLIENT EDUCATION (MSM), mixtures with MSM, or other
synovial lining cells. • Medical therapy is palliative and the supplements (e.g., Dasuquin® Advanced,
• Bacterial culture of synovial fluid or condition is likely to progress. GlycoFlex® 2, Synflex).
synovium—negative. • Describe identifying signs of flare-ups and
CONTRAINDICATIONS
• Biopsy of synovial tissue to rule out importance of getting it under control
• NSAIDs must not be given with steroids.
neoplasia or immune-mediated arthropathy quickly.
• Acetaminophen must not be given to cats.
(lymphocytic plasmacytic synovitis, systemic • Discuss management options, daily
lupus erythematosus). exercise, activity level, and diet. PRECAUTIONS
• NSAIDs may cause gastric ulceration.
PATHOLOGIC FINDINGS SURGICAL CONSIDERATIONS
• Cyclooxygenase-2 (COX-2)-selective drugs
• Fibrillation or erosion of articular cartilage. • Arthrotomy—used to remove aggravating
• Eburnation and sclerosis of subchondral bone. causes (e.g., fragmented coronoid process, may interfere with liver function when used
• Thickening and fibrosis of joint capsule. ununited anconeal process, osteochondral flaps). outside of dosage range
• When switching NSAIDs—wait 3 days for
• Synovial fluid can be grossly normal to thin • Arthroscopy—used to diagnose and remove
and watery, usually increased volume. aggravating causes. washout before starting new drug.
• Synovial villous hypertrophy and hyperplasia. • Reconstructive procedures—used to POSSIBLE INTERACTIONS
• Osteophytes and enthesiophytes at joint eliminate joint instability and correct Steroids with NSAIDS.
capsule attachments and adjacent to the joint. anatomic problems (cruciate ligament
• Neovascularization or pannus in severe rupture, patella luxation, angular deformity). ALTERNATIVE DRUG(S)
cases over joint surfaces. • Free-radical scavengers.
• Joint removal—femoral head and neck
• Amantadine (3–5 mg/kg PO q24h)—best
ostectomy, temperomandibular joint arthro-
plasty. used in combination with another analgesic
• Joint replacement—total hip replacement is
such as NSAID. Only analgesic (other than
widely used, total elbow and stifle replace- NSAID) with scientific evidence for usage
TREATMENT ment are used with less frequency, total ankle with OA.
APPROPRIATE HEALTH CARE • Gabapentin (5–10 mg/kg PO q8-12h)—no
and shoulder replacment are experimental
• Medical—usually tried initially. and used infrequently at this time. scientific evidence for usage with OA.
• Surgical options—to improve joint geometry • Codeine (1–2 mg/kg PO q 8–12h)—no
• Joint fusion (arthrodesis)—in selected
or remove bone-on-bone contact areas through chronic cases and for joint instability, scientific evidence for usage with OA;
total joint arthroplasty, ostectomy, or joint fusion. complete or partial; carpus, hock: generally suggested for short-term use during flare-ups.
• Glucocorticoids—inhibit inflammatory
NURSING CARE excellent outcome; shoulder, elbow, stifle: less
predictable outcome. mediators and cytokines; however, chronic
• Physical rehabilitation—very beneficial use delays healing and initiates damage to
during periods of flare-ups. articular cartilage; potential systemic side
• Maintaining or increasing joint motion— effects documented; goal is low dose (dogs,
active and passive range of motion exercises, 0.5–2 mg/kg; cats, 2–4 mg/kg) q48h.
stretching, massage, therapeutic exercises, and MEDICATIONS • Prednisone—initial dose 1–2 mg/kg PO q24h
hydrotherapy. for dogs and 4 mg/kg PO q24h for cats.
• Pain management—cold and heat therapy,
DRUG(S) OF CHOICE
• Triamcinolone hexacetonide—intra-articular
transcutaneous electrical stimulation (TENS), Nonsteroidal Anti-inflammatory Drugs injection of 5 mg in dogs showed a protective
and acupuncture. (NSAIDs) and therapeutic effect in one model.
• Muscle tone/strengthening—daily leash • Inhibit prostaglandin synthesis through • Hyaluronic acid—intra-articular injection
walking, incorporation of inclines/declines, cyclooxygenase enzymes. (15–30 mg/joint) used as a series of 3
stair ascent and stair descent, walking on • Deracoxib (3–4 mg/kg PO q24h, chewable). separated by 1 week or in combination
uneven terrain, open water swimming, • Carprofen (2.2 mg/kg PO q12h or q24h). with an intra-articular steroid.
underwater and land treadmill. • Meloxicam (load 0.2 mg/kg PO, then • Platelet-rich plasma—intra-articular
• Maintenance of a lean body weight through 0.1 mg/kg PO q24h, liquid). injection to decrease inflammatory mediators;
both diet and daily exercise. • Tepoxalin (load 20 mg/kg, then 10 mg/kg many patients need more than 1 injection
ACTIVITY PO q24h). separated by 2 weeks; weak scientific evidence
• During periods of calmness, daily leash • Cats—meloxicam (0.1 mg/kg PO q24h, for efficacy.
walks to work up to twice-daily level flat liquid) or robenacoxib (1 mg/kg PO q24h for
ground for 20 minutes before incorporation 3 days).
of increased time or terrain. • Inhibit prostaglandin synthesis at receptor
• Limitation of daily activity that minimizes specific sites.
• Grapiprant (2.0 mg/kg PO q24h, chewable). FOLLOW-UP
aggravation of clinical signs during periods of
flare-up (avoidance of running, chasing, PATIENT MONITORING
Disease-Modifying Osteoarthritis Agents
jumping, and playing). • During flare-up recheck 2 weeks later; pain
(DMOAs) should be better controlled at this time; then
DIET • Host of products, many with little produc- recheck every 4–6 weeks until flare-up under
• Weight reduction for obese patients— tion oversight so effects vary widely. Supply control.
decreases stress placed on arthritic joints. polysulfated glycosaminoglycan (PSGAG) • Recheck OA patients every 4–6 months
Begin by feeding 60% of calories needed to molecules to repair and regenerate cartilage. for life.
maintain current body weight. • Adequan®—clinical study in dogs with hip • Any clinical deterioration could indicate a
• Omega n-3 fatty acids decrease production of dysplasia; 4.4 mg/kg IM every 3–5 days for 8 flare-up—need to change drug selection or
certain prostaglandins and modulate inflamma- injections had positive, temporary effect. dosage; may indicate need for intra-articular
tion. Dosage should be 150–175 mg/kg DHA/ • Glucosamine and chondroitin sulfate—oral
EPA daily. Cosequin®, oral methylsulfonylmethane
(continued) Arthritis (Osteoarthritis) A
injection, formal rehabilitation therapy, or • MSM = methylsulfonylmethane. symptoms: a randomized, double-blind,

surgical intervention. • NSAID = nonsteroidal anti-inflammatory placebo-controlled study using acetami-
PREVENTION/AVOIDANCE drug. nophen as a side comparator. Arthritis
Early identification of predisposing causes • OA = osteoarthritis. Rheum 2007, 56(2):555–567.
and prompt treatment to help reduce • OCD = osteochondritis dessicans. Johnston SJ. Osteoarthritis joint anatomy,
progression of secondary conditions, e.g., • PSGAG = polysulfated glycosaminoglycan. physiology and pathobiology. Vet Clin
surgical removal of osteochondral lesions. Suggested Reading North Am 1997, 27:699–723.
Aragon CL, Hofmeister EH, Budsberg SC. Mlacnik E, Bockstahler BA, Muller M, et al.
EXPECTED COURSE AND PROGNOSIS Effects of caloric restriction and a moderate
• Slow progression of disease likely.
Systematic review of clinical trials of
treatments for osteoarthritis in dogs. J Am or intense physiotherapy program for
• Some form of medical or surgical treatment treatment of lameness in overweight dogs
usually allows a good quality of life when Vet Med Assoc 2007, 230(4):514–521.
Baime MJ. Glucosamine and chondroitin with osteoarthritis. J Am Vet Med Assoc
managed appropriately and aggressively. 2006, 229(11):1756–1760.
sulphate did not improve pain in osteoar-
thritis of the knee. Evid Based Med 2006, Van Der Kraan PM, Van Den Berg WB.
11(4):115. Osteophytes: relevance and biology.
Budsberg SC, Bartges JW. Nutrition and Osteoarthritis Cartilage 2007, 15(3):237–244.
MISCELLANEOUS osteoarthritis in dogs: does it help? Vet Clin Author David Dycus
North Am Small Anim Pract 2006, Consulting Editor Mathieu M. Glassman
SYNONYMS Acknowledgment The author and book
• Degenerative arthritis. 36(6):1307–1323.
Glass GG. Osteoarthritis. Dis Mon 2006, editors acknowledge the prior contribution of
• Degenerative joint disease. Walter C. Renberg.
• Osteoarthritis. 52(9):343–362 (human review).
• Osteoarthrosis. Hampton T. Efficacy still uncertain for widely
used supplements for arthritis. J Am Med Client Education Handout
ABBREVIATIONS Assoc 2007 297(4):351–352.
• ANA = antinuclear antibody. available online
Herrero-Beaumont G, Ivorra JA, Del Carmen
• COX-2 = cyclooxygenase-2. Trabado M, et al. Glucosamine sulfate in
• DMOA = disease-modifying osteoarthritis agent. the treatment of knee osteoarthritis
A Arthritis, Septic
• Localized joint heat. • Decreased range of Synovial Fluid Culture
motion. • Local lymphadenopathy. • Pyrexia. • Positive culture is definitive but not
CAUSES necessary for diagnosis; negative culture does
BASICS not rule out infection. • Must be collected
• Aerobic bacterial organisms—most common:
DEFINITION staphylococci, streptococci, coliforms, and aseptically; requires heavy sedation or
Pathogenic microorganisms within the closed Pasteurella. • Anaerobic organisms—most general anesthesia. • Place fluid sample in
space of one or more synovial joints. common: Propionibacterium, Peptostreptococcus, aerobic and anaerobic culturettes and in
Fusobacterium, and Bacteroides. • Spirochete— blood culture medium. • Use 1 : 9 dilution
PATHOPHYSIOLOGY of synovial fluid to blood culture media.
• Usually caused by contamination associated Borrelia burgdorferi. • Mycoplasma. • Fungal
• Culturette samples—cultured immediately
with traumatic injury (e.g., a direct penetrating agents—Blastomyces, Cryptococcus, and
Coccidioides. • Rickettsial—Anaplasma, upon arrival at the laboratory. • Blood
injury such as bite, gunshot wound, foreign culture medium—reculturing after 24 hours
object), a sequela to surgery, arthrocentesis or Ehrlichia, Rickettsia. • Leishmania.
• Feline calicivirus.
of incubation increases accuracy by 50% and
joint injection, hematogenous spread of is the preferred method. • Mycoplasma,
microorganisms from a distant septic focus, RISK FACTORS bacterial L-forms, and protozoa require
or less commonly the extension of primary • Predisposing factors for hematogenous specific culture procedures—contact
osteomyelitis. • Primary sources of infection—diabetes mellitus, hypoadreno laboratory prior to sample collection.
hematogenous infection—urogenital, corticism (Addison’s disease), immuno
integumentary (including ears and anal sacs), Other
suppression. • Penetrating trauma to the joint
respiratory, cardiac, and gastrointestinal • Synovial biopsy—to rule out immune-
including surgery. • Existing osteoarthritis or
systems. other joint damage. • Intra-articular mediated joint disease; no more effective than
injection, particularly if steroid injected. incubated blood culture medium for growing
SYSTEMS AFFECTED bacterial organisms. • Blood and urine
Musculoskeletal—usually affects one joint. cultures if hematogenous source is suspected.
GENETICS PATHOLOGIC FINDINGS
N/A • Synovium—thickened; discolored; often
INCIDENCE/PREVALENCE DIAGNOSIS very proliferative. • Histology—evidence of
Relatively uncommon cause of monoarticular DIFFERENTIAL DIAGNOSIS hyperplastic synoviocytes. • Increased
arthritis in dogs and cats. • Osteoarthritis. • Trauma. • Immune- numbers of neutrophils, macrophages, and
GEOGRAPHIC DISTRIBUTION mediated arthropathy. • Postvaccinal transient fibrinous debris. • Cartilage—loss of
May be an increased incidence in areas with polyarthritis. • Greyhound polyarthritis. proteoglycan, destruction of articular surface,
endemic Lyme disease. • Feline progressive polyarthritis. • Crystal- pannus formation.
induced joint disease. • Synovial sarcoma.
SIGNALMENT
Species
• Hemogram—inflammatory left shift in
• Most common in dogs. • Rare in cats.
some cases. • Other results normal. TREATMENT
Breed Predilections
OTHER LABORATORY TESTS APPROPRIATE HEALTH CARE
Any; medium to large breeds—most
Serologic testing for specific pathogens. • Inpatient—initial stabilization; initiate
commonly German shepherds, Dobermans,
and Labrador retrievers. IMAGING systemic antibiotic therapy as soon as fluid is
obtained for bacterial culture; consider joint
Mean Age and Range Radiography drainage/lavage as soon as possible to minimize
Any age; usually between 4 and 7 years. • Early disease—may reveal thickened and intra-articular injury. • Analgesia with anti-
Hematogenous—more common in dense periarticular tissues; may see evidence inflammatory medications if appropriate, and
immature animals. of synovial effusion. Often difficult to intravenous opioid. • Identify and treat source
diagnose early disease radiographically. • Late if hematogenous spread is suspected.
Predominant Sex
disease—reveals bone destruction, osteolysis, • Outpatient—long-term management.
Male
irregular joint space, discrete erosions, and
SIGNS periarticular osteophytosis. NURSING CARE
Alternating heat and cold packing—beneficial
General Comments DIAGNOSTIC PROCEDURES in promoting increased blood flow and
Always consider the diagnosis in patients decreased swelling.
Synovial Fluid Analysis
with acute, monoarticular lameness
• Increased volume. • Turbid fluid. ACTIVITY
associated with soft tissue swelling, heat,
• Decreased viscosity. • Decreased mucin Restricted until resolution of symptoms.
and pain.
clot reaction. • Make slides immediately;
Historical Findings if additional fluid is obtained, place in EDTA DIET
• Lameness—acute onset most common, tube. • Elevated white blood cell (WBC) N/A
but can present as chronic lameness. count—i.e., >80% neutrophils with CLIENT EDUCATION
• Lethargy. • Anorexia. • May report >40,000/mm3 (normal joint fluid <10% • Discuss probable cause. • Warn client about
previous trauma—dog bite, penetrating neutrophils and <3,000/mm3) • Neutrophils the need for long-term antibiotics and the
injury, prior surgery or other invasive may show degenerative changes (chromatolysis, likelihood of residual degenerative joint disease.
procedure of the joint. vacuolation, nuclear swelling, loss of
segmentation). • Neutrophils with SURGICAL CONSIDERATIONS
Physical Examination Findings • Acute disease with minimal radiographic
• Monoarticular lameness, rarely polyarticular. phagocytosed bacteria—definitive diagnosis
or bacteria in the synovial fluid. changes—joint drainage and lavage via
• Joint pain and effusion—commonly carpus,
needle arthrocentesis, arthroscopic lavage,
stifle, hock, shoulder, or cubital joint.
(continued) Arthritis, Septic A
or arthrotomy; an irrigation catheter ABBREVIATIONS

(ingress/egress) can be placed in larger • NSAID = nonsteroidal anti-inflammatory
joints. • Chronic disease—may require drug.
open arthrotomy with debridement of the FOLLOW-UP • WBC = white blood cell.
synovium and copious lavage; if approp PATIENT MONITORING Suggested Reading
riate, an irrigation catheter (ingress/egress) • If drainage and irrigation catheters have Benzioni H, Shahar R, Yudelevitch S, Milgram J.
may be placed to lavage the joint been placed—may be removed after 4–6 days Bacterial infective arthritis of the coxofemo
postoperatively. • Lavage—use warmed or after reassessment of synovial fluid cytology. ral joint in dogs with hip dysplasia. Vet
physiologic saline or lactated Ringer’s • Duration of antibiotic therapy—2 weeks Comp Orthop Traumatol 2008,
solution (2–4 mL/kg q8h) until effluent is following resolution of clinical signs; total 21:262–266.
clear; do not add povidone/iodine or treatment may be 4–8 weeks or longer, Clements DN, Owen MR, Mosely JR, et al.
chlorhexidine to lavage fluid. • Effluent depending on clinical signs and pathogenic Retrospective study of bacterial infective
fluid—cytologically monitored daily for organism. • Persistent synovial inflammation arthritis in 31 dogs. J Small Anim Pract
existence and character of bacteria and without viable bacterial organisms (dogs)— 2005, 46:171–176.
neutrophils. • Removal of catheters—when may be caused by antigenic bacterial fragments Ellison RS. The cytologic examination of
effluent fluid has no bacteria and the or antigen antibody deposition. • Systemic synovial fluid. Semin Vet Med Surg Small
neutrophils are cytologically healthy. corticosteroid therapy (after joint sepsis has Anim 1988, 3:133–139.
• Arthroscopy allows for visual assessment been resolved) and aggressive physical Fitch RB, Hogan TC, Kudnig ST. Hematogenous
of articular cartilage, lavage, and biopsy, and therapy—may be needed to maximize normal septic arthritis in the dog: results of five
is a less invasive method of thorough joint joint dynamics. patients treated nonsurgically with
lavage than arthrotomy. • Recent reports antibiotics. J Am Anim Hosp Assoc 2003,
suggest there may be no difference between 39:563–566.
If clinical signs recur, early (within 24–48
combined medical and surgical management Luther JF, Cook JL, Stoll MR. Arthroscopic
hours) treatment provides the greatest
and medical management alone. exploration and biopsy for diagnosis of
benefit.
septic arthritis and osteomyelitis of the
coxofemoral joint in a dog. Vet Comp
• Chronic disease—severe degenerative joint
Orthop Traumatol 2005, 18:47–51.
disease. • Recurrence of infection. • Limited
MEDICATIONS Machevsky AM, Read RA. Bacterial septic
range of joint motion. • Generalized sepsis.
arthritis in 19 dogs. Aust Vet J 1999,
DRUG(S) OF CHOICE • Osteomyelitis.
77:233–237.
• Pending culture susceptibility data— EXPECTED COURSE AND PROGNOSIS MacWilliams PS, Friedrichs KR. Laboratory
bactericidal antibiotics, such as first-generation • Acutely diagnosed disease (within 24–48 evaluation and interpretation of synovial
cephalosporin or amoxicillin–clavulanic acid, hours) responds well to antibiotic therapy. fluid. Vet Clin Small Anim 2003,
preferred. • Choice of antimicrobial drugs— • Delayed diagnosis or resistant or highly 33:153–178.
primarily depends on in vitro determination virulent organisms—guarded to poor Mielko B, Comerford E, English K, et al.
of susceptibility of microorganisms; toxicity, prognosis. Spontaneous septic arthritis of canine
frequency, route of administration, and elbows: twenty-one cases. Vet Comp
expense also considered; most penetrate the Orthop Traumatol 2018, 31:488–493.
synovium well; need to be given for a Montgomery RD, Long IR, Milton JL.
minimum of 4–8 weeks. • Nonsteroidal Comparison of aerobic culturette, synovial
anti-inflammatory drugs (NSAIDs)—may MISCELLANEOUS membrane biopsy, and blood culture
help decrease pain and inflammation. ASSOCIATED CONDITIONS medium in detection of canine bacterial
CONTRAINDICATIONS N/A arthritis. Vet Surg 1989, 18:300–303.
Avoid fluorinated quinolones in pediatric AGE-RELATED FACTORS Scharf VF, Lewis ST, Wellehan JF, et al.
patients, as their use has induced cartilage N/A Retrospective evaluation of the efficacy of
lesions experimentally. isolating bacteria from synovial fluid in dogs
ZOONOTIC POTENTIAL with suspected septic arthritis. Aust Vet J
PRECAUTIONS N/A 2015, 93:200–203.
Failure to respond to conventional antibiotic
PREGNANCY/FERTILITY/BREEDING Author Sherisse A. Sakals
therapy—may indicate anaerobic disease,
N/A Consulting Editor Mathieu M. Glassman
other unusual cause (fungal, spirochete), or
aseptic arthritides. SYNONYMS
• Infectious arthritis. • Joint ill.
POSSIBLE INTERACTIONS Client Education Handout
N/A SEE ALSO available online
• Osteomyelitis.
ALTERNATIVE DRUG(S)
• Polyarthritis, Erosive, Immune-Mediated.
N/A
A Ascites
• Ultrasonography of the liver, spleen,
pancreas, kidney, bladder, and abdomen can
often determine cause.
BASICS DIAGNOSIS • Stages of ascites:
DEFINITION DIFFERENTIAL DIAGNOSIS ◦ Stage I—minimal ascites: detected by
The escape of fluid, either transudate or ultrasound only.
Differentiating Abdominal Distension
exudate, into the abdominal cavity between ◦ Stage II—moderate ascites: abdominal
the parietal and visceral peritoneum. without Effusion distention visible and/or noted on
• Organomegaly—hepatomegaly, splenomegaly, ballottement.
PATHOPHYSIOLOGY renomegaly, and hydrometra. ◦ Stage III—significant ascites: marked
• Ascites can be caused by the following: • Abdominal neoplasia. abdominal distention; patient uncomfort-
◦ Congestive heart failure (CHF) and • Pregnancy. able, possibly with labored breathing.
associated interference in venous return. • Bladder distension.
◦ Depletion of plasma proteins associated • Obesity. DIAGNOSTIC PROCEDURES
with inappropriate loss of protein from • Gastric dilatation. Ascitic Fluid Evaluation
renal or gastrointestinal disease—protein- Exfoliative cytologic examination and
losing nephropathy or enteropathy, Differentiating Diseases
• Transudate—nephrotic syndrome, cirrhosis bacterial culture and antibiotic sensitivity—
respectively. remove approximately 3–5 mL of abdominal
◦ Obstruction of the vena cava or portal
of liver, right-sided CHF, hypoproteinemia,
and ruptured bladder. fluid via aseptic technique.
vein, or lymphatic drainage due to
neoplastic occlusion. • Exudate—peritonitis, abdominal neoplasia, Transudate
◦ Overt neoplastic effusion.
and hemorrhage. • Clear and colorless.
◦ Peritonitis—infective or inflammatory. CBC/BIOCHEMISTRY/URINALYSIS • Protein <2.5 g/dL.
◦ Electrolyte imbalance, especially • Neutrophilic leukocytosis occurs in patients • Specific gravity <1.018.
hypernatremia. with systemic infection. • Cells <1,000/mm3—neutrophils and
◦ Liver cirrhosis. • Albumin is low in patients with impaired mesothelial cells.
SYSTEMS AFFECTED liver synthesis, gastrointestinal loss, or renal Modified Transudate
• Cardiovascular.
loss. • Red or pink; may be slightly cloudy.
• Cholesterol is low in patients with impaired • Protein 2.5–5 g/dL.
• Gastrointestinal.
• Hemic/lymph/immune.
liver synthesis. • Specific gravity >1.018.
• Renal/urologic. Liver Enzymes • Cells <5,000/mm3—neutrophils, mesothelial
• Low to normal in patients with impaired cells, erythrocytes, and lymphocytes.
SIGNALMENT
• Dog and cat.
liver synthesis. Exudate (Nonseptic)
• High in patients with liver inflammation, • Pink or white; cloudy.
• No species or breed predisposition.
hyperadrenocorticism, gallbladder obstruc- • Protein 2.5–5 g/dL.
SIGNS tion, and chronic passive congestion. • Specific gravity >1.018.
• Episodic weakness. • Cells 5,000–50,000/mm3—neutrophils,
• Lethargy. Total and Direct Bilirubin
• Low to normal in patients with impaired mesothelial cells, macrophages, erythrocytes,
• Abdominal fullness. and lymphocytes.
• Abdominal discomfort when palpated.
liver synthesis.
• Dyspnea from abdominal distension or • High in patients with biliary obstruction Exudate (Septic)
associated pleural effusion. caused by tumor, gallbladder distension, or • Red, white, or yellow; cloudy.
• Anorexia.
obstruction. • Protein >4.0 g/dL.
• Vomiting. Blood Urea Nitrogen (BUN) • Specific gravity >1.018.
• Weight gain. • Cells 5,000–100,000/mm3—neutrophils,
and Creatinine
• Scrotal or preputial edema. mesothelial cells, macrophages, erythrocytes,
• High in patients with renal failure.
• Groaning when lying down. lymphocytes, and bacteria.
• BUN low in patients with impaired liver
synthesis or hyperadrenocorticism. Hemorrhage
CAUSES
• Red; spun supernatant clear and sediment
• Nephrotic syndrome. Glucose
• Cirrhosis of liver.
red.
Low in patients with impaired liver • Protein >5.5 g/dL.
• Right-sided CHF. synthesis. • Specific gravity 1.007–1.027.
• Hypoproteinemia.
• Ruptured bladder. OTHER LABORATORY TESTS • Cells consistent with peripheral blood.
• To detect hypoproteinemia—protein • Does not clot.
• Peritonitis.
• Abdominal neoplasia.
electrophoresis and immune profile. Chyle
• To detect proteinuria—urinary protein : • Pink, straw, or white.
• Abdominal hemorrhage.
creatinine ratio (normal <0.5 : 1). • Protein 2.5–7 g/dL.
RISK FACTORS • To detect liver ascites—analysis of serum • Specific gravity 1.007–1.040 and above.
N/A ascites albumin gradient. • Cells <10,000/mm3—neutrophils,
IMAGING mesothelial cells, and large population of
• Thoracic and abdominal radiography is small lymphocytes.
sometimes helpful.
(continued) Ascites A
• Other—fluid in tube separates into Large-Volume Paracentesis

cream-like layer when refrigerated; fat • Stage III treatment.
droplets stain with Sudan III. • Pretreat patient with hetastarch (6%)
@ 1–2 mL/kg for 2 hours. MISCELLANEOUS
Pseudochyle
• Abdominal tap (paracentesis), until AGE-RELATED FACTORS
• White.
• Protein >2.5 g/dL.
drainage slows. N/A
• Post-treat patient with hetastarch (6%)
• Specific gravity 1.007–1.040. PREGNANCY/FERTILITY/BREEDING
• Cells <10,000/mm3—neutrophils, meso-
@ 1–2 mL/kg for 4 hours.
N/A
thelial cells, and small lymphocytes.
SYNONYMS
• Other—fluid in tube does not separate into
Abdominal effusion.
cream-like layer when refrigerated; does not
stain with Sudan III. MEDICATIONS SEE ALSO
• Cirrhosis and Fibrosis of the Liver.
Urine DRUG(S) OF CHOICE
• Congestive Heart Failure, Right-Sided.
• Clear to pale yellow. • Patients with liver insufficiency or CHF—
• Hypoalbuminema.
• Protein >2.5 g/dL. restrict sodium and give a diuretic combination
• Nephrotic Syndrome.
• Specific gravity 1–1.040 and above. of furosemide (1–2 mg/kg q8h PO) and
• Cells 5,000–50,000/mm3—neutrophils, spironolactone (1–2 mg/kg q12h PO); if control ABBREVIATIONS
erythrocytes, lymphocytes, and macrophages. is inadequate, hydrochlorothiazide (1–4 mg/kg • BUN = blood urea nitrogen.
• Other—if the urinary bladder ruptured q12h PO) can be added (cautiously); must • CHF = congestive heart failure.
<12 hours before, urinary glucose and protein monitor serum potassium concentration to Suggested Reading
could be negative; if bladder ruptured >12 prevent potassium imbalances. Gompf RE. The history and physical examina-
hours before, urine becomes a dialysis • Additionally for patients in CHF— tion. In: Smith FWK, Tilley LP, Oyama MA,
medium with ultrafiltrate of plasma, and pimobendan (0.3 mg/kg q12h PO) and an Sleeper MM, eds., Manual of Canine and
urine contains glucose and protein. angiotensin-converting-enzyme inhibitor Feline Cardiology, 5th ed. St. Louis, MO:
Bile (e.g., enalapril 0.25-0.5 mg/kg q12h PO). Saunders Elsevier, 2016, pp. 3–24.
• Slightly cloudy and yellow. • Patients with hypoproteinemia, nephrotic Kramer RE, Sokol RJ, Yerushalmi B, et al.
• Protein >2.5 g/dL. syndrome, and associated ascitic fluid Large-volume paracentesis in the management
• Specific gravity >1.018. accumulation—can treat as above with the of ascites in children. J Ped Gastro Nutr
• Cells 5,000–750,000/mm3—neutrophils, addition of hetastarch (6% hetastarch in 2001; 33:245–249.
erythrocytes, macrophages, and lymphocytes. 0.9% NaCl); administer an IV bolus (dogs, Kumar KS, Srikala D. Ascites with right
• Other—bilirubin confirmed by urine 20 mL/kg; cats, 10–15 mL/kg) slowly over ~1 heart failure in a dog: diagnosis and manage-
dipstick; nonicteric patient may have gall- hour; hetastarch increases plasma oncotic ment. J Adv Vet Anim Res 2014,
bladder rupture, biliary tree leakage, or pressure and pulls fluid into the intravascular 1(3):140–144.
rupture in the proximal bowel. space for up to 24–48 hours. Lewis LD, Morris ML Jr, Hand MS. Small
• Systemic antibiotic therapy is dictated by Animal Clinical Nutrition, 3rd ed. Topeka,
bacterial identification and sensitivity testing KS: Mark Morris Associates, 1987.
in patients with septic exudate ascites. Li MK. Management of ascites. Hong Kong
Med Di 2009; 14:27–29.
TREATMENT Pradham MS, Dakshinkar NP, Waghaye UG,
• Can design treatment on an outpatient basis,
Bodkhe AM. Successful treatment of ascites
with follow-up or inpatient care, depending on of hepatic origin in dog. Vet World 2008;
physical condition and underlying cause. FOLLOW-UP
1(1):23.
• If patients are markedly uncomfortable PATIENT MONITORING Runyon BA. Management of adult patients
when lying down or become more dyspneic • Varies with the underlying cause. with ascites due to cirrhosis. Hepatol 2004;
with stress, consider removing enough ascites • Check sodium, potassium, BUN, creati- 39:1–16.
to reverse these signs. nine, and weight fluctuations periodically if Saravanan M, Sharma K, Kumar M, et al.
• Dietary salt restriction may help control the patient is maintained on a diuretic. Analysis of serum ascites albumin gradient
transudate fluid accumulation due to CHF, test in ascitic dogs. Vet World 2012,
cirrhosis, or hypoproteinemia. 5(5):285–287.
Aggressive diuretic administration may
• For exudate ascites control, address the
cause hypokalemia, which could predispose Author Jerry A. Thornhill
underlying cause; corrective surgery is often Consulting Editor Michael Aherne
to metabolic alkalosis and exacerbation of
indicated, followed by specific therapeutic
hepatic encephalopathy in patients with
management (e.g., patient with splenic
underlying liver disease; alkalosis causes a
tumor: tumor removed, abdominal Client Education Handout
shift from ammonium (NH4) to ammonia
bleeding controlled, blood transfusion available online
(NH3).
administered).
A Aspergillosis, Disseminated Invasive
• Ocular—uveitis, chorioretinitis, hyphema, • Definitive diagnosis by fungal culture from
panophthalmitis. normally sterile body fluids and tissues (urine,
• Nonspecific—fever, weight loss, weakness, bone, cerebrospinal fluid (CSF), blood, lymph
BASICS vomiting, lymphadenopathy. node, pleural effusions, intervertebral disc
OVERVIEW Cats aspirates, kidney, spleen); urine culture
• Opportunistic fungal infection caused by • Usually nonspecific signs (e.g., lethargy,
positive in 50% of dogs.
Aspergillus spp., common molds that are vomiting, and diarrhea). • Culture on Sabouraud’s dextrose agar
ubiquitous in the environment, forming • Ocular—exophthalmos.
(requires 5–7 days).
spores in dust, straw, grass clippings, hay. • Antibody serology is highly insensitive for
• Disseminated disease does not appear to be CAUSES & RISK FACTORS diagnosis of disseminated aspergillosis.
related to nasal form of disease. • Caused by Aspergillus species, most commonly • Galactomannan antigen ELISA (urine or
• Disseminated disease—usually A. terreus or A. terreus or A. deflectus, but other species have serum)—good sensitivity (89%) and
A. deflectus, but other Aspergillus species have also been described (e.g., A. niger, A. flavipes, A. specificity (89%); pulmonary and ocular
also been described; A. fumigatus causes nasal versicolor, A. lentulus, A. alabamensis). infections have lower sensitivity; false positive
or pulmonary disease; typically does not • A. felis recently reported to cause fungal in dogs treated with Plasmalyte or with other
disseminate. rhinosinusitis in cats, sinoorbital aspergillosis mycotic infections (Penicillium, Paecilomyces,
• Portal of entry not definitively established, in cats, disseminated disease in dogs, Cladosporidium, Geotrichum, Histoplasma,
possibly through respiratory tract or gastro- pulmonary aspergillosis in humans. Cryptococcus).
intestinal tract, with subsequent hematog- • German shepherd dogs, purebred dogs, • Cats—test for FeLV and feline immuno
enous spread. immunosuppressed animals at higher risk. deficiency virus (FIV).
• Most commonly affects intervertebral • Geographic/environmental conditions—may
be factor, as some regions have higher incidence IMAGING
discs, bones, thoracic lymph nodes, lung,
renal pelvis; localized respiratory (broncho- (e.g., California, Louisiana, Michigan, Georgia, Radiographic Findings
pulmonary aspergillosis) or, rarely, cornea or Florida, Virginia in the United States; Western • Spinal views may show end-plate lysis,
ear canal disease can occur, often with Australia; Barcelona; Milan). productive lesions with bridging spondylosis,
Aspergillus species other than A. terreus or A. • Cats—described in association with feline lysis of vertebral bodies.
deflectus. infectious peritonitis (FIP), feline panleuko- • Bony proliferation, lysis, periosteal reaction
• Sinoorbital aspergillosis has been described penia virus, feline leukemia virus (FeLV), typical of osteomyelitis of diaphyseal region
in cats; may be caused by variety of species diabetes mellitus, chemotherapy. of long bones.
including Aspergillus felis. • Pulmonary involvement rare; mixed interstitial/
alveolar pattern, enlarged sternal and/or
SIGNALMENT tracheobronchial lymph nodes, pleural
Dogs effusion; productive and destructive lesions of
DIAGNOSIS sternebrae; cavitary pulmonary lesions in dogs
• Considerably more common in dogs than
in cats. DIFFERENTIAL DIAGNOSIS with chronic pulmonary localization.
• German shepherd dogs, and less so • Bacterial osteomyelitis/discospondylitis.
Ultrasonographic Findings
Rhodesian ridgebacks, overrepresented, but • Spinal neoplasia.
• Kidneys—most common site to detect
reported sporadically in many breeds; average • Intervertebral disc disease.
changes; renal pelvis dilation ± echogenic
age 3 years (range 2–8 years); females three • Skeletal neoplasia.
debris within pelvis, loss of corticomedullary
times more likely to develop disease than males. • Bacterial pyelonephritis.
distinction, renal distortion with mottled
• Bacterial pneumonia.
Cats appearance of parenchyma, dilation of
• Other causes of vestibular abnormalities or
• Persians—overrepresented for sinoorbital proximal ureter, renomegaly, nodules or
seizures.
aspergillosis. masses, hydronephrosis.
• Other causes of uveitis (see Anterior
• Disseminated cases mostly affect lungs and/ • Spleen—hypoechoic, lacy, sharply demar-
Uveitis—Cats; Anterior Uveitis—Dogs).
or gastrointestinal tract. cated areas with no Doppler signal (suggestive
CBC/BIOCHEMISTRY/URINALYSIS of infarct), nodules/masses, mottled paren-
SIGNS • Nonspecific. chyma, splenic venous thrombosis.
Dogs • CBC: • Other—abdominal lymphadenomegaly,
• May develop acutely or slowly over a period ◦ Dogs—mature neutrophilic leukocytosis, diffuse hepatic hypoechogenicity, ascites, or
of several months. sometimes with eosinophilia and monocyto- evidence of venous thrombosis.
• Lameness—fungal osteomyelitis, with focal sis; one-third have normocytic, normo
MRI Findings
pain and swelling. chromic, nonregenerative anemia.
Useful for further defining brain lesions in
• Neurologic—fungal discospondylitis ◦ Cats—may have nonregenerative anemia,
animals with CNS abnormalities; changes
causing paraparesis, paraplegia, spinal pain; leukopenia.
similar to other infectious and noninfectious
central signs—vestibular signs, circling, • Biochemistry—variable hyperglobulinemia,
inflammatory brain diseases; may identify
seizures, hemiparesis, mental dullness, ataxia, increases in activity of alkaline phosphatase
subtle vertebral lesions in dogs with disco-
vision impairment. (ALP), alanine aminotransferase (ALT), and
spondylitis.
• Renal involvement—polyuria/polydipsia, amylase; increased concentrations of serum,
vomiting, inappetence, weight loss. creatinine, phosphate, blood urea nitrogen DIAGNOSTIC PROCEDURES
• Respiratory—cough, increased respiratory (BUN), and calcium. Area to collect sample relies on clinical
effort, decreased lung sounds due to pleural • Urinalysis—possible isosthenuria, microscopic presentation, but may include CSF tap,
effusion. hematuria, pyuria, fungal hyphae in sediment. intervertebral disc space aspirates, abdomino
• Cardiac—arrhythmias. centesis/thoracocentesis, aspirate of various
• Gastrointestinal—abdominal distension, organs (spleen, liver, kidney) or lymph nodes.
• Methods of detection include cytology,
anorexia, vomiting, diarrhea. culture, histopathology.
(continued) Aspergillosis, Disseminated Invasive A
PATHOLOGIC FINDINGS amphotericin B (dogs, 2–3 mg/kg IV

• Hyphae that branch at 45-degree angle; 3 days/week for 9–12 treatments, to
special stains assist organism detection. cumulative dose of 24–27 mg/kg)—treatment
• Focal osteomyelitis with multiple pale of choice. FOLLOW-UP
granulomas in kidneys, spleen, lymph node, • Itraconazole monotherapy has achieved • Disseminated—monitor serial radiographs
myocardium, pancreas, liver. remission for months to 1–2 years in small every 1–2 months, renal function, and urine
• Pyogranulomatous inflammation can be number of dogs. cultures.
found in lungs, eyes, thyroid, uterus, brain, • New triazoles—voriconazole and • Prognosis poor, especially in purebred dogs
prostate; contain numbers of septate, branch- posaconazole both have activity against that lack other reasons for immune compromise.
ing hyphae that may have characteristic Aspergillus; some dogs treated with them have
lateral branching aleuriospores (A. terreus). gone into remission for many months;
• Best visualized with periodic acid-Schiff, Aspergillus spp. and other molds are
Gomori’s methenamine silver, or Crocott’s stain. intrinsically resistant to fluconazole, so it MISCELLANEOUS
should not be used.
• Terbinifine (5–10 mg/kg PO q24h) alone ZOONOTIC POTENTIAL
or in combination with triazoles has been None
used to treat resistant infections, with unclear ABBREVIATIONS
TREATMENT benefit. • ALP = alkaline phosphatase.
DOGS • β-glucan synthase inhibitors caspofungin, • ALT = alanine transaminase.
• Treatment rarely curative; may result in micafungin, anidulafungin—limited clinical • BUN = blood urea nitrogen.
partial clinical remission or halt progression information in dogs, but efficacious in • CSF = cerebrospinal fluid.
of clinical signs; severely ill dogs have poor invasive aspergillosis in humans. • FeLV = feline leukemia virus.
prognosis. • FIP = feline infectious peritonitis.
• Fluid therapy—indicated by volume status, • FIV = feline immunodeficiency virus.
degree of renal compromise. INTERACTIONS
• Pulmonary lobectomy followed by systemic • Amphotericin B—contraindicated in dogs Suggested Reading
with preexisting renal compromise or failure; Maddison JE, Page SW, Church DB. Small
antifungals has been successful in dogs with
amphotericin B lipid complex reduces likeli- Animal Clinical Pharmacology, 2nd ed.
cavitary lesions without evidence of dissem-
hood of nephrotoxicity. Edinburgh: Saunders, 2008, pp. 186–197.
ination.
• Oral azoles—nausea, intermittent anorexia, Sykes, JE. Canine and Feline Infectious
CATS liver enzyme elevation. Diseases. Philadelphia, PA: Saunders, 2014,
Disseminated—likely difficult to treat; • Avoid midazolam and cisapride with pp. 639–647.
limited data. azoles—fatal drug reactions noted in Author Jane E. Sykes
humans. Consulting Editor Amie Koenig
• Hepatotoxicity and ulcerative dermatitis Acknowledgment The author and editors
more likely to occur at doses of itraconazole acknowledge the prior contributions of
MEDICATIONS ≥10 mg/kg/day; discontinue itraconazole if Hannah N. Pipe-Martin and Stephen C. Barr.
adverse effects occur; may be able to reinstitute
DRUG(S) OF CHOICE at lower dose once side effects have resolved.
• Combination itraconazole (5–10 mg/kg Client Education Handout
PO q24h or divided q12h) and available online
A Aspergillosis, Nasal
• Sino-orbital disease in cats—stertor, exoph- • Rostrocaudal or skyline frontal sinus view
thalmos, exposure keratitis, hard palate may show increased soft tissue density in the
ulceration, facial asymmetry, loss of nasal airflow. frontal sinus.
BASICS • Cannot evaluate cribriform.
CAUSES
DEFINITION • No underlying cause identified, although DIAGNOSTIC PROCEDURES
Nasal fungal disease caused by opportunistic preexisting foreign body or trauma is
ubiquitous saprophytic fungi that are members Rhinoscopy
occasionally implicated. • Allows for visualization of fungal plaques
of the Aspergillus fumigatus species complex. • Likely due to inhalation of a large bolus (white, yellow, black, or light green) on the
PATHOPHYSIOLOGY of fungus from the environment, most mucosa of the nasal cavity and/or frontal sinus.
• Inhalation of fungus leads to disease in the commonly from the Aspergillus fumigatus • Rigid rhinoscopy—examination of the
nasal cavity with destruction of turbinates, species complex—A. fumigatus in sinonasal nasal cavity alone; good visualization is
formation of plaque lesions, and disease, A. felis in sino-orbital disease. possible due to large airspaces caused by
overproduction of mucus, causing clinical RISK FACTORS turbinate lysis; excessive mucus and bleeding
signs of nasal disease; does not result in Unknown can make full examination difficult.
systemic mycosis. • Flexible rhinoscopy in dogs allows exam-
• In dogs, confined to nasal cavity and frontal ination of the nasopharynx and frontal sinus
sinus—sinonasal form. if the opening of the nasofrontal duct is
• In cats, can result in sinonasal or sino- destroyed by fungal infection.
orbital disease. DIAGNOSIS • Sinuscopy—may be required to confirm the
SYSTEMS AFFECTED DIFFERENTIAL DIAGNOSIS diagnosis in dogs that lack nasal cavity plaques.
• Respiratory—sinonasal form in dogs and cats. • Foreign body.
PATHOLOGIC FINDINGS
• Ophthalmic—sino-orbital form in cats. • Oronasal fistula.
• Biopsies obtained of affected area under
• Lymphoplasmacytic rhinitis.
GENETICS direct rhinoscopic visualization using cup
• Neoplasia.
Unknown biopsy instruments.
• Nasopharyngeal polyp or
• Samples placed in formalin, routinely
INCIDENCE/PREVALENCE cryptococcosis—cats.
processed.
Unknown, but a common diagnosis in dogs CBC/BIOCHEMISTRY/URINALYSIS • Identification of septate, branching hyphae,
with nasal discharge in many locations. • Often normal. and conidia on histopathology with
GEOGRAPHIC DISTRIBUTION • Possible inflammatory leukogram. surrounding inflammation.
Worldwide OTHER LABORATORY TESTS • Blind biopsies in an unaffected area of the
SIGNALMENT nasal cavity can result in a false diagnosis of
Serology inflammation.
Species • Detects fungi-specific serum antibodies.
Dogs and cats (less common). • Agar gel immunodiffusion (AGID)—
Breed Predilections commercially available; 98% specificity, 67%
• Dogs—dolichocephalic and mesocephalic
sensitivity in dogs; 43% sensitivity in cats.
Serial serology does not appear to correlate TREATMENT
breeds.
• Cats—brachycephalic breeds may be
with clinical status. APPROPRIATE HEALTH CARE
• ELISA—88% sensitivity, 97% specificity in Overnight hospitalization advised after
overrepresented.
dogs; 90% sensitivity in cats. topical treatment or surgery.
Mean Age and Range • Counter-immunoelectrophoresis—85%
Predominantly young to middle-aged. specificity in dogs. NURSING CARE
• Serum galactomannan—unreliable. Maintain the nares free of nasal discharge.
Predominant Sex
None identified. Culture ACTIVITY
• Tissue fungal culture—visualized biopsy Restriction of activity is not required if no
SIGNS bleeding is documented.
sample taken from a region of suspected
Historical Findings fungal growth showed 100% specificity, 81% DIET
• Unilateral or bilateral nasal discharge— sensitivity in dogs. N/A
typically mucoid, mucopurulent, or • Culture of nasal discharge is less sensitive
serosanguinous; may be primarily epistaxis. CLIENT EDUCATION
and specific. • Dogs—inform client that multiple topical
• Sneezing.
• Typically chronic signs—several months. IMAGING treatments may be necessary for cure.
• Many patients will have been treated with • No established protocols for treatment in cats.
CT
antibiotics for a possible bacterial infection, • Imaging method of choice. SURGICAL CONSIDERATIONS
with variable response. • Allows for evaluation of the cribriform plate. Endoscopic Debridement
Physical Examination Findings • Cavitated turbinate lysis, thickening of the Extensive curettage and removal of fungal
• Unilateral or bilateral nasal discharge. mucosa along the nasal turbinates. material from the nose and frontal sinus are
• Typically increased nasal airflow on the • Frontal sinus proliferative mass effect. essential for efficacy of topical medication.
affected side. • Cats—soft tissue mass in the choana or
• Depigmentation with ulceration of the nasopharynx. Trephination of the Frontal Sinus
• May be required for dogs with frontal sinus
nasal planum. Skull Radiography
• Facial pain.
involvement where access cannot be established
• Intraoral dorsoventral radiograph of the via rhinoscopy.
• Ipsilateral mandibular lymphadenopathy. nasal cavity shows turbinate lysis.
(continued) Aspergillosis, Nasal A
• Performed using a Jacob’s chuck and doxycycline 5 mg/kg PO q12h for refractory POSSIBLE COMPLICATIONS
intramedullary pin. disease; complete remission reported in • Topical therapy—monitor for any complica-
Surgical Debridement and/or 7/10 dogs, partial clinical remission in 3/10 tions such as swelling of oropharynx,
dogs; 2/10 dogs relapsed after cessation of neurologic signs, infection/swelling of trephine
Exenteration therapy. site.
• Rhinotomy for debridement in some dogs. • Voriconazole 5 mg/kg PO q12h in dogs; • Triazoles can cause anorexia and can be
• Exenteration in some cats with sino-orbital efficacy has not been established; neurotoxic hepatotoxic.
disease. in cats. • Amphotericin B can be nephrotoxic.
• Fluconazole is not recommended due to
resistance. • The prognosis in dogs is good, though
CONTRAINDICATIONS multiple topical treatments may be needed;
MEDICATIONS • A breach in the cribriform plate was recurrence or reinfection can occur years after
DRUG(S) OF CHOICE thought to be a contraindication to topical supposedly successful therapy.
• Clotrimazole and enilconazole are the most treatment; two recent retrospective studies • The prognosis for cats with sinonasal
widely used drugs topically in different showed no adverse neurologic effects after disease is better than with the sino-orbital
formulations and protocols. topical treatment in dogs with lysis of the form.
• Treatment is usually performed during the cribriform and/or frontal sinus floor.
same anesthesia as diagnostics, after debride- • Sino-orbital disease in cats necessitates the
ment. use of systemic therapy.
• No consensus regarding the most effective PRECAUTIONS MISCELLANEOUS
therapy; three protocols are described here. Topical clotrimazole and enilconazole are ASSOCIATED CONDITIONS
Clotrimazole Solution Infusion caustic to mucosal surfaces; all staff in close N/A
• Clotrimazole solution 1% infused through contact should wear protective gear.
catheters placed into the nasal cavity and ZOONOTIC POTENTIAL
ALTERNATIVE DRUG(S) No documented cases of human infection
frontal sinus via trephination, or in the nasal
Homeopathic remedy—aurum metallicum from an affected dog or cat.
cavity only; reported efficacy of up to 87% in
reported to have resulted in a resolution of
dogs with multiple treatments. PREGNANCY/FERTILITY/BREEDING
clinical signs and clearance of organisms in a
• Has been used in cats with sinonasal disease N/A
dog unresponsive to topical therapy.
with varying success.
ABBREVIATIONS
Combined Clotrimazole Irrigation • AGID = agar gel immunodiffusion.
and Depot Therapy Suggested Reading
Frontal sinus trephination with flushing of
1% clotrimazole solution followed by 1% FOLLOW-UP Barrs VR, Talbot JJ. Feline aspergillosis. Vet
Clin North Am 2014, 44(1):51–73.
clotrimazole cream instilled as a depot agent; PATIENT MONITORING Friend E, Anderson DM, White RAS.
reported efficacy of 86% with multiple Dogs Combined clotrimazole irrigation and depot
treatments needed in one dog. • Reduction of clinical signs does not therapy for canine nasal aspergillosis. J
Debridement and Clotrimazole Depot establish resolution of disease. Small Anim Pract 2006, 47(6):312–315.
Therapy under Rhinoscopic Guidance • Follow-up rhinoscopy with possible Mathews KG, Davidson AP, Koblik PD, et al.
Debridement and sinus and nasal depot histopathology and culture is recommended Comparison of topical administration of
therapy with 1% clotrimazole cream under to establish a response to treatment. clotrimazole through surgically placed
rhinoscopic guidance; reported efficacy of • Serial serology (AGID) appears not to versus nonsurgically placed catheters for
100% with multiple treatments. correlate with disease status. treatment of nasal aspergillosis in dogs:
• Repeat CT should be considered for 60 cases (1990–1996). J Am Vet Med Assoc
Systemic Therapy reassessment of the cribriform plate before 1998, 213:501–506.
• Antifungal triazole drugs should be repeat topical treatment if worsening clinical Sharman M, Mansfield CS. Sinonasal
considered if the cribriform is not intact; can signs are seen. aspergillosis in dogs: a review. J Small Anim
also be combined with topical therapy. Pract 2012, 53:434–444.
• Used as primary therapy in some cats. Dogs and Cats
• Monitor liver enzymes on triazole therapy. Vedrine B, Fribourg-Blanc L-A. Treatment of
• May be cost-prohibitive.
• Monitor renal parameters on amphotericin B. sinonasal aspergillosis by debridement and
• Itraconazole 5 mg/kg PO q12h in dogs;
sinonasal deposition therapy with clotrimazole
reported efficacy of 60–70%; 10 mg/kg PO PREVENTION/AVOIDANCE under rhinoscopic guidance. J Am Anim
q24h in cats. N/A Hosp Assoc 2018, 54:103–110.
• Posaconazole 5 mg/kg PO q12h with
Author Jill S. Pomrantz
terbinafine 30 mg/kg PO q12h and Consulting Editor Elizabeth Rozanski
A Aspirin Toxicosis
• Leukocytosis. depression, and coma are poor prognostic
• Hypoproteinemia. indicators.
• Elevated liver enzymes.
BASICS • Elevated renal values (rare).
OVERVIEW OTHER LABORATORY TESTS
• Given for its antipyretic, analgesic, anti- • Initial respiratory alkalosis followed by MISCELLANEOUS
inflammatory, and antiplatelet effects. marked metabolic acidosis. • Be sure that history of “aspirin” medication
• Aspirin inhibits cyclooxygenase, reducing the • High ketones and pyruvic, lactic, and does not refer to other available pain
synthesis of prostaglandins and thromboxanes. amino acid levels. medications.
• Gastric irritation and hemorrhage can occur. • Decreased sulfuric and phosphoric acid • Question owner about any preexisting
• Repeated doses can produce gastrointestinal renal clearance. painful condition that may have prompted
ulceration and perforation and hepatic injury; the aspirin administration.
renal injury is uncommon. IMAGING
• Toxic hepatitis, marked metabolic acidosis, • Abdominal imaging (perforation). ABBREVIATIONS
and anemia can occur, especially in cats (long DIAGNOSTIC PROCEDURES • PCV = packed cell volume.
half-life). • Salicylic acid concentrations in serum. Suggested Reading
• Hepatic damage may not be dose related. Plumb DC. Aspirin. In: Plumb DC, ed.,
SIGNALMENT Plumb’s Veterinary Drug Handbook, 9th
Cats and less commonly dogs. ed. Ames, IA: Wiley-Blackwell, 2018,
TREATMENT pp. 92–96.
SIGNS Talcott PA, Gwaltney-Brant SM. Nonsteroidal
• Depression, lethargy. • Inpatient—following general principles of
poisoning management. anti-inflammatories. In: Peterson ME,
• Anorexia. Talcott PA, eds. Small Animal Toxicology,
• Vomiting ± blood. • Induced gastric emptying—gastric lavage or
induced emesis. 3rd ed. St. Louis, MO: Elsevier, 2013,
• Diarrhea ± blood; melena. pp. 698–700.
• Tachypnea. • Correction of acid-base balance—continuous
IV fluids; assisted ventilation and supplemental Author Lisa A. Murphy
• Hyperthermia. Consulting Editor Lynn R. Hovda
• Pallor. oxygen for severely affected animals.
• Polyuria/polydipsia (rare). • Whole blood transfusions for severe cases of
• Muscular weakness and ataxia. hemorrhage and hypotension.
• Ataxia, coma, seizures, and death in 1 or • Peritoneal dialysis and hemodialysis are
more days. advanced procedures that will increase
salicylate clearance in severe cases.
• Owners employing human dosage guide-
lines to medicate cats and dogs.
• Dogs—single 25 mg/kg dose has resulted in
gastric bleeding. MEDICATIONS
• Cats have a decreased ability to conjugate DRUG(S) OF CHOICE
salicylate with glycine and glucuronic acid • No specific antidote available.
due to a deficiency in glucuronyl transferase. • Activated charcoal—1–2 g/kg PO with a
• Half-life increases with dosage—cats, 22–27 cathartic (sorbitol); monitor sodium
hours for 5–12 mg/kg and approximately 44 concentration.
hours for 25 mg/kg; responsible for higher risk • 5% dextrose IV to correct dehydration.
in cats. Dogs, half-life = 7.5 hours. • Gastrointestinal protectants—sucralfate and
• Elimination is slower in neonatal and an H2 blocker or proton pump inhibitor;
geriatric patients. misoprostol for patients at higher risk for
• Patients with hypoalbuminemia may be at gastrointestinal hemorrhage.
higher risk of toxicity because aspirin is highly • Sodium bicarbonate 1 mEq/kg IV in severe
protein bound to plasma albumin. ingestions—alkalinizes urine; must closely
monitor acid-base status.
• Diazepam 0.5–1 mg/kg IV or rectal as
needed for seizures.
DIAGNOSIS CONTRAINDICATIONS/POSSIBLE
DIFFERENTIAL DIAGNOSIS INTERACTIONS
• Ethylene glycol or alcohol. N/A
• Anticoagulant rodenticides.
• Other causes of liver failure, including
acetaminophen, iron, metaldehyde, and
blue-green algae.
FOLLOW-UP
CBC/BIOCHEMISTRY/URINALYSIS • Maintaining renal function and acid-base
• Cats—prone to Heinz body formation. balance is vital.
• Decreased packed cell volume (PCV); may • Severe acid-base disturbances, severe
be marked, especially in cats. dehydration, toxic hepatitis, bone marrow
Asthma, Bronchitis—Cats A
• Increased tracheal sensitivity is common. CT

• Chest auscultation may reveal crackles and/ Bronchial wall thickening, patchy alveolar
or expiratory wheezes, but can be normal. patterns, and bronchiectasis.
BASICS • Labored breathing with an abdominal push Echocardiography
DEFINITION on expiration, increase in expiratory effort. Useful to document heartworm disease or
• Chronic bronchitis—neutrophilic inflamma- CAUSES secondary pulmonary hypertension.
tion of the lower airways (bronchi and Triggers of airway inflammation unknown.
bronchioles) lacking a specific etiology; chronic DIAGNOSTIC PROCEDURES
daily cough of greater than 2 months in RISK FACTORS Transoral Tracheal Wash (TOTW)
duration. • Asthma—acute or chronic airway • Cigarette smoke, poor environmental Use a sterile endotracheal tube and polypro-
inflammation associated with increased airway hygiene, dusty cat litter, hair sprays, and air pylene or red rubber catheter to collect airway
responsiveness to various stimuli, airway fresheners can exacerbate disease. • Use of fluids at the level of the carina.
narrowing due to smooth muscle hypertrophy potassium bromide—implicated in causing
signs of bronchitis/asthma in some cats. Bronchoscopy
or constriction, reversibility of airway constric- Allows visualization of trachea and bronchi.
tion, and presence of eosinophils, lymphocytes, Excessive amounts of thick mucus are
and mast cells within the airways. • Bronchitis common with bronchitis. Mucosa of the
is thought to result in airflow obstruction due to airways is typically hyperemic and edematous.
airway remodeling, while asthma is associated DIAGNOSIS
with airway constriction; however, clinically the Cytology of TOTW or Bronchoscopy/
two disease processes can appear similar. No DIFFERENTIAL DIAGNOSIS Bronchoalveolar Lavage (BAL)
• Rule out infectious pneumonia
physical examination findings or biomarkers can • Eosinophils and neutrophils are most
distinguish between the two syndromes, (Mycoplasma, Toxoplasma, bacterial or fungal prominent cell types. • Up to 20% eosino-
although reversal of airflow obstruction pneumonia). • Consider Dirofilaria immitis phils on BAL cytology can be found in
following administration of a beta‐agonist is and primary lung parasites (Aelurostrongylus normal cats. • A mixed inflammatory cell
suggestive of the asthmatic form of disease. abstrusus, Capillaria aerophilia, Paragonimus population occurs in about 21% of cats.
kellicotti, Troglostrongylus brevior). More
PATHOPHYSIOLOGY common in southern and midwest United Bacterial Cultures
• Lower airway inflammation likely results from States, and in outdoor and hunting cats in • Quantitated cultures recommended; positive
inhalation of irritant substances. • Bronchiolar some geographic regions. • Primary or cultures frequently encountered, but bacterial
smooth muscle constriction—can resolve metastatic neoplasia can have similar clinical colony counts >100–300 cfu/mL uncommon
spontaneously or with treatment. • Increase in and radiographic appearance. • Clinical with bronchitis. • Specific Mycoplasma cultures
mucosal goblet cells, mucus production, and presentation of idiopathic pulmonary fibrosis and PCR for species detection.
edema of bronchial wall associated with may appear similar to feline bronchitis. Biopsy
inflammation. • Excessive mucus can cause Keyhole biopsy—can differentiate between
bronchiolar obstruction, atelectasis, or bronchi- CBC/BIOCHEMISTRY/URINALYSIS
Frequently normal; ~40% of cats with idiopathic pulmonary fibrosis, neoplasia, and
ectasis. • Smooth muscle hypertrophy implies bronchitis if needed; rarely performed.
chronicity—usually not reversible. • Chronic bronchial disease have peripheral
inflammation leads to airway remodeling and eosinophilia. PATHOLOGIC FINDINGS
irreversible airflow obstruction. OTHER LABORATORY TESTS Hyperplasia/hypertrophy of goblet cells,
• Fecal exams—flotation for Capillaria, hypertrophy of airway smooth muscle, epithelial
SYSTEMS AFFECTED erosion, and inflammatory infiltrates.
• Respiratory. • Cardiac—pulmonary hyper-
sedimentation for Paragonimus, Baermann for
tension rarely. Aelurostrongylus; false‐negative results are common.
• Heartworm antigen and antibody testing,
GEOGRAPHIC DISTRIBUTION particularly if coughing occurs in conjunction
Worldwide with vomiting. • Radioallergosorbent testing TREATMENT
SIGNALMENT or intradermal skin testing—no correlation
between skin allergies and respiratory disease APPROPRIATE HEALTH CARE
Species currently documented. • Remove patient from environment that
Cat exacerbates disease. • Hospitalize for acute
IMAGING respiratory distress.
Breed Predilections
Siamese overrepresented. Radiography NURSING CARE
• Classically, diffuse bronchial wall thicken- • Oxygen therapy, bronchodilators, and
Mean Age and Range ing; interstitial or patchy alveolar patterns also
Any age; more common between 2 and 8 sedatives in an acute crisis. • Minimize
possible. • Severity of radiographic changes manipulation in order to lessen stress and
years. does not necessarily correlate with clinical oxygen needs of the animal.
Predominant Sex severity or duration, and normal radiographs
One study showed females overrepresented. can be found. • Hyperinflation of lung ACTIVITY
fields—flattened and caudally displaced Usually self‐limited by patient.
SIGNS
diaphragm, increased distance between the DIET
Historical Findings heart and diaphragm, extension of lungs to Calorie restriction for obese cats.
• Coughing, tachypnea, labored breathing or the first lumbar vertebrae thought to reflect
wheezing. • Signs are typically episodic and bronchoconstriction. • Collapse of right CLIENT EDUCATION
can be acute or chronic. • Most causes are chronic and progressive.
middle lung lobe due to mucus plugging and
• Do not discontinue medical therapy when
Physical Examination Findings atelectasis reported in 11% of cases.
• Pulmonary lobar arterial enlargement is
clinical signs have resolved—subclinical
• Severely affected cats present with open‐ inflammation is common and can lead to
mouth breathing, tachypnea, and cyanosis. suspicious for heartworm disease.
A Asthma, Bronchitis—Cats (continued)
progression of disease; lifelong medication Anthelminthics will be refractory to treatment; these carry a
and environmental changes usually necessary. • Empirical therapy is indicated for cats with much worse prognosis.
• Some clients can be taught to give terbuta- clinical signs of bronchial disease and
line subcutaneously and corticosteroid eosinophilic airway cytology in an appropriate
injections at home for a crisis situation. geographic location. • Consider fenbendazole,
ivermectin, praziquantel, or milbemycin. MISCELLANEOUS
Antibiotics ASSOCIATED CONDITIONS
Use based on a positive quantitative culture and Cor pulmonale can be a sequela to chronic
MEDICATIONS susceptibility testing or Mycoplasma isolation. lower airway disease.
DRUG(S) OF CHOICE CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING
Emergency Treatment
Beta‐2 antagonists (e.g., propranolol) are Glucocorticoids are contraindicated in the
• Oxygen and a parenteral bronchodilator—
contraindicated because of their ability to block pregnant animal; bronchodilators should be
injectable terbutaline (0.01 mg/kg IV/SC); sympathetically mediated bronchodilation. used with caution.
repeat if no clinical improvement (decrease in PRECAUTIONS SYNONYMS
respiratory rate or effort) in 20–30 minutes. • Long‐term use of steroids increases risk of
• Allergic bronchitis. • Asthmatic bronchitis.
• A sedative can aid in decreasing anxiety development of diabetes mellitus and predisposes • Feline lower airway disease. • Extrinsic
(butorphanol tartrate at 0.2–0.4 mg/kg IV/ to immunosuppression. • Use of corticosteroids asthma. • Eosinophilic bronchitis.
IM, buprenorphine at 0.01 mg/kg IV/IM, or in cats may precipitate congestive heart failure.
acepromazine at 0.01–0.05 mg/kg SC). • A • Beta agonists could cause tachycardia and SEE ALSO
short‐acting parenteral corticosteroid may exacerbate underlying cardiac disease. • Heartworm Disease—Cats.
also be required—dexamethasone sodium • Respiratory Parasites.
ALTERNATIVE DRUG(S)
phosphate (0.1–0.25 mg/kg IV/SC). • Leukotriene receptor blockers and inhibitors of ABBREVIATIONS
Long‐Term Management generation—no evidence to support use. • BAL = bronchoscopy/bronchoalveolar lavage.
• Tyrosine kinase inhibitors—masitinib is no • MDI = metered‐dose inhaler. • PU/PD =
Corticosteroids
• Decrease inflammation. • Oral treatment is longer on the market; side effects were dose polyuria/polydipsia. • RIT = rush immuno-
preferred over injectable for closer monitoring limiting. • Antiserotonin and antihistamine therapy. • TOTW = transoral tracheal wash.
of dose and duration. • Prednisolone—0.5– drugs—no evidence to support use. INTERNET RESOURCES
1 mg/kg PO q12h; begin to taper dose (50% • Immunotherapy—allergen‐specific rush • www.aerokat.com • www.fritzthebrave.com
each week) after 1–2 weeks if clinical signs immunotherapy (RIT) shows promise in treating
asthma. • Omega 3 fatty acids/neutraceuticals— Suggested Reading
have improved; maintenance therapy Chang C, Cohn L, DeClue A, et al. Oral
0.5–1 mg/kg PO q24–48h. • Longer‐acting diminished hyperresponsiveness of airway, but
did not resolve airway eosinophilia. glucocorticoids diminish the efficacy of allergen‐
parenteral steroids (Vetalog® or Depo‐Medrol®) specific immunotherapy in experimental
should be reserved only for situations where feline asthma. Vet J 2013, 197:268–272.
owners are unable to administer oral or inhaled Chang DG, Dodam HR, Cohn LA, et al. An
medication on a routine basis. experimental janus kinase (JAK) inhibitor
Inhaled Corticosteroids FOLLOW‐UP suppresses eosinophilic airway inflammation in
• Requires a form‐fitting facemask, spacer, and PATIENT MONITORING feline asthma. ACVIM Forum Proceedings, 2013.
metered‐dose inhaler (MDI); veterinary brand— • Owners should report any increase in Cohn LA, DeClue AE, Cohen RL, Reinero CR.
Aerokat ® (Trudell Medical). • The most coughing, sneezing, wheezing, or respiratory Effects of fluticasone propionate dosage in an
common corticosteroid used as an MDI is distress; medications should be increased experimental model of feline asthma. J Feline
fluticasone propionate (Flovent®)—110 μg appropriately, or additional therapy initiated Med Surg 2010, 12(2):91–96.
Flovent MDI is recommended (1–2 actuations, if clinical signs worsen. • Follow‐up radiographs Crisi P, DiCesare A, Boari A. Feline
7–10 breaths q12h); in one study, use of 44 μg may be helpful to detect onset of new disease. troglostrongylosis: current epizootiology,
Flovent decreased BAL eosinophil counts in • Owner should watch for signs of polyuria/ clinical features, and therapeutic pptions. Front
cats with experimentally induced lower airway polydipsia (PU/PD) that could indicate Vet Sci 2018, 5:126.
disease. • Flovent is used for long‐term control diabetes mellitus or renal disease; monitor Kirschvink J, Leemans J, Delvaux F, et al. Inhaled
of airway inflammation; takes 10–14 days to blood glucose and urine cultures. fluticasone reduces bronchial responsiveness
reach peak effect; use oral steroids concurrently and airway inflammation in cats with mild
during this time. • Results in some suppression chronic bronchitis. J Feline Med Surg 2006,
Eliminate any environmental factors that can
of the hypothalamic–pituitary axis, but 8(1):45–54.
trigger a crisis situation (see Risk Factors);
systemic side effects appear to be limited. Schulz BS, Richter P, Weber K, et al. Detection of
change furnace and air‐conditioner filters on
Bronchodilators feline Mycoplasma species in cats with feline
a regular basis; consider dust‐free litters.
• Methylxanthines—sustained‐release
asthma and chronic bronchitis. J Feline Med
POSSIBLE COMPLICATIONS Surg 2014, 16(12): 943–949.
theophylline formulations recommended, and
• Acute episodes can be life‐threatening. Author Karah Burns DeMarle
pharmacokinetics can vary greatly; only
• Right‐sided heart disease develops rarely as Consulting Editor Elizabeth Rozanski
compounded generic currently available; dose
a result of long‐term bronchitis. Acknowledgment The author and book
at 15–20 mg/kg PO once daily in the evening.
• Beta‐2 agonists (terbutaline, albuterol)— EXPECTED COURSE editors acknowledge the prior contribution of
reverse smooth muscle constriction; oral Carrie J. Miller and Lynelle R. Johnson.
AND PROGNOSIS
terbutaline dose is 1/4 of a 2.5 mg tablet; • Long‐term therapy should be expected.
initial albuterol dose is 1–2 puffs; avoid • Most cats do well if recurrence of clinical
giving beta‐2 agonists daily as tachyphylaxis Client Education Handout
signs is carefully monitored and medical
may develop. available online
therapy appropriately adjusted. • A few cats
Astrocytoma A
tumor, based on tumor characteristics and increase in hepatic enzymes on serum

highlighted in specific sequences. biochemical panel. • CBC and platelet
DIAGNOSTIC PROCEDURES count are recommended 7–10 days after
BASICS chemotherapy and immediately before
• Neurologic exam. • Ophthalmic exam.
OVERVIEW • MRI. • CSF analysis. • Tumor biopsy for
each dose of chemotherapy to monitor
• Glial cell neoplasm, most commonly definitive diagnosis, when specific antineo- myelosuppression. • Chemotherapy has
affecting the brain and rarely the spinal cord. plastic treatment is sought (surgery, curative- the potential to be synergistic with
• Neoplastic cells are of astrocytic origin. • The intent radiation therapy, experimental radiation therapy. Timely referral to a
most common intraaxial (situated inside of the therapies). specialty center with neurosurgery,
brain parenchyma) intracranial neoplasm of dogs, radiation therapy, and medical oncology
but is rarely diagnosed in cats. • Tumors are often capabilities is important for patients
located in the pyriform area of the temporal lobe, seeking more than palliative care.
the cerebral hemispheres, the thalamus, hypo-
thalamus, or midbrain. • Biologic behavior of TREATMENT
this tumor is dictated by the histopathologic • Surgery. • Radiation therapy can be very
grade (I–IV, from best to worst prognosis) and effective in improving neurologic signs.
• Chemotherapy with lomustine, procar- FOLLOW-UP
anatomic involvement. • Tumors typically
do not penetrate the ventricular system or bazine, or temozolomide might exert cyto- PATIENT MONITORING
metastasize outside of the cranial vault. reductive activities. • Anti-inflammatory • Blood phenobarbital concentration should
dosing with corticosteroids to reduce be assessed after 7–10 days of treatment, with
SIGNALMENT peritumoral edema. • Consultation with a modifications to dosages for achieving target
• Dog—often brachycephalic breeds >5 years of neurosurgeon and a radiation oncologist is plasma concentrations. • Serial MRIs should
age; no sex predilection reported. • Cat—usually essential for appropriate patient management. be considered for documenting response if
>9 years; no sex or breed predilection reported. multimodality therapy is used. • Serial CBC
SIGNS and platelet counts should be performed to
• Location and growth kinetic dependent. monitor myelotoxicity associated with
• Seizures. • Behavioral changes. • Apathy MEDICATIONS chemotherapy.
toward normal activities, including eating, EXPECTED COURSE AND PROGNOSIS
playing, and societal interactions. DRUG(S) OF CHOICE
• Long-term prognosis is guarded.
• Disorientation. • Loss of conscious Seizure Control • Median survival after chemotherapy plus
proprioception. • Cranial nerve abnormal • Status epilepticus—diazepam (0.5–1 mg/kg medical management may be up to 7 months.
ities. • Head muscle atrophy. • Upper IV, up to three times to achieve effect); if no • Median survival after radiation therapy
motor neuron tetraparesis. response to diazepam, use pentobarbital has been reported to be as high as 12
(5–15 mg/kg IV slowly to effect). • Long- months.
term management—phenobarbital (1–4 mg/kg
PO q12h) with or without adjuvant potassium
DIAGNOSIS bromide (20 mg/kg PO q24h).
DIFFERENTIAL DIAGNOSIS Tumor Control MISCELLANEOUS
• Other primary tumors arising from tissues • Timely consultation with a neurosurgeon is of
paramount importance for appropriate manage- SEE ALSO
of the central nervous system. • Metastatic • Seizures (Convulsions, Status Epilepticus)—
neoplasia with brain tropism such as hemangio- ment of the patient. • Radiation therapy may
be effective, and consultation with a radiation Cats
sarcoma. • Granulomatous meningoencepha- • Seizures (Convulsions, Status Epilepticus)—
litis. • Trauma. Cerebrovascular infarction. oncologist is recommended. Stereotactic
radiosurgery or intensity-modulated radiation Dogs
• Meningitis.
therapy may be considered as first-line ABBREVIATIONS
CBC/BIOCHEMISTRY/URINALYSIS treatment options. • Chemotherapy may be • CSF = cerebrospinal fluid.
Usually unremarkable. effective for treating dogs. Potential drugs that
may exert measurable anticancer effects include Suggested Reading
OTHER LABORATORY TESTS Bentley RT, Ober CP, Anderson KL, et al.
Cerebrospinal fluid (CSF) analysis may show CCNU (60–70 mg/m2 PO every 3 weeks) or
temozolomide (100–120 mg/m2 PO q24h for Canine intracranial gliomas: relationship
albumin-cytologic dissociation (high protein between magnetic resonance imaging criteria
with low number of nucleated cells). The CSF 5 days every 3 weeks). • Prednisone (1 mg/kg
and tumor type and grade. Vet J 2013,
analysis is indicated to exclude infectious q24h) may be effective in reducing peritumoral
198(2):463–471.
etiology, not to diagnose astrocytoma. edema and improving neurologic signs. Patients
Stoica G, Levine J, Wolff J, Murphy K.
may need to be on steroids long term, even after
IMAGING the definitive treatment of the tumor.
Canine astrocytic tumors: a comparative
• MRI of brain is ideal for mass lesion review. Vet Pathol 2011, 48(1):266–275.
confirmation, as it is superior to CT CONTRAINDICATIONS/POSSIBLE Troxel MT, Vite CH, Van Winkle TJ, et al.
scanning for detecting lesions in the middle INTERACTIONS Feline intracranial neoplasia: retrospective
and caudal fossae. MRI is more sensitive • Prednisone and phenobarbital may cause review of 160 cases (1985–2001). J Vet Intern
than CT for detection infarcts, bleeding, and polyphagia, polydipsia, and polyuria. Med 2003, 17:850–859.
edema. • Brain MRI is useful in establishing • Phenobarbital may cause sedation for up Author Nick Dervisis
a tentative differential diagnosis of a glial to 2 weeks after initiation of treatment, Consulting Editor Timothy M. Fan
A Ataxia
• Bilateral vestibular disease is uncommon and Vestibular—CNS
most often peripheral in origin. Typical • Infectious—FIP; canine distemper virus;
vestibular signs are absent. Wide swinging back rickettsial diseases.
BASICS and forth head motions and poor to absent • Inflammatory, idiopathic, immune-
DEFINITION physiologic nystagmus are characteristic. mediated—meningoencephalomyelitis of
• A sign of sensory dysfunction causing loss Cerebellar
undetermined etiology.
of coordination of the limbs, head, and/or • Nutritional—thiamine deficiency.
• The cerebellum regulates, coordinates, and
trunk. • Toxic—metronidazole.
modulates motor activity.
• Three clinical types—sensory (proprioceptive), • Proprioception is normal because the Vestibular—Peripheral Nervous System
vestibular, and cerebellar. All cause limb ascending proprioceptive pathways to the • Infectious—otitis media interna;
incoordination, but only vestibular and cortex are intact; weakness does not occur Cryptococcus granuloma (cats).
cerebellar ataxia cause head and neck because the upper motor neurons are intact. • Inflammatory—nasopharyngeal (middle
incoordination. • While strength is preserved, affected ear) polyps (cats).
PATHOPHYSIOLOGY animals have uncoordinated motor activity of • Idiopathic—geriatric vestibular disease
limbs, head, and neck manifested by hyper- (dogs); idiopathic vestibular syndrome
Sensory (Proprioceptive) (cats).
metria; dysmetria; head tremors; intention
• Proprioceptive pathways in the spinal cord
tremors; and truncal sway. Menace responses • Metabolic—hypothyroidism.
(i.e., fasciculus gracilis, fasciculus cuneatus, • Neoplastic—squamous cell carcinoma,
may be absent without visual dysfunction.
and spinocerebellar tracts) relay limb and bone tumors.
trunk positions to the brain. SYSTEMS AFFECTED
• Traumatic.
• When the spinal cord is slowly compressed, Nervous—spinal cord (and brainstem and
proprioceptive deficits are usually the first signs cortex), cerebellum, vestibular system. Spinal Cord
observed, because these tracts or pathways are • Degenerative—degenerative myelopathy
SIGNALMENT
located more superficially in the white matter Any age, breed, or sex. (old German shepherd, pug, boxer, Welsh
and their larger axons are more susceptible to corgi, others); degenerative disc disease.
compression than are other tracts. SIGNS • Vascular—fibrocartilaginous embolic
• Limb weakness (paresis) will occur if more • Important to define the type of ataxia to myelopathy.
centrally located motor tracts or pathways localize the problem. • Anomalous—hemivertebrae; dens hypo-
become involved; weakness is not always • Only one limb involved—rule out a plasia with atlantoaxial subluxation-luxation;
obvious early in the course of the disease. musculoskeletal problem. Chiari-like malformation; cervical
• Ataxia can occur with spinal cord, brainstem, • Only hind limbs affected—likely a spinal cord spondylomyelopathy; spinal subarachnoid
and cerebral lesions. Ataxia can be mild to disorder affecting the spinocerebellar tracts. diverticulum; other spinal cord and vertebral
absent with unilateral brainstem lesions, and • All limbs or ipsilateral limbs affected— malformation.
subtle to absent with unilateral cerebral lesions. cervical spinal cord or cerebellar • Neoplastic—primary bone tumors; multiple
localization. myeloma and metastatic tumors that infiltrate
Vestibular • Head tilt and/or nystagmus—vestibular localiz- the vertebral body; meningioma; others.
• Changes in balance and head and neck ation. • Infectious—discospondylitis; myelitis.
positions are detected by vestibular receptors • Traumatic—intervertebral disc herniation;
of the inner ear, relayed to the vestibulo CAUSES
fracture or luxation; atlantoaxial subluxation-
cochlear nerve, which is connected to Cerebellar luxation.
vestibular nuclei in the brainstem. • Degenerative—abiotrophy (Kerry blue
• The inner ear’s vestibular receptors and nerve terrier, Gordon setter, rough-coated collie, Metabolic
are components of the peripheral nervous Australian kelpie, Airedale, Bernese mountain • Anemia.
system, whereas brainstem vestibular nuclei are dog, Finnish harrier, Brittany spaniel, border • Polycythemia.
components of the central nervous system. collie, beagle, Samoyed, wirehaired fox terrier, • Electrolyte disturbances—especially
• Vestibular ataxia should be localized to Labrador retriever, Great Dane, chow chow, hypokalemia, hypocalcemia, and hypoglycemia.
either the peripheral or central vestibular Rhodesian ridgeback, domestic shorthair Miscellaneous
nervous system, because prognosis and cats); storage diseases often have cerebello • Drugs—acepromazine; antihistamines;
rule-outs differ for these two locations. medullary involvement. antiepileptic drugs; flea and tick products.
• Both locations of vestibular disease cause • Anomalous—hypoplasia secondary to • Respiratory compromise.
various degrees of vestibular ataxia, often perinatal infection with panleukopenia virus • Cardiac compromise—reverse patent
manifested by head tilt and leaning, falling, (cats); malformed cerebellum due to ductus arteriosus, aortic thromboembolism.
or even rolling toward the side of the lesion. herpesvirus infection (newborn puppies);
• Central vestibular disease usually has arachnoid or epidermoid cyst located near RISK FACTORS
vertical nystagmus or changing types of • Intervertebral disc disease—dachshund,
fourth ventricle.
nystagmus; somnolence, stupor, or coma (due • Neoplastic—any CNS tumor (primary or
poodle, cocker spaniel, beagle, and others.
to involvement of the nearby ascending • Cervical spondylomyelopathy—Doberman
secondary) localized to the cerebellum.
reticular activating system); multiple cranial • Infectious—canine distemper virus; feline
pinscher and Great Dane.
nerve signs (e.g., trigeminal or facial nerve • Fibrocartilaginous embolism—young,
infectious peritonitis (FIP); and any other
deficits); proprioceptive deficits and CNS infection affecting the cerebellum. large-breed dogs and miniature schnauzers.
quadriparesis or hemiparesis. • Dens hypoplasia and atlantoaxial luxation—
• Inflammatory, idiopathic, immune-
• Peripheral vestibular disease does not mediated—meningoencephalomyelitis of small-breed dogs, poodles.
typically show changes in mental status, • Chiari-like malformation—cavalier King
undetermined etiology.
vertical nystagmus, proprioceptive deficits, • Toxic—metronidazole.
Charles spaniel, small-breed dogs.
quadriparesis, or hemiparesis.
(continued) Ataxia A
• Bullae radiography—if peripheral vestibular POSSIBLE COMPLICATIONS

disease suspected; CT or MRI superior; for • Spinal cord—progression to weakness and
inner ear disease, MRI superior to CT. possibly paralysis.
DIAGNOSIS • Thoracic radiography—for older patients • Hypoglycemia—seizures.
DIFFERENTIAL DIAGNOSIS and patients suspected to have neoplasia or • Cerebellar disease—head tremors and
• Differentiate the types of ataxia. systemic fungal infection. bobbing.
• Differentiate from other disease processes • CT or MRI—if cerebellar disease suspected; • Brainstem disease—stupor, coma, death.
that can affect gait—musculoskeletal, MRI superior to CT.
metabolic, cardiovascular, respiratory. • Abdominal ultrasonography—if hepatic,
• Musculoskeletal disorders—typically renal, adrenal, or pancreatic dysfunction
produce lameness, pain, and a reluctance to suspected.
MISCELLANEOUS
move; degenerative joint disease signs often DIAGNOSTIC PROCEDURES
improve with increased movements. SEE ALSO
• Cerebrospinal fluid analysis—helps confirm
• Systemic illness and endocrine, cardiovascular, • Cerebellar Degeneration.
nervous system etiology.
and metabolic disorders—can cause intermittent • Head Tilt.
• Cerebrospinal fluid culture, antibody titer,
ataxia, especially of the pelvic limbs; with fever, • Paralysis.
or polymerase chain reaction—helps confirm
weight loss, murmurs, arrhythmias, hair loss, or nervous system infectious etiology. ABBREVIATIONS
collapse with exercise, suspect a non-neurologic • FIP = feline infectious peritonitis.
cause; obtain minimum data from hemogram,
biochemistry, and urinalysis. Suggested Reading
• Head tilt or nystagmus—likely vestibular
Cherubini GB, Lowrie M, Anderson J. Pelvic
localization. TREATMENT limb ataxia in the older dog. In Pract 2008,
• Intention tremors of the head or hyper- • Usually outpatient, depending on severity 30:386–391.
metria—likely cerebellar localization. and acuteness of clinical signs. Davies C, Shell L. Neurological problems. In:
• All four limbs affected—lesion is in the • Exercise—decrease or restrict if ataxia Davies C, Lawrence T, Shell L, eds.,
cervical spinal cord, cerebellum, or is multifocal originates from spinal cord disease. Common Small Animal Medical Diagnoses:
to diffuse. • Client should monitor gait for increasing An Algorithmic Approach. Philadelphia,
• Only pelvic limbs affected—lesion is dysfunction or weakness; if paresis worsens or PA: Saunders, 2002, pp. 36–59.
anywhere below the second thoracic vertebra. paralysis develops, other testing is warranted. Lowrie M. Vestibular disease: anatomy,
• Avoid drugs that could contribute to the physiology, and clinical signs. Compend
CBC/BIOCHEMISTRY/URINALYSIS problem; may not be possible in patients on Contin Educ Vet 2012, 34:E1–5.
Normal unless metabolic cause (e.g., hypo- antiepileptic drugs for seizures. Penderis J. The wobbly cat: diagnostic and
glycemia, electrolyte imbalance, anemia, therapeutic approach to generalised ataxia. J
polycythemia). Fel Med Surg 2009, 11:349–359.
OTHER LABORATORY TESTS Rossmeisl JH Jr. Vestibular disease in dogs
• Hypoglycemia—determine serum insulin and cats. Vet Clin North Am Small Anim
concentration on sample that has low glucose
MEDICATIONS Pract 2010, 40:81–100.
value; low glucose and higher than expected DRUG(S) OF CHOICE Author Linda G. Shell
insulin value suggest insulin-secreting tumor. Not recommended until the source or cause
• Anemia—differentiate as nonregenerative or of the problem is identified.
regenerative on the basis of the reticulocyte count. Client Education Handout
• Electrolyte imbalance—correct the problem; available online
see if ataxia resolves.
• Antiepileptic drugs—if being administered,
FOLLOW-UP
evaluate serum concentration for toxicity.
PATIENT MONITORING
IMAGING Periodic neurologic examinations to assess
• Spinal radiography, myelography, CT,
condition.
or MRI—if spinal cord dysfunction suspected.
A Atlantoaxial Instability
BASICS DIAGNOSIS TREATMENT

• Prior to treatment, consultation with a
OVERVIEW DIFFERENTIAL DIAGNOSIS
• Results from malformation or disruption of • Differential diagnoses are consistent with
board-certified neurologist or surgeon should
the articulation between the first and second various causes of cervical myelopathies, be pursued.
cervical vertebrae (atlas and axis, respectively); including: • Improper treatment can lead to irreversible
causes spinal cord compression. ◦ Other congenital malformation.
deterioration in neurologic function.
• Can result in spinal cord trauma or ◦ Trauma. MEDICAL
compression at the junction between atlas and ◦ Meningitis or meningomyelitis, infectious • Neck brace (splint) to stabilize cervical
axis—may cause neck pain and/or varying or noninfectious (granulomatous vertebral column in extension.
degrees of general proprioceptive (GP) ataxia/ meningoencephalomyelitis). ◦ Fiberglass cast material positioned
upper motor neuron (UMN) tetraparesis, ◦ Fibrocartilaginous embolic myelopathy. ventrally from rostral aspect of mandible to
tetraplegia (with or without nociception), and ◦ Disk herniation. xiphoid and incorporated into bandage
death from respiratory arrest. ◦ Neoplasia. material, which immobilizes head and
Etiology CBC/BIOCHEMISTRY/URINALYSIS neck.
◦ Strict exercise restriction (cage confine-
• Congenital—anomaly of the dens (aplasia, Normal
hypoplasia, or malformation [dorsal angulation] ment) for minimum of 8 weeks.
IMAGING ◦ Frequent bandage/splint changes are
of the dens) and its ligamentous attachments. • Plain radiography of the cervical vertebral
• Acquired—consequence of traumatic
needed.
column: • Adjunctive medication (see below).
injury. ◦ Lateral view—caudal and dorsal displace-
SIGNALMENT ment of the axis in relationship to the atlas, Overall Prognosis
• Successful outcome observed in 62.5%
• Congenital—toy-breed dogs (Yorkshire resulting in increased distance between
terrier, miniature or toy poodle, Chihuahua, vertebrae. of dogs.
Pekingese, and Pomeranian). • Improved prognosis associated with acute
◦ Ventral dorsal or oblique view—may
• Age at onset—usually before 12 months. reveal absence, hypoplasia, or malformation onset and short duration of clinical signs
• Uncommon in larger-breed dogs, dogs >1 (dorsal angulation) of the dens. (<30 days).
year old, and cats. • Surgery recommended to treat animals that
• Cross-sectional imaging:
• No sex predilection. ◦ MRI.
fail to improve or experience recurrence of
◦ Diagnosis based on observation of caudal
signs following medical treatment.
SIGNS
• Intermittent or progressive ambulatory
and dorsal displacement of the axis in SURGERY
tetraparesis, usually with neck pain—most relationship to the atlas, as evidenced by the • Treatment of choice in majority of cases.
common. following features of the atlantoaxial • Surgical approach; ventral method is
• Neurologic signs vary from mild to
articulation: (1) dorsal: displacement of the preferred.
moderate GP/UMN ambulatory tetraparesis spinous process of the axis; (2) ventral: • Ventral approach—variety of methods:
to nonambulatory GP/UMN tetraparesis, or increased size of the occipito-atlas-axis joint ◦ Transarticular pinning or lag screw
tetraplegia, depending on degree of spinal cavity. technique; ventral tips of pins incorporated
cord compression and secondary pathology ◦ Allows identification of spinal cord in polymethylmethacrylate to prevent pin
(i.e., edema, hemorrhage, or gliosis). compression. migration.
◦ Allows recognition of secondary spinal ◦ Transarticular pinning and ventral
• Animals may have only neck pain without
concurrent neurologic deficits. cord pathology such as edema, hemorrhage, cortical screws or K-wires in bodies of atlas
• Episodes of collapse secondary to weakness.
or gliosis, which may impact prognosis. and axis ± K-wires applied longitudinally
• CT—may provide detailed visualization of and wired to screws; screw heads and
• Abnormal postural reactions with spinal
reflexes that are normal to exaggerated, with bony structures, which allows for creation of K-wires incorporated in polymethylmeth-
normal to increased muscle tone in all four three-dimensional reconstructed image to acrylate to provide fixation.
limbs. help surgical planning. • Dorsal approach—use wire or synthetic
• Precautions: suture material to fix spinous process of axis
• Acute death may occur when accompanied
by trauma and respiratory arrest (uncommon). ◦ Proper positioning will require sedation to dorsal arch of atlas; provides less rigid
or general anesthesia. fixation and may be associated with greater
CAUSES & RISK FACTORS ◦ Sedation or general anesthesia carries implant failure.
• Usually caused by abnormal development significant risk for iatrogenic trauma. • Strict exercise restriction required for
of the dens and/or ligamentous support ◦ Care needs to be exercised when first month postoperatively, followed by
structures, resulting in subluxation of the positioning animals. gradual return to activity over additional
atlantoaxial joint. ◦ Avoid excessive flexion of the neck! month.
• Fracture of the axis. ◦ Flexion may exacerbate compression, • Adjunctive medication (see below).
• Clinical signs often occur as a result of mild which may worsen clinical signs or cause • Overall prognosis ranges from 63% to 91%
or insignificant trauma (e.g., jumping or death due to spinal cord trauma. success—improved prognosis associated with
playing). ◦ To protect against neck flexion during young (<24 months) dogs, duration of clinical
• Clinical signs may be exacerbated by recovery, affected animals should be closely signs <10 months, and mild neurologic
activity such as flexion of the neck. monitored until they are capable of deficits.
• Toy-breed dogs—at risk for congenital maintaining normal head and neck carriage.
malformation of the dens.
(continued) Atlantoaxial Instability A
• Complications: Suggested Reading

◦ Failure to improve/worsening of neuro- Beaver DP, Ellison GW, Lewis DD. Risk
logic deficits. factors affecting the outcome of surgery for
◦ Implant failure/infection. FOLLOW-UP atlantoaxial subluxation in dogs: 46 cases
◦ Respiratory—respiratory arrest, dyspnea, • Dogs treated medically require frequent (1978–1998). J Am Vet Med Assoc 2000,
cough, and aspiration pneumonia. (weekly) bandage changes for associated soft 216(7):1104–1109.
◦ Death. tissue trauma. Havig ME, Cornell KK, Hawthorne JC, et al.
• All dogs should be reevaluated at 1 and 3 Evaluation of nonsurgical treatment of
months (postoperatively or after neck brace atlantoaxial subluxation in dogs: 19 cases
removal) and then monthly until neurologic (1992–2001). J Am Vet Med Assoc 2005,
deficits resolve or remain static over 2–3 227(2):257–262.
MEDICATIONS months. McCarthy RJ, Lewis DD, Hosgood G.
DRUG(S) OF CHOICE • More frequent rechecks may be needed for Atlantoaxial subluxation in dogs. Compend
• Anti-inflammatory medication: dogs experiencing complications or recur- Contin Educ Pract Vet 1995, 17:215–226.
◦ Corticosteroids—prednisone 0.5– rence of signs. Platt SR, Casimiro da Costa R. Cervical
1.0 mg/kg PO divided twice daily for • Untreated animals may experience vertebral column. In: Johnston SA, Tobias
2 weeks, followed by tapering regime. deterioration in neurologic function, KM, eds., Textbook of Small Animal
Suggested protocol following initial dose: catastrophic acute spinal cord trauma, Surgery, 2nd ed. St. Louis, MO: Elsevier,
0.5 mg/kg PO daily for 5 days, followed by respiratory arrest, and death. 2018, pp. 438–485.
0.5 mg/kg PO every other day for 5 days. Platt SR, Chambers JN, Cross A. A modified
◦ Nonsteroidal anti-inflammatory drug ventral fixation for surgical management of
(NSAID)—1- to 4-week course. atlantoaxial subluxation in 19 dogs. Vet
• Analgesia: MISCELLANEOUS Surg 2004, 33(4):349–354.
◦ Tramadol 2.0–4.0 mg/kg PO q6–8h— • Rehabilitation may play a significant role Sanders SG, Bagley RS, Silver GM, et al.
questionable efficacy. in ultimate neurologic functional level of Outcomes and complications associated
◦ Gabapentin 10–20 mg/kg PO q6–8h. patient. with ventral screws, pins, and polymethyl
◦ Pregabalin 3–4 mg/kg (begin with 2 mg/ • Rehabilitation should only be considered methacrylate for atlantoaxial instability in
kg) PO q8–12h. in dogs >30 days postoperatively or after 12 dogs. J Am Anim Hosp Assoc 2004,
CONTRAINDICATIONS/POSSIBLE neck brace (splint) removal. 40:204–210.
Schulz KS, Waldron DR, Fahie M.
INTERACTIONS ABBREVIATIONS Application of ventral pins and polymethyl-
• Corticosteroid—use caution when given in • GP = general proprioceptive.
methacrylate for the management of
conjunction with medical treatment; may • NSAID = nonsteroidal anti-inflammatory
atlantoaxial instability: results in nine dogs.
reduce pain, resulting in increased activity drug. Vet Surg 1997, 26(4):317–325.
and spinal cord trauma. • UMN = upper motor neuron.
Author Mathieu M. Glassman
• Avoid NSAIDs in combination with
INTERNET RESOURCES Consulting Editor Mathieu M. Glassman
corticosteroids in all patients—increases risk
www.acvs.org/small-animal/
of life-threatening gastrointestinal
atlantoaxial-instability
hemorrhage.
A Atopic Dermatitis
Highland white terrier, wirehaired fox DIAGNOSTIC PROCEDURES
terrier, Labrador retriever. • Feline— • Diagnosis made by history, physical exam
Abyssinian, Devon Rex, domestic ination, and ruling out differential diagnoses.
BASICS shorthaired cats. • Serology/intradermal test (IDT) not meant for
DEFINITION Mean Age and Range diagnosis. • Greatest treatment success noted
• Genetically predisposed skin disease • Canine—6 months to 3 years. • Feline—6 when immunotherapy based on results of both
characterized by inflammation and pruritus. months to 2 years, commonly under 3 years. serum and intradermal testing.
Clinical signs associated with immunoglobulin Serologic Allergy Tests
(Ig) E and most commonly directed against Predominant Sex
None reported. • Measures allergen-specific IgE in serum.
environmental allergens. • Differentiate from • Advantages—readily available; clipping/
atopic-like dermatitis, in which clinical signs SIGNS sedation not required; concurrent/recent
identical to atopic dermatitis but IgE response medications and infections less likely to affect
General Comments
to environmental or other allergens cannot be results; similar hyposensitization success to
Cutaneous changes caused by self-induced
demonstrated. IDT. • Disadvantages—fewer allergens tested;
trauma; primary lesions usually unrecognized.
PATHOPHYSIOLOGY quality control/reliability varies with laboratory.
Historical Findings
• Allergen exposure in susceptible animals IDT
• Pruritus. • Early age of onset. •History in
results in IgE production. Upon reexposure to • Test allergens injected intradermally causing
related individuals. • May be initially
allergen, mast cell degranulation and activation wheal formation. • Advantages—tests
seasonal. • Recurring skin or ear infection.
of TH2 lymphocytes allow release of affected organ, results available immediately,
• Temporary response to glucocorticosteroids.
inflammatory cytokines, chemokines, many allergens tested; preferred where
• Signs worsen with time.
histamine, proteolytic enzymes, and other available. • Disadvantages—requires
chemical mediators. • Genetic defects—dogs: Physical Examination Findings experience to interpret results, clipping and
gene expression upregulated or downregulated; • Most common (dogs)—interdigital spaces,
sedation needed, difficult to interpret in cats;
cats: not well documented. • Barrier function carpal/tarsal areas, muzzle, periocular, drug withdrawal periods recommended,
defects—dogs: impaired epidermal lipid axillae, abdomen, pinnae; >40% can be concurrent infection may affect results.
barrier can lead to enhanced allergen generalized. • Most common (cats)—head
penetration and increased transepidermal and neck, mouth, abdomen, lateral thorax, PATHOLOGIC FINDINGS
water loss (TEWL); filaggrin defect thought hind limbs. • Lesions (dogs)—none to Skin biopsy—rule out other differential
to be associated; cats: may not be as relevant salivary staining, alopecia, erythema, papules, diagnoses; results not pathognomonic;
as with dogs. • Immunologic defects—dogs: crusts, hyperpigmentation, lichenification, superficial perivascular dermatitis with
acute lesions characterized by increased TH2 seborrhea sicca/oleosa, and/or hyperhidrosis. lymphocytic exocytosis ± eosinophils, mast
lymphocyte activity, while TH1 cytokines • Lesions (cats)—miliary dermatitis (small cells; often with secondary bacterial folliculitis.
predominate in chronic lesions; TH2:TH1 crusted papules), alopecia, eosinophilic
imbalance proposed; aberrant regulatory granuloma complex (indolent ulcers,
T-cell function reported; cats: TH2-mediated eosinophilic granulomas, eosinophilic
dysfunction suspected, but cytokine pathways plaques). • Chronic relapsing bacterial and TREATMENT
need further investigation. • Bacterial yeast skin/ear infections (common).
superantigens, auto-antigens released via • Respiratory symptoms, conjunctivitis, and APPROPRIATE HEALTH CARE
keratinocyte damage, and Malassezia may blepharitis possible. Outpatient
play role in inflammation. CAUSES ACTIVITY
SYSTEMS AFFECTED • Pollens. • Mold spores. • Malassezia. Avoid offending allergens when possible.
• Ophthalmic. • Respiratory. • Skin/exocrine. • House dust and storage mites. • Animal/ DIET
human dander. • Insects. Diets rich in essential fatty acids may be beneficial.
GENETICS
• Dogs—inherited predisposition. • Cats— RISK FACTORS CLIENT EDUCATION
inherited predisposition less clear. • Environments with long allergy seasons and Explain inheritable, progressive, and incurable
high pollen and mold spore levels. • Concurrent nature of condition.
hypersensitivities (summation effect). • Born
• Canine—3–27% of canine population
during allergy season. • Breed predisposition.
estimated. • Feline—lower than for dogs.
Canine—worldwide; local factors influence MEDICATIONS
seasonality, severity, and duration of signs. DRUG(S) OF CHOICE
DIAGNOSIS
SIGNALMENT Immunotherapy (Hyposensitization)
Species • Subcutaneous or sublingual administration
• Adverse food reaction. • Flea bite hyper
Dogs and cats. of causative allergens. • Allergen selection
sensitivity. • Sarcoptic mange. • Bacterial
based on allergy test results, patient history,
Breed Predilections folliculitis. • Yeast dermatitis. • Contact
and knowledge of local exposure.
• United States—Boston terrier, boxer, dermatitis (allergic or irritant).
• Immunotherapy protocols not standardized
Cairn terrier, Chinese Shar-Pei, cocker CBC/BIOCHEMISTRY/URINALYSIS and vary widely between clinicians.
spaniel, Dalmatian, English bulldog, English Eosinophilia—rare in dogs without concurrent • Preferred treatment in most cases.
and Irish setter, American Staffordshire flea infestations; common in cats. • Successfully reduces pruritus in 50–90%
terrier, Lhasa apso, miniature schnauzer, of dogs and cats. • 3 months to 1 year for full
pug, Sealyham terrier, Scottish terrier, West effect. • May continue lifelong if effective.
(continued) Atopic Dermatitis A
Cyclosporine (Atopica® Preferred) use in dogs under 1 year of age; may cause PREGNANCY/FERTILITY/BREEDING
• Cyclosporine, modified (dogs, 5 mg/kg/ existing parasitic skin infestations and/or • Corticosteroids—contraindicated during
day; cats, 7 mg/kg/day). • 1–4 weeks for prevent resolution of infections. pregnancy. • Affected animals should not be
effect—frequency of dosing may be reduced POSSIBLE INTERACTIONS used for breeding.
to maintain control of symptoms. Concurrent use of cyclosporine and ketoconazole SYNONYMS
• Monitoring recommended. • Cats—drug
permits 50% dose reduction of each drug. • Atopy. • Canine atopic disease.
blood level monitoring recommended; keep
indoors, do not feed raw meat. ALTERNATIVE DRUG(S) SEE ALSO
• Frequent bathing (once to twice weekly) in • Eosinophilic Granuloma Complex.
Corticosteroids
cool water with antipruritic, antibacterial, • Flea Bite Hypersensitivity and Flea Control.
• For short-term relief or taper to lowest
antifungal, and/or moisturizing shampoos can • Food Reactions, Dermatologic.
dosage/frequency. • Dogs—e.g., prednisolone be beneficial. • Fatty acids—diets rich in • Otitis Externa and Media.
(1 mg/kg PO q24h). • Cats—e.g., essential fatty acids typically provided higher • Pyoderma.
prednisolone (2 mg/kg q24h). amounts than with oral supplements. ABBREVIATIONS
Antihistamines • Pentoxifylline 25 mg/kg q12h. • Topical
• IDT = intradermal test.
• Less effective than corticosteroids. • 2 weeks hydrocortisone or triamcinolone spray • Ig = immunoglobulin.
for effect. • Dogs—cetirizine (1 mg/kg PO 0.015% (short-term use). • TEWL = transepidermal water loss.
q12–24h), chlorpheniramine (0.4 mg/kg PO
q8–12h), diphenhydramine (2.2 mg/kg PO Suggested Reading
q8–12h), amitriptyline (1–2 mg/kg q12h). Botoni LS, Torres SMF, Koch SN, et al.
• Cats—cetirizine (5 mg/cat q24h), Comparison of demographic data, disease
chlorpheniramine (2 mg/cat PO q12h), FOLLOW-UP severity, and response to treatment, between
amitriptyline (5–10 mg/cat q24h); PATIENT MONITORING dogs with atopic dermatitis and atopic-like
diphenhydramine may cause paradoxical • Examination every 2–8 weeks initially; once dermatitis: a retrospective study. Vet Derm
excitation in cats. acceptable level of control achieved, examine 2019, 30:10–e4.
every 3–6 months. • Monitor pruritus, self- Gedon NK, Mueller RS. Atopic dermatitis
Oclacitinib (Apoquel®)
trauma, development of secondary infection, in cats and dogs: a difficult disease for
• Dogs—onset time/response similar to
possible adverse drug reactions. • CBC/blood animals and owners. Clin Transl Allergy
glucocorticoids (0.4–0.6 mg/kg q12h for 14 2018, 8:41.
days, then q24h for maintenance). • Cats— chemistry/urinalysis with culture—
recommended every 3–12 months for Lappin MR, VanLare KA, Seewald W, et al.
not licensed; limited short-term studies report Effect of oral administration of cyclosporine
effectiveness, but higher doses may be needed. patients on chronic corticosteroid,
cyclosporine, or oclacitinib therapy. on Toxoplasma gondii infection status of
Lokivetmab (Cytopoint®) cats. Am J Vet Res 2015, 76(4):351–357.
Dogs only—anti-IL-31 monoclonal antibody PREVENTION/AVOIDANCE
Miller WH, Griffin CE, Campbell KL.
• Avoidance of allergens seldom possible.
injectable; repeated as needed up to frequency Muller & Kirk’s Small Animal Dermatology,
• Minimize other sources of pruritus.
of every 4–6 weeks. 7th ed. St. Louis, MO: Elsevier Mosby,
PRECAUTIONS POSSIBLE COMPLICATIONS 2013.
• Secondary bacterial folliculitis or Noli C, Matricoti I, Schievano C. A double
• Immunotherapy—anaphylaxis rare
(accompanied by diarrhea, weakness, Malassezia dermatitis. • Concurrent blinded, randomized, methylprednisolone-
collapse), hives, facial swelling; monitor for hypersensitivities. controlled study on the efficacy of oclacitinib
1 hour post injection; increased pruritus EXPECTED COURSE AND PROGNOSIS in the management of pruritus in cats with
after injection may indicate change in • Pruritus and duration of signs usually nonflea nonfood induced hypersensitivity
schedule needed; pain or swelling at worsen over time without intervention. dermatitis. Vet Derm 2019,
injection site uncommon. • Cyclosporine— • Some cases spontaneously resolve. 30(2):110–e30.
may affect glucose homeostasis; increased Author Heather D. Edginton
incidence of urinary tract infection; Consulting Editor Alexander H. Werner
vomiting and diarrhea most common side Resnick
effects; gingival hyperplasia, papillomavirus, Acknowledgment The author acknowledges
and hirsutism possible; risk of fatal toxoplasmosis
MISCELLANEOUS the prior contribution of Alexander H.
in naïve cats. • Corticosteroids—avoid ASSOCIATED CONDITIONS Werner Resnick.
iatrogenic hyperglucocorticism/ • Hypersensitivity (flea, food). • Bacterial
hyperadrenocorticism; possible aggravation folliculitis. • Malassezia dermatitis. • Otitis
of pyoderma and induction of demodicosis. externa. Client Education Handout
• Antihistamines—can produce drowsiness, available online
AGE-RELATED FACTORS
rarely anorexia, vomiting, diarrhea, increased Severity worsens with age.
pruritus; use with caution in patients with
cardiac arrhythmias. • Oclacitinib—not for
A Atrial Fibrillation and Atrial Flutter
conduction of subsequent electrical impulses; CAUSES
electrical impulses are conducted through the • Myxomatous valve disease. • Cardiomyopathy.
AV junction irregularly, producing an irregular • Congenital heart disease. • Digoxin toxicity.
BASICS ventricular rhythm. • Atrial flutter—probably • Idiopathic. • Ventricular preexcitation
DEFINITION originates from one site of reentry that moves (atrial flutter).
• Atrial fibrillation—rapid, irregularly irregular continuously throughout the atrial myocar-
supraventricular rhythm. Two forms recognized: dium and frequently and regularly stimulates
primary atrial fibrillation, an uncommon disease the AV node. When the atrial rate becomes
that occurs mostly in large dogs with no under- sufficiently fast, the refractory period of the AV
node exceeds the cycle length (P to P interval)
DIAGNOSIS
lying cardiac disease; and secondary atrial
fibrillation, which occurs in dogs and cats of the supraventricular tachycardia (SVT), and DIFFERENTIAL DIAGNOSIS
secondary to underlying cardiac disease. • Atrial some atrial depolarizations are blocked from • Frequent atrial (supraventricular) premature
flutter is similar to atrial fibrillation, but the traversing the AV node (functional second- depolarizations. • Supraventricular tachy
atrial rate is generally slower and is character- degree AV block). cardia with AV block. • Multifocal atrial
ized by saw-toothed flutter waves in the baseline tachycardia (irregular).
SYSTEMS AFFECTED
of the ECG. The ventricular response is generally CBC/BIOCHEMISTRY/URINALYSIS
rapid, but may be regular or irregular. Cardiovascular
N/A
Loss of atrial contraction may result in
ECG Features decreased stroke volume and cardiac output, OTHER LABORATORY TESTS
Atrial Flutter depending on heart rate; high heart rate may N/A
• Atrial rhythm usually regular; rate approx- result in deterioration in myocardial function IMAGING
imately 300–400 bpm. • P waves usually (tachycardia-induced myocardial failure). • Echocardiography and radiography may
discerned as either discrete P waves or “saw- characterize type and severity of underlying
GENETICS
toothed” baseline. • Ventricular rhythm and cardiac disease; moderate to severe heart
No breeding studies available.
rate generally depend on atrial rate and enlargement common. • Typically normal in
atrioventricular (AV) nodal conduction, but SIGNALMENT
patients with primary atrial fibrillation,
are generally regular or regularly irregular and Species although mild left atrial enlargement may
rapid. • Conduction pattern to ventricles is Dog and cat. accompany hemodynamic alterations
variable—in some cases every other atrial imposed by arrhythmia.
depolarization produces a ventricular Breed Predilections
depolarization (2 : 1 conduction ratio), giving Large- and giant-breed dogs more prone to DIAGNOSTIC PROCEDURES
a regular ventricular rhythm (Figure 1); other primary atrial fibrillation. A baseline 24-hour Holter is recommended
times the conduction pattern appears Mean Age and Range to determine if arrhythmia is chronic or
random, giving an irregular ventricular N/A paroxysmal. If it is chronic, drug therapy may
rhythm that can mimic atrial fibrillation. be indicated.
Predominant Sex
Secondary Atrial Fibrillation N/A
• No P waves present—baseline may be
SIGNS
flat or may have small irregular undulations
(“f ” waves); some undulations may look like General Comments TREATMENT
P waves. • Ventricular rate often elevated— • Generally relate to underlying disease
usually 180–240 bpm in dogs and >220 bpm process and/or congestive heart failure
• Patients with fast (secondary) atrial
in cats. • Interval between QRS complexes is (CHF) rather than arrhythmia itself, but
fibrillation are treated medically to slow the
irregularly irregular; QRS complexes usually previously stable animals may decompensate.
ventricular rate. Converting the atrial
appear normal (Figure 2). • Patients with primary atrial fibrillation are
fibrillation to sinus rhythm would be ideal, but
generally asymptomatic, but may demonstrate
Primary Atrial Fibrillation mild exercise intolerance.
such attempts in patients with severe underly-
Similar to secondary atrial fibrillation, except ing heart disease or left atrial enlargement are
ventricular rate usually in normal range. Historical Findings generally futile because of a low success rate
• Coughing/dyspnea/tachypnea. • Exercise and high rate of recurrence. Consider electrical
PATHOPHYSIOLOGY
intolerance. • Rarely, syncope. • Dogs with cardioversion to sinus rhythm for a dog with
• Atrial fibrillation—caused by numerous
primary atrial fibrillation are typically primary atrial fibrillation and minimal
small reentrant pathways creating a rapid
asymptomatic. structural heart disease. • Patients with primary
(>500 depolarizations/minute) and disorgan-
Physical Examination Findings atrial fibrillation may be converted back to
ized depolarization pattern in the atria that
• On auscultation, patients with atrial normal sinus rhythm. The success rate depends
results in cessation of atrial contraction.
fibrillation have an erratic heart rhythm that on chronicity. Patients that have been in atrial
Depolarizations continuously bombard the AV
sounds like “tennis shoes in a dryer.” • First fibrillation for >4 months generally have a
nodal tissue, which acts as a filter and does not
heart sound intensity in atrial fibrillation is lower success rate and a higher rate of
allow all depolarizations to conduct to the
variable; second heart sound only heard on recurrence. In these patients, rate control, if
ventricles. Many atrial depolarizations activate
beats with effective ejection, not on every beat. necessary, is the recommended treatment.
only a part of the atria, because the rapid rate
• Third heart sounds (gallop sounds) may • Electrical (DC) cardioversion—application
renders portions of the atria refractory, and
be present. • Patients with atrial fibrillation of a transthoracic electrical shock at a specific
thus they cannot reach the AV junction. Other
have pulse deficits and variable pulse quality. time in the cardiac cycle; requires special
atrial impulses penetrate into the AV junc-
• Signs of CHF often present (e.g., cough, equipment, trained personnel, and general
tional tissue, but do not penetrate the entire
dyspnea, cyanosis). anesthesia. Using a monophasic defibrillator:
length. Blocked impulses affect the conduction
start with 4 J/kg; if no conversion occurs,
properties of the AV junctional tissue and alter
(continued) Atrial Fibrillation and Atrial Flutter A
Figure 1.
Atrial flutter with 2 : 1 conduction at a ventricular rate of 330/minute in a
dog with an atrial septal defect. This supraventricular tachycardia was associ-
ated with a Wolff-Parkinson-White pattern. (Source: From Tilley LP.
Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore, MD:
Williams & Wilkins, 1992. Reprinted with permission of Wolters Kluwer.)
increase dose by 50 J and repeat until a max of signs. • Sustained conversion to sinus Dogs
360 J. Using a biphasic defibrillator: start with rhythm is unlikely with secondary atrial • Digoxin—maintenance oral dose
1–2 J/kg; if no cardioversion occurs, increase fibrillation. 0.005–0.01 mg/kg PO q12h; to achieve
dose by 50 J and repeat until max of 360 J. SURGICAL CONSIDERATIONS therapeutic serum concentration more
• For atrial flutter, conversion to sinus rhythm
N/A rapidly, maintenance dose can be doubled
can be accomplished by drug therapy, electrical for the first day. If digoxin is administered
cardioversion, or rapid atrial pacing (trans- alone and heart rate remains high, check
venous pacing electrode). digoxin level and adjust dose to bring level
NURSING CARE into therapeutic range. If heart rate remains
As indicated for CHF.
MEDICATIONS high, consider adding calcium channel
DRUG(S) OF CHOICE blocker or β-adrenergic blocker.
ACTIVITY • Diltiazem—initially administered at dose
• Digoxin, β-adrenergic blockers, esmolol,
Restrict activity until tachycardia is controlled. of 0.5 mg/kg PO q8h, then titrated up to
and calcium channel blockers (diltiazem) are
DIET frequently used to slow conduction through maximum of 1.5 mg/kg PO q8h or until
Mild to moderate sodium restriction if CHF. the AV node; definition of an adequate heart adequate response is obtained. • Therapy
rate response varies among clinicians, but in for atrial flutter is aimed at suppressing
CLIENT EDUCATION atrial reentry circuit using sotalol, amiodar-
• Secondary atrial fibrillation and atrial dogs is generally 130–150 bpm. • For atrial
flutter, therapy is aimed at suppressing the one, or procainamide. Conversion to
flutter are usually associated with severe normal sinus rhythm is usually
underlying heart disease; goal of therapy is atrial reentry circuit using sotalol, amiodar-
one, or procainamide. unsuccessful.
to lower heart rate and control clinical
Figure 2.
“Coarse” atrial fibrillation in a dog with patent ductus arteriosus. The f waves are prominent.
(Source: From Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore, MD:
Williams & Wilkins, 1992. Reprinted with permission of Wolters Kluwer.)
A Atrial Fibrillation and Atrial Flutter (continued)
Cats after transthoracic cardioversion of dogs

• Diltiazem (1–2.5 mg/kg PO q8h) or with naturally occurring atrial fibrillation.
atenolol (6.25–12.5 mg/cat PO q12–24h) J Vet Intern Med 2008, 22(1):114–119.
are drugs of choice in most cats. • If the FOLLOW-UP Gelzer RM, Kraus MS. Management of atrial
heart rate is not sufficiently slowed with PATIENT MONITORING fibrillation. Vet Clin North Am Small Anim
these drugs or myocardial failure is present, • Monitor heart rate and ECG closely. • As Pract 2004, 34:1127–1144.
digoxin (5 μg/kg PO q24–48h) can be heart rates in the hospital and those measured Gelzer ARM, Kraus MS, Moise NS, et al.
added. on the surface ECG may be inaccurate (due Assessment of antiarrhythmic drug efficacy
CONTRAINDICATIONS to patient anxiety and other environmental to control heart rate in dogs with atrial
• Digoxin, diltiazem, propranolol, and factors), Holter monitoring provides a more fibrillation using 24-hour ambulatory
atenolol should not be used in patients with accurate means for assessing the need for electrocardiographic (Holter) recordings.
preexisting AV block. • Use of calcium heart rate control and/or the efficacy of J Vet Intern Med 2004, 18(5):779.
channel blockers in combination with beta medical therapy for heart rate control. Tilley LP, Smith FWK, Jr. Electrocardiography.
blockers should be avoided because clinically In: Smith FWK, Tilley LP, Oyama M,
significant bradyarrhythmias and/or AV Sleeper M., eds., Manual of Canine and
Worsening of cardiac function with onset of
block can develop. Feline Cardiology, 5th ed. St. Louis, MO:
arrhythmia.
PRECAUTIONS EXPECTED COURSE AND PROGNOSIS Santilli R, Moise NS, Pariaut R, Perego M.
• Calcium channel blockers and β-adrenergic • Secondary atrial fibrillation—often Electrocardiography of the Dog and Cat:
blockers, both negative inotropes, should be associated with severe structural heart disease, Diagnosis of Arrhythmias, 2nd ed. Milan:
used cautiously in animals with myocardial so a guarded to poor prognosis. • Primary Edra, 2018.
failure. • Using high-dose oral quinidine for atrial fibrillation with normal ultrasound Tilley LP, Smith, F.W. Essentials of
conversion to sinus rhythm carries a risk of findings—generally a good prognosis. Electrocardiography: Interpretation and
quinidine toxicity (e.g., hypotension, weak- Treatment, 4th ed. Ames, IA: Wiley-
ness, ataxia, and seizures)—administration of Blackwell, 2016.
diazepam intravenously controls seizures; Willis R, Oliveira P, Mavropoulou A. Guide
other signs abate within several hours of to Canine and Feline Electrocardiography.
discontinuing quinidine administration. MISCELLANEOUS Ames, IA: Wiley-Blackwell, 2018.
POSSIBLE INTERACTIONS ABBREVIATIONS Author Larry P. Tilley
Quinidine raises the digoxin level, generally • AV = atrioventricular. Consulting Editor Michael Aherne
necessitating a digoxin dose reduction. • CHF = congestive heart failure.
• SVT = supraventricular tachycardia.
Suggested Reading Client Education Handout
Bright JM, Brunnen J. Chronicity of atrial available online
fibrillation affects duration of sinus rhythm
Atrial Premature Complexes A
dogs; commonly seen in dogs with atrial

enlargement secondary to chronic mitral
valvular insufficiency; may also be observed
BASICS in dogs or cats with any atrial disease. • May DIAGNOSIS
DEFINITION not cause hemodynamic problems; the DIFFERENTIAL DIAGNOSIS
Premature atrial complexes or beats (APC) clinical significance relates to their frequency, • Marked sinus arrhythmia. • Ventricular
that originate outside the sinoatrial node and timing relative to other complexes, and the premature complexes when aberrant
disrupt the normal sinus rhythm for 1 or underlying clinical problems. • Can presage ventricular conduction follows an APC.
more beats. more serious rhythm disturbances (e.g., atrial
fibrillation, atrial flutter, or atrial tachycardia).
ECG Features N/A
• Heart rate usually normal; rhythm irregular SYSTEMS AFFECTED
due to the premature P wave (called a P′ Cardiovascular
N/A
wave) that disrupts the normal P wave GENETICS
rhythm (Figure 1). • Ectopic P′ wave— IMAGING
N/A
premature; configuration differs from that of Echocardiography and Doppler ultrasound
the sinus P waves and may be negative, INCIDENCE/PREVALENCE may reveal the type and severity of the under-
positive, biphasic, or superimposed on the Not documented. lying heart disease.
previous T wave. • QRS complex— SIGNALMENT DIAGNOSTIC PROCEDURES
premature; configuration usually normal • ECG. • Holter monitor to quantify APC
Species
(same as that of the sinus complexes). If the frequency and event monitor/Holter ECG to
Dog and cat.
P′ wave occurs during the refractory period of correlate symptoms with rhythm.
the atrioventricular (AV) node, ventricular Breed Predilections
conduction does not occur (nonconducted Small-breed dogs. PATHOLOGIC FINDINGS
APCs), so no QRS complex follows the P′ Atrial enlargement; other features vary
Mean Age and Range depending on underlying cause.
wave. If there is partial recovery in the AV Geriatric animals, except those with
node or intraventricular conduction systems, congenital heart disease.
the P′ wave is conducted with a long P′–R
interval or with an abnormal QRS configura- SIGNS
tion (aberrant conduction). The more Historical Findings TREATMENT
premature the complex, the more marked the • No signs. • Congestive heart failure (CHF).
aberration. • In the P–QRS relationship, the • Coughing and dyspnea. • Exercise
• Treat animal as inpatient or outpatient.
P′–R interval is usually as long as, or longer intolerance. • Syncope.
• Treat the underlying CHF, cardiac disease,
than, the sinus P′–R interval. • A noncom-
Physical Examination Findings or other causes.
pensatory pause—when the R–R interval of
• Myxomatous valve disease. • Cardiac murmur.
the two normal sinus complexes enclosing an NURSING CARE
• Gallop sound. • Signs of CHF.
APC is less than the R–R intervals of three Usually not necessary; varies with underlying
consecutive sinus complexes—usually follows CAUSES & RISK FACTORS cause.
an APC (Figure 2). The ectopic atrial impulse • Chronic valvular disease. • Congenital
ACTIVITY
discharges the sinus node and resets the cycle. heart disease. • Cardiomyopathy. • Atrial
Restrict if symptomatic.
myocarditis. • Electrolyte disorders.
PATHOPHYSIOLOGY DIET
• Neoplasia. • Hyperthyroidism. • Toxemias.
• Mechanisms—an increase in automaticity No modifications unless required for
• Drug toxicity (e.g., digitalis). • Normal
of atrial myocardial fibers or a single reentrant management of underlying condition
variation in aged animals.
circuit. • May be normal finding in aged (i.e., low-salt diet).
Figure 1.
APCs in a dog. P′ represents the premature P wave. The premature QRS resembles the normal (sinus) QRS. The upright P′ wave is superimposed on the T wave
of the preceding complex. (Source: From Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992. Reprinted with
permission of Wolters Kluwer.)
A Atrial Premature Complexes (continued)
Figure 2.
APCs in bigeminy in a cat under general anesthesia. The second complex of each pair is an APC and the first is a sinus complex. The abnormality in rhythm
disappeared after the anesthetic was stopped. (Source: From Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore: Williams & Wilkins,
1992. Reprinted with permission of Wolters Kluwer.)
CLIENT EDUCATION POSSIBLE INTERACTIONS SYNONYMS

APCs may not cause hemodynamic abnormali- N/A • Atrial extrasystoles. • Atrial premature
ties; may be precursors of serious arrhythmias. ALTERNATIVE DRUG(S) contractions. • Atrial premature impulses.
• Premature atrial complexes/contractions.
SURGICAL CONSIDERATIONS N/A
N/A SEE ALSO
Supraventricular Tachycardia.
ABBREVIATIONS
FOLLOW-UP • APC = atrial premature complex.
MEDICATIONS PATIENT MONITORING
• AV = atrioventricular.
• CHF = congestive heart failure.
DRUG(S) OF CHOICE Monitor heart rate and rhythm with serial
Treat CHF and correct any electrolyte or ECG. Suggested Reading
acid/base imbalances. Jackson BL, Lehmkuhl LB, Adin DB. Heart
rate and arrhythmia frequency of normal
Dogs N/A
cats compared to cats with asymptomatic
• Digoxin (0.005–0.01 mg/kg PO q12h,
POSSIBLE COMPLICATIONS hypertrophic cardiomyopathy. J Vet Cardiol
maintenance dosage), diltiazem (0.5–1.5 mg/ Frequent APCs may further diminish cardiac 2014, 16:215–225.
kg PO q8h), or atenolol (0.25–1 mg/kg PO output in patients with underlying heart Santilli R, Moise NS, Pariaut R, Perego M.
q12h) are used to treat clinically significant disease and worsen clinical symptoms. Electrocardiography of the Dog and Cat:
arrhythmias. • Digoxin—treatment of
EXPECTED COURSE AND PROGNOSIS Diagnosis of Arrhythmias, 2nd ed. Milan:
choice. • CHF is treated with appropriate
Even with optimal antiarrhythmic drug Edra, 2018.
dosage of diuretic, angiotensin-converting
therapy, some animals have an increased Tilley LP, Smith FWK Jr. Electrocardiography.
enzyme inhibitor, and pimobendan; approp-
frequency of APCs or deteriorate to more In: Smith FWK, Tilley LP, Oyama M,
riate management of CHF may reduce APC
severe arrhythmia as the underlying disease Sleeper M, eds., Manual of Canine and
frequency.
progresses. Feline Cardiology, 5th ed. St. Louis, MO:
Cats Saunders Elsevier, 2016, pp. 49–76.
• Cats with hypertrophic cardiomyopathy— Willis R, Oliveira P, Mavropoulou A. Guide
diltiazem (1–2.5 mg/kg PO q8h) or atenolol to Canine and Feline Electrocardiography.
(6.25–12.5 mg PO q12–24h). • Cats Ames, IA: Wiley-Blackwell, 2018.
with dilated cardiomyopathy—digoxin MISCELLANEOUS Author Larry P. Tilley
(one-fourth of a 0.125 mg digoxin tablet ASSOCIATED CONDITIONS Consulting Editor Michael Aherne
q24h or q48h). None
CONTRAINDICATIONS AGE-RELATED FACTORS Client Education Handout
Negative inotropic agents (e.g., propranolol) Typically occurs in geriatric dogs. available online
should be avoided in animals with CHF.
PRECAUTIONS N/A
Use digoxin, diltiazem, atenolol, or propranolol
cautiously in animals with underlying atrio-
ventricular block or hypotension.
Atrial Septal Defect A
Physical Examination Findings CATHETER-BASED THERAPY

• Soft systolic murmur over left base due • Amplatzer® atrial septal occluder (ASO)
to increased blood flow across normal device delivered percutaneously through jugular
BASICS pulmonic valve. • Split S2 (fixed) due to vein possible for some secundum-type defects.
OVERVIEW delayed closure of pulmonic valve. • Hybrid procedure involving surgical access
• Congenital defect in which interatrial septum • Cyanosis with right-to-left shunting. and transatrial delivery of ASO device under
fails to develop normally, resulting in communi- • Ascites and jugular vein distension inflow occlusion reported.
cation between atria. Unknown cause; genetic with right CHF.
basis suspected. Acquired atrial septal defects
(ASD) secondary to atrial rupture reported with
canine degenerative mitral valve disease. MEDICATIONS
• Comprises 0.7–3.7% of congenital heart DIAGNOSIS See Congestive Heart Failure, Left-Sided;
defects in dogs, <10% of congenital heart Congestive Heart Failure, Right-Sided; and
defects in cats. Significantly higher incidence CBC/BIOCHEMISTRY/URINALYSIS
• Typically normal. • Polycythemia with Hypertension, Pulmonary.
(37.7%) noted in one study. • Three major
types of ASD classified based on the location right-to-left shunting.
of the defect within the interatrial septum— IMAGING
ostium primum ASD (most apical portion of
Radiographic Findings FOLLOW-UP
septum, adjacent to the atrioventricular [AV]
• None with small defects. • Right heart
valves), ostium secundum ASD (central portion PATIENT MONITORING
enlargement and vascular pattern (pulmonary
of the septum, region of fossa ovalis), and sinus • Periodic evaluation to assess cardiac
overcirculation) with significant shunting.
venosus ASD (adjacent to cranial or caudal vena structure and function. • Recheck when
cava). • Secundum ASD with left-to-right Echocardiographic Findings decompensation or other clinical signs
shunting is most common (98.7% in one • Right atrial and/or right ventricular develop.
study of dogs and cats). • Ostium primum dilation. • Septal dropout (artifactual septal
ASD typically large; possible component of AV dropout is common and may lead to misdiag- EXPECTED COURSE AND PROGNOSIS
canal defect. • Sinus venosus ASD typically nosis). • Shunting across ASD by color-flow • Dependent on ASD size and coexisting defects.
located at junction of cranial vena cava (less or spectral Doppler. • Increased pulmonic • Small, isolated defects unlikely to cause
commonly caudal vena cava) and right atrium. flow velocity. • Dilation of pulmonary trunk. clinical signs. • Defects >12 mm more likely
Right pulmonary veins may be directed at to cause CHF.
right atrium through the defect. May be
associated with anomalous pulmonary venous Electrocardiography
connections of some/all pulmonary veins. • Usually normal. • Right atrial and
ventricular enlargement (tall P wave, deep
• Isolated ASD typically shunts left to right.
S waves in lead II), right axis deviation.
MISCELLANEOUS
Magnitude of flow dependent on ASD size,
relative systemic and pulmonary resistance, and • Arrhythmias and intraventricular conduc- SEE ALSO
relative ventricular compliance. Small restrictive tion disturbances possible. • Congestive Heart Failure, Left-Sided.
defects allow atria to maintain normal differen- • Congestive Heart Failure, Right-Sided.
tial pressure. Large defects may have significant • Hypertension, Pulmonary.
left-to-right shunting, causing volume overload to ABBREVIATIONS
right heart and pulmonary vessels. Secondary TREATMENT • ACE = angiotensin-converting enzyme.
pulmonary hypertension can reverse shunting • ASD = atrial septal defect.
(i.e., right to left), termed Eisenmenger’s GENERAL • ASO = atrial septal occluder.
physiology. ASD with concurrent defects causing • Long-term prognosis for small ASD is • AV = atrioventricular.
increased right atrial pressure (i.e., pulmonic good; treatment typically unnecessary. • CHF = congestive heart failure.
stenosis, tricuspid valve dysplasia, tricuspid valve • Large ASD with hemodynamically
significant shunting and right-sided enlarge- Suggested Reading
stenosis) may have balanced or reversed shunting. Bonagura JD, Lehmkuhl LB. Congenital
ment warrants closure.
SIGNALMENT heart disease. In: Fox PR, Sisson D, Moïse
• Dog and cat. • Various breeds affected; MEDICAL THERAPY ND, eds., Textbook of Canine and Feline
higher prevalence in boxer and standard • Standard treatment of CHF—furosemide, Cardiology, 2nd ed. Philadelphia, PA:
poodle. • No sex predisposition. pimobendan, angiotensin-converting enzyme Saunders 1999, pp. 471–535.
(ACE) inhibitor). • Treatment of poly- Chetboul V, Charles V, Nicolle A, et al.
SIGNS cythemia (right-to-left shunting) if clinically Retrospective study of 156 atrial septal
General Comments indicated. defects in dogs and cats (2001–2005). J Vet
• Typically asymptomatic (73.7% in one SURGICAL THERAPY Med Assoc 2006, 53(4):179–184.
study). • Severe cases may show signs of • Open heart surgery under cardiopulmo- Author Sandra P. Tou
congestive heart failure (CHF). • Generalized nary bypass (surgical closure using patch Consulting Editor Michael Aherne
cyanosis possible with reversed shunting. graft). • Pulmonary artery banding as
Historical Findings palliative measure to limit left-to-right
Clinical signs related to concurrent heart shunting.
disease, CHF, or cyanosis; exercise intoler-
ance, syncope, and dyspnea.
A Atrial Standstill
Mean Age and Range IMAGING
Most animals with persistent atrial standstill Echocardiogram and electromyography if
are young; animals with hypoadrenocorticism persistent atrial standstill suspected—
BASICS are usually young to middle-aged. cardiomegaly and depressed contractility may
DEFINITION Predominant Sex be seen.
ECG rhythm characterized by absence of P Hypoadrenocorticism more common in DIAGNOSTIC PROCEDURES
waves; condition can be temporary (e.g., females (69%). Skeletal muscle biopsy in animals with
associated with hyperkalemia or drug induced), persistent atrial standstill, particularly if
terminal (e.g., associated with severe hyper- SIGNS
skeletal muscle wasting noted.
kalemia or dying heart), or persistent. Historical Findings
• Vary with underlying cause. PATHOLOGIC FINDINGS
ECG Features
• Lethargy common; syncope may occur. Persistent Atrial Standstill
Persistent Atrial Standstill • Patients with persistent atrial standstill • Greatly enlarged and paper-thin atria; usually
• P waves absent.
may show signs of congestive heart failure biatrial involvement, although one case of only
• Heart rate usually slow (<60 bpm).
(CHF). left atrial involvement was reported.
• Rhythm regular with supraventricular-type
Physical Examination Findings • Severe scapular and brachial muscle wasting
QRS complexes.
• Vary with underlying cause. in some dogs.
• Heart rate does not increase with atropine
• Bradycardia common. • Marked fibrosis, fibroelastosis, chronic
administration.
• Patients with persistent atrial standstill may mononuclear cell inflammation, and
Hyperkalemic Atrial Standstill have skeletal muscle wasting of the antebra- steatosis throughout the atria and interatrial
• Heart rate normal or slow. septum.
chium and scapula.
• Rhythm regular or irregular.
• QRS complexes tend to be wide and CAUSES
become wider as the potassium level rises; • Hyperkalemia.
with severe hyperkalemia (potassium • Atrial disease, often associated with
>10 mEq/L), the QRS complexes are replaced atrial distension (e.g., cats with cardio- TREATMENT
by a smooth biphasic curve. myopathy). APPROPRIATE HEALTH CARE
• Heart rate may increase slightly with atropine. • Atrial myopathy (persistent atrial
Persistent Atrial Standstill
standstill).
PATHOPHYSIOLOGY Not life-threatening condition; animal can be
RISK FACTORS treated as an outpatient.
Persistent Atrial Standstill • Hyperkalemic atrial standstill.
Caused by an atrial muscular dystrophy/ • Hypoadrenocorticism.
Hyperkalemic Atrial Standstill
cardiomyopathy; skeletal muscle involvement • Conditions leading to obstruction or
Potentially life-threatening; often requires
common. rupture of the urinary tract. aggressive treatment.
Hyperkalemic Atrial Standstill • Oliguric or anuric renal failure. NURSING CARE
Generally occurs with serum potassium levels Aggressive fluid therapy with 0.9% saline
>8.5 mEq/L; value influenced by serum often required to correct hypovolemia
sodium and calcium levels and acid-base status. and lower serum potassium levels (see
Hyperkalemic patients with atrial standstill Hyperkalemia) in patients with hyperkalemic
have sinus node function, but impulses do not
DIAGNOSIS atrial standstill.
activate atrial myocytes; thus, the associated DIFFERENTIAL DIAGNOSIS ACTIVITY
rhythm is termed a sinoventricular rhythm. • Slow atrial fibrillation.
Restrict activity in patients with persistent
Since the sinus node is functional, an irregular • Sinus bradycardia with small or hidden
atrial standstill and signs of CHF or syncope.
rhythm may be due to sinus arrhythmia. P waves.
DIET
SYSTEMS AFFECTED CBC/BIOCHEMISTRY/URINALYSIS N/A
Cardiovascular Persistent Atrial Standstill
CLIENT EDUCATION
GENETICS Normal
None Persistent Atrial Standstill
Hyperkalemic Atrial Standstill
Clinical signs generally improve after
INCIDENCE/PREVALENCE • Hyperkalemia.
pacemaker implantation; signs of CHF
Rare rhythm disturbance. • Hyponatremia and sodium : potassium
may develop, and weakness and lethargy
ratio <27 if atrial standstill secondary to
GEOGRAPHIC DISTRIBUTION may persist even after heart rate and
hypoadrenocorticism. rhythm are corrected with the pacemaker.
None
• Azotemia and hyperphosphatemia
SIGNALMENT with hypoadrenocorticism, renal failure, SURGICAL CONSIDERATIONS
Species and rupture or obstruction of the urinary Persistent Atrial Standstill
Dog and cat. tract. Implant permanent ventricular pacemaker to
Breed Predilections OTHER LABORATORY TESTS regulate rate and rhythm.
Persistent atrial standstill—most common in Adrenocorticotropic hormone (ACTH) Hyperkalemic Atrial Standstill
English springer spaniels; other breeds stimulation test if hypoadrenocorticism Hyperkalemia secondary to urinary tract
occasionally affected. suspected. obstruction or rupture may require surgery.
(continued) Atrial Standstill A
Figure 1.
Atrial standstill in a dog with a potassium of 9 mEq/L. Note the absence of P waves and wide QRS complexes.
• Monitor electrolytes in patients with PREGNANCY/FERTILITY/BREEDING

hyperkalemic atrial standstill. N/A
• Monitor patients with persistent atrial
MEDICATIONS SYNONYMS
standstill for signs of CHF. Silent atrium.
DRUG(S) OF CHOICE PREVENTION/AVOIDANCE SEE ALSO
Persistent Atrial Standstill N/A • Digoxin Toxicity.
Treat with standard therapy (pimobendan, POSSIBLE COMPLICATIONS • Hyperkalemia.
diuretics, and angiotensin-converting enzyme CHF in patients with persistent atrial • Hypoadrenocorticism (Addison’s Disease).
(ACE) inhibitor, e.g., enalapril or benazepril) standstill. • Urinary Tract Obstruction.
if CHF develops.
EXPECTED COURSE AND PROGNOSIS ABBREVIATIONS
Hyperkalemic Atrial Standstill • ACE = angiotensin-converting enzyme.
• Treat the underlying cause (e.g., oliguric Persistent Atrial Standstill
• Clinical signs generally improve after • ACTH = adrenocorticotropic hormone.
renal failure, hypoadrenocorticism). • CHF = congestive heart failure.
• Aggressive fluid therapy with 0.9% saline and pacemaker implantation. Signs of CHF may
possibly sodium bicarbonate or insulin with develop, and weakness and lethargy may Suggested Reading
dextrose, as discussed under Hyperkalemia. persist even after heart rate and rhythm are Cervenec RM, Stauthammer CD, Fine DM,
• Calcium gluconate—counters the cardiac corrected with the pacemaker. et al. Survival time with pacemaker
effects of hyperkalemia; can be used in life- • Signs related to muscular dystrophy may implantation for dogs diagnosed with
threatening situations while instituting persist. persistent atrial standstill. J Vet Cardiol
treatment to lower potassium concentration. • Median survival in 20 dogs with atrial 2017, 19(3):240–246.
standstill treated with a pacemaker was 866 days Kraus MS, Gelzer ARM, Moïse NS.
CONTRAINDICATIONS and was not influenced by breed or presence of Treatment of cardiac arrhythmias and
Avoid potassium-containing fluids or heart failure at time of implantation. conduction disturbances. In: Smith FWK,
medications that increase potassium Tilley LP, Oyama MA, Sleeper MM, eds.,
concentration in hyperkalemic patients. Hyperkalemic Atrial Standstill
Long-term prognosis is excellent if underlying Manual of Canine and Feline Cardiology,
PRECAUTIONS cause can be corrected and hyperkalemia reversed. 5th ed. St. Louis, MO: Saunders Elsevier,
Diuretics lower preload and may worsen 2016, pp. 313–329.
weakness in dogs with persistent atrial Tilley LP, Smith FWK Jr. Electrocardiography.
standstill and CHF unless a pacemaker has In: Smith FWK, Tilley LP, Oyama MA,
been implanted. Sleeper MM, eds., Manual of Canine and
MISCELLANEOUS Feline Cardiology, 5th ed. St. Louis, MO:
ASSOCIATED CONDITIONS Saunders Elsevier, 2016, pp. 49–76.
N/A
Diseases causing hyperkalemia (e.g., hypo- Author Francis W.K. Smith, Jr.
ALTERNATIVE DRUG(S) adrenocorticism, urethral obstruction or Consulting Editor Michael Aherne
N/A urinary tract tear, acidosis, and drugs).
AGE-RELATED FACTORS Client Education Handout
Persistent atrial standstill—usually diagnosed available online
in young animals; hypoadrenocorticism—
FOLLOW-UP usually diagnosed in young to middle-aged
PATIENT MONITORING animals.
• Monitor ECG during treatment of hyper- ZOONOTIC POTENTIAL
kalemia and periodically in animals with a None
permanent ventricular pacemaker.
A Atrial Wall Tear
Physical Examination Findings • Actual tear often not identified, though
• Collapse. associated thrombus occasionally visualized
• Tachycardia. within LA.
BASICS • Weak pulses or pulsus paradoxus. • Evidence of cardiac tamponade.
DEFINITION • Pale, muddy, or ashen mucous membranes; • Signs of advanced myxomatous mitral valve
• Endocardial splitting is a linear defect prolonged capillary refill time (CRT). disease with moderate to severe LA enlarge-
limited to the atrial endocardium (typically • Other signs of significant cardiac disease ment expected.
left atrium [LA]) resulting from distension of (e.g., murmur, gallop sound, arrhythmia, DIAGNOSTIC PROCEDURES
the atrial wall beyond its elastic limits. cough, dyspnea) typically present.
• Atrial tear results if the split extends • May have signs of right CHF (e.g., ascites, ECG
through the myocardium and epicardium, jugular venous distension). • Sinus tachycardia.
resulting in a full-thickness atrial wall defect • Heart sounds may be muffled, or if • Atrial or ventricular arrhythmias.
and hemorrhage into the pericardial space. murmur was heard before atrial wall tear • Possible dampened QRS complexes.
occurred, it may be reduced in intensity. • Electrical alternans.
PATHOPHYSIOLOGY • ST-segment abnormalities.
• Endocardial splitting typically results from CAUSES • Possible left ventricular or LA enlargement
increased LA pressure secondary to severe • Myxomatous mitral valve disease.
pattern.
mitral regurgitation and mechanical trauma • Chordae tendineae rupture.
from the regurgitant jet; primary endocardial • Chest trauma. PATHOLOGIC FINDINGS
degeneration may also play a role. • Cardiac catheterization. • Endocardial splitting is noted grossly as
• If split is incomplete, fibrin may seal the pale linear depression in atrial endocardium.
RISK FACTORS • Atrial wall tears appear as full-thickness
defect temporarily; either heals as a linear • Severe mitral regurgitation; LA enlargement.
depression in endocardial surface or subse- defects extending through atrial endocar-
• May be precipitated by excitement, stress,
quently extends through myocardium, dium, myocardium, and epicardium;
or activity. associated thrombus may or may not be
resulting in complete tear.
• LA tear results in peracute bleeding into present. Caudolateral aspect of LA most
pericardial sac and acute cardiac tamponade. commonly affected, with many tears
• If tear occurs in interatrial septum, an occurring at atrio-auricular junction.
acquired atrial septal defect may form. DIAGNOSIS • Hemorrhagic pericardial effusion or peri-
• Tearing of either atrium may also rarely occur cardial thrombus with acute tears.
secondary to blunt trauma, or iatrogenically during • Myxomatous valve disease characterized by
• Other causes of acute cardiovascular
pericardiocentesis or cardiac catheterization. thickened leaflets with rolled edges; may have
collapse or syncope.
chordae tendineae rupture; possibly atrial jet
SYSTEMS AFFECTED • Pericardial effusion from other causes
lesions.
• Cardiovascular. (e.g., neoplastic, idiopathic).
• Cardiomegaly with severe LA enlargement
• Respiratory. • CHF.
expected.
• Severe arrhythmias.
GENETICS
Unknown CBC/BIOCHEMISTRY/URINALYSIS
• Elevations in serum lactate; metabolic
INCIDENCE/PREVALENCE acidosis.
A rare cause of hemorrhagic pericardial • Increased alanine aminotransferase/ TREATMENT
effusion in the dog encompassing approxi- aspartate aminotransferase in some patients. APPROPRIATE HEALTH CARE
mately 2% of pericardial effusion cases. • Prerenal azotemia; hyponatremia or other • If LA tear suspected, perform pericardio-
SIGNALMENT electrolyte derangements may be seen. centesis only if effusion causing symptomatic,
Species OTHER LABORATORY TESTS life-threatening cardiac tamponade, since
Dog; uncommon in cat. NT-proBNP and cardiac troponin I (cTnI) further hemorrhage into pericardial sac or
levels may be elevated. exsanguination may occur once pericardial
Breed Predilections fluid removed; remove only enough fluid to
• Any breed predisposed to degenerative valve IMAGING improve clinical signs.
disease. Radiography • Pericardiocentesis likely difficult given small
• If traumatic, any breed may be represented. • Usually moderate to severe LA enlargement; volume of effusion typically present, severe
Mean Age and Range cardiac silhouette may be rounded and cardiomegaly, and small size of most dogs
Middle-aged to older dogs. further enlarged compared with previous with LA rupture; ultrasound guidance and
radiographs. continuous ECG monitoring highly
Predominant Sex recommended.
• Interstitial to alveolar pulmonary infiltrates
Male dogs may be overrepresented. • Best practices for management of LA tear have
if left-sided CHF present.
SIGNS • Pleural effusion, ascites, hepatomegaly, and not been clearly established; however, aggressive
Historical Findings large caudal vena cava if right-sided CHF. medical management to lower LA pressure using
• Acute weakness and collapse; may progress
afterload and preload reducers recommended
ECG
quickly to respiratory or cardiopulmonary arrest. based on author’s clinical experience.
• Pericardial effusion—volume may be
• If fibrin clot forms over defect, patient may
• History of chronic cardiac disease; signs of relatively small as pericardium remains
congestive heart failure (CHF) in most patients. stabilize and recover.
inelastic due to acute nature of bleed;
• Acute worsening of cough or dyspnea is characteristic linear, hyperechoic thrombus NURSING CARE
commonly observed. may be seen within pericardial sac. • Administer oxygen to dyspneic or hemody-
• Possible history of blunt trauma. namically unstable dogs.
(continued) Atrial Wall Tear A
• Administer IV fluids only if evidence of • Pimobendan (0.25–0.3 mg/kg PO q12h) EXPECTED COURSE AND PROGNOSIS
hypovolemia present; most dogs volume may result in further LA pressure reduction, Prognosis is guarded; however, some animals can
overloaded and further intravascular volume though studies have not specifically examined do well for several months or more with exercise
expansion will increase LA pressure and its use in setting of LA rupture. restriction and optimal medical management.
potentially worsen tamponade. • Once patient is stable, angiotensin-
ACTIVITY converting enzyme inhibitors (e.g., enalapril
Strict cage rest in acute period, followed by 0.5 mg/kg q12–24h) should be implemented
for chronic management of accompanying
chronic exercise restriction.
CHF.
MISCELLANEOUS
DIET ASSOCIATED CONDITIONS
Sodium restriction may be indicated for CONTRAINDICATIONS
• Myxomatous mitral valve disease.
• Antithrombotic medications.
animals with advanced myxomatous valve • CHF.
disease with cardiomegaly. • Arterial vasodilators, if significant hypoten-
• Mainstem bronchial compression.
sion present.
CLIENT EDUCATION AGE-RELATED FACTORS
LA tear typically accompanies advanced PRECAUTIONS
Middle-aged to older dogs are predisposed.
• Aggressive fluid therapy unwarranted;
cardiac disease and chronic medical therapy is
further volume expansion may increase LA ZOONOTIC POTENTIAL
necessary; though prognosis is guarded for
pressure, worsen cardiac tamponade, and N/A
surviving acute event, some dogs have lived
more than a year after the incident. contribute to hemodynamic compromise. PREGNANCY/FERTILITY/BREEDING
• Best practices for management of LA tear N/A
SURGICAL CONSIDERATIONS not clearly established; choice of whether to
Exploratory thoracotomy may be considered perform pericardiocentesis, and whether to SYNONYMS
if hemorrhage persists or recurs, but should administer preload and/or afterload reducers, • Atrial rupture.
be undertaken cautiously given advanced state should be based on assessment of volume • Atrial splitting.
of cardiac disease typically present. status, blood pressure, and clinical stability of SEE ALSO
patient. • Atrial Septal Defect.
POSSIBLE INTERACTIONS • Congestive Heart Failure, Left-Sided.
Sodium nitroprusside should not be admin- • Congestive Heart Failure, Right-Sided.
MEDICATIONS istered concurrently with phosphodiesterase- • Myxomatous Mitral Valve Disease.
DRUG(S) OF CHOICE V inhibitors (e.g., sildenafil, tadalafil) due to • Pericardial Disease.
• Atrial tears occur secondary to elevated LA potential for life-threatening systemic • Syncope.
pressure; thus medical therapy should be hypotension. ABBREVIATIONS
focused on lowering LA pressures to reduce ALTERNATIVE DRUGS • CHF = congestive heart failure.
continued hemorrhage into pericardial space N/A • CRT = capillary refill time.
and permit fibrin clot formation at the tear; • cTnI = cardiac troponin I.
this may be accomplished with preload (e.g., • LA = left atrium/atrial.
diuretics, nitroglycerin paste) and/or afterload INTERNET RESOURCES
reducers (arterial vasodilators). James Buchanan Cardiology Library: https://
• Preload and afterload reduction must be FOLLOW-UP
www.vin.com/apputil/content/defaultadv1.
undertaken cautiously to avoid worsening of PATIENT MONITORING aspx?pId=84
hemodynamic compromise. • Recommend close monitoring of respira-
• If concurrent CHF present, afterload tory rate and effort, mucous membrane color Suggested Reading
reduction may be achieved by conservative and CRT, pulse quality, and heart rate; blood Nakamura RK, Tompkins E, Russell NJ, et al.
doses of sodium nitroprusside; low starting CRI pressure monitoring recommended if arterial Left atrial rupture secondary to myxoma-
dose of 0.5–1 μg/kg/min recommended to vasodilators are implemented. tous mitral valve disease in 11 dogs. J Am
decrease LA pressure without precipitating • Follow-up examination with echocardiog- Anim Hosp Assoc 2014, 50:405–408.
significant hypotension; dose may be uptitrated raphy helps determine resolution of pericardial Peddle GD, Buchanan JW. Acquired atrial
as necessary every 15–30 min up to maximum effusion and resorption of atrial or pericar- septal defects secondary to rupture of the
of 10 μg/kg/min to improve clinical signs and/ dial clot. atrial septum in dogs with degenerative
or reduce blood pressure by 10–15 mmHg. • Close follow-up every 2–3 months thereafter mitral valve disease. J Vet Cardiol 2010,
• Alternatively, amlodipine may be started at recommended for repeat pericardial fluid 12:129–134.
0.1–0.2 mg/kg PO q24h; chronic amlodipine checks and medication adjustments as Reineke EL, Burkett DE, Drobatz KJ. Left
therapy may be implemented in normoten- indicated. atrial rupture in dogs: 14 cases (1990–2005).
sive or hypertensive animals to reduce regurg- J Vet Emerg Crit Care 2008, 18:158–164.
itant fraction and lower LA pressure. PREVENTION/AVOIDANCE Author Suzanne M. Cunningham
• Cautious diuretic use, if needed, to treat Avoid strenuous physical activity and Consulting Editor Michael Aherne
dyspnea associated with concomitant CHF excitement.
(e.g., 1–2 mg/kg furosemide IV as needed); POSSIBLE COMPLICATIONS
signs of left-sided CHF may worsen as cardiac • Even if the tear seals, patient is prone to further
tamponade resolves due to augmented preload— tears because of underlying cardiac disease.
more aggressive diuretic therapy may then be • Most dogs have or will develop concurrent
required. CHF.
A Atrioventricular Block, Complete (Third Degree)
Not documented.
BASICS GEOGRAPHIC DISTRIBUTION DIAGNOSIS
N/A
DEFINITION DIFFERENTIAL DIAGNOSIS
• All atrial impulses are blocked at the SIGNALMENT • Advanced second-degree AV block. • Atrial
atrioventricular (AV) junction; atria and Species standstill. • Accelerated idioventricular
ventricles beat independently. A secondary Dog and cat. rhythm.
“escape” pacemaker site (junctional or CBC/BIOCHEMISTRY/URINALYSIS
Breed Predilections
ventricular) stimulates the ventricles. • Atrial • Abnormal serum electrolytes (e.g., hyper-
• Cocker spaniel—can have idiopathic fibrosis.
rate normal. • Idioventricular escape rhythm kalemia, hypokalemia) possible. • High white
• Pug and Doberman pinscher—can have
slow. blood cell count with left shift in animals
associated sudden death, AV conduction
ECG Features defects, and bundle of His lesions. with bacterial endocarditis.
• Ventricular rate slower than atrial rate
Mean Age and Range OTHER LABORATORY TESTS
(more P waves than QRS complexes)— • High serum digoxin concentration if AV
Geriatric animals, except congenital heart
ventricular escape rhythm (idioventricular) block due to digoxin toxicity. • Lyme titer
disease patients. Median age for cats—
usually <40 bpm; junctional escape rhythm and accompanying clinical signs if AV block
14 years.
(idiojunctional) 40–60 bpm in dogs and due to Lyme disease.
60–100 bpm in cats. • P waves—usually Predominant Sex
normal configuration (Figures 1 and 2). Intact female dogs. IMAGING
• QRS complex—wide and bizarre when Echocardiography and Doppler ultrasound
SIGNS
pacemaker located in the ventricle, or in the to assess cardiac structure and function.
lower AV junction in a patient with bundle Historical Findings
branch block; normal when escape pacemaker • Exercise intolerance. • Weakness or
• Electrocardiography. • His bundle electro-
in the lower AV junction (above the syncope. • Occasionally, congestive heart
gram to determine the site of the AV block is
bifurcation of the bundle of His) in a patient failure (CHF).
possible. • Long-term (Holter) ambulatory
without bundle branch block. • No Physical Examination Findings recording if AV block is intermittent.
conduction between the atria and the • Bradycardia. • Variable third and fourth
ventricles; P waves have no constant relation- PATHOLOGIC FINDINGS
heart sounds. • Variation in intensity of first
ship with QRS complexes; P–P and R–R Degeneration or fibrosis of the AV node
heart sounds. • Signs of CHF possible.
intervals relatively constant (except for a sinus and its bundle branches, associated with
• Intermittent “cannon” A waves in jugular
arrhythmia). endocardial and myocardial fibrosis and
venous pulses. • Often bounding arterial
organized endomyocarditis.
PATHOPHYSIOLOGY pulses.
Slow ventricular escape rhythms (<40 bpm) CAUSES & RISK FACTORS
result in low cardiac output and eventual • Isolated congenital defect. • Idiopathic
heart failure, often when animal is excited or fibrosis. • Infiltrative cardiomyopathy
exercised, since demand for greater cardiac (amyloidosis or neoplasia). • Hypertrophic TREATMENT
output is not satisfied. As the heart fails, signs cardiomyopathy in cats. • Digitalis toxicity. APPROPRIATE HEALTH CARE
increase with mild activity. • Hyperthyroidism in cats. • Myocarditis. • Temporary or permanent cardiac
SYSTEMS AFFECTED • Endocarditis. • Electrolyte disorder. pacemaker—only effective treatment in
Cardiovascular • Myocardial infarction. • Other congenital symptomatic patients. • Carefully monitor
heart defects. • Lyme disease. • Chagas asymptomatic patients without a pacemaker
GENETICS disease. for development of clinical signs.
Can be an isolated congenital defect.
Figure 1.
Complete heart block in a dog. The P waves occur at a rate of 120, independent of the ventricular rate of 50. The QRS configuration is a right bundle branch block
pattern. (Source: From Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore: Williams & Wilkins, 1992. Reprinted with permission of
Wolters Kluwer.)
(continued) Atrioventricular Block, Complete (Third Degree) A
Figure 2.
Complete heart block in a cat. The P wave rate is 240/minute, independent of the ventricular rate of 48/minute. QRS configuration is a left bundle branch block
pattern. (Source: From Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore: Williams & Wilkins, 1992. Reprinted with permission of
Wolters Kluwer.)
NURSING CARE stabilize hemodynamics. • If CHF—diuretic

Cage rest prior to pacemaker implantation; and vasodilator therapy may be needed
when the pulse generator is implanted into a before pacemaker implantation.
subcutaneous pocket, a nonconstricting MISCELLANEOUS
CONTRAINDICATIONS
bandage is placed around the ventral neck or Avoid digoxin, xylazine, acepromazine, beta ASSOCIATED CONDITIONS
abdomen for 3–5 days to prevent seroma blockers (e.g., propranolol and atenolol), and None
formation or pacemaker movement. calcium channel blockers (e.g., verapamil and ABBREVIATIONS
ACTIVITY diltiazem); ventricular antiarrhythmic agents • AV = atrioventricular.
Restrict if symptomatic. are dangerous because they suppress lower • CHF = congestive heart failure.
DIET escape foci.
Suggested Reading
No modifications unless required to manage PRECAUTIONS Kellum HB, Stepien RL. Third-degree
underlying condition (e.g., low-salt diet). Vasodilators—may cause hypotension in atrioventricular block in 21 cats (1997–2004).
CLIENT EDUCATION animals with complete AV block; monitor J Vet Intern Med 2006, 20:97–103.
• Temporary or permanent cardiac
closely if used, especially prior to pacemaker Santilli R, Moise NS, Pariaut R, Perego M.
pacemaker—only effective treatment in implantation. Electrocardiography of the Dog and Cat:
symptomatic patients. • Asymptomatic Diagnosis of Arrhythmias, 2nd ed. Milan:
patients without a pacemaker—must be Edra, 2018.
carefully monitored for development of Schrope DP, Kelch WJ. Signalment, clinical
clinical signs. FOLLOW-UP signs, and prognostic indicators associated
with high-grade second or third-degree
SURGICAL CONSIDERATIONS PATIENT MONITORING atrioventricular block in dogs: 124 cases
• Most patients—at high anesthetic • Monitor—pacemaker function with serial (January 1, 1997–December 31, 1997).
cardiopulmonary risk; usually paced electrocardiograms. • Radiographs—following J Am Vet Med Assoc 2006,
preoperatively with a temporary external pacemaker implantation, to confirm the 228:1710–1717.
pacemaker system. • The small size of cats position of the lead and generator. Tilley LP, Smith FWK Jr. Electrocardiography.
makes pacemaker implantation more In Smith FWK, Tilley LP, Oyama M,
difficult than in dogs. Sleeper M, eds., Manual of Canine and
N/A
Feline Cardiology, 5th ed. St. Louis, MO:
POSSIBLE COMPLICATIONS Saunders Elsevier, 2016, pp. 49–76.
Pulse generators—pacemaker replacement Willis R, Oliveira P, Mavropoulou A. Guide
necessary if battery becomes depleted, pulse
MEDICATIONS generator malfunction occurs, or exit block
to Canine and Feline Electrocardiography.
Ames, IA: Wiley-Blackwell, 2018.
DRUG(S) OF CHOICE develops; pacemaker leads can become Author Larry P. Tilley
• Treatment with drugs—usually of no dislodged and infected. Consulting Editor Michael Aherne
value. Traditionally used to treat complete EXPECTED COURSE AND PROGNOSIS
AV block: atropine, isoproterenol, cortico Poor long-term prognosis if no cardiac pace-
steroids, and dobutamine. • Intravenous maker implanted, especially when the animal has Client Education Handout
isoproterenol infusion may help increase the clinical signs. Cats can sometimes survive >1 available online
rate of the ventricular escape rhythm to year without a permanent pacemaker.
A Atrioventricular Block, First Degree
Breed Predilections agents (bethanechol, physostigmine,
American cocker spaniel, dachshund, pilocarpine), and severe procainamide or
brachycephalic dogs, Persian cats. quinidine toxicity.
BASICS • Degenerative disease of the conduction
Mean Age and Range
DEFINITION • May occur in young, otherwise healthy system.
Refers to a delay in conduction that occurs dogs as a manifestation of high vagal tone. • Hypertrophic cardiomyopathy.
between atrial and ventricular activation. • Intra-atrial conduction delay involving • Myocarditis (especially Trypanosoma cruzi,
the right atrium may be seen with Borrelia burgdorferi, Rickettsia rickettsii).
ECG Features
congenital heart disease, especially AV • Infiltrative diseases (tumors, amyloid).
• Rate and rhythm—usually normal.
septal defects. • Atropine administered intravenously may
• Usually there are regularly occurring
• May be noted in aged patients with briefly prolong the PR interval.
normal P waves and QRS complexes
(Figures 1 and 2). degenerative conduction system disease, RISK FACTORS
• Prolonged, consistent PR intervals— particularly cocker spaniels and Any condition or intervention that raises
dogs, >0.13 sec; cats, >0.09 sec (Figures 1 dachshunds. vagal tone.
and 2). • Persian cats of any age with high vagal tone
and in cats of any age with hypertrophic
PATHOPHYSIOLOGY cardiomyopathy.
• Virtually never causes clinical signs.
• May become a more severe atrioventricular SIGNS DIAGNOSIS
(AV) conduction disturbance in some animals. Historical Findings DIFFERENTIAL DIAGNOSIS
• Normally the PR interval tends to shorten • Most animals are asymptomatic. P waves superimposed upon preceding
with rapid heart rates. • If drug induced, may have a history of T waves because of first-degree AV block
• May be the result of intra-atrial conduction clinical signs related to drug toxicity—anorexia, should be differentiated from bifid T waves.
delay (prolongation of the PA interval on vomiting, and diarrhea with digoxin; weakness
surface ECG and simultaneous His bundle with calcium channel blockers or β-adrenergic CBC/BIOCHEMISTRY/URINALYSIS
electrogram) or delay of conduction within • Serum electrolytes—hypokalemia and
antagonists.
the AV node itself (prolongation of the AH hyperkalemia may predispose to AV
interval on His bundle electrogram). Physical Examination Findings conduction disturbances.
Normal—unless also signs of more general- • Leukocytosis—may be noted with bacterial
SYSTEMS AFFECTED ized myocardial disease, drug toxicity, or endocarditis or myocarditis.
Cardiovascular noncardiac disease.
GENETICS CAUSES • Serum digoxin concentration—may be high.
N/A • May occur in normal animals. • T. cruzi, B. burgdorferi, R. rickettsii titers—
INCIDENCE/PREVALENCE • Enhanced vagal stimulation resulting from may be high.
Common noncardiac diseases—usually accompanied by • Thyroxine (T4)—may be high in cats if
sinus arrhythmia, sinus arrest, and/or Mobitz associated with thyrotoxic myocardial disease.
GEOGRAPHIC DISTRIBUTION type I second-degree AV block.
None • Pharmacologic agents—e.g., digoxin,
IMAGING
SIGNALMENT β-adrenergic antagonists, calcium channel Echocardiographic examination—may reveal
blocking agents, propafenone, amiodarone, hypertrophic or infiltrative myocardial
Species disorder.
Dog and cat. α2-adrenergic agonists, parasympathomimetic
Figure 1.
Lead II ECG rhythm strip recorded from a cat with hypertrophic cardiomyopathy. There is sinus bradycardia (120 bpm) and first-degree AV conduction block.
The PR interval is 0.12 second (paper speed = 50 mm/s).
(continued) Atrioventricular Block, First Degree A
Figure 2.
Lead II ECG rhythm strip recorded from a dog showing sinus tachycardia (175 bpm) and first-degree AV conduction block. Because the heart rate is rapid, P waves
are superimposed on the downslope of the preceding T waves. The PR interval exceeds 0.16 second (paper speed = 50 mm/s).
DIAGNOSTIC PROCEDURES • Avoid drugs likely to impair impulse PREGNANCY/FERTILITY/BREEDING

May be needed to identify causes of high conduction further (calcium channel blocking N/A
vagal tone—upper airway disease, cervical agents, β-adrenergic antagonists, α2-adrenergic SEE ALSO
and thoracic masses, gastrointestinal agonists, amiodarone, propafenone). • Atrioventricular Block, Complete
disorders, and high intraocular pressure. PRECAUTIONS (Third Degree).
PATHOLOGIC FINDINGS Drugs with vagomimetic action (e.g., digoxin, • Atrioventricular Block, Second Degree—
Variable—depend on underlying cause. bethanechol, physostigmine, pilocarpine) may Mobitz Type I.
potentiate first-degree block. • Atrioventricular Block, Second Degree—
POSSIBLE INTERACTIONS Mobitz Type II.
N/A ABBREVIATIONS
TREATMENT ALTERNATIVE DRUG(S) • AV = atrioventricular
N/A • T4 = thyroxine
• Remove or treat underlying cause(s). Suggested Reading
• Hospitalization may be necessary to manage Berger MG, Rubenstein JC, Roth JA. Cardiac
the underlying cause (e.g., cardiomyopathy, arrhythmias. In: Benjamin IJ, Griggs RC,
gastrointestinal disease, airway disease). Wing EJ, Fitz JG, eds., Andreoli and
FOLLOW-UP Carpenter’s Cecil Essentials of Medicine,
NURSING CARE PATIENT MONITORING 9th ed. Philadelphia, PA: Saunders, 2016,
N/A Except in healthy young animals, monitor pp. 110–135.
ACTIVITY ECG to detect any progression in conduction Miller MS, Tilley LP, Smith FWK, Fox PR.
Unrestricted; unless restriction required for an disturbance. Electrocardiography. In: Fox PR, Sisson D,
underlying condition. PREVENTION/AVOIDANCE Moïse NS, eds., Textbook of Canine and
DIET N/A Feline Cardiology. Philadelphia, PA:
No modifications or restrictions, unless Saunders, 1999, pp. 67–106.
POSSIBLE COMPLICATIONS Santilli R, Moïse NS, Pariaut R, Perego M.
required to manage an underlying condition. N/A Electrocardiography of the Dog and Cat:
CLIENT EDUCATION EXPECTED COURSE AND PROGNOSIS Diagnosis of Arrhythmias, 2nd ed. Milan:
Generally unnecessary. • Depends on underlying cause. Edra, 2018.
SURGICAL CONSIDERATIONS • Prognosis usually excellent if no significant Tilley LP, Smith FWK Jr. Electrocardiography.
None, unless required to manage an under- underlying disease is present. In: Smith FWK, Tilley LP, Oyama M,
lying condition. Sleeper M, eds., Manual of Canine and
Feline Cardiology, 5th ed. St. Louis, MO:
Willis R, Oliveira P, Mavropoulou A. Guide
MISCELLANEOUS to Canine and Feline Electrocardiography.
MEDICATIONS ASSOCIATED CONDITIONS Ames, IA: Wiley-Blackwell, 2018.
DRUG(S) OF CHOICE None Authors Francis W.K. Smith, Jr. and Larry P.
Medications used only if needed to manage Tilley
AGE-RELATED FACTORS
an underlying condition. Consulting Editor Michael Aherne
PR interval—tends to lengthen with
CONTRAINDICATIONS advancing age.
• Avoid hypokalemia—increases sensitivity ZOONOTIC POTENTIAL Client Education Handout
to vagal tone; may potentiate AV conduction None available online
delay.
A Atrioventricular Block, Second Degree—Mobitz Type I
SIGNALMENT
Species
BASICS Dog; uncommon in cat. DIAGNOSIS
Second-degree atrioventricular (AV) block N/A • Nonconducted P waves from supraventricu-
refers to failure of one or more P waves but Mean Age and Range lar premature impulses or supraventricular
not all P waves to be conducted. Mobitz type • Usually occurs in young, otherwise healthy tachycardias should be distinguished from
I second-degree AV block occurs when AV dogs as a manifestation of high vagal tone. second-degree AV block.
transmission is progressively delayed prior to • Occasionally occurs in older dogs with • Type II second-degree AV block (no
a blocked P wave. abnormally strong vagal tone. variation in PR intervals).
ECG Features • Rarely noted in old dogs with degenerative CBC/BIOCHEMISTRY/URINALYSIS
• PR interval—becomes progressively conduction system disease. Hypokalemia may predispose to AV
longer prior to the appearance of a P wave SIGNS conduction disturbances.
that is not followed by a QRS complex OTHER LABORATORY TESTS
Historical Findings
(Figure 1). Serum digoxin concentration—may be high.
• Most animals are asymptomatic.
• Heart rate and QRS morphology—usually
• If drug induced, owner may report signs of IMAGING
normal.
drug toxicity—anorexia, vomiting, and N/A
• Often cyclic.
diarrhea with digoxin; weakness with calcium
PATHOPHYSIOLOGY channel blockers or β-adrenergic antagonists. DIAGNOSTIC PROCEDURES
• Frequently associated with high resting • If heart rate is abnormally slow, syncope or • May be necessary to identify specific
vagal tone and sinus arrhythmia in dogs. weakness may occur. causes of enhanced vagal tone (e.g., upper
• Generally not pathologic or hemodynami- airway disease, cervical and thoracic masses,
Physical Examination Findings gastrointestinal disorders, and high intraocu-
cally significant.
• May be normal unless signs of more lar pressure).
• This type of AV block usually results
generalized myocardial disease or noncardiac • Atropine response test—administer
from conduction delay within the AV
disease are present. 0.04 mg/kg atropine IM and repeat ECG in
node itself (rather than delay in other
• Intermittent pauses in the cardiac rhythm. 20–30 minutes; may be used to determine
segments of the AV conducting system) and
• First heart sound may become progressively whether AV block is due to vagal tone;
is characterized by a progressive increase in
softer, followed by a pause. resolution of AV block with atropine
AH interval, with eventual block between
• An audible S4 may be heard unaccompa- supports vagal cause.
the A and H deflections on a His bundle
nied by S1 and S2 when block occurs. • Electrophysiologic studies are generally
recording.
CAUSES unnecessary, but will confirm this type of
SYSTEMS AFFECTED second-degree AV block if surface ECG is
• Occasionally noted in normal animals.
Cardiovascular equivocal.
• Enhanced vagal stimulation resulting from
GENETICS noncardiac diseases—usually accompanied by PATHOLOGIC FINDINGS
N/A sinus arrhythmia, sinus arrest. Generally, no gross or histopathologic findings.
INCIDENCE/PREVALENCE • Pharmacologic agents—digoxin, β-adrenergic
Radiotelemetry studies have shown that this antagonists, calcium channel blocking agents,
arrhythmia occurs in 64% of healthy adult propafenone, amiodarone, α2-adrenergic
dogs and 100% of healthy puppies 8–12 agonists, opioids.
weeks of age. RISK FACTORS
TREATMENT
Any condition or intervention that enhances APPROPRIATE HEALTH CARE
vagal tone. • Treatment usually unnecessary.
N/A
• Treat or remove underlying cause(s).
Figure 1.
Lead II ECG strip recorded from a dog with Mobitz type I, second-degree AV block. The PR intervals become progressively longer, with the longest PR intervals
preceding nonconducted P waves (typical Wenckebach phenomenon) (paper speed = 50 mm/s).
(continued) Atrioventricular Block, Second Degree—Mobitz Type I A
NURSING CARE ABBREVIATIONS

Generally unnecessary. • AV = atrioventricular.
ACTIVITY FOLLOW-UP Suggested Reading
Unrestricted Branch CE, Robertson BT, Williams JC.
PATIENT MONITORING Frequency of second-degree atrioventricular
DIET Typically not necessary.
Modifications or restrictions only to manage heart block in dogs. Am J Vet Res 1975,
an underlying condition. PREVENTION/AVOIDANCE 36:925–929.
N/A Kittleson MD. Electrocardiography. In:
CLIENT EDUCATION Kittleson MD, Kienle RD, eds., Small
Explain that any treatment is directed POSSIBLE COMPLICATIONS
Animal Cardiovascular Medicine. St. Louis,
toward reversing or eliminating an under N/A
MO: Mosby, 1998, pp. 72–94.
lying cause. Santilli R, Moïse NS, Pariaut R, Perego M.
SURGICAL CONSIDERATIONS Electrocardiography of the Dog and Cat:
N/A except to manage an underlying Diagnosis of Arrhythmias, 2nd ed. Milan:
condition. MISCELLANEOUS Edra, 2018.
Tilley LP, Smith FWK Jr. Electrocardiography.
In: Smith FWK, Tilley LP, Oyama M,
N/A
Sleeper M, eds., Manual of Canine and
AGE-RELATED FACTORS Feline Cardiology, 5th ed. St. Louis, MO:
MEDICATIONS N/A Saunders Elsevier, 2016, pp. 49–76.
DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING Willis R, Oliveira P, Mavropoulou A. Guide
Only as needed to manage an underlying N/A to Canine and Feline Electrocardiography.
condition. Ames, IA: Wiley-Blackwell, 2018.
SYNONYMS Authors Francis W.K. Smith, Jr. and Larry P.
CONTRAINDICATIONS • Wenckebach block. Tilley
Drugs with vagomimetic action (e.g., digoxin, • Wenckebach periodicity. Consulting Editor Michael Aherne
bethanechol, physostigmine, pilocarpine) may • Wenckebach phenomenon.
potentiate block.
SEE ALSO
PRECAUTIONS • Atrioventricular Block, Complete Client Education Handout
Hypokalemia increases the sensitivity to vagal (Third Degree). available online
tone and may potentiate AV conduction delay. • Atrioventricular Block, First Degree.
POSSIBLE INTERACTIONS • Atrioventricular Block, Second Degree—
N/A Mobitz Type II.
A Atrioventricular Block, Second Degree—Mobitz Type II
SYSTEMS AFFECTED • Degenerative change within the cardiac
• Cardiovascular. conduction system—replacement of AV
• Central nervous or musculoskeletal systems nodal cells and/or Purkinje fibers by
BASICS if inadequate cardiac output. fibrotic and adipose tissue in old cats
DEFINITION GENETICS and dogs.
Second-degree atrioventricular (AV) block • Pharmacologic agents (e.g., digoxin,
May be heritable in pugs.
refers to failure of one or more P waves, but β-adrenergic antagonists, calcium channel
not all P waves, to be conducted. Mobitz type INCIDENCE/PREVALENCE blocking agents, propafenone, α2-adrenergic
II second-degree AV block occurs when one or Unknown agonists, muscarinic cholinergic agonists,
more P waves are blocked without a preceding GEOGRAPHIC DISTRIBUTION or severe procainamide or quinidine
progressive delay in AV transmission. N/A toxicity).
• Infiltrative myocardial disorders (neoplasia,
ECG Features SIGNALMENT amyloid).
• One or more P waves not followed by a
Species • Endocarditis (particularly involving the
QRS complex; PR interval is constant, but
Dog and cat. aortic valve).
may be either normal or consistently
• Myocarditis (viral, bacterial, parasitic,
prolonged (Figure 1). Breed Predilections
American cocker spaniel, pug, dachshund, idiopathic).
• Ventricular rate—usually slow.
• Cardiomyopathy (especially in cats).
• Fixed ratio of P waves to QRS complexes Airedale terrier, Doberman pinscher.
• Trauma.
may occur (e.g., 2 : 1, 3 : 1, 4 : 1 AV block). Mean Age and Range • Atropine administered intravenously may
• High-grade (advanced) second-degree AV Generally occurs in older animals. cause a brief period of first- or second-degree
block is characterized by two or more
Predominant Sex heart block before increasing the heart rate.
consecutively blocked P waves.
• In second-degree AV block with a 2 : 1 con- N/A RISK FACTORS
duction ratio or higher, it is impossible to SIGNS Any condition or intervention that enhances
observe prolongation of the PR interval before vagal tone.
Historical Findings
the block, so a designation of Mobitz type I
• Presenting complaint may be syncope,
vs. II is not appropriate.
collapse, weakness, or lethargy.
• QRS complexes may appear normal, but
• Some animals are asymptomatic.
may also be wide or have an abnormal DIAGNOSIS
• Animals may show signs of the underlying
morphology due to aberrant intraventricular
disease process if present. DIFFERENTIAL DIAGNOSIS
conduction or ventricular enlargement.
• Abnormally wide QRS complexes may Physical Examination Findings • High-grade (advanced) form must be
indicate serious, extensive cardiac disease. • ± weakness. distinguished from complete AV block.
• Bradycardia common. • Nonconducted P waves arising from
PATHOPHYSIOLOGY refractoriness of the conduction system
• May be intermittent pauses in the cardiac
• Rare in healthy animals. during supraventricular tachycardias must
rhythm.
• May be hemodynamically important when be differentiated from pathologic conduction
• An S4 may be audible in lieu of the normally
ventricular rate is abnormally slow. block.
expected heart sounds (i.e., S1, S2) when the
• May progress to complete AV block, parti-
block occurs. CBC/BIOCHEMISTRY/URINALYSIS
cularly when accompanied by wide QRS
• If associated with digoxin intoxication, there • Serum electrolytes—hypokalemia and
complexes.
may be vomiting, anorexia, and diarrhea. hyperkalemia may predispose to AV.
• Typically this type of AV block results from
• May be other abnormalities reflecting the • Conduction disturbances.
conduction delay within the AV node itself
underlying etiology. • Leukocytosis—may be noted with bacterial
(rather than delay in another segment of the
AV conducting system) that is characterized CAUSES endocarditis or myocarditis.
by normal or prolonged AH intervals, with • Heritable in pugs. • Electrolyte abnormalities (e.g., severe
intermittent block between A and H deflec- • Enhanced vagal stimulation from noncardiac hypokalemia, hyperkalemia, or hypercalce-
tions on a His bundle electrogram. diseases. mia) may predispose to AV block.
Figure 1.
Lead II ECG rhythm strip recorded from a dog with both first- and second-degree AV block. The second-degree AV block is high grade, with both 2 : 1 and 3 : 1
block resulting in variation in the RR intervals. The PR interval for the conducted beats is prolonged but constant (0.28 second) (paper speed = 25 mm/s).
(continued) Atrioventricular Block, Second Degree—Mobitz Type II A
OTHER LABORATORY TESTS • Pharmacologic agents may not be effective EXPECTED COURSE AND PROGNOSIS
• Serum digoxin concentration—may be high. long term. Variable—depends on cause. If degenerative
• High thyroxine (T4) in cats—if associated SURGICAL CONSIDERATIONS disease of the cardiac conduction system,
with hyperthyroidism. Permanent pacemaker may be required for often progresses to complete (third-degree)
• High arterial blood pressure—if associated long-term management of symptomatic patients. AV block.
with hypertensive heart disease.
• Positive Borrelia, Rickettsia, or Trypanosoma
cruzi titers—if associated with one of these
infectious agents.
• Blood cultures may be positive in patients MEDICATIONS MISCELLANEOUS
with vegetative endocarditis. DRUG(S) OF CHOICE ASSOCIATED CONDITIONS
• Atropine (0.02–0.04 mg/kg IV/IM) or May be noted in cats with primary or
IMAGING
glycopyrrolate (5–10 μg/kg IV/IM) may be secondary myocardial disease.
Echocardiographic examination may reveal
structural heart disease (e.g., endocarditis, used short term if positive atropine response. AGE-RELATED FACTORS
neoplasia, or cardiomyopathy). • Chronic anticholinergic therapy (propan- N/A
theline 0.5–2 mg/kg PO q8–12h or ZOONOTIC POTENTIAL
hyoscyamine 3–6 μg/kg q8h)—indicated for N/A
• Atropine response test—administer
symptomatic patients if improved AV
0.04 mg/kg atropine IM and repeat ECG in PREGNANCY/FERTILITY/BREEDING
conduction with atropine response test.
20–30 minutes; may be used to determine N/A
• Isoproterenol (0.04–0.09 μg/kg/min IV to
whether AV block is due to high vagal tone.
effect) or dopamine (2–5 μg/kg/min IV to SEE ALSO
• Electrophysiologic testing is generally
effect) may be administered in acute, life- • Atrioventricular Block, Complete (Third
unnecessary, but can be done to confirm this
threatening situations to enhance AV conduc- Degree).
type of AV block if surface ECG findings are
tion and/or accelerate an escape focus. • Atrioventricular Block, Second Degree—
equivocal.
CONTRAINDICATIONS Mobitz Type I.
PATHOLOGIC FINDINGS
• Drugs with vagomimetic action (e.g., ABBREVIATIONS
• Variable—depend on underlying cause.
digoxin, bethanechol, physostigmine, • AV = atrioventricular.
• Old animals with degenerative change of
pilocarpine) may potentiate block. • T4 = thyroxine.
the conduction system may have focal
• Avoid drugs likely to impair impulse
mineralization of the interventricular septal Suggested Reading
conduction further or depress a ventricular
crest visible grossly; chondroid metaplasia of Kittleson MD. Electrocardiography. In:
escape focus (e.g., procainamide, quinidine,
the central fibrous body and increased fibrous Kittleson MD, Kienle RD, eds., Small
lidocaine, calcium channel blocking agents,
connective tissue in the AV bundle is noted Animal Cardiovascular Medicine. St. Louis,
β-adrenergic blocking agents).
histopathologically. MO: Mosby, 1998, pp. 72–94.
PRECAUTIONS Santilli R, Moise NS, Pariaut R, Perego M.
Hypokalemia—increases sensitivity to vagal Electrocardiography of the Dog and Cat:
tone and may potentiate AV conduction delay. Diagnosis of Arrhythmias, 2nd ed. Milan:
TREATMENT POSSIBLE INTERACTIONS Edra, 2018.
N/A Tilley LP, Smith FWK Jr. Electrocardiography.
APPROPRIATE HEALTH CARE In: Smith FWK, Tilley LP, Oyama M,
• Treatment—may be unnecessary if heart ALTERNATIVE DRUG(S) Sleeper M, eds., Manual of Canine and
rate maintains adequate cardiac output. N/A Feline Cardiology, 5th ed. St. Louis, MO:
• Positive dromotropic interventions are Saunders Elsevier, 2016, pp. 49–76.
indicated for symptomatic patients. Willis R, Oliveira P, Mavropoulou A. Guide
• Treat or remove underlying cause(s). to Canine and Feline Electrocardiography.
NURSING CARE FOLLOW-UP Ames, IA: Wiley-Blackwell, 2018.
Generally unnecessary. Authors Larry P. Tilley and Francis W.K.
PATIENT MONITORING
Smith, Jr.
ACTIVITY Periodic ECG because risk of progression to
Consulting Editors Michael Aherne
Cage rest advised for symptomatic patients. complete (third-degree) AV block.
DIET PREVENTION/AVOIDANCE
Modifications or restrictions only to manage N/A Client Education Handout
an underlying condition. available online
CLIENT EDUCATION Prolonged bradycardia may cause secondary
• Need to seek and specifically treat under- congestive heart failure or inadequate renal
lying cause. perfusion.
A Atrioventricular Valve Dysplasia
hypotension or ventricular arrhythmias in cases
with severe dynamic outflow obstruction.
BASICS GENETICS DIAGNOSIS
TVD appears to be inherited as an autosomal
DEFINITION recessive trait in dogues de Bordeaux and an DIFFERENTIAL DIAGNOSIS
A congenital malformation of the mitral or autosomal dominant with incomplete • Except for age of onset, congenital AV valve
tricuspid valve apparatus. penetrance trait in Labrador retrievers. insufficiency resembles acquired degenerative
PATHOPHYSIOLOGY AV valve insufficiency with regard to history,
INCIDENCE/PREVALENCE physical examination findings, and clinical
• Atrioventricular valve dysplasia (AVVD) These are common congenital cardiac
can result in valvular insufficiency, valvular sequelae.
anomalies in cats (17% of reported congenital • The right-sided murmur of tricuspid
stenosis, or dynamic outflow tract obstruc- cardiac defects in one study). Mitral valve
tion, depending on the anatomic abnormality. insufficiency may be confused with the
malformations often are noted in cats with right-sided murmur of a ventricular septal
AVVD may occur alone or in association with hypertrophic cardiomyopathy. Less frequently
abnormalities of the ipsilateral outflow tract defect.
diagnosed in dogs. • Ascites caused by silent tricuspid regurgita-
(e.g., valvular or subvalvular aortic or pulmonic
stenosis). It is not uncommon for mitral and SIGNALMENT tion or tricuspid valve stenosis is often
tricuspid valve dysplasia to occur together in attributed to pericardial effusion, hepatic
Species
the same patient. disease, or caudal vena caval obstruction.
Dog and cat.
• Dogs and cats with cor triatriatum share
• Valvular insufficiency results in ipsilateral atrial
Breed Predilections many of the clinical features of AV valve
dilation, eccentric hypertrophy of the associated
• TVD—increased risk for Labrador retriever, stenosis.
ventricle, and, if severe, signs of congestive heart
German shepherd dog, great Pyrenees, • There is no certain way to distinguish outflow
failure (CHF). Cardiomyopathy of chronic
possibly Old English sheepdog; also common tract obstruction due to MVD and obstructive
volume overload and elevated atrial pressures are
in cats. hypertrophic cardiomyopathy. If the obstruction
the end result, culminating in pulmonary
• MVD—increased risk in bull terrier, can be abolished with adrenergic beta blockers
congestion (with mitral valve dysplasia [MVD])
Newfoundland, Labrador retriever, Great and LV hypertrophy resolves, it is likely that the
or systemic congestion (with tricuspid valve
Dane, golden retriever, Dalmatian, and primary abnormality was MVD.
dysplasia [TVD]).
Siamese cat.
• Valvular stenosis results in atrial dilation IMAGING
and hypertrophy and, if severe, hypoplasia of Mean Age and Range
Radiographic Findings
the receiving ventricle. The end result is atrial Variable; signs most often manifest within the
• Ipsilateral atrial and ventricular enlarge-
pressure elevation, also resulting in pulmo- first few years after birth.
ment with valvular insufficiency. Isolated
nary congestion (mitral stenosis) or systemic Predominant Sex atrial enlargement with valvular stenosis.
congestion (tricuspid stenosis). Right-to-left Males are more likely to experience CHF. Mild left atrial (LA) enlargement with
shunting may occur in cases of tricuspid dynamic LV outflow obstruction. Cardiac
stenosis if there is an atrial septal defect or SIGNS
silhouette may appear globoid with pro-
patent foramen ovale. Pulmonary hyperten- Historical Findings nounced enlargement in cases of severe TVD.
sion is a common complication in animals • Exercise intolerance. • Evidence of left CHF—distended
with mitral valve stenosis. • Abdominal distention, weight loss, and pulmonary veins, interstitial or alveolar
• Dynamic outflow tract obstruction may stunting may be observed with severe TVD. edema in severe MVD.
occur in patients with MVD, with resultant • Labored respiration common with severe • Evidence of right CHF—dilated caudal
concentric left ventricular (LV) hypertrophy MVD. vena cava, hepatosplenomegaly, or ascites in
that is proportional to the severity of the • Syncope and collapse if critical atrioven- severe TVD.
obstruction. tricular (AV) valve stenosis, severe outflow
• Ebstein’s anomaly is a rare form of TVD, tract obstruction, associated arrhythmias, or Echocardiography
characterized by apical displacement of the CHF. • Valvular insufficiency results in ipsilateral
basal tricuspid leaflet attachments and atrial dilation and eccentric ventricular
Physical Examination Findings hypertrophy. Doppler echocardiography
resultant right atrial (RA) enlargement, with a
• A holosystolic murmur is heard over the demonstrates a high velocity retrograde
small right ventricle (“atrialized” right
ipsilateral cardiac apex. In severe cases the systolic jet and modestly increased transmitral
ventricle). It can be accompanied by varying
murmur is accompanied by a thrill or gallop or transtricuspid inflow velocities.
degrees of insufficiency or stenosis.
heart sounds. In animals with valvular stenosis, • Valvular stenosis results in ipsilateral atrial
SYSTEMS AFFECTED a soft diastolic murmur may be present in the dilation, while the associated ventricular
• Cardiovascular—chronic volume overload same location, but many have no audible dimensions are normal or small. Valve
from valvular insufficiency and/or inflow murmur. A labile systolic ejection murmur may leaflets are often thickened, relatively
obstruction due to valvular stenosis result in be audible in animals with dynamic outflow immobile, and fused. Doppler echocardiog-
elevated pulmonary (MVD) or systemic tract obstruction. Silent tricuspid regurgitation raphy demonstrates a high-velocity
(TVD) venous pressures. is well documented in cats with a large regurg transmitral or transtricuspid diastolic jet
• Respiratory—pulmonary edema may itant orifice and laminar regurgitant flow. with a reduced EF slope. There may also be
develop secondary to MVD; pulmonary • Jugular venous distension/pulsation may be evidence of concurrent AV valvular
hypertension is a common complication in evident in patients with TVD. insufficiency, secondary pulmonary hyper-
animals with mitral stenosis. • Evidence of left CHF (tachypnea, dyspnea, tension (in cases of mitral stenosis), or
• Neurologic—collapse and/or loss of conscious- pulmonary crackles, cyanosis) in animals with right-to-left shunting across a patent
ness, most often with exercise, may occur severe MVD. foramen ovale or associated atrial septal
with severe disease due to low cardiac output/ • Evidence of right CHF (ascites, peripheral defect (in cases of tricuspid stenosis).
edema) with severe TVD.
(continued) Atrioventricular Valve Dysplasia A
• With MVD, the LV papillary muscles are SURGICAL CONSIDERATIONS

typically flattened and displaced dorsally. • Valve repair or replacement is available in a
Chordae tendineae are often short and few centers.
thickened. With TVD, papillary muscles • Balloon valvuloplasty is sometimes effective MISCELLANEOUS
and chordae tendineae may be fused, for valvular stenosis. ASSOCIATED CONDITIONS
creating a curtain-like appearance of the • MVD commonly accompanies valvular or
tricuspid valve. subvalvular aortic stenosis as well as TVD.
• Dynamic LV outflow obstruction in • TVD commonly accompanies pulmonic
patients with MVD is characterized by systolic stenosis as well as MVD.
motion of the anterior mitral leaflet toward
MEDICATIONS
DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING
the interventricular septum, increased LV
• For patients with CHF, furosemide Breeding should be avoided—heritable defect
outflow tract velocities, eccentric mitral regur-
(1–4 mg/kg q12–24h) and enalapril (0.5 mg/ and possibility of causing decompensated or
gitation, and concentric LV hypertrophy.
kg q12h) are used to control congestion, with worsening CHF.
Cardiac Catheterization
the addition of pimobendan (0.3 mg/kg SEE ALSO
• Indicated only for cases in which diagnosis
q12h) in cases of valvular insufficiency. • Congestive Heart Failure, Left-Sided.
cannot be confirmed by echocardiography or
• Supraventricular tachyarrhythmias may be • Congestive Heart Failure, Right-Sided.
if surgical correction anticipated.
managed using digoxin (2–4 μg/kg q12h), a ABBREVIATIONS
• Hemodynamic measurements should
calcium channel blocker such as diltiazem • AV = atrioventricular.
include ipsilateral atrial and ventricular
(1–1.5 mg/kg q8h), or a beta blocker such • AVVD = atrioventricular valve dysplasia.
pressures. Additional measurements in
as atenolol (0.5–1.5 mg/kg q12–24h). • CHF = congestive heart failure.
cases of MVD include pulmonary capillary
Heart rate should be maintained below • LA = left atrial.
wedge pressure (in lieu of direct LA
150 bpm. • LV = left ventricular.
pressure measurement), pulmonary artery
• For dynamic outflow tract obstruction, beta
pressures, and, in cases of dynamic • MVD = mitral valve dysplasia.
blockers such as atenolol (0.5–1.5 mg/kg • RA = right atrial.
obstruction, simultaneous aortic and LV
q12–24h) may be used to abolish or diminish • TVD = tricuspid valve dysplasia.
pressure recording with medical provo
severity of outflow obstruction; however,
cation. Contrast studies are best Suggested Reading
benefit has not been proven.
performed with ventricular injection in Bonagura JD, Lehmkuhl LB. Congenital
cases of valvular insufficiency, and direct PRECAUTIONS heart disease. In: Fox PR, Sisson D, Moise
atrial injection in cases of valvular stenosis. Standard patient monitoring for cardiac NS. Textbook of Canine and Feline
medication side effects (e.g., digitalis toxicity, Cardiology: Principles and Clinical Practice,
azotemia). 2nd ed. Philadelphia, PA: Saunders, 1999,
ECG
pp. 520–526.
• Findings usually reflect pattern of chamber
Oyama MA, Sisson DD, Thomas WP,
enlargement.
Bonagura JD. Congenital heart disease.
• Severe defects may be accompanied by
arrhythmias, particularly atrial premature FOLLOW-UP In: Ettinger SJ, Feldman EC, eds., Textbook
of Veterinary Internal Medicine, 7th ed.
beats, supraventricular tachycardia, or atrial PATIENT MONITORING
St. Louis, MO: Elsevier, 2010,
fibrillation. • Recheck yearly if no signs of CHF.
pp. 1250–1298.
• Recheck every 3 months if signs of CHF
Strickland KN, Oyama MA. Congenital heart
(consider thoracic radiographs, ECG, and
disease. In: Tilley LP, Smith FWK, Oyama
echocardiography).
MA, Sleeper MM, eds., Manual of Canine
TREATMENT PREVENTION/AVOIDANCE and Feline Cardiology, 5th ed. St. Louis,
Do not breed affected animals. MO: Saunders Elsevier, 2016, pp. 218–238.
Inpatient treatment required for CHF. POSSIBLE COMPLICATIONS Author Michael Aherne
• CHF—left-sided with MVD; right-sided Consulting Editor Michael Aherne
DIET Acknowledgment The author and book
with TVD.
Sodium restricted if overt or pending CHF. editors acknowledge the prior contribution of
• Collapse or syncope with exercise.
CLIENT EDUCATION • Paroxysmal supraventricular tachycardia or David D. Sisson.
Owners should be informed of heritability atrial fibrillation with severe disease.
and advised against breeding.
EXPECTED COURSE AND PROGNOSIS Client Education Handout
• Depends on severity of underlying defect. available online
• Guarded to poor with serious defects.
A Atrioventricular Valvular Stenosis
INCIDENCE/PREVALENCE RISK FACTORS
Rare Breed predispositions (see above); see Risk
GEOGRAPHIC DISTRIBUTION Factors for Endocarditis, Infective; permanent
BASICS transvenous pacing.
Worldwide
DEFINITION
Atrioventricular (AV) valvular stenosis is a SIGNALMENT
pathologic narrowing of the mitral or Species
tricuspid valve orifice or the presence of an Dog and cat. DIAGNOSIS
obstructive, supravalvular ring.
Breed Predilections DIFFERENTIAL DIAGNOSIS
PATHOPHYSIOLOGY • MS is overrepresented in bull terriers and AV valvular stenosis must be differentiated
• AV stenosis increases the resistance to Newfoundlands, and in Siamese cats. from the more common causes of mitral and
ventricular filling. • TS has been reported most often in Old tricuspid regurgitation in the absence of
• Ventricular filling in clinically significant English sheepdogs and Labrador retrievers. stenosis. These include both congenital and
disease requires a persistent diastolic pressure acquired lesions of the AV valves and support
Mean Age and Range
gradient between atrium and ventricle. apparatus. Cor triatriatum dexter, cor
Most patients are presented at a young
• Concomitant valvular regurgitation is triatriatum sinister and double outlet right
age, although exceptions occur, especially
common. atrium can mimic some of the clinical
in cats.
• The increased atrial pressure leads to atrial findings of pure tricuspid and mitral valvular
dilation, venous congestion, and often to Predominant Sex
stenosis, respectively.
congestive heart failure (CHF). Pulmonary N/A
edema occurs with mitral stenosis (MS); CBC/BIOCHEMISTRY/URINALYSIS
SIGNS
whereas ascites, pleural effusion, and chylo- May be normal or reflect changes related to
thorax can develop in cases of severe tricuspid Historical Findings CHF or drug therapy for CHF.
stenosis (TS). • Exercise intolerance.
IMAGING
• The foramen ovale can remain patent • Syncope.
(PFO) in patients with TS, allowing right- • Exertional dyspnea or tachypnea. Thoracic Radiography
• Cough—MS. • Atrial enlargement is the most common
to-left shunting with signs of cyanotic heart
disease. • Cyanosis. and outstanding feature; may see generalized
• Partial AV septal defect (primum atrial • Abdominal distention—TS. cardiomegaly, especially with AV valve
septal defect [ASD] and abnormal AV valve) • Acute posterior paresis—cats with MS and regurgitation.
arterial thromboembolism. • MS—may see pulmonary venous conges-
is observed in some cats with supravalvular
mitral (ring) stenosis. • Stunted growth. tion and pulmonary edema; intrapulmonary
• Cardiac output and therefore exercise • Hemoptysis from rupture of intrapulmonary hemorrhage can be misinterpreted as
capacity are limited. vessels—MS. pneumonia or another parenchymal disease.
• TS—may see hepatomegaly; increased
• The atrial pressure increases disproportion- Physical Examination Findings
ally with faster heart rates, thereby creating diameter of caudal vena cava.
• Soft diastolic murmur with point of
the risk for “flash” pulmonary edema in dogs maximal intensity over left apex (MS) or right Echocardiography
or cats with MS. hemithorax (TS). • Diagnostic test of choice.
• Development of atrial tachyarrhythmias, • Holosystolic murmur of mitral or tricuspid • Two-dimensional echocardiography reveals a
especially atrial fibrillation (AF), is associated regurgitation is more often detected. markedly dilated atrium and attenuated valve
with cardiac decompensation. • Tachypnea, dyspnea from pulmonary excursion during diastole, often with thickened,
• Pulmonary hypertension (PH) can develop edema or pleural effusion. irregular AV valve leaflets; valve leaflets may
consequent to MS, leading to exercise • Crackles from pulmonary edema. appear to “dome” during diastole (see Web Video
intolerance and right ventricular hypertrophy. • Jugular distention, jugular pulses, ascites, 1). A supravalvular obstructing ring also may be
This can be severe, especially in cats. hepatomegaly with TS, or biventricular CHF evident, as well as other lesions (see Causes).
associated with pulmonary hypertension and • Color-flow imaging reveals a turbulent
SYSTEMS AFFECTED
• Respiratory—with MS: bronchial compres- AF in chronic MS. diastolic jet that originates proximal to the
sion from enlarged left atrium, pulmonary • Cyanosis from right-to-left shunting with stenotic valve and projects toward the apex of
edema from left heart failure; potential for TS and PFO or from pulmonary edema the ventricle (see Web Video 2); AV valve
hemoptysis due to rupture of pulmonary with MS. regurgitation is often present (see Web Videos
venous–bronchial venous connections; pleural 3 and 4). Concurrent defects may also be
CAUSES
effusion with atelectasis in TS or in long- noted, such as PFO, ASD, or bridging septal
• Usually due to congenital dysplasia of
standing MS complicated by PH or AF. leaflet (see Web Video 5).
mitral or tricuspid valve.
• M-mode studies show an enlarged atrium
• Hepatobiliary—with TS: hepatic • Supravalvular obstructing rings of tissue
congestion, ascites. and concordant motion of the AV valve
have been associated with AV stenosis; this is
leaflets, indicating commissural fusion (see
GENETICS especially important in cats.
Web Figure 1); the E-to-F slope is decreased.
• Uncertain in most cases. • Infective endocarditis, intracardiac neoplasia,
• Spectral Doppler studies show increased
• Tricuspid valve dysplasia in Labrador retrievers and hypertrophic cardiomyopathy with
diastolic transvalvular flow velocities;
has been localized to a defect in dog chromo- scarring are rare causes of acquired AV valve
prolonged calculated pressure half-time is a
some 9, inherited as an autosomal dominant stenosis.
hallmark feature; E-wave/A-wave amplitude
trait with reduced penetrance. In dogue de • Acquired TS has been observed due to
reversal is often evident in cases still in
Bordeaux, tricuspid valve dysplasia has been fibrous scarring of the tricuspid valve in dogs
normal sinus rhythm (see Web
identified as an autosomal recessive trait. with transvenous pacing leads.
Figures 2, 3, 4).
(continued) Atrioventricular Valvular Stenosis A
• Right-sided chamber enlargement in MS • Surgical or catheter-based interventions can • Angiotensin-converting enzyme (ACE)
with pulmonary hypertension or with chronic be considered once heart failure has been inhibitor—enalapril or benazepril: dogs,
AF (see Web Figure 4). stabilized. 0.25–0.5 mg/kg PO q12h; cats, 0.25–
• Control of heart rhythm disturbances, 0.5 mg/kg PO q12–24h; see Follow-Up for
Angiography especially AF, is also important. patient monitoring.
• Right atrium—injection demonstrates • These patients are typically complicated • Nitroglycerin paste (1/4 to 1 inch topically
markedly dilated atrium in TS; with and consultation with a cardiologist is highly q12h) to reduce pulmonary venous pressures,
concurrent PFO or ASD, opacification of the recommended. but this has not been evaluated critically.
left atrium is also observed following right • Electrocardioversion of AF should be
atrial injection. Atrial Tachyarrhythmias
considered, but advanced atrial disease can • Digoxin—dogs, 3–5 μg/kg PO q12h; cats,
• Might visualize thickened, irregular valve render the procedure less effective or limit the
leaflets or a stenotic valve funnel. one-fourth of a 0.125 mg tablet PO
duration of sinus rhythm. q24–48h; adjust dosage based on serum
• Ventricular injection often reveals valvular
regurgitation. NURSING CARE concentrations.
• There can be delayed opacification of the • Sedation with butorphanol is appropriate • Beta blockers such as atenolol or the
ventricles and great vessels. for dyspneic patients. calcium channel blocker diltiazem for
• Oxygen therapy should be administered to suppression of frequent atrial premature
Cardiac Catheterization patients with dyspnea or hypoxemia from complexes and for heart rate control in atrial
• A diastolic pressure gradient is identified left-sided CHF. tachyarrhythmias such as atrial tachycardia/
between atrium and ventricle. A large “A” • Fluid therapy is typically contraindicated in flutter/fibrillation. Beware when using these
wave is common if atrial function is patients with overt CHF, except in cases of drugs in uncontrolled CHF.
preserved. moderate to severe azotemia, renal • Typical atenolol dosages—dogs, 0.25–
• High left atrial, pulmonary capillary compromise, or severe dehydration. Therapeutic 1.0 mg/kg q12h; cats, 6.25–12.5 mg/cat
wedge, and pulmonary artery pressures paracentesis may be considered in patients q12–24h; start low and titrate to effect.
occur in MS. with pleural effusion or tympanic ascites. • Diltiazem dosages—dogs, 2–6 mg/kg daily
• High right atrial and central venous in two (long-acting diltiazem) or three
pressures are present in TS. ACTIVITY
divided dosages; start low and titrate to effect;
• Ventricular pressure may be normal in the
Exercise restriction is important to
cats, 7.5 mg diltiazem HCl PO q8h. Higher
absence of concurrent defects. recommend for any animal with this
dosages are sometimes needed.
condition, because tachycardia increases the
DIAGNOSTIC PROCEDURES • Sotalol for intractable/recurrent arrhythmias—
mean gradient across the stenotic valve,
dogs, 1–2.5 mg/kg PO q12h; cats,
ECG predisposing to pulmonary edema or venous
10–20 mg/cat q12h.
• Variable enlargement and ventricular congestion (see Web Figures 3 and 4). Cage
• Dogs can be referred for electrocardiover-
conduction patterns are observed. Widened rest is ideal for patients with CHF.
sion to convert AF to sinus rhythm (with
or tall P-waves are commonly observed. DIET follow-up therapy with sotalol or amiodar-
• Splintered R-waves are present in some Feed a sodium-restricted diet to patients in one); however, reversion to AF is common
dogs with tricuspid dysplasia. CHF. owing to marked atrial dilatation.
• Axis deviation due to hypertrophy or
ventricular conduction disturbances is CLIENT EDUCATION Pulmonary Hypertension
relatively common in cats with mitral valve Clients must be advised of symptoms • Sildenafil—dogs, 0.5–3 mg/kg PO q8–12
malformation. associated with CHF and the urgency of hours.
• Ectopic rhythms, especially of atrial origin, treatment, particularly with left-sided CHF.
CONTRAINDICATIONS
are often observed. AF is the most important Likelihood of recurrent bouts of CHF should
Primary afterload reducers such as hydralazine
rhythm disturbance as atrial contribution to also be discussed.
or amlodipine should be avoided in treatment
filling is lost and the R-to-R intervals vary SURGICAL CONSIDERATIONS of heart failure from pure MS due to risk of
with short cycles, increasing the mean • Surgical valve replacement or repair hypotension.
diastolic gradient. requires cardiopulmonary bypass or
PRECAUTIONS
PATHOLOGIC FINDINGS hypothermia; cost, availability, and high
• As a general rule, pimobendan is
• The AV valve is abnormal, with thickened complication and mortality rates are greatly
relatively contraindicated in pure valvular
leaflets and fused commissures. Other lesions limiting factors.
stenosis; however, many dogs and cats with
may be identified such as a supramitral ring • Balloon valvuloplasty is an alternative referral
advanced CHF have been treated with this
(see Causes). treatment and has been used successfully for
drug with apparent success, especially when
• Many cases also have abnormal chordae managing some cases of AV stenosis.
there is combined stenosis/regurgitation of
tendineae and papillary muscles. the valve.
• Atrial dilation and hypertrophy are common. • Use ACE inhibitors or other vasodilators
• PFO with TS or partial AV septal defect judiciously in patients with CHF; cardiac
(primum ASD and bridging septal leaflet) MEDICATIONS output is limited and vasodilation may induce
with supravalvular mitral (ring) stenosis. hypotension. Monitor arterial blood pressure
DRUG(S) OF CHOICE
and renal function.
CHF
• Diuretic—Furosemide: dogs, 2–4 mg/kg POSSIBLE INTERACTIONS
IV/IM/SC/PO q8–24h; cats, 1–4 mg/kg IV/ • Furosemide and ACE inhibitors can affect
TREATMENT IM/SC/PO q8–24h. Torsemide: dogs, kidney function, alter blood electrolytes, and
APPROPRIATE HEALTH CARE 0.2–0.5 mg/kg PO q12–24h; cats, 1.25 mg reduce blood pressure; these parameters
• Patients in overt CHF should be treated PO q12–48h. should be monitored.
with inpatient medical management.
A Atrioventricular Valvular Stenosis (continued)
• Sildenafil can also reduce systemic blood EXPECTED COURSE AND SEE ALSO
pressure and should not be used with nitro- PROGNOSIS • Atrioventricular Valve Dysplasia.
glycerin paste or other nitrates. • Morbidity is high; except for mild cases, • Endocarditis, Infective.
ALTERNATIVE DRUG(S) prognosis is generally poor once an animal ABBREVIATIONS
Spironolactone (2 mg/kg PO q12–24h) becomes symptomatic. However, some • ACE = angiotensin-converting enzyme.
should be considered as an ancillary diuretic animals will live for many years even with • AF = atrial fibrillation.
and for its antifibrotic benefit (as an relatively severe stenosis of the mitral or • ASD = atrial septal defect.
aldosterone antagonist). tricuspid valve. • AV = atrioventricular.
• Surgical intervention or balloon valvulo- • CHF = congestive heart failure.
plasty might alter course of disease, but data • MS = mitral stenosis.
are limited. • PFO = patent foramen ovale.
• PH = pulmonary hypertension.
FOLLOW-UP
• TS = tricuspid stenosis.
PATIENT MONITORING
• Thoracic radiographs for pulmonary edema
Suggested Reading
or pleural effusion.
MISCELLANEOUS Arndt JW, Oyama MA. Balloon valvuloplasty
• Echocardiography with Doppler studies— ASSOCIATED CONDITIONS of congenital mitral stenosis. J Vet Cardiol
to estimate pulmonary pressures and Concurrent congenital defects are common, 2013, 15:147–151.
subjectively assess right heart function if on e.g., subaortic stenosis in MS, PFO in TS, Brown WA, Thomas WP. Balloon valvulo-
sildenafil. primum ASD in cats with supravalvular plasty of tricuspid stenosis in a Labrador
• Digoxin level—check 7–10 days following mitral (ring) stenosis. retriever. J Vet Intern Med 1995,
institution of therapy; 8- to 12-hour trough 9:419–424.
PREGNANCY/FERTILITY/BREEDING Campbell FE, Thomas WP. Congenital
should be 0.8–1.5 ng/mL. The possibility that this may be a heritable
• Renal function, electrolyte status, and
supravalvular mitral stenosis in 14 cats. J
defect must be considered in assessing Vet Cardiol 2012, 14:281–292.
arterial blood pressure when on diuretic and/ suitability of the animal for breeding,
or ACE inhibitor. Lehmkuhl LB, Ware WA, Bonagura JD.
particularly in breeds with a predilection for Mitral stenosis in 15 dogs. J Vet Intern Med
• Standard rhythm ECG or Holter (ambula- this defect. The additional hemodynamic
tory ECG) if arrhythmias are present. 1994, 8:2–17.
burden of gestation may be poorly tolerated Stamoulis ME, Fox PR. Mitral valve stenosis
POSSIBLE COMPLICATIONS by an already compromised heart. In general, in three cats. J Small Anim Pract 1993,
• CHF. breeding is strongly discouraged. 34:452–456.
• Atrial fibrillation. SYNONYMS Authors Lora S. Hitchcock and John D.
• Syncope. • AV dysplasia with stenosis. Bonagura
• Arterial thromboembolism—cats with MS. • Supravalvular mitral ring. Consulting Editor Michael Aherne
• Pulmonary hemorrhage with MS.
Azotemia and Uremia A
SIGNALMENT nonsteroidal anti-inflammatory drugs,

Dog and cat. diuretics, antihypertensive medications;
SIGNS failure to adjust dosage of drugs primarily
BASICS eliminated by the kidneys to correspond with
DEFINITION General Comments decline in renal function.
• Azotemia is an excess of urea, creatinine, or Azotemia may not be associated with • Toxins—ethylene glycol, grapes (dogs),
other nonprotein nitrogenous substances in historical or physical abnormalities. Unless lilies (cats).
blood, plasma, or serum. patient has uremia, clinical findings are
• Uremia is the polysystemic toxic syndrome limited to disease responsible for azotemia.
resulting from marked loss in kidney functions. Historical Findings
Uremia occurs simultaneously in animals • Weight loss. DIAGNOSIS
with increased quantities of urine constituents • Declining appetite or anorexia.
in blood (azotemia), but azotemia may occur • Depression. DIFFERENTIAL DIAGNOSIS
in the absence of uremia. • Fatigue. • Dehydration, poor peripheral perfusion, low
• Weakness. cardiac output, history of recent fluid loss,
PATHOPHYSIOLOGY high-protein diet—rule out prerenal azotemia.
• Azotemia can be caused by (1) increased • Vomiting.
• Diarrhea. • Recent onset of altered urine output (high
production of nonprotein nitrogenous or low), clinical signs consistent with uremia,
substances, (2) decreased glomerular filtration • Halitosis.
• Constipation. exposure to possible nephrotoxicants or
rate (GFR), or (3) reabsorption of urine that ischemic renal injury, or kidney size normal or
has escaped from the urinary tract into the • Polyuria.
• Changes in urine volume. enlarged—rule out acute kidney injury (AKI).
bloodstream. High production of nonprotein • Progressive weight loss, polyuria, polydipsia,
nitrogenous waste substances may result from • Poor haircoat or unkempt appearance.
small kidneys, disparate kidney size (cats—
high intake of protein (diet or gastrointestinal Physical Examination Findings big kidney and little kidney), pallor, and signs
bleeding) or accelerated catabolism of endo- • Muscle wasting/sarcopenia/cachexia. of uremia that have developed over several
genous proteins. GFR may decline because of • Mental depression. weeks to months—rule out chronic kidney
reduced renal perfusion (prerenal azotemia), • Dehydration. disease (CKD).
acute or chronic kidney disease (renal • Weakness. • Abrupt decline in urine output and onset of
azotemia), or urinary obstruction (postrenal • Pallor. signs of uremia; disparate kidney size, dysuria,
azotemia). Reabsorption of urine into the • Petechiae and ecchymoses. stranguria, and hematuria; large urinary
systemic circulation may also result from • Dull and unkempt haircoat. bladder or fluid-filled abdomen—rule out
leakage of urine from the excretory pathways • Uremic breath. postrenal azotemia.
(also a form of postrenal azotemia). • Uremic stomatitis (including oral ulcers,
• Pathophysiology of uremia—incompletely infarctions of the tongue). CBC/BIOCHEMISTRY/URINALYSIS
understood; may be related to (1) metabolic • Scleral and conjunctival injection. CBC
and toxic systemic effects of waste products • Relative hypothermia. • Nonregenerative anemia (normocytic,
retained because of renal excretory failure, (2) normochromic)—often present with CKD.
CAUSES
deranged renal regulation of fluid, electrolytes, • Hemoconcentration—often present with
and acid-base balance, and (3) impaired renal Prerenal Azotemia prerenal azotemia; can also be seen with AKI
production and degradation of hormones and • Reduced renal perfusion due to low blood and postrenal azotemia.
other substances (e.g., erythropoietin and volume or low blood pressure.
1,25-dihydroxycholecalciferol). • Accelerated production of nitrogenous waste Biochemistry
products because of enhanced catabolism of • Serial determinations of serum urea
SYSTEMS AFFECTED nitrogen and creatinine concentrations
tissues in association with infection, fever,
• Uremia affects all body systems. may help differentiate the cause of azotemia.
trauma, corticosteroid excess, or burns.
• Cardiovascular—arterial hypertension, left Appropriate therapy to restore renal perfusion
• Increased gastrointestinal digestion and
ventricular hypertrophy, heart murmur, typically yields a dramatic reduction in
absorption of protein sources (diet or gastro-
cardiomegaly, cardiac rhythm disturbances. azotemia in patients with prerenal azotemia
intestinal hemorrhage).
• Endocrine/metabolic—renal secondary (typically within 24–48 hours). Correcting
hyperparathyroidism, inadequate production Renal Azotemia obstruction to urine flow or a rent in the
of calcitriol and erythropoietin, hypergas- Acute or chronic kidney diseases (primary excretory pathway typically is followed by a
trinemia, weight loss. kidney disease affecting glomeruli, renal rapid reduction in the magnitude of azotemia.
• Gastrointestinal—anorexia, nausea, tubules, renal interstitium, and/or renal • Hyperkalemia may be consistent with
vomiting, diarrhea, uremic stomatitis, vasculature) that impair at least 75% of postrenal azotemia, primary renal azotemia
xerostomia, uremic breath, constipation. kidney function (GFR). due to oliguric renal failure, or prerenal
• Hemic/lymph/immune—anemia and Postrenal Azotemia azotemia associated with hypoadrenocorticism.
immunodeficiency. Urinary obstruction; rupture of excretory • Increased serum albumin and globulin
• Neuromuscular—dullness, lethargy, fatigue, pathway. concentration suggest prerenal component.
irritability, tremors, gait imbalance, flaccid
muscle weakness, myoclonus, behavioral RISK FACTORS Urinalysis
• Medical conditions—kidney disease, • Urine specific gravity (USG) ≥1.030 (dog)
changes, dementia, isolated cranial nerve
deficits, seizures, stupor, coma, impaired hypoadrenocorticism, low cardiac output, and ≥1.035 (cat) supports a diagnosis of
thermoregulation (hypothermia). hypotension, fever, sepsis, liver disease, pyometra, prerenal azotemia. Administration of fluid
• Ophthalmic—scleral and conjunctival hypoalbuminemia, dehydration, acidosis, therapy before urine collection may interfere
injection, retinopathy, acute-onset blindness. exposure to nephrotoxic chemicals, gastrointesti- with interpretation of USG.
nal hemorrhage, urolithiasis, urethral plugs in • Azotemic patients that have not been treated
• Respiratory—dyspnea.
• Skin/exocrine—pallor, bruising, increased cats, urethral trauma, and neoplasia. with fluids and have USG <1.030 (dog) and
shedding, unkempt appearance, loss of • Advanced age may be a risk factor. <1.035 (cat) typically have primary renal
normal sheen to coat. • Drugs—potentially nephrotoxic drugs, azotemia. A notable exception is glomerular
A Azotemia and Uremia (continued)
disease, which is sometimes characterized by that may develop during solute diuresis
glomerulotubular imbalance, where adequate that follows correction of postrenal
urine-concentrating ability may persist despite azotemia.
sufficient renal glomerular damage to cause • Fluid therapy—indicated for most FOLLOW-UP
primary renal azotemia; these patients are azotemic patients; isotonic balanced PATIENT MONITORING
recognized by moderate to marked proteinuria crystalloid is preferred replacement fluid, Serum urea nitrogen and creatinine concen-
in the absence of hematuria and pyuria. followed by hypotonic maintenance fluid trations 24 hours after initiating fluid
• USG is not useful in identifying postrenal administration. Determine fluid volume to administration; also urine production, blood
azotemia. administer on basis of severity of dehydra- pressure, body weight, and hydration status.
OTHER LABORATORY TESTS tion or volume depletion. If no clinical
Endogenous or exogenous creatinine, iohexol, dehydration is evident, cautiously assume
• Failure to correct prerenal azotemia caused
or inulin clearance tests or other specific tests that patient is <5% dehydrated and
by renal hypoperfusion rapidly could result in
of GFR may be used to confirm that azotemia administer corresponding volume of fluid.
ischemic primary kidney disease.
is caused by reduced GFR. Provide 25% of calculated fluid deficit in
• Primary renal azotemia can progress to uremia.
first hour. Thereafter, serially monitor
IMAGING • Failure to restore normal urine flow in
perfusion (capillary refill time, pulse
• Abdominal radiographs—used to deter- patients with postrenal azotemia can result in
pressure, heart rate, and temperature of
mine kidney size (small kidneys consistent progressive renal damage or death due to
feet), blood pressure, and urine output to
with CKD; mild-to-moderate enlargement of hyperkalemia and uremia.
assess adequacy of fluid therapy. If perfusion
kidneys may be consistent with AKI or has not improved, additional fluid should
urinary obstruction) and to rule out urinary be administered. Provide the remaining
obstruction (marked dilation of urinary fluid deficit over the next 12–24 hours.
bladder or mineral densities within excretory Fluid therapy should be cautiously MISCELLANEOUS
pathway). administered to patients with overt or
• Ultrasonography—may detect changes in ASSOCIATED CONDITIONS
suspected cardiac failure and patients that
echogenicity of renal parenchyma and size An association may exist between hypoka-
are oliguric or anuric.
and shape of kidneys; useful to rule out lemia and azotemia in cats.
• Consider feeding diets formulated for
postrenal azotemia characterized by kidney disease to reduce magnitude of AGE-RELATED FACTORS
distension of excretory pathway and uroliths azotemia, hyperphosphatemia, and acidosis. Primary renal failure may occur in animals of
or masses within or impinging on excretory any age, but geriatric dogs and cats appear to
pathway and intra-abdominal fluid accumu- be at substantially higher risk for both acute
lation (with rupture of excretory pathway). and chronic kidney disease; these patients are
• Excretory urography, pyelography, or also at higher risk for prerenal and postrenal
cystourethrography—may help establish MEDICATIONS causes of azotemia.
diagnosis of postrenal azotemia due to urinary DRUG(S) OF CHOICE ZOONOTIC POTENTIAL
obstruction or rupture of excretory pathway. • Symptomatic therapy for myriad manifesta- Leptospirosis
DIAGNOSTIC PROCEDURES tions of uremia.
• Omeprazole (1 mg/kg q12h) may be used PREGNANCY/FERTILITY/BREEDING
Renal biopsy can confirm the diagnosis of
to reduce gastric hyperacidity. • Data on azotemia and pregnancy are very
primary kidney disease, to differentiate acute
• Antiemetics such as maropitant (1 mg/kg limited.
from chronic kidney disease, and to attempt
q24h) are indicated for vomiting. • Pregnant azotemic animals—pharmacologic
to establish the underlying disease process
agents excreted by nonrenal pathways are
responsible for kidney disease. CONTRAINDICATIONS preferred.
Administration of nephrotoxic drugs.
SEE ALSO
PRECAUTIONS • Acute Kidney Injury.
• Use caution when administering drugs • Chronic Kidney Disease.
TREATMENT requiring renal excretion. Consult approp • Urinary Tract Obstruction.
• Prerenal azotemia caused by impaired renal riate references concerning dose-reduction
perfusion—correct the underlying cause of schedules or adjustments of maintenance ABBREVIATIONS
renal hypoperfusion; aggressiveness of intervals. • AKI = acute kidney injury.
treatment depends on severity of underlying • Cautiously administer fluids to oligoanu- • CKD = chronic kidney disease.
condition. ric patients. Monitor urine production • GFR = glomerular filtration rate.
• Primary renal azotemia and associated rates and body weight during fluid therapy • USG = urine specific gravity.
uremia—(1) specific therapy directed at to minimize likelihood of inducing over- INTERNET RESOURCES
halting or reversing primary disease process hydration. International Renal Interest Society (IRIS):
affecting the kidneys, and (2) symptomatic, • Stop fluid therapy in overhydrated oliguric/ www.iris-kidney.com.
supportive, and palliative therapies that anuric patients. Use caution in administering
ameliorate clinical signs of uremia; minimize drugs that may promote hypovolemia or
Suggested Reading
Polzin D. Chronic kidney disease. In: Ettinger
clinical impact of deficits and excesses in hypotension (e.g., diuretics); carefully
SJ, Feldman EC, eds., Textbook of Veterinary
fluid, electrolyte, acid-base balances; monitor response to such drugs by assessing
Internal Medicine, 7th ed. Philadelphia, PA:
minimize effects of inadequate renal hydration status, peripheral perfusion, and
Saunders, 2010, pp. 2036–2067.
biosynthesis of hormones and other blood pressure, with serial evaluation of renal
Ross L. Acute renal failure. In: Bonagura JD,
substances; and maintain adequate function tests.
Twedt DC, eds. Kirk’s Veterinary Therapy
nutrition. • Corticosteroids may worsen azotemia by
XIV. Philadelphia, PA: Saunders, 2009,
• Postrenal azotemia—eliminate urinary increasing catabolism of endogenous proteins.
pp. 879–882.
obstruction or repair rents in excretory ALTERNATIVE DRUG(S) Author David J. Polzin
pathway; supplemental fluid administra- N/A Consulting Editor J.D. Foster
tion often required to prevent dehydration
Babesiosis
B
SIGNS B. canis rossi, B. gibsoni, and B. vulpes.
• Similar in dogs and cats. • Peracute, acute, • Bilirubinuria is common.
or chronic. • Some carrier animals have no • Hemoglobinuria is detected less commonly
BASICS detectable clinical signs. • Dogs—lethargy, in United States than in Africa.
OVERVIEW anorexia, pale mucous membranes, fever, OTHER LABORATORY TESTS
• Caused by protozoal parasites of the genus splenomegaly, lymphadenomegaly, pigmenturia, • Microscopic examination of stained thin or
Babesia. Babesia spp. infect mammalian red icterus, weight loss, discolored stool. thick blood smears—can provide definitive
blood cells (RBCs). • Large Babesia spp. that • Cats—lethargy, anorexia, pale mucous diagnosis (not to species level); sensitivity
infect dogs: ◦ Babesia vogeli is transmitted by membranes, icterus. depends on microscopist experience and
Rhipicephalus sanguineus and has a worldwide staining technique; most success using a quick
distribution. ◦ Babesia canis is transmitted by CAUSES & RISK FACTORS
• History of tick attachment. • Splenectomized modified Wright stain; capillary blood may
Dermacentor reticulatus and is primarily found enhance sensitivity. • Indirect fluorescent
in Europe. ◦ Babesia rossi is transmitted by animals develop more severe clinical disease.
• History of splenectomy or chemotherapy antibody (IFA)—serum antibody test; cross-
Haemaphysalis leachi and is primarily found reactive antibodies can prevent differentiation
in Africa. ◦ Babesia sp. (Coco)—tick vector is is risk factor for Babesia sp. (Coco)
infection. • Immune suppression may cause of species and subspecies; some infected
unknown; identified primarily in splenec animals, particularly young dogs, may have no
tomized and immune-suppressed dogs in the clinical signs and increased parasitemia in
chronically infected dogs. • History of recent detectable antibodies. • PCR—identifies
United States. • Small Babesia spp. (2–5 μm) presence of Babesia DNA in a biologic sample
that infect dogs: ◦ B. gibsoni—worldwide dog-bite wound is risk for B. gibsoni (Asia)
infection. • Recent blood transfusion from (usually ethylenediaminetetra-acetic acid
distribution; most common Babesia sp. [EDTA] anticoagulated whole blood); can
disease in the United States. subclinically infected donor.
differentiate subspecies and species.
◦ B. conradae (also B. gibsoni [United States/
California])— only reported in California.
◦ Babesia vulpes (also Theileria Vulpes,
Spanish dog piroplasm, and B. microti-like DIAGNOSIS
parasite)—reported in Europe and the United TREATMENT
States. • Several case reports of novel Babesia DIFFERENTIAL DIAGNOSIS • Inpatient or outpatient care depending on
sp. and other piroplasms (i.e., T. equi) • Any cause of immune-mediated severity of disease. • Hypovolemic animals
infecting dogs. • Small piroplasms (2–5 μm) hemolytic anemia or thrombocytopenia, should receive aggressive fluid therapy.
that infect cats: ◦ B. felis—reported in including idiopathic immune-mediated • Severely anemic animals require blood
Africa. ◦ Cytauxzoon felis—reported in the hemolytic anemia or thrombocytopenia, transfusion.
United States. • Infection may occur either ehrlichiosis, Rocky Mountain spotted
by tick transmission, direct transmission via fever, systemic lupus erythematosus,
blood transfer during dog bites, blood neoplasia, endocarditis, hemotropic
transfusions, or transplacentally. mycoplasmosis (haemobartonellosis), and
cytauxzoonosis. • A positive Coombs’ test
MEDICATIONS
• Incubation period averages approximately
2 weeks, but some cases are not clinically does not rule out babesiosis, since many DRUG(S) OF CHOICE
diagnosed for months to years. • Piroplasms animals with babesiosis are also Coombs’ • Combination therapy of azithromycin
infect and replicate in red blood cells (RBCs), positive. • Non-immune-mediated (10 mg/kg PO q24h for 10 days) and
resulting in both direct and immune- hemolytic anemia, including microangio atovaquone (13.5 mg/kg PO q8h for 10 days)
mediated hemolytic anemia. • Immune- pathic anemia, caval syndrome, splenic is the treatment of choice and the only
mediated hemolytic anemia is more clinically torsion, disseminated intravascular treatment that can potentially clear B. gibsoni
important than parasite-induced RBC coagulation (DIC), Heinz body anemia, (Asia) infections in dogs; in a controlled study,
destruction, since severity of signs does not pyruvate kinase deficiency, phosphofructo 85% of dogs cleared the infection after
depend on degree of parasitemia. kinase deficiency. • Hepatic and posthepatic treatment. • Imidocarb dipropionate (FDA
jaundice. approved; 6.6 mg/kg SC/IM every 1–2
Systems Affected weeks) and diminazine aceturate (not FDA
• Hemic/lymphatic/immune—anemia, CBC/BIOCHEMISTRY/URINALYSIS
approved; 3.5–7 mg/kg SC/IM every 1–2
thrombocytopenia (bleeding tendencies rare), • Anemia—absent to severe; usually
weeks) decrease morbidity and mortality in
fever, splenomegaly, lymphadenomegaly, regenerative (reticulocytosis) unless signs are
affected animals; they may completely clear
vasculitis. • Hepatobiliary—mild to very acute; in severe cases, packed cell volume
B. canis and B. vogeli infections, but not B.
moderate increase in liver enzyme activities. (PCV) <10%. • Thrombocytopenia—usually
gibsoni. • A combination of clindamycin
• Nervous—cerebral babesiosis, weakness, moderate to severe; some animals have thrombo-
(25 mg/kg PO q12h), metronidazole (15 mg/
disorientation, collapse (most common with cytopenia without anemia; most common
kg PO q12h), and doxycycline (5 mg/kg PO
B. canis rossi). • Renal/urologic—renal failure hematologic abnormality. • Both leukocytosis
q12h) had been associated with elimination
(B. rossi and B. vulpes). and leukopenia reported. • Hyperbilirubinemia,
or reduction of parasite below the limit of
depending on rate of hemolysis.
SIGNALMENT detection of PCR testing in dogs;
• Hyperglobulinemia is common in chronic
• Any age or breed of dog can be infected. unfortunately, a well-defined treatment
infections and may be the only biochemical
• B. vogeli infections are more prevalent in course has not been established, with
abnormality in some animals. • Mildly
greyhounds. • B. gibsoni infections are more treatment times ranging from 24 to 92 days;
elevated liver enzyme activities from anemia/
prevalent in American pit bull terriers. • Any minimum duration of therapy of 90 days
hypoxia. • Proteinuria and hypoalbuminemia
age or breed of cat can be infected, but to recommended. • Combination of
(protein-losing nephropathy) may occur.
date, only C. felis has been reported in the doxycycline (7–10 mg/kg PO q24h),
• Azotemia and metabolic acidosis secondary
United States. enrofloxacin (2–2.5 mg/kg PO q12h), and
to renal failure have been reported with
Babesiosis (continued)
B
metronidazole (5–15 mg/kg PO q12h) for
6 weeks was associated with clinical
remission in 85% of dogs, but PCR was not
performed to assess effect on parasitemia. FOLLOW-UP MISCELLANEOUS
• Metronidazole (25–50 mg/kg PO q24h for • Recheck CBC and biochemistry as needed to All potential blood donors should test
7 days), clindamycin (12.5–25 mg/kg PO monitor resolution of anemia, thrombocyto negative for Babesia spp.
q12h for 7–10 days), or doxycycline (10 mg/kg penia, icterus, etc. • Most patients have clinical ZOONOTIC POTENTIAL
PO q12h for 7–10 days) as single-agent response within 1–2 weeks of treatment. • 2–3 N/A
treatments may decrease clinical signs but consecutive negative PCR tests beginning 2
months post treatment should be performed to PREGNANCY/FERTILITY/BREEDING
not clear infections. • Primaquine phosphate
rule out treatment failure and persistent Transplacental transmission.
(1 mg/kg IM single injection) is the
treatment of choice for B. felis. • Since the parasitemia; IFA titers are not recommended ABBREVIATIONS
anemia and thrombocytopenia are often for follow-up because titers may persist for • DIC = disseminated intravascular
immune mediated, immunosuppressive years. • Long-term follow-up of B. conradae, coagulation.
agents, such as prednisone (2.2 mg/kg/day B. vulpes, or B. felis after treatment has not been • EDTA = ethylenediaminetetra-acetic acid.
PO), may be indicated in some cases that reported. • When a dog housed in a multidog • IFA = indirect fluorescent antibody.
are not responding to antiprotozoal kennel is diagnosed with babesiosis, all dogs in • PCV = packed cell volume.
treatments alone; prolonged immune that kennel should be screened, since there is a • RBC = red blood cell.
suppressive therapy before specific high percentage of carrier animals in kennel
situations. • Coinfection with other vector- Suggested Reading
antiprotozoal therapy is contraindicated. Birkenheuer AJ, Correa MT, Levy MG,
• Antibabesial drugs (imidocarb and transmitted pathogens (e.g., Ehrlichia,
hemotropic Mycoplasma, Leishmania) should be Breitschwerdt EB. Geographic distribution
diminazene) can cause cholinergic signs that of babesiosis among dogs in the United
can be minimized by administering atropine considered, especially in animals that fail to
respond to treatment. States and association with dog bites: 150
(0.02 mg/kg SC 30 min prior to administration). cases (2000–2003). J Am Vet Med Assoc
CONTRAINDICATIONS/POSSIBLE PREVENTION/AVOIDANCE 2005, 227(6):942–947.
Recent studies suggest that using acaracides Solano-Gallego L, Baneth G. Babesiosis in
INTERACTIONS
can reduce transmission with Babesia spp. All dogs and cats—expanding parasitological
High doses of antibabesial drugs (imidocarb
attached ticks should be removed as soon as and clinical spectra. Vet Parasitol 2011,
and diminazene) have resulted in liver and
possible. Vaccines for B. canis and B. rossi are 181(1):48–60.
kidney failure.
available in Europe, but may not confer Author Adam J. Birkenheuer
protection against other Babesia spp. Tick Consulting Editor Amie Koenig
control is important for disease prevention.
Baclofen Toxicosis
B
• Pulse oximetry (hypoxemia). • End tidal consider additional doses of 1.5 mL/kg IV
CO2 (hypercapnia or hypoventilation). q4–6h for initial 24 hours; if after 3–5 boluses
• Baclofen serum or urine concentrations to no clinical response is seen, discontinue use; do
BASICS confirm exposure; not helpful for case not exceed 8 mL/kg/day.
OVERVIEW management. CONTRAINDICATIONS/POSSIBLE
• Baclofen is centrally acting skeletal muscle IMAGING INTERACTIONS
relaxant used to prevent spasticity in people Thoracic radiographs (aspiration pneumonia • Use acepromazine cautiously due to risk of
with multiple sclerosis, cerebral palsy, and spinal secondary to severe sedation). hypotension. • Use all sedatives cautiously as
disorders. • Binds to gamma-aminobutyric acid
baclofen also causes sedation. • Avoid drugs that
(GABAB) receptors and prevents release of
cause respiratory depression (e.g., phenobarbital).
inhibitory neurotransmitters and substances.
• Has been used extra-label in dogs to reduce
urethral resistance (1–2 mg/kg PO q8h), but is TREATMENT
rarely recommended due to narrow margin of • Many cases quickly become serious and
safety; use in cats not recommended. • Oral referral to a 24-hour critical care center FOLLOW-UP
doses as low as 0.7 mg/kg in dogs have caused should be considered. • Treatment focused
on decontamination and supportive care. PATIENT MONITORING
depression, dyspnea, and hypothermia. • Death • Serious cases require intense, consistent
has been documented in dogs at 2.3 mg/kg, but • Induce emesis following recent (<1 hour)
ingestion in asymptomatic patients only if patient monitoring including vital signs, blood
more likely at 8–16 mg/kg. • These organ pressure, blood gas analysis, pulse oximetry, and
systems are predominantly affected: have not already vomited; consider gastric
lavage for very large ingestions. • One dose of end tidal CO2. • Nursing care should include
◦ Cardiovascular. ◦ Gastrointestinal. turning/repositioning q6h, ocular lubrication,
◦ Musculoskeletal. ◦ Nervous. ◦ Respiratory. activated charcoal with sorbitol. • IV fluid
crystalloids at 1.5–2.5 × maintenance to support keeping patient dry/clean, passive range of
SIGNALMENT organ perfusion and enhance elimination. motion of limbs, and soft bedding.
• Accidental exposure in dogs is more • Monitor for cardiac arrhythmias, hypo PREVENTION/AVOIDANCE
frequently reported than in cats, but any ventilation, and aspiration pneumonia. Educate pet owners about risks of leaving
animal may be at risk for poisoning. • Oxygen if respiratory depression; ventilator prescription drugs accessible to pets.
• Cats are extremely sensitive to baclofen. support if severe respiratory depression/failure. POSSIBLE COMPLICATIONS
SIGNS • Monitor body temperature and provide
Aspiration pneumonia due to combination of
• Signs begin within 15–90 minutes of warming/cooling measures as needed. vomiting, sedation, seizures, and paralysis of
ingestion but, rarely, may be delayed several • Hemodialysis and hemoperfusion have diaphragm/intercostal muscles.
hours. • Common signs—vocalization, successfully shortened elimination half-life and
vomiting, ataxia, disorientation, hypersalivation, led to full recovery. EXPECTED COURSE AND PROGNOSIS
depression, weakness, coma, flaccid paralysis, • Patients suffering serious intoxications may
recumbency, seizures, and hypothermia. take 5–7 days to fully recover. • Recovery
• Life-threatening signs—dyspnea, respiratory often occurs with no residual effects.
depression, and arrest secondary to • Prognosis good with early and appropriate
diaphragmatic/intercostal muscle paralysis.
MEDICATIONS care, but becomes poor if medical care
DRUG(S) OF CHOICE delayed; seizures and aspiration pneumonia
CAUSES & RISK FACTORS associated with guarded prognosis.
• Atropine for bradycardia (0.02–0.04 mg/kg
Pet owners with medical conditions such as
IM/IV/SC PRN for dogs or cats). • Antiemetics
multiple sclerosis, cerebral palsy, and spinal
as needed (e.g., maropitant 1 mg/kg SC q24h).
disorders are more likely to have baclofen in
• Diazepam (0.25–1.0 mg/kg IV to effect) or
the home.
midazolam (0.1–0.3 mg/kg IV/IM) for seizures;
use lowest effective dose. • For seizures refractory MISCELLANEOUS
to bolus diazepam or midazolam, use CRI of ABBREVIATIONS
diazepam (0.1–0.5 mg/kg/h), midazolam • GABA = gamma-aminobutyric acid.
DIAGNOSIS (0.05–0.5 mg/kg/h), levetiracetam (dogs, • ILE = intravenous lipid emulsion.
DIFFERENTIAL DIAGNOSIS 30–60 mg/kg IV; cats, 20 mg/kg IV), propofol • PCP = phencyclidine.
• Toxic—barbiturates, benzodiazepines,
(1–8 mg/kg IV to effect, followed by CRI dose
of 0.1–0.6 mg/kg IV for dogs or cats), or INTERNET RESOURCES
depressants, ethanol, ethylene glycol, cannabis/ http://www.petpoisonhelpline.com/poison/
marijuana, illicit drugs (LSD, phencyclidine inhalant anesthesia. • Agitation may be treated
with diazepam or midazolam; acepromazine baclofen
[PCP], hallucinogenic mushrooms), methanol,
opioids, propylene glycol, tranquilizers, xylitol. (0.05–0.2 mg/kg IV/IM/SC PRN for cats or Suggested Reading
• Lower motor neuron disease (e.g., botulism,
dogs) should be used with caution. Khorzad R, Lee JA, Whelan M, et al. Baclofen
• Cyproheptadine for vocalization/disorientation toxicosis in dogs and cats: 145 cases
Neospora, tick paralysis, Toxoplasma). • Metabolic
(e.g., hepatic encephalopathy, hypoglycemia, etc.). (dogs, 1.1 mg/kg PO or rectally q4–6h; cats, (2004–2010). J Am Vet Med Assoc 2012,
2–4 mg total dose q4–6h). • IV lipid emulsion 241(8):1059–1064.
CBC/BIOCHEMISTRY/URINALYSIS (ILE) has successfully treated dogs suffering Author Ahna G. Brutlag
No specific abnormalities expected, but from baclofen intoxication; should be reserved Consulting Editor Lynn R. Hovda
should be used to rule out other causes. for critical cases; doses vary; using 20%
OTHER LABORATORY TESTS emulsion, give 1.5 mL/kg IV bolus followed by
• Arterial blood gas analysis (hypoxemia, CRI of 0.25 mL/kg/min for 30–60 min; if Client Education Handout
oxygenation, and ventilation). initial bolus fails to produce desired effect, available online
Bartonellosis
B
◦ Good specificity, poor sensitivity. ◦ Acutely
ill bacteremic animals may not have
detectable antibodies.
BASICS • PCR amplification of bacterial DNA—on MISCELLANEOUS
blood, body fluids, fresh or fresh frozen • One episode appears to confer lifelong
OVERVIEW
• Small, facultative, fastidious intracellular tissue; for cases with negative culture and immunity. • Bacillary angiomatosis—vascular
argyrophilic, hemotrophic Gram-negative rod serology. • Bartonella alpha proteobacteria proliferative disease of skin; may be caused by
(bacilli) bacteria. • Emerging, vector- growth medium (BAPGM) culture—of B. henselae; responds to antimicrobial drugs.
transmitted (fleas, ticks); adapted to reservoir blood, cerebrospinal fluid, joint fluid, ZOONOTIC POTENTIAL
hosts, establishes chronic, intraerythrocytic effusions, or tissue biopsies; enriched • Risk of transfer of organisms from infected
bacteremia. • Cats—usually asymptomatic, media, requires 14–30 days; obtain culture dogs and cats to people unknown. • Infected
reservoir host. • Dogs—emerging clinical before antibiotic therapy. • Combination cats likely serve as source of organisms for fleas
syndrome. • Seasonal—more cases reported BAPGM and PCR enhances diagnostic that transmit infection to humans (i.e., cat
between July and January. • Human syndrome— sensitivity. scratch disease). • Dogs may be chronically
variable; cat scratch disease most common; infected reservoirs for Bartonella species.
worldwide, estimate >25,000 cases/year in PATHOLOGIC FINDINGS • Veterinarians are at occupational risk of
United States; few fatalities. • Histopathology of lymph nodes—nonspecific infection from exposure. • Human disease
inflammatory reaction: granulomas, micro- manifested as erythema followed by unilateral
SIGNALMENT abscesses, and necrosis. • Warthin–Starry
Dogs and cats. regional lymphadenopathy (painful, often
silver stain—bacilli in lesions. suppurative) in 3–10 days. Infection may be
SIGNS • Immunohistochemistry, alone or with PCR accompanied by fever, malaise, myalgia, nausea.
Cats
to identify bacteria. Atypical infections may result in encephalopathy,
• May have no clinical signs. • Lymphoid meningitis, palpebral conjunctivitis, endocarditis,
hyperplasia, uveitis, endocarditis (rare), hepatitis, other systemic manifestations.
self-limiting fever. • Between 5 and 60% ABBREVIATIONS
seropositive, depending on geographic area. • BAPGM = Bartonella alpha proteobacteria
TREATMENT growth medium.
Dogs Supportive care.
Nonspecific; include lethargy, fever, lymphad- INTERNET RESOURCES
enomegaly, uveitis, or chorioretinitis, and may • www.cdc.gov/bartonella/index.html
include signs consistent with endocarditis (e.g. • www.abcdcatsvets.org/feline-bartonellosis
weakness, cardiac arrhythmias), encephalitis • www.galaxydx.com
(e.g. seizures, ataxia), myocarditis, vasculitis,
rhinitis, angioproliferative lesions, or arthritis. MEDICATIONS Suggested Reading
DRUG(S) OF CHOICE Álvarez-Fernández A, Breitschwerdt EB,
CAUSES & RISK FACTORS Solano-Gallego L. Bartonella infections in
• Optimal protocols for treating Bartonella
• Dogs—flea and tick exposure, rural cats and dogs including zoonotic aspects.
environment. • Bartonella associated with spp. have not been established; likely long-
term (4–6 weeks) antibiotics required. Parasit Vectors 2018, 11(1):624.
clinical illness in dogs and cats include Lappin MR. Update on flea and tick
• Difficult to completely eliminate organism
Bartonella henselae, B. clarridgeiae, associated diseases of cats. Vet Parasitol
B. koehlerae, B. quintana, B. vinsonii ssp. in cats; treatment reserved for symptomatic
animals or those owned by immunocompromised 2018, 254:26–29.
berkhoffii, B. rochalimae, B. elizabethae. Pultorak EL, Maggi RG, Breitschwerdt EB.
• Human disease associated with contact with
people. • Single-agent antibiotic therapy not
efficacious. • Antibiotic therapy: ◦ Cats— Bartonellosis: a one health perspective. In:
cats (>90%), particularly young cats with fleas. Yamada A, ed. Confronting Emerging
doxycycline, amoxicillin–clavulanate,
fluoroquinolones, and azithromycin have Zoonoses. Tokyo: Springer, 2014, pp. 113–149.
been used. ◦ Dogs—fluoroquinolone + Author J. Paul Woods
doxycycline good first choice; amoxicillin, Consulting Editor Amie Koenig
DIAGNOSIS gentamicin/amikacin, rifampin,
DIFFERENTIAL DIAGNOSIS erythromycin, azithromycin also options.
Other tick-borne infections (Ehrlichia, ◦ Macrolides not recommended as first
Babesia). Due to the broad spectrum of line due to rapid development of resistance.
diseases associated with Bartonella, many
differentials possible.
• Anemia, thrombocytopenia, eosinophilia.
FOLLOW-UP
• Hyperglobulinemia, signs of liver dysfunc PREVENTION/AVOIDANCE
tion, hypoglycemia possible. • Immunocompromised people should avoid
young cats. • Flea prevention.
• Serology—indirect fluorescent antibody, POSSIBLE COMPLICATIONS
ELISA, and western immunoblot. Caution with fluoroquinolones in cats and
◦ Fourfold rise in antibody titer over a young dogs.
2–3-week period consistent with infection.
Basal Cell Tumor

B
DIAGNOSTIC PROCEDURES Cowell RL, Tyler RD, Meinkoth JH.
• Cytologic evaluation of fine-needle Diagnostic Cytology and Hematology of
aspiration sample reveals aggregates of round the Dog and Cat. St. Louis, MO: Mosby,
BASICS cells with basophilic cytoplasm; mitoses are 1999, pp. 40–42.
OVERVIEW not uncommon despite benign nature. In Ho NT, Smith KC, Dobromylskyj MJ.
• Originates from the basal epithelial cells of basal cell carcinomas, mitotic activity may be Retrospective study of more than 9000
both epidermal and adnexal origin. low to high with atypical mitotic figures. feline cutaneous tumours in the UK:
• Majority of them are benign (e.g., basal cell • When clinically indicated, fine-needle 2006–2013. J Feline Med Surg 2018,
epithelioma and basaloid tumor), with aspiration of draining lymph nodes to confirm 20(2):128–134.
smaller occurrences of malignant (e.g., basal or deny the presence of regional metastases. Pakhrin B, Kang MS, Bae IH, et al.
cell carcinoma) tumors. • Histopathologic examination required for Retrospective study of canine cutaneous
• Metastasis is rare with the benign forms, definitive diagnosis; when highly pigmented, tumors in Korea. J Vet Sci 2007,
and uncommon with malignant. immunohistochemistry occasionally required 8:229–236.
to differentiate from melanoma. Ramos-Vara JA, Miller MA, Johnson GC,
SIGNALMENT
et al. Melan A and S100 protein immuno-
• Most common skin tumor in cats (10–26%) PATHOLOGIC FINDINGS histochemistry in feline melanomas: 48
and second to third most common skin tumor • Histologic cellular patterns vary from solid cases. Vet Pathol 2002, 39:127–132.
in dogs (4–12%). to cystic to ribbon appearance. Simeonov R, Simeonova G. Nucleomorphometric
• Median age—dogs, 6–9 years; cats, 10–11 • Tumor cells may contain melanin pigment analysis of feline basal cell carcinomas. Res
years. ation; may have a fine eosinophilic stroma. Vet Sci 2008, 84:440–443.
• Cocker spaniels, Kerry blue terriers, Siberian • Nuclear criteria might help predict risk of Author Jason Pieper
huskies, English springer spaniels, and poodles local recurrence in feline basal cell carcinomas. Consulting Editor Timothy M. Fan
are predisposed for dogs. Persian, British Blue,
Norwegian Forest Cat, Himalayan, and
editors acknowledge the prior contribution of
Siamese are predisposed for cats.
Louis-Philippe de Lorimier.
SIGNS
• Solitary, well-circumscribed, firm, often
TREATMENT
• Surgical excision treatment of choice and
hairless, intradermal raised mass, typically
located on the head, neck, limbs, or generally curative for fully resectable tumors.
• Cryosurgery or plesiotherapy with
shoulders.
• Can vary greatly in size from a few milli-
strontium-90 can be used for smaller, superficial
meters to many centimeters in diameter. lesions (<1 cm).
• Feline basal cell tumors are frequently
heavily pigmented, and occasionally cystic or
ulcerated.
CAUSES & RISK FACTORS MEDICATIONS
• Breed (see Signalment). DRUG(S) OF CHOICE
• Contrary to human basal cell tumors, N/A
chronic ultraviolet exposure does not appear
to play a role in pets. CONTRAINDICATIONS/POSSIBLE
• Possible association with papillomavirus in INTERACTIONS
dogs and cats. N/A
DIAGNOSIS FOLLOW-UP
• Complete surgical excision is usually
DIFFERENTIAL DIAGNOSIS curative and associated with an excellent
• Other skin tumors including mast cell prognosis.
tumor, extramedullary plasmacytoma, • Majority of tumors are locally confined and
melanoma, hemangioma, hemangiosarcoma, nonmetastatic. Long-term follow-up is
histiocytoma. generally unnecessary.
• Melanoma is an especially important
differential with the pigmented feline basal
cell tumors.
• Intradermal cysts.
MISCELLANEOUS
Normal Suggested Reading
Carpenter JL, Andrews LK, Holzworth J.
OTHER LABORATORY TESTS Tumors and tumor-like lesions. In:
N/A Holzworth J, ed., Diseases of the Cat:
IMAGING Medicine and Surgery. Philadelphia, PA:
N/A Saunders, 1987, pp. 406–596.
Battery Toxicosis
B
• Endoscopy—pending severity of signs,
evaluate extent of damage to esophagus; may
be able to remove battery or casing; use
BASICS caution and do not damage esophagus. FOLLOW-UP
OVERVIEW PATIENT MONITORING
• Alkaline/acid-based batteries (generally Consider endoscopy 2 weeks post exposure to
referred to as dry cell batteries)—gastro assess condition of esophagus.
intestinal tract (GIT) ulcers from leaking TREATMENT POSSIBLE COMPLICATIONS
corrosive contents, oral injury from chewing • Lavage oral cavity for 10–15 minutes for Esophageal perforation, esophageal stricture,
on casing, rarely heavy metal toxicity from alkaline batteries; for disc batteries give gastrointestinal obstruction, heavy metal
breakdown of casing in the GIT. 10–20 mL of water every 15 minutes until toxicity.
• Disc/button/lithium ion batteries—rapid battery is out of esophagus.
necrosis to the esophagus and stomach due to EXPECTED COURSE AND PROGNOSIS
• Do not induce vomiting, as this may expose
electric current from the battery; significant • Nonruptured dry cell battery—excellent;
esophagus to further injury. most pets pass on own within 48 hours.
necrosis can occur 15 minutes after contact. • NPO or slurry feeding for 24–48 hours if
• Ruptured dry cell battery—guarded,
SIGNALMENT oral ulcerations are present. pending location of corrosive exposure and
Dogs, cats, birds, and small mammals. Young • Ulceration may not be visible in the oral
amount of time before removal; esophageal
animals are more commonly affected. cavity until 48 hours post exposure. injury worsens prognosis.
• Wear gloves when cleaning up battery
SIGNS • Disc/button/lithium ion battery—guarded,
• Historical—finding chewed-up electronic
debris, as leaked acid could cause injury to rapid removal is needed; significant injury,
equipment without the battery; chewed or hands. including esophageal or gastric perforation,
• Small, intact dry cell batteries in stomach
mangled battery or battery packaging. can occur within 15 minutes of ingestion.
• Black debris in the oral cavity is evidence of
should pass within 48 hours; evaluate all
leaked dry cell battery contents. stools and if battery has not passed the
• Physical:
pylorus in 48 hours, surgical removal is
◦ Oral ulcerations.
recommended.
• Punctured dry cell batteries and disc/ MISCELLANEOUS
◦ Oral injury from chewing on battery
casing. button/lithium ion batteries should be
immediately removed by endoscopy or ASSOCIATED CONDITIONS
◦ Anorexia, drooling, regurgitation, vomiting, • Heavy metal toxicity.
diarrhea, melena, progressive weakness, surgery.
• Esophagitis.
dyspnea, coughing, stridor, pleuritis, • Esophageal stricture.
pyothorax, and pneumo-mediastinum. • Esophageal perforation.
• Gastrointestinal obstruction.
MEDICATIONS ABBREVIATIONS
DRUG(S) OF CHOICE • FBO = foreign body obstruction.
DIAGNOSIS • Analgesics: • GIT = gastrointestinal tract.
DIFFERENTIAL DIAGNOSIS ◦ Dogs—butorphanol 0.1–0.5 mg/kg IV/ • NSAID = nonsteroidal anti-inflammatory
• Diagnosis based on history, complete oral IM/SC; tramadol 4–10 mg/kg PO q6–8h. drug.
exam, and full (esophagus and abdominal ◦ Cats—buprenorphine 0.01–0.03 mg/kg
GIT) survey radiographs. buccal/IV/IM q6–8h.
Suggested Reading
Angle CA. Batteries. In: Osweiler GD, Hovda
• Nonsteroidal anti-inflammatory drugs • Antiemetics—maropitant 1 mg/kg PO/SC/
LR, Brutlag AG, et al., eds. Blackwell’s
(NSAIDs), foreign body obstruction (FBO), IV q12h PRN.
Five-Minute Clinical Companion, Small
pancreatitis, and other corrosive compounds • H2 blockers—pantoprazole 0.7–1 mg/kg
Animal Toxicology. Ames, IA: Wiley-
(cleaning agents, drain cleaners, pool IV over 15 min q24h; ranitidine 1–2 mg/kg
Blackwell, 2016, pp. 617–623.
shocking agents, etc.). PO/SC/IM/IV q8–12h; famotidine 0.5–
Yamashita M, Saito S, Koyama K, et al.
CBC/BIOCHEMISTRY/URINALYSIS 1.1 mg/kg PO q12h.
Esophageal electrochemical burn by
• Sucralfate 0.25–1 g PO q8h on empty
• Anemia—secondary to bleeding GI button-type alkaline batteries in dogs. Vet
ulceration. stomach.
Hum Toxicol 1987, 29:226–230.
• Antibiotics—as needed to prevent
• Leukocytosis—inflammation and secondary Author Tyne Hovda
infection. secondary infection when ulcers are present.
• Elevated total proteins/prerenal azotemia— CONTRAINDICATIONS/ Acknowledgment The author and book
secondary to dehydration. POSSIBLE INTERACTIONS editors acknowledge the prior contribution of
• Elevated liver enzymes secondary to heavy • Emetics—emesis should not be performed Catherine A. Angle.
metal toxicity from breakdown of casing. as it may worsen damage to the esophagus.
IMAGING • Steroids—may reduce risk of esophageal
• Full survey radiographs—determine if a stricture, but expected to slow healing time. Client Education Handout
battery was swallowed, assess location and • NSAIDs—–aid in pain management and available online
condition of battery and casing; look for swelling reduction, but may increase risk of
evidence of perforation and/or obstruction. gastric ulceration/perforation.
Baylisascariasis
B
• Larval form—ophthalmoscopic examina- • Larval form—infected puppies pose no
tion may show migratory tracks in retina, zoonotic threat.
may use advanced imaging methods to • Alert owner of potential risk to people who
BASICS visualize lesions in soft tissue or brain. may frequent similar habitats to raccoons.
OVERVIEW Suggested Reading
• Disease caused by the raccoon roundworm, Bauer C. Baylisascariosis—infections of
Baylisascaris procyonis. animals and humans with “unusual”
• Two forms reported in dogs—intestinal roundworms. Vet Parasitol 2013,
infection occurring in adults; visceral disease TREATMENT
• Intestinal form—may treat as inpatient to
193:404–412.
caused by larval migration in puppies. Kazacos KR. Baylisascaris Larva Migrans. US
• Infection of raccoons occurs by ingestion prevent environmental contamination with
eggs and to ensure proper disposal (as Geological Survey, Circular 1412, 2016.
of eggs or larvae in tissues of mammalian doi: 10.3133/cir1412
paratenic hosts. biohazard) or destruction (incineration) of
fecal material and worms after treatment. Rowley HA, Uht RM, Kazacos KR, et al.
• Dogs are infected by ingestion of infective Radiologic-pathologic findings in raccoon
eggs or paratenic hosts, from which they • Larval form—no treatment to date.
• Client education—alert owner of potential
roundworm (Baylisascaris procyonis)
develop patent infections with adult worms in encephalitis. Am J Neuroradiol 2000,
small intestine; puppies, probably infected by risk to people who may frequent similar
habitats to raccoons. 21:415–420.
the ingestion of eggs, develop visceral disease. Author Dwight D. Bowman
• Dogs with intestinal infection are typically Consulting Editor Amie Koenig
without signs; puppies with larval baylisasca-
riasis show signs of neurologic disease.
SIGNALMENT MEDICATIONS
• Dogs.
DRUG(S) OF CHOICE
• Intestinal form—adult animals.
• Larval form—puppies; suspect only severe Intestinal Form
cases have been reported; infection with only • Pyrantel pamoate—5–10 mg/kg PO.
a few larvae probably does not cause severe • Fenbendazole (50 mg/kg q24h PO) for
disease in most puppies. 3 days, repeat in 2 weeks.
• Febantel (25–35 mg/kg PO) with pyrantel
SIGNS
pamoate (5–7 mg/kg PO) and praziquantel
• Intestinal form—none.
(5–7 mg/kg PO); Drontal Plus® label dose
• Larval form—weakness, ataxia, dysphagia,
PO q24h for 5 days.
circling, recumbency.
• Ivermectin (5 μg/kg PO) with pyrantel
CAUSES & RISK FACTORS pamoate (5 mg/kg PO); Heartguard®
Sharing space with areas frequented by raccoons. approved label dosage, once monthly.
• Milbemycin (0.5–0.9 mg/kg PO), with
lufenuron (10 mg/kg PO); Sentinel® approved
label dosage, once monthly.
DIAGNOSIS Larval Form
DIFFERENTIAL DIAGNOSIS Corticosteroids and long-term albendazole
• Intestinal form—eggs in feces can be
(25–50 mg/kg/day PO for 10 days) may
distinguished from those of either Toxocara or prove beneficial.
Toxascaris. CONTRAINDICATIONS/POSSIBLE
• Larval form—rabies, canine distemper, INTERACTIONS
congenital neurologic defect, other infectious N/A
or inflammatory neurologic disease.
Usually normal; eosinophilia has been reported.
OTHER LABORATORY TESTS FOLLOW-UP
N/A • Intestinal form—check feces 2 weeks after
deworming and again 1 month later.
IMAGING
• Larval form—disease has proven fatal.
• Larval form—based on lesions of toxocaria-
sis or baylisascariasis in humans, lesions may
appear on abdominal ultrasound or CT scans
as small, single or multiple, ill-defined, oval
or elongated, low-attenuating lesions in liver MISCELLANEOUS
parenchyma. ZOONOTIC POTENTIAL
• In neurologic lesions, MRI reveals diffuse
• Intestinal form—eggs are not infectious
periventricular white matter disease with atrophy. when passed, but can develop in the
DIAGNOSTIC PROCEDURES environment in several days; ingestion of eggs
• Intestinal form—direct fecal smear or fecal containing infective larvae by humans can
flotation (Web Figure 1). cause severe disease, i.e., larval baylisascariasis.
Benign Prostatic Hyperplasia

B
CBC/BIOCHEMISTRY/URINALYSIS CONTRAINDICATIONS/POSSIBLE
• CBC and biochemistry—normal in BPH. INTERACTIONS
• Urinalysis—may be normal or reveal • Potential for glucocorticoid insufficiency
BASICS hematuria; pyuria and bacteriuria absent during stressful events for unspecified period
OVERVIEW unless concurrent bacterial infection. after delmadinone acetate treatment.
• Age-related pathologic change in prostate OTHER LABORATORY TESTS • GnRH agonists contraindicated in breeding
gland, making it nonpainfully large. Elevated serum concentration of canine dogs as will inhibit fertility.
• Occurs in two phases, glandular and complex. prostate-specific arginine esterase correlates
• Glandular phase characterized by high with histologic evidence of BPH.
number of large prostatic cells and symmetri
cally large prostate gland. IMAGING
• Complex phase characterized by glandular • Radiography—abdominal radiographs FOLLOW-UP
reveal prostatomegaly. • Castration is treatment of choice for
hyperplasia and atrophy, small cyst formation,
chronic inflammation, and squamous • Ultrasonography—reveals enlarged prostate nonbreeding dogs, will result in 80%
metaplasia of epithelium. gland with uniform prostatic parenchymal reduction in prostate volume within 12
echogenicity; small, fluid-filled cysts. weeks.
SIGNALMENT • Finasteride is treatment of choice for
Prevalence increases with age; 60% of intact DIAGNOSTIC PROCEDURES
breeding males. Side effects in dogs reported.
male dogs affected by 6 years and 95% of Prostatic fluid obtained by ejaculation or
Prostate reduced 50–70% between 16 and
intact male dogs affected by 9 years of age. prostatic massage may be clear or hemorr
53 weeks of treatment. Testosterone preserved,
hagic; red blood cell count high; white blood
SIGNS thus finasteride not associated with decline in
cell count normal; culture reveals <100,000
libido or semen quality. BPH will recur after
Historical Findings colony-forming units of bacteria/mL unless
withdrawal of finasteride; time until clinical
• None in most dogs. dog has concurrent bacterial infection.
signs recur is variable.
• Serosanguinous urethral discharge.
• Hemospermia.
• Hematuria.
• Dysuria. TREATMENT
• Dyschezia. • Not required if asymptomatic.
MISCELLANEOUS
• Ribbon-like stools. • Castration—most effective and prevents ASSOCIATED CONDITIONS
Physical Examination Findings recurrence; if BPH complicated by acute • Bacterial prostatitis and prostatic
• Symmetric, nonpainfully enlarged prostate bacterial prostatitis, delay surgery until carcinoma.
gland. infection resolved. • Prostatomegaly in castrated dog strongly
• Prostatic pain in dogs with complication of • Finasteride, if castration not desired, as long suggests prostatic carcinoma, as other
bacterial infection or prostatic carcinoma. as dog is to remain intact. prostatic diseases unlikely to occur in absence
of androgenic influence.
• Dihydrotestosterone (DHT; strongly) and SEE ALSO
testosterone (weakly). • Prostatic Cysts.
• Estrogens. • Prostatitis and Prostatic Abscess.
MEDICATIONS • Prostatomegaly.
• Aging as intact male.
• Risk eliminated by castration. DRUG(S) OF CHOICE
ABBREVIATIONS
• If castration not acceptable, the
• BPH = benign prostatic hyperplasia.
following are the most available and
• DHT = dihydrotestosterone.
clinically useful:
• GnRH = gonadotropin-releasing hormone.
◦ Finasteride (0.1 mg/kg/day, not to exceed
DIAGNOSIS 5 mg/dog/day) for as long as dog remains Suggested Reading
DIFFERENTIAL DIAGNOSIS intact—inhibits conversion of testosterone Christensen, BW. Canine prostate disease. Vet
• Acute bacterial prostatitis—fever, to DHT by enzyme 5-α-reductase. Clinics North Am Small Anim Pract 2018,
depression, pain on rectal palpation, neutro- ◦ Osaterone acetate (0.25 mg/kg PO once 48(4):701–719.
philia, pyuria, and bacteriuria; occurs daily for 7 days)—competitively binds to Smith J. Canine prostatic disease: a review of
concurrently with and secondary to benign androgen receptors, reduces 5-α-reductase, anatomy, pathology, diagnosis, and treatment.
prostatic hyperplasia (BPH). inhibits testosterone transport into Theriogenology 2008, 70:375–383.
• Chronic bacterial prostatitis—recurrent lower prostate cells. Author Bruce Christensen
urinary tract infections and subfertility; occurs ◦ Delmadinone acetate (3 mg/kg SC Consulting Editor J.D. Foster
concurrently with and secondary to BPH. once)—antiandrogenic activity due to Acknowledgments The author and book
• Prostatic adenocarcinoma—poor appetite, competitive binding to androgen receptors. editors acknowledge the prior contributions
weight loss, hind limb weakness, dysuria, ◦ Deslorelin acetate (subcutaneous implant of Carl A. Osborne and Jeffrey S. Klausner.
hematuria, and dyschezia; may see carcinoma administered every 6–12 months)—
cells in urine sediment. gonadotropin-releasing hormone (GnRH)
• Prostatic and paraprostatic cysts—can cause agonist to inhibit hypothalamic–pituitary–
palpable abdominal cystic mass filled with gondal axis by negative feedback.
yellow to orange fluid.
Benzodiazepine and Other Sleep Aids Toxicosis

B
paradoxical reactions were seen at 0.34 mg/kg
or greater.
BASICS SYSTEMS AFFECTED DIAGNOSIS
• Gastrointestinal—vomiting.
DEFINITION • Hepatic—acute necrosis and failure in cats DIFFERENTIAL DIAGNOSIS
• Toxicosis due to ingestion of sleep aids or with diazepam and clonazepam. • CNS depression—barbiturates, ivermectin,
antianxiety medications commonly used in • Nervous—CNS depression and/or ethylene glycol, alcohols (e.g., ethanol,
human and veterinary medicine. paradoxical reactions, ataxia, coma. methanol), marijuana, opioids, and anti
• Benzodiazepine class—alprazolam (Xanax®), • Respiratory—depression. depressants (low doses).
clonazepam (Klonopin®), diazepam (Valium®), • Paradoxical reactions—amphetamines,
lorazepam (Ativan®), midazolam (Versed®), GENETICS pseudoephedrine, methylxanthines, cocaine,
temazepam (Restoril®), triazolam (Halcion®), N/A phenylpropanolamine, and serotonin
and many more. INCIDENCE/PREVALENCE syndrome (secondary to antidepressants).
• Imidazopyridine class—eszopiclone Commonly prescribed drugs, so exposure is CBC/BIOCHEMISTRY/URINALYSIS
(Lunesta®), zaleplon (Sonata®), and zolpidem common. • No abnormalities expected in acute
(Ambien®, Ambien CR, Intermezzo®, overdoses.
Zolpimist®). • In cats with idiopathic liver failure, elevated
None
PATHOPHYSIOLOGY liver enzymes and bilirubin.
SIGNALMENT
• Benzodiazepines and imidazopyridines bind
to receptors near the gamma-aminobutyric Species
• Benzodiazepines can be detected in blood,
acid (GABA) receptor/chloride channel on Dogs and cats—acute toxicity; cats—
urine, and liver; over-the-counter (OTC)
neurons; they potentiate GABA’s effect, which idiosyncratic hepatic failure with chronic oral
drug-testing kits may be used to confirm
increases the opening of the chloride channel, dosing of diazepam or clonazepam possible.
exposure, but the label should be examined
leading to hyperpolarization of the nerve and Breed Predilections closely to be certain all benzodiazepines are
decreased excitation. None included in the test kit.
• Imidazopyridines bind near the receptor
Mean Age and Range • Imidazopyridines can be detected in blood
subset that is responsible for sedation, while and urine; OTC drug-testing kits are not yet
benzodiazepines bind to all receptor subsets None
readily available.
and so not only mediate sedation, but are also Predominant Sex
anticonvulsant and anxiolytic. None DIAGNOSTIC PROCEDURES
• Paradoxical reactions can occur and are N/A
SIGNS
typically described as excitement, irritability, PATHOLOGIC FINDINGS
and aberrant demeanor in cats and excitement General Comments No gross or histologic changes are expected.
in dogs, when the expected effect is seizure • Benzodiazepines can cause sedation with
control or sedation. virtually any exposure (even at therapeutic
• Both classes are well absorbed orally and doses).
have rapid onset of actions, often less than 30 • Imidazopyridines cause sedation at low
minutes. doses, but likelihood of paradoxical reaction TREATMENT
• Duration of action depends on the drug increases with increasing dose, especially in APPROPRIATE HEALTH CARE
and may last for hours to days. dogs. • Outpatient—most mildly affected animals
• Both classes have wide margins of safety; Historical Findings can be managed at home with confinement
lethal exposures are rare if a single agent is • Evidence of accidental ingestion of (to avoid injury due to falls) and minimizing
involved. medication. stimulation.
• Benzodiazepines—signs can be seen at • Therapeutic use of drug. • Inpatient—animals who are comatose or
therapeutic doses; however, the drugs have a • Lethargy. showing paradoxical reactions.
wide margin of safety, with the minimal lethal • Ataxia. NURSING CARE
dose being approximately 1,000 times the • Sedation. • Intravenous fluids.
therapeutic dose. Cats may develop idiosyn • Agitation. • Monitor and control body temperature.
cratic hepatic failure with chronic oral dosing
Physical Examination Findings • Good bedding and frequent turning for
of diazepam and clonazepam.
• Depression. recumbent patients.
• Zaleplon—based on a review of the
• Ataxia. • Minimize sensory stimulation, especially
American Society for the Prevention of
• Sedation. with paradoxical reactions.
Cruelty to Animals’ Animal Poison Control
Center (ASPCA APCC) Antox database: in • Hypothermia. ACTIVITY
dogs, doses >0.11 mg/kg have been associated • Agitation. Restrict until recovered to avoid injury.
with restlessness and hyperactivity; in cats, • Hyperthermia (secondary to agitation).
• Tachycardia. DIET
doses of >1.25 mg/kg caused paradoxical Cats with liver failure may require forced or
reactions. • Icterus (in cats with idiopathic liver failure).
tube feeding for support.
• Zolpidem—based on a review of the CAUSES
ASPCA APCC Antox database: in dogs, Accidental exposure, inappropriate admini CLIENT EDUCATION
dosages >0.2 mg/kg can cause mild sedation stration, or therapeutic use. • Make all clients aware of proper storage of
and ataxia; doses >0.6 mg/kg can cause all medications.
RISK FACTORS • If prescribing diazepam or clonazepam to
paradoxical reactions. In cats, signs of
• Younger and older animals. cats, have owner closely monitor the cat for
• Animals with preexisting conditions. the first week.
Benzodiazepine and Other Sleep Aids Toxicosis (continued)

B
SURGICAL CONSIDERATIONS PREVENTION/AVOIDANCE • Ethylene Glycol Toxicosis.
N/A Secure medications out of reach of dogs and • Ivermectin and Other Macrocyclic Lactones
cats. Toxicosis.
POSSIBLE COMPLICATIONS ABBREVIATIONS
No long-term complications expected. • ASPCA APCC = American Society for the
Prevention of Cruelty to Animals’ Animal
MEDICATIONS EXPECTED COURSE
Poison Control Center.
DRUG(S) OF CHOICE AND PROGNOSIS • GABA = gamma-aminobutyric acid.
• Acepromazine 0.01–0.2 mg/kg IV/IM as • Prognosis for acute overdose is excellent • OTC = over-the-counter.
needed to control paradoxical reactions. with symptomatic care.
• Prognosis for acute hepatic failure in cats INTERNET RESOURCES
• Cyproheptadine 1.1 mg/kg PO q4–6h or
with diazepam is poor. • http://www.aspca.org/pet-care/
rectally for dogs; 2–4 mg/cat q4–6h for
animal-poison-control
control of paradoxical reactions.
• http://www.petpoisonhelpline.com/poison/
• Flumazenil—a benzodiazepine reversal
lunesta
agent: 0.01 mg/kg IV q1–2h as needed; it can
be used to reverse both excessive sedation and MISCELLANEOUS Suggested Reading
paradoxical reaction; however, flumazenil can Center SA, Elston TH, Rowland PH, et al.
cause seizures, so its use is generally restricted ASSOCIATED CONDITIONS Fulminant hepatic failure associated with
to life-threatening situations. N/A oral administration of diazepam in 11 cats.
AGE-RELATED FACTORS J Am Vet Med Assoc 1996,
CONTRAINDICATIONS
• Young animals and those with preexisting 209(3):618–625.
Do not give other benzodiazepines to control
liver disease may have prolonged signs due to Czopowicz M, Szalus-Jordanow O, Frymus T.
paradoxical reactions.
reduced ability to clear the drugs. Zolpidem poisoning in a cat. Aust Vet J
PRECAUTIONS • Younger animals may be more prone to 2010, 88(8):326–327.
N/A paradoxical reactions. Lancaster AR, Lee JA, Hovda LR, et al. Sleep
POSSIBLE INTERACTIONS aid toxicosis in dogs: 317 cases (2004–2010).
ZOONOTIC POTENTIAL
Care when using other depressant medic J Vet Emerg Crit Care 2011, 21(6):658–665.
None
ations (e.g., barbiturates, phenothiazines), as Author Eric K. Dunayer
these can potentiate the depressant effects of PREGNANCY/FERTILITY/BREEDING Consulting Editor Lynn R. Hovda
these drugs. Benzodiazepines are considered teratogenic.
SEE ALSO
• Amphetamine and ADD/ADHD
Medication Toxicosis.
• Antidepressant Toxicosis—SSRIs and
FOLLOW-UP SNRIs.
PATIENT MONITORING • Antidepressant Toxicosis—Tricyclic.
TPR, blood pressure, respiratory effort. • Ethanol Toxicosis.
Beta Receptor Antagonist (Beta Blockers) Toxicosis

B
DIAGNOSTIC PROCEDURES potassium chloride to keep potassium
• ECG—first, second, and third degree AV concentrations within normal range.
block; prolonged PR, QRS, and QT intervals. • Calcium gluconate 10% 0.5–1.5 ml/kg IV
BASICS • Echocardiogram—negative inotropy, over 10–20 min, followed by CRI 0.1–
OVERVIEW decreased cardiac output. 0.15 ml/kg/h. May increase calcium available
• Beta receptor antagonists—class II anti- for heart muscle contraction.
dysrhythmics used to treat hypertrophic or • Glucagon—0.05–0.2 mg/kg slow IV bolus
hypertrophic obstructive cardiomyopathy in followed by CRI of 0.1–0.15 mg/kg/h. May
cats and hypertension and tachydysrhythmias not be as effective as IFE or HIE therapy.
TREATMENT • Sympathomimetics or vasopressin should only
in dogs and cats. • Emesis if asymptomatic and recent
• β1 receptors—primarily located in heart, be used in cases refractory to other treatments.
ingestion (<2 hours).
eye, and kidney. • Consider gastric lavage if decreased mental CONTRAINDICATION/POSSIBLE
• β2 receptors—primarily located in bronchial status and large number of pills ingested. INTERACTIONS
smooth muscle, gastrointestinal tract, pancreas, • Volume resuscitation with IV fluid bolus Vasopressors/sympathomimetics may not be
liver, skeletal muscle, vascular smooth muscle, over 15–20 minutes for hypotension—cats, as effective as other therapy and may make
and endothelium. 10–20 mL/kg for cats; dogs, 20–30 mL/kg. patients less responsive to treatment.
• Systems affected include: • Consider temporary cardiac pacing and
◦ Cardiovascular—bradycardia, hypotension. hemodialysis (drug removal) in severe
◦ Respiratory—bronchospasm. intoxications.
◦ Nervous—decreased mentation, seizures.
◦ Endocrine/metabolic—hypoglycemia, FOLLOW-UP
metabolic acidosis secondary to hypo- PATIENT MONITORING
perfusion. • Monitor for 8 hours with immediate release
◦ Renal/urologic—acute kidney injury MEDICATIONS preparations and 12–24 hours for extended
secondary to prolonged hypoperfusion. DRUG(S) OF CHOICE release (ER) preparations.
SIGNALMENT • Activated charcoal (1–2 g/kg) within 2 • Heart rate/ECG.
Dogs and cats equally affected with no breed, hours post exposure; repeat activated charcoal • Blood pressure.
age, or sex predilection. for ER formulations. • Potassium levels.
• Atropine (0.02–0.04 mg/kg IV) for sinus • Blood glucose.
SIGNS
bradycardia.
• Bradycardia, atrioventricular (AV) block. POSSIBLE COMPLICATIONS
• Intravenous fat emulsion (IFE)—may bind
• Hypotension. Renal failure can occur secondary to
lipid-soluble drugs, increase Ca available for
• Decreased mentation. prolonged hypoperfusion.
muscle contraction, and provide energy source
• Respiratory distress/bronchospasm. EXPECTED COURSE AND PROGNOSIS
for heart muscle. IFE 20% dose—1.5 mL/kg
• Seizures. • Ingestion of immediate release preparations
IV bolus over 1 min followed by CRI of
• Coma. typically result in clinical signs in 6 hours.
0.25 mL/kg/min for 30–60 min. Additional IV
• Death. • Sustained release (SR) or ER preparations may
doses—1.5 ml/kg every 4–6 hours or CRI of
CAUSES & RISK FACTORS 0.5 mL/kg/h; monitor serum for lipemia every take 12–24 hours for clinical signs to develop.
Therapeutic overdose or ingestion of 2–4 hours to determine if additional dosing • Prognosis depends on dose ingested and
medication. needed. response to therapy, but generally good.
• High-dose insulin euglycemia (HIE)
treatment—may provide energy for heart
muscle and increase Ca available for muscle
DIAGNOSIS contraction. Recommended treatment: MISCELLANEOUS
◦ Check blood glucose (BG) concentration
DIFFERENTIAL DIAGNOSIS and administer dextrose if BG <100 mg/dL. ABBREVIATIONS
• Calcium channel blocker overdose. ◦ Administer regular insulin at 1 unit/kg IV • AV = atrioventricular.
• Cardiac disease with bradyarrhythmias. followed by CRI at 0.5–2 units/kg/h. Increase • BG = blood glucose.
• Cardiovascular drug overdose (e.g., every 10 min as needed up to maximum dose • ER = extended release.
clonidine, digoxin toxicosis). of 10 units/kg/h. When clinical signs resolve, • HIE = high-dose insulin euglycemia.
• Sedative overdose (e.g., opioid or baclofen decrease insulin by 1–2 units/kg/h. • IFE = intravenous fat emulsion.
toxicosis). ◦ Monitor BG every 10 min while titrating • SR = sustained release.
• Sick sinus syndrome. insulin dosing. Once insulin dosing is
• Hyperkalemia. Suggested Reading
stabilized, check BG every 30–60 min.
• Decompensated shock. Engebretsen KM, Kaczarek KM, Morgan J,
Dextrose supplementation IV will be needed
Holger JS. High dose insulin therapy in
CBC/CHEMISTRY/URINALYSIS to maintain normal BG concentrations.
beta-blocker and calcium channel-blocker
• Hypoglycemia. Central line placement recommended for
poisoning. Clin Toxicol 2011, 49(4):277–283.
• Hyperkalemia (mild). frequent glucose monitoring and dextrose
Author Katherine L. Peterson
• Azotemia and elevated liver enzymes with administration during HIE treatment. May
prolonged hypoperfusion. need to continue dextrose supplementation up
to 24 hours after discontinuation of insulin.
OTHER LABORATORY TESTS ◦ Monitor potassium concentration every hour Client Education Handout
Blood gas—metabolic acidosis. during titration, then every 6 hours. Administer available online
Beta-2 Agonist Inhaler Toxicosis

B
• Potassium phosphate if phosphorus <1 mg/
dL—0.01–0.03 mM/kg/h IV.
• Lidocaine for ventricular arrhythmias—
BASICS DIAGNOSIS dogs, 2–4 mg/kg IV (max 8 mg/kg over 1–2
OVERVIEW DIFFERENTIAL DIAGNOSIS mins) followed by CRI of 25–100 μg/kg/min;
• Beta-2 agonist inhaler toxicosis occurs • Amphetamines and related drugs such as cats, 0.25–0.5 mg/kg IV slowly (special
when dogs chew and puncture pressurized those used for attention deficit hyperactivity caution for use in cats due to predilection for
inhalers containing albuterol (salbutamol), disorder (ADHD). CNS and CV toxicity).
levalbuterol, or salmeterol. • Sympathomimetics (e.g., phenylpropano CONTRAINDICATIONS/POSSIBLE
• Loss of beta-2 adrenergic selectivity with lamine, pseudoephedrine, phenylephrine,
INTERACTIONS
overdose results in beta-1 stimulation (sinus ephedrine).
N/A
tachycardia). Failure of the myocardium to • Methylxanthines (e.g., caffeine, theobromine).
effectively oxygenate during extreme periods • Metaldehyde.
of tachycardia can result in other tachyarrhy • Illicit drugs including methamphetamine.
thmias such as ventricular premature • Thyroxine.
contractions (VPCs) and ventricular • Tremorgenic mycotoxins. FOLLOW-UP
tachycardia. • Hops (Humulus lupulus). PATIENT MONITORING
• Generalized adrenergic stimulation • Nicotine. • Electrolytes (potassium, phosphorus) q12h
releases catecholamines that exacerbate CBC/BIOCHEMISTRY/URINALYSIS or PRN if ECG changes, weakness (potassium),
cardiovascular (CV) stimulation, stimulate • Hypokalemia. hemolysis (phosphorus). Note: Monitor for
the CNS and respiratory systems, and can • Hypophosphatemia. rebound hyperkalemia.
result in significant intracellular trans • ECG.
location of potassium and phosphorus. DIAGNOSTIC PROCEDURES
• Mentation.
• Propellants are now hydrofluoroalkanes ECG to confirm, monitor for arrhythmias.
(HFAs) and are expected to sensitize the POSSIBLE COMPLICATIONS
myocardium less to catecholamines than older • Rarely fatal. Persistent, severe tachycardia
chlorofluorocarbon propellants. can result in myocardial hypoxia and more
serious arrhythmias or other cardiac sequelae.
Systems Affected TREATMENT • Catecholamine depletion can result in weakness
• Behavioral—hyperactivity, apprehension, • Inpatient treatment—initiate medical and depression once the stimulatory effects wane.
nervousness, restlessness. management and emergency care as soon as
• Cardiovascular—sinus tachycardia, other possible following exposure. EXPECTED COURSE AND PROGNOSIS
tachyarrhythmias. • Nursing care required—fluid support.
Excellent prognosis with prompt and appropriate
• Endocrine/metabolic—hypokalemia, • Altered activity—cage rest, quiet environment.
treatment in an otherwise healthy patient.
hypophosphatemia. • NPO if vomiting.
• Gastrointestinal—mild vomiting. • Discuss with owner timing of presentation
• Musculoskeletal—tremors, weakness with relative to exposure; patients that have
catecholamine depletion. delayed presentation and prolonged, MISCELLANEOUS
• Nervous—anxiety, apprehension untreated CNS and CV stimulation may be
initially, depression with catecholamine PREGNANCY/FERTILITY/BREEDING
at greater risk for more serious arrhythmias
depletion. • Albuterol crosses the placenta. Overdose
and slower recovery.
• Neuromuscular—tremors. effects are expected to be similar for the fetus.
• No surgical or anesthetic considerations.
• Respiratory—tachypnea. Hypoxia with cardiac compromise in the
bitch may harm the fetus.
SIGNALMENT • No adverse effects expected with regard to
Young dogs are overrepresented due to their fertility.
predilection for dietary indiscretion. MEDICATIONS ABBREVIATIONS
SIGNS DRUG(S) OF CHOICE • ADHD = attention deficit hyperactivity
• Tachycardia, other tachyarrhythmias. • Benzodiazepines PRN for anxiety, nervousness, disorder.
• Lethargy, weakness, depression. tremors—diazepam: 0.5–1 mg/kg IV or 1 mg/ • CV = cardiovascular.
• Hyperactivity, apprehension, nervousness, kg rectally, repeat PRN; midazolam: 0.1– • HFA = hydrofluoroalkane.
restlessness. 0.3 mg/kg IV, IM, repeat PRN. • VPC = ventricular premature contraction.
• Tachypnea. • Beta blockers for severe tachycardia (HR Suggested Reading
• Vomiting. >160 in large dogs; >200 in miniature breeds), Mensching D, Volmer PA. Breathe with ease
• Tremors. hypokalemia—propranolol (preferred, nonspecific when managing beta-2 agonist inhaler
blocker): dogs, 0.02–0.06 mg/kg IV to effect; toxicoses in dogs. Vet Med, 2007,
CAUSES & RISK FACTORS esmolol (blocks beta-1 only; ultra-short acting): June:369–373.
• Puncture of inhalers containing beta-2 dogs, 0.25–0.5 mg/kg IV as slow bolus then Author Lynn R. Hovda
agonists. CRI of 0.01–0.2 mg/kg/min. Consulting Editor Lynn R. Hovda
• Pets prone to dietary indiscretion with • Potassium chloride supplementation—up Acknowledgments The author and book
access to inhalers. to 0.5 mEq potassium/kg/h IV maximum, editors acknowledge the prior contribution of
based on degree of hypokalemia. Donna Mensching.
Bile Duct Carcinoma

B
OTHER LABORATORY TESTS CONTRAINDICATIONS/POSSIBLE
• α-fetoprotein (an oncofetal glycoprotein) is INTERACTIONS
elevated in 55% of dogs with bile duct Medications requiring metabolism by
BASICS carcinoma; may differentiate neoplastic from hepatobiliary system should be used with
OVERVIEW non-neoplastic lesions in dogs. • Coagulation caution if evidence of dysfunction is present.
• Epithelial neoplasia that arises from the profile (prothrombin time [PT], partial
cells lining the biliary ducts or gallbladder. thromboplastin time [PTT]) recommended
• Second most common malignant hepatic before biopsy or surgical procedures.
tumor in dogs, representing 22–41% of all • Pre- and postprandial bile acids can help
malignant canine liver tumors. • Most assess hepatobiliary function. FOLLOW-UP
common malignant hepatobiliary tumor in IMAGING PATIENT MONITORING
cats, but less common than benign biliary • Abdominal radiography—may localize a Periodic physical examination, lab work,
cystadenoma. • Benign biliary cystadenomas mass to the liver, show displacement of the abdominal ultrasonography, and thoracic
may undergo malignant transformation into stomach, or demonstrate loss of detail in radiography after tumor resection.
cystadenocarcinomas, although time period over patients with peritoneal effusion. • Abdominal PREVENTION/AVOIDANCE
which this occurs is unknown. • Common ultrasonography—can be used to assess Anthelmintic therapy is warranted due to
metastatic sites include lungs, regional lymph location and character of lesion, detect and potential association between canine bile duct
nodes, and peritoneum (carcinomatosis); other sample peritoneal effusion, and guide tumor carcinoma and infection with hookworms or
metastatic sites include intestine, pancreas, biopsy. • Thoracic radiography—should be whipworms.
heart, spleen, kidney, spinal cord, urinary used to screen for pulmonary metastasis.
bladder, bone, and rarely bone marrow. • CT and MRI—more sensitive techniques POSSIBLE COMPLICATIONS
that are more likely to detect smaller lesions • Tumor rupture/hemorrhage, esp. if the
SIGNALMENT
not visible on ultrasound and radiography. massive form. • Biliary obstruction.
• Dogs and cats. • Possible predilection for
Labrador retrievers. • Affected animals DIAGNOSTIC PROCEDURES EXPECTED COURSE AND PROGNOSIS
typically >10 years of age. • Possible • Abdominocentesis and cytologic evaluation • Aggressive tumor with a guarded to poor
predisposition for female dogs. of peritoneal fluid. • Cytology or needle core prognosis, especially if nonresectable. • High
(Tru-Cut®) biopsy samples via ultrasound rate of metastasis (up to 88%) in both dogs
SIGNS
guidance. • Laparoscopy or laparotomy may and cats; widespread intraperitoneal carcino-
Historical Findings matosis common in cats. • Most patients die
be needed to obtain larger samples for
• Anorexia. • Lethargy. • Weight loss. within 6 months of surgery due to local
definitive diagnosis.
• Vomiting. • Polyuria/polydipsia. • Icterus. recurrence or metastasis.
• Abdominal distension. PATHOLOGIC FINDINGS
• Gross findings—morphologic types include
massive (37–46%), nodular (0–21%), or
• Hepatomegaly/cranial abdominal mass
diffuse (17–54%). Can be intrahepatic (most
effect. • Ascites. • Icterus. • Paraneoplastic MISCELLANEOUS
common in dogs), extrahepatic, or within the
alopecia (ventral abdomen) associated with
gall bladder (rare). • Histopathology PREGNANCY/FERTILITY/BREEDING
feline biliary carcinoma.
findings—histologic subtypes include solid Chemotherapy drugs may be carcinogenic
CAUSES & RISK FACTORS (cholangiocarcinoma) and cystic (biliary and mutagenic.
• Potential association between canine cystadenocarcinoma); subtype does not
cholangiocarcinoma and trematode influence prognosis; immunohistochemistry ABBREVIATIONS
(hookworms, whipworms) infection. (hepatocyte paraffin-1 and Claudin-7) can • PT = Prothrombin time.
• Canine biliary carcinoma has been distinguish poorly differentiated hepatocel- • PTT = Partial thromboplastin time.
experimentally induced by lular carcinoma from biliary carcinoma. Suggested Reading
N-ethyl-N′-nitro-N-nitrosoguanidine. Kinsey JR, Gilson SD, Hauptman J, et al.
Factors associated with long-term survival in
dogs undergoing liver lobectomy for liver
tumors. Can Vet J 2015, 56:598–604.
TREATMENT Liptak JM. Hepatobiliary tumors. In:
DIAGNOSIS • Complete surgical excision is treatment of
Withrow SJ, Vail DM, eds., Small Animal
choice; surgery not applicable for nodular/ Clinical Oncology, 5th ed. St. Louis, MO:
diffuse forms. • Up to 80% of liver can be Saunders Elsevier, 2013, pp. 405–410.
• Hepatocellular adenoma (hepatoma).
resected if remaining liver tissue is functional. Selmic LE. Hepatobiliary neoplasia. Vet Clin
• Hepatocellular carcinoma. • Biliary
• Interventional techniques (chemoemboliza-
adenoma/cystadenoma. • Nodular hyperplasia. Small Anim Pract 2017, 47:725–735.
tion) may be utilized as palliative procedures Authors Christine Mullin and Craig A.
• Cirrhosis. • Chronic active hepatitis.
for nonresectable solitary tumors. Clifford
• Hepatic myelolipoma. • Carcinoids.
• Hepatic abscess. Consulting Editor Timothy M. Fan
• Anemia. • Leukocytosis. • Elevated serum
enzyme (alkaline phosphatase [ALP], MEDICATIONS
gamma-glutamyl transferase [GGT], alanine DRUG(S) OF CHOICE
aminotransferase [ALT], aspartate • Chemotherapy—no effective protocol
aminotransferase [AST]) activity. identified. Tyrosine kinase inhibitors have
• Hyperbilirubinemia. been used anecdotally.
Bile Duct Obstruction (Extrahepatic)

B
Physical Examination Findings CBC/BIOCHEMISTRY/URINALYSIS
• Depend on underlying cause.
CBC
• Weight loss.
BASICS • Anemia—mild nonregenerative (chronic
• Severe jaundice.
disease) or regenerative (enteric bleeding,
DEFINITION • Hepatomegaly unless biliary cirrhosis.
Heinz body hemolysis).
Extrahepatic bile duct obstruction (EHBDO) • Cranial mass effect—extrahepatic biliary
• Microcytosis—uncommon.
is biliary tree obstruction at the level of either structures (small dogs and cats) or pancreatic • Leukogram—variable, neutrophilic
the common bile duct (CBD) or the hepatic involvement. leukocytosis, left‐shifted leukogram with
ducts, where it may involve one, several, or all • Vague cranial abdominal discomfort.
sepsis.
hepatic ducts. Obstruction may be partial or • Acholic feces—unless enteric bleeding
• Plasma—markedly jaundiced.
complete. (hemoglobin pigment evolves pigmented feces).
• Bleeding tendencies and bruising—chronic Biochemistry
PATHOPHYSIOLOGY EHBDO. • Liver enzymes—variable; marked increases
• EHBDO caused by abnormalities within in alkaline phosphatase (ALP) and gamma
• Orange urine—severe bilirubinuria.
biliary system or secondary to diseases affecting glutamyltransferase (GGT) reflect ductal
organs surrounding biliary tree; see Causes. CAUSES & RISK FACTORS injury; high alanine aminotransferase (ALT)
• Serious hepatobiliary injury follows within • Diverse primary disorders.
and aspartate transaminase (AST) reflect
weeks of complete duct obstruction. • Cholelithiasis.
periportal hepatocyte injury or multifocal
• Gallbladder (GB) bile may become colorless • Choledochitis.
injury associated with sepsis.
(white bile) if canalicular green pigmented • Neoplasia.
• Total bilirubin—moderate to markedly
hepatic bile not diverted into GB. • Bile duct malformations—DPM pheno-
high; less than observed with hemolysis or
• Increased risk of bacterial infection of bile types: choledochal cysts (cats), Caroli’s HL; hyperbilirubinemia markedly escalated
with stasis of bile flow. malformation (dogs, cats), rare cystadenoma subsequent to blood transfusion.
• EHBDO progresses to biliary cirrhosis encroaching on porta hepatis (cats). • Albumin—variable, usually normal
within 6 weeks; exception is pancreatitis • Parasitic infestation—flukes (cats).
except when EHBDO >6 weeks (biliary
causing EHBDO that may self‐resolve within • Extrinsic compression—lymph nodes,
cirrhosis); low albumin reflects synthetic
2–3 weeks. neoplasia, pancreatitis, CBD entrapment in failure or loss into abdominal effusion if
diaphragmatic hernia; foreign body syndrome complicated by GB rupture,
SYSTEMS AFFECTED obstruction of sphincter of Oddi in
Hepatobiliary suppurative hepatitis, or hepatic fibrosis
duodenum. leading to ascites.
SIGNALMENT • Duct fibrosis—trauma, peritonitis,
• Globulins—normal or increased.
Species pancreatitis; major duct involvement in feline • Glucose—normal or low if biliary cirrhosis
Dog and cat. cholangitis/cholangiohepatitis syndrome or sepsis; high if diabetes with pancreatitis.
(CCHS). • Hypercholesterolemia—common.
Breed Predilection • Duct stricture—blunt trauma, iatrogenic
• Some breeds predisposed to pancreatitis, surgical manipulations, e.g., after cholecystec- Urinalysis
choleliths, GB mucocele (GBM), dyslipi- tomy. • Bilirubinuria and bilirubin crystal
demias. formation.
• Animals with large duct ductal plate • Absence of urobilinogen—unless enteric
malformation (DPM) phenotypes—predis- bleeding; unreliable test for EHBDO.
posed to infection and cholelithiasis.
DIAGNOSIS OTHER LABORATORY TESTS
• Choleliths appear more common in small‐
• Serum bile acids—always markedly
breed dogs and cats. DIFFERENTIAL DIAGNOSIS increased; superfluous test if hepatobiliary
• Neoplasia involving CBD more common in • Mass lesions—primary or metastatic jaundice already suspected.
older animals and cats with chronic inflam- hepatobiliary neoplasia; adjacent viscera. • Coagulation abnormalities—within 10 days
mation of biliary tree. • Diffuse infiltrative liver disease— of EHBDO develop vitamin K deficiency;
Mean Age and Range neoplastic, inflammatory, hepatic lipidosis may develop disseminated intravascular
Middle‐aged to old animals with acquired (HL), amyloid (rare). coagulation (DIC).
disease; younger animals with DPM. • Infectious hepatitis—bacterial, viral, • Fecal examination—acholic stools consistent
trematodes, protozoal. with EHBDO, but may be masked by
Predominant Sex • Severe hepatic fibrosis/cirrhosis.
None small‐volume melena; trematode eggs may be
• Decompensated chronic hepatitis. verified in fluke infestation (cats).
SIGNS • Copper‐associated hepatopathy.
• Fulminant hepatic failure. IMAGING
Historical Findings • Abdominal radiography—inconsistent
• Biliary cysts—DPM phenotypes: chole-
• Depend on underlying disorder and hepatomegaly; variable mass effect in area of
dochal (cats), cystadenoma compressing CBD
“completeness” of EHBDO. gallbladder or CBD, pattern consistent with
at porta hepatis.
• Progressive lethargy and vague illness pancreatitis, mineralized cholelith(s).
• Pancreatitis—CBD stenosis/stricture,
associated with progressive jaundice. • Cholecystography—rarely provides
choleliths in cats: fused bile and pancreatic
• Pale (acholic) stools—complete EHBDO in additional practical information.
ducts.
absence of enteric bleeding. • Abdominal ultrasonography—evidence of
• HL—cats: canalicular collapse causes
• Polyphagia—complete EHBDO causes obstruction in 72–96 hours (distended,
jaundice.
nutrient malassimilation (fat). tortuous CBD, cystic duct, intrahepatic bile
• CCHS—cats, lymphocytic sclerosing or
• Bleeding tendencies—within 10 days of ducts); may disclose underlying or primary
destructive cholangitis.
complete EHBDO, more severe/overt in cats. disorder (e.g., pancreatitis, cystic lesions, mass
(continued) Bile Duct Obstruction (Extrahepatic)

B
lesions, choleliths). Caution: GB bile “sludge” • Restrict fat if overt fat malassimilation recognized in biopsy sections; bile, biliary debris,
and full GB common in anorectic or fasted caused by lack of enteric bile acids in chronic and GB wall: more likely to harbor bacteria.
patients—do not mistake for EHBDO. EHBDO—rare. • Sclerosing or destructive feline cholangitis
• Caution: Feline CBD serpiginous compared • Supplement fat‐soluble vitamins—vitamins (intrahepatic ductopenia associated with
to canine—always inspect liver image for E and K most urgent; supplements of vitamins lymphocytic or nonsuppurative or suppura-
distended intrahepatic bile ducts and confirm D and A can lead to toxicity, thus careful use tive CCHS) may clinically emulate EHBDO;
that “tubes” are ducts rather than vasculature only in chronic unresolvable EHBDO. does not respond to biliary tree decompres-
with color flow Doppler. • Water‐soluble vitamin E—necessary in sion; liver biopsy necessary for definitive
DIAGNOSTIC PROCEDURES chronic EHBDO (see Drug(s) of Choice). diagnosis.
• Vitamin K—parenteral only, use SC or IM
• Hepatic aspiration cytology—used to rule
in HL (cats) or sample mass lesions; most routes only.
clinicians avoid aspiration of obstructed CLIENT EDUCATION
biliary structures to avoid iatrogenic bile • Inform client that surgical biliary decom- MEDICATIONS
leakage and peritonitis. pression essential (unless resolvable pancreati-
DRUG(S) OF CHOICE
• Ultrasound‐guided needle biopsy— tis or cholelith obstruction).
strongly contraindicated; may cause • Warn client that surgical success contingent Vitamin K1
iatrogenic bile peritonitis. on underlying cause, results of liver biopsy, • Provide 12–36h before surgery—0.5–1.5 mg/
• Laparotomy—best approach; allows tissue infection, and individual variables. kg IM/SC, 3 doses at 12h intervals. Caution:
biopsy; biliary decompression; mass excision: avoid IV, may cause anaphylaxis.
cholelith or inspissated bile removal; cholecyst- • If chronic EHBDO not resolvable,
• Surgical exploration—imperative for
ectomy or creation of biliary‐enteric parenteral vitamin K1 given chronically with
determining underlying cause and for
anastomosis; CBD stent insertion. frequency titrated using prothrombin time
implementing definitive treatment unless
• Laparoscopic procedures not prioritized (PT); too much vitamin K1 causes hemolytic
obvious pancreatitis with hope for resolution.
because of need to completely evaluate (Heinz body) anemia in cats.
• Excise masses, remove choleliths and
biliary structures, ensure bile duct patency, • Oral vitamin K ineffectual owing to low
inspissated bile; ensure common duct patency.
and provide biliary decompressive surgeries. bioavailability in EHBDO.
• Resect GB—if necrotizing cholecystitis,
PATHOLOGIC FINDINGS GBM, or GB cholelithiasis. Vitamin E
• Gross—distended, tortuous bile duct, • Biliary‐enteric anastomosis—if irresolvable • If chronic EHBDO nonresolvable, use
distended GB: cause often grossly apparent; occlusion of CBD: e.g., fibrosing pancreatitis, water‐soluble vitamin E (d‐α‐tocopheryl
obstruction >2 weeks: large, dark green to or neoplasia; anastomotic stoma at least 2.5 cm polyethylene glycol succinate [TPGS]‐vita-
dark mahogany‐colored liver; chronic wide; chronic recurrent infection likely after min E)—10 U/kg/day PO.
complete obstruction often associates with biliary‐enteric anastomosis; warn clients that • Treat early to allow response before invasive
white or clear GB bile. temporary stenting instead of biliary‐enteric catheterizations, sampling, or surgical procedures.
anastomosis may be complicated by infection Antibiotics
and stent obstruction, esp. in cats. Before surgery—broad‐spectrum antimicrobi-
• Hypotension and bradycardia (vasovagal als for potential biliary infection because
reflex)—may develop during biliary tree
TREATMENT manipulation; ensure availability of emer-
surgical manipulations may disseminate
bacteremia; initially use antibiotics with wide
APPROPRIATE HEALTH CARE gency drugs (anticholinergics) and ventilatory spectrum, e.g., triad of ticarcillin 25 mg/kg
Inpatient—surgical intervention for EHBDO support for rescue endeavors. IV q8h, metronidazole 7.5 mg/kg IV/PO
unless the cause is pancreatitis with prospect • Cholangiovenous reflux—bacteria and q12h, enrofloxacin 5 mg/kg PO q12–24h
for resolution with supportive care. endotoxins during surgery from biliary tree (24h dose in cats no greater than 5 mg/
NURSING CARE manipulations in septic conditions; contrib- kg/24h to avoid retinopathy).
• Fluid therapy—depends on underlying utes to perioperative hypotension; all
suspected EHBDO patients should be given Antioxidants
conditions; rehydrate and provide mainte- • Vitamin E (α‐tocopherol acetate)—10–
nance fluids before general anesthesia and broad‐spectrum IV antimicrobials pre‐, intra‐,
and postoperatively (during surgery after 100 IU/kg; a larger than normal (normal =
surgical interventions. 10 IU/kg/day) oral dose needed in chronic
• Water‐soluble vitamins—in IV fluids; B tissue and bile collection for bacterial culture).
• Ensure IV catheter access and volume EHBDO if fat‐soluble vitamin used; lower
complex (2 mL/L polyionic fluids). dose used with water‐soluble vitamin E
• Initiate antibiotic therapy before surgery— expansion before surgery—use colloids only
when plasma unavailable; be prepared for (preferred, see previous).
see Drug(s) of Choice. • S‐adenosylmethionine (SAMe)—20‐40 mg/
• Vitamin K1—parenteral administration if hemorrhage (have whole blood or packed red
blood cells [RBCs] available). kg/day PO enteric‐coated tablet 1–2h before
EHBDO >5–7 days (see Drug(s) of Choice) feeding; choleretic with high‐dose adminis
before surgical interventions, abdominal or • Surgical biopsies—submit tissue and
particulate bile for aerobic and anaerobic tration via glutathione (GSH) provoked bile
visceral aspiration cytology, placement of flow.
central lines or urinary catheters. bacterial culture; submit tissue for histology.
Culture biliary debris; if GB removed, scrape Ursodeoxycholic Acid
ACTIVITY wall to collect mucoid wall adherent material. • 10–15 mg/kg PO per day—after biliary
Depends on patient status and coagulopathy. Also collect GB wall, liquid bile, and liver decompression as a choleretic; ensure adequate
DIET tissue for culture. Combine all samples into a hydration to achieve choleresis; inappropriate
• Maintain nitrogen balance—avoid protein single culture for best bacterial recovery. before biliary decompression: can accelerate
restriction. • Cytology—tissue and bile; cytology may liver injury in EHBDO.
detect bacterial infection and fluke eggs not
Bile Duct Obstruction (Extrahepatic) (continued)

B
• Beneficial effects: antifibrotic, anti‐ enzyme supplementation; cannot rely on
endotoxic, hepatoprotectant, anti‐apoptotic, trypsin‐like immunoreactive (TLI)
immunomodulator. substance to estimate pancreatic exocrine
adequacy in this circumstance; sequentially MISCELLANEOUS
Bowel Preparation before Surgery
• Mechanical cleansing of colon with water
evaluate body weight and condition, check ASSOCIATED CONDITIONS
or crystalloid fluids—may reduce endotox- feces for steatorrhea; only relevant if animal • See Causes.
emia potentiating perioperative hypotension. is fed a normal fat‐containing diet; if • Sclerosing or destructive lymphocytic
• Acutely alter enteric flora to reduce enteric
steatorrheic after biliary‐enteric anastomosis cholangitis (cats) and destructive suppurative
translocation of opportunistic pathogen with and patient is anicteric, reduce dietary fat cholangitis causing ductopenia and idiopathic
medications given either PO or by high intake and supplement pancreatic enzymes. or toxic ductopenia are confused with EHBDO.
enema instillation—neomycin 22 mg/kg q8h; Warning: pancreatic enzymes can induce
SEE ALSO
lactulose 1–2 mL/kg q8h; metronidazole oral or esophageal injury, especially in
• Cholangitis/Cholangiohepatitis Syndrome.
7.5 mg/kg q12h; enrofloxacin 2.5 mg/kg cats—must be mixed in food or adminis-
• Gallbladder Mucocele.
q12h PO; rifaximin 5–10 mg/kg q12h, at tered in capsule or tablet form, followed by
liquid or food to prevent mucosal adherence ABBREVIATIONS
present limited experience with rifaximin in
and injury. • ALP = alkaline phosphatase.
dogs and cats; probiotic bacteria, empirical
• ALT = alanine aminotransferase.
product dose but has unproven efficacy. POSSIBLE COMPLICATIONS
• AST = aspartate transaminase.
• Bile peritonitis.
Gastrointestinal Protectants • CBD = common bile duct.
• Restenosis of bile duct—if not bypassed
• Agents reducing gastric acidity—omepra- • CCHS = cholangitis/cholangiohepatitis
zole or pantoprazole (pump inhibitors) or and only stented to achieve biliary
syndrome.
famotidine (H2 blocker) combined with decompression.
• DIC = disseminated intravascular coagulation.
sucralfate for local cytoprotection if PO • Stenosis of biliary‐enteric anastomosis.
• DPM = ductal plate malformation.
medications tolerated and enteric bleeding • Severe enteric hemorrhage with EHBDO—
• EHBDO = extrahepatic bile duct
recognized (stagger sucralfate administration hypertensive enteric vasculopathy with
obstruction.
from other oral medications to avoid drug coagulopathy (vitamin K deficiency).
• GB = gallbladder.
interactions). • Hemorrhage during surgery.
• GBM = gallbladder mucocele.
• Septic bacteremia or systemic inflamma-
• Antiemetics—maropitant (Cerenia®) or • GGT = gamma glutamyltransferase.
ondansetron. tory response syndrome (SIRS) during or
• GSH = glutathione.
after surgery.
CONTRAINDICATIONS • HL = hepatic lipidosis.
• Perioperative unresponsive hypotension—
• Provide biliary decompression before • PT = prothrombin time.
persistent vasovagal reflex or sepsis related.
institution of ursodeoxycholic acid. • RBC = red blood cell.
• Vasovagal reflex.
• Take care to reduce drug dosages for • SAMe = S‐adenosylmethionine.
• Cholangiovenous reflux.
medications eliminated in bile if EHBDO. • SIRS = systemic inflammatory response
• Avoid invasive procedures—sampling, biopsy, EXPECTED COURSE AND PROGNOSIS syndrome.
surgical interventions before vitamin K1. • Depends on underlying disease. • TLI = trypsin‐like immunoreactive.
• Prognosis good if fibrosing pancreatitis and • TPGS‐Vitamin E = d‐α‐tocopheryl
PRECAUTIONS pancreatic inflammation resolve; bile duct polyethylene glycol succinate.
See Surgical Considerations. patency may return without surgery.
• Beware: biliary tree distention often persists
Suggested Reading
Center SA. Diseases of the gallbladder and
(ultrasound imaging) after EHBDO resolution.
biliary tree. Vet Clin North Am Small Anim
• Permanent peribiliary fibrosis from
Pract 2009, 39(3):543–598.
FOLLOW‐UP EHBDO.
Mehler SJ, Mayhew PD, Drobatz KJ, et al.
• Cats with sclerosing cholangitis or
PATIENT MONITORING Variables associated with outcome in dogs
ductopenia mimic EHBDO but show no
• Depends on underlying condition. undergoing extrahepatic biliary surgery: 60 cases
response to biliary decompression; liver
• Total bilirubin values acutely reflect biliary (1988–2002). Vet Surg 2004, 33:644–649.
biopsy is essential for diagnosis.
decompression; values normalize within days. Author Sharon A. Center
• Liver enzyme activities—decline slowly. Considerations/Precautions Consulting Editor Kate Holan
• CBC—repeat q2–3 days initially if septic. • Anticipate bleeding tendencies, vasovagal
• Bile peritonitis—evaluate abdominal girth, reflex, and cholangiovenous reflux during
body weight, and fluid accumulation. surgical procedures. Client Education Handout
• Determine necessity for pancreatic • Always submit liver and biliary tree biopsies available online
enzyme supplementation based on site of for histology; all tissues, crushed choleliths,
biliary‐enteric anastomosis; patients with and biliary debris for bacterial culture (aerobic,
cholecystojejunostomy may benefit from anaerobic).
Bile Peritonitis
B
cholecystitis, choledochitis, neoplasia, GBM, • Acellular mucinous material reflects biliary
neoplasia, blunt trauma. mucin production; GBM material may be
• Conditions causing EHBDO—e.g., free within abdominal cavity.
BASICS neoplasia, choleliths, pancreatitis, duct • Ratio of bilirubin in effusion : serum
OVERVIEW stricture/fibrosis. usually ≥2–3 : 1.
• Chemical peritonitis due to release of free • Sepsis or endotoxemia. • Bacterial aerobic/anaerobic culture and
bile into the abdominal cavity. • Ascites—in jaundiced cirrhotic patient. sensitivity—effusion, GB wall, liver, GB
• Can involve focal or diffuse peritoneal • Nonhepatic conditions causing abdominal contents; Gram-negative enteric opportunists
inflammation, depending on chronicity and effusion and jaundice. and anaerobes most common; polymicrobial
causal factors, and omental adhesions. CBC/BIOCHEMISTRY/URINALYSIS infection possible.
• Exploratory laparotomy—appropriate for
SIGNALMENT CBC definitive diagnosis and treatment; permits
• More common in dog than in cat. Inflammatory leukogram—left shift and toxic cholecystectomy, cholecysto-enterostomy,
• No age, breed, or sex predilection. neutrophils if necrotizing cholecystitis or duct or GB repair.
SIGNS sepsis; nonregenerative anemia if chronic • Liver biopsy—important, evaluates for
inflammation. antecedent or coexistent disease, sample
Historical Findings
• Acute presentation if septic peritonitis. Biochemistry distant to the GB to avoid artifacts.
• May have chronic illness if nonseptic. • High liver enzymes, especially alkaline PATHOLOGIC FINDINGS
• Rare asymptomatic biliary rupture associated phosphatase (ALP); hyperbilirubinemia; ± Depend on cause and site of rupture.
with omental encapsulation of leakage. hypoalbuminemia; ± prerenal azotemia.
• Abdominal discomfort—vague. • Electrolyte, fluid, and acid-base distur-
• Lethargy. bances; hyponatremia common.
• Gastrointestinal signs—anorexia, vomiting, Urinalysis
diarrhea. TREATMENT
Bilirubinuria • Inpatient—expediency of surgery depends
• Weight loss.
• ± Abdominal distention. OTHER LABORATORY TESTS on patient condition: achieve euhydration,
• Variable jaundice. Coagulation tests—abnormal if sepsis correct electrolyte and acid-base status,
• Collapse, if septic. syndrome, disseminated intravascular provide preoperative antimicrobial treatment
coagulation (DIC), or chronic EHBDO. for best survival.
Physical Examination Findings • Abdominal lavage to reduce peritoneal
• Lethargy. IMAGING
contamination if surgery delayed; use warm
• Variable (cranial) abdominal pain. • Abdominal radiography—reduced
polyionic fluids and aseptic technique.
• Jaundice. abdominal detail, generalized or focal in GB
• Surgical experience important for best
• Abdominal effusion. area; cranial abdominal mass effect; rare
outcome—complicated resections and
• ± Fever. mineralized cholelith or biliary gas
anastomoses may be required.
• ± Endotoxic shock, if septic. (emphysematous cholecystitis).
• Need for cholecystectomy decided at
• Thoracic radiography—rare bicavity
CAUSES & RISK FACTORS surgery; discolored GB wall indicates
effusion (pleural effusion), signs of trauma
• Limited arterial perfusion (cystic artery) to ischemic devitalized wall.
(e.g., fractured rib, hernia).
gallbladder (GB) fundus predisposes to • Abdominal ultrasonography—effusion;
ischemic necrosis and GB rupture. EHBDO—distended GB or CBD; cholecysti-
• Trauma to biliary structures—automobile tis/choledochitis— thick GB or duct wall;
injuries, surgical, animal bites, gunshot wounds, necrotizing cholecystitis—segmental GB wall MEDICATIONS
cystic artery laceration during cholecystocentesis. hyperechogenicity, laminated wall (represents
• Common bile duct (CBD)—frequent site DRUG(S) OF CHOICE
necrosis); pericholecystic fluid; hepatic/ • Antimicrobials—in all patients, initiate
of rupture with blunt trauma. pancreatic mass effect: common with bile
• Cholecystitis/choledochitis—may derive broad-spectrum antimicrobials before
peritonitis; choleliths or GBM (“kiwifruit surgical intervention; enteric Gram-
from GB mucocele (GBM); sepsis more sign”); gas in GB or bile ducts (emphysematous
common with necrotizing cholecystitis. negative and anaerobic organisms most
inflammation, implicates gas-forming common opportunists (good initial choices:
• Extrahepatic bile duct obstruction organisms) casting acoustic shadow; ruptured
(EHBDO)—may derive from neoplasia, ticarcillin, piperacillin, or third-generation
GB may be difficult to image; liver size usually cephalosporins, with enro-floxacin and
cholelithiasis, pancreatitis, duct stricture. normal; variable parenchymal echogenicity
• Focal, small-volume, bile peritonitis— metronidazole); customized antimicrobial
reflects hepatic pathology (e.g., ascending treatment, thereafter based on cultures;
associated with cholecystitis; may reflect cholangitis/cholangiohepatitis [CCHS]).
omental entrapment of bile or transmural continue antimicrobials ≥4–8 weeks if signs
bile leakage without rupture. DIAGNOSTIC PROCEDURES of infection confirmed by culture or on
• Chemical peritonitis due to bile—predisposes • Abdominocentesis—physicochemical, cytology.
to septic peritonitis. cytologic, and culture evaluations; ultrasound • Vitamin K1 (0.5–1.5 mg/kg IM/SC q12h
guidance optimizes sampling; sample close to for up to 3 doses)—all jaundiced patients
biliary structures but avoid structure before surgery.
penetration. • Prepare for blood component ± synthetic
• Cytology—impression smears of GB, liver, colloid therapy.
DIAGNOSIS and bile (with particulate material) used for • Antiemetics if patient is vomiting—
DIFFERENTIAL DIAGNOSIS immediate detection of infection and metoclopramide (0.2–0.5 mg/kg PO/SC
• Conditions promoting inflammation/ neoplasia; modified transudate or exudate, q6–8h or 1–2 mg/kg/24h IV by CRI);
devitalization of biliary structures—e.g., phagocytized/free bile, and bilirubin. ondansetron (0.5–1.0 mg/kg q12h IV/PO
Bile Peritonitis (continued)

B
30 min before feeding); maropitant (1.0 mg/kg/ • Repeat abdominocentesis to assess continued • CBD = common bile duct.
day IV/SC/PO max 5 days). infection and/or bile leakage as indicated. • CCHS = cholangitis/cholangiohepatitis.
• Proton pump inhibitor if gastric bleeding— • DIC = disseminated intravascular
pantoprazole (0.7–1.0 mg/kg IV q12–24h); • Cholangitis/cholangiohepatitis.
coagulation.
omeprazole (0.5–1.0 mg/kg PO q12–24h); • Pancreatitis. • EHBDO = extrahepatic bile duct
H2-receptor antagonists if proton pump • Recurrent bacterial cholangitis if biliary-
obstruction.
inhibitor is not available: famotidine enteric anastomosis required. • GB = gallbladder.
(0.5–2.0 mg/kg PO/IV/SC q12–24h); • GBM = GB mucocele.
sucralfate (0.25–1.0 g PO q8–12h). EXPECTED COURSE AND PROGNOSIS • SAMe = S-adenosylmethionine.
• Ursodeoxycholic acid as choleretic and • High survival rate for dogs with sterile bile
peritonitis, if successful surgery, depending on Suggested Reading
hepatoprotectant if GBM, choleliths, CCHS, Mayhew PD, Holt DE, McLear RC, et al.
or chronic hepatitis—may administer underlying cause.
• Higher mortality in septic bile peritonitis
Pathogenesis and outcome of extrahepatic
chronically if GBM or cholelithiasis: biliary obstruction in cats. J Small Anim
10–15 mg/kg PO daily, divided, with food (up to 73%).
• Anticipate slow clinical recovery and
Pract 2002, 43:247–253.
for best bioavailability. Mehler SJ. Complications of the extrahepatic
• Antioxidants—vitamin E (10 IU/kg/24h); normalization of liver enzymes, but rapid
resolution of hyperbilirubinemia with biliary surgery in companion animals. Vet
S-adenosylmethionine (SAMe, with proven Clin North Am Small Anim Pract 2011,
bioavailability and efficacy) 20 mg/kg PO successful surgery.
41:949–967.
daily 2h before feeding until enzymes Mehler SJ, Mayhew PD, Drobatz KJ, et al.
normalize, indefinitely if chronic hepatitis or Variables associated with outcome in dogs
CCHS, GBM, inspissated bile syndrome; undergoing extrahepatic biliary surgery: 60
choleretic influence requires higher dose MISCELLANEOUS cases (1988–2002). Vet Surg 2004,
(40 mg/kg/day). 33:644–649.
SEE ALSO
• Cholecystitis and Choledochitis. Author Sharon A. Center
• Cholelithiasis. Consulting Editor Kate Holan
• Gallbladder Mucocele.
FOLLOW-UP • Hepatitis, Chronic.
PATIENT MONITORING ABBREVIATIONS
• Sequential hematologic, biochemical, and • ALP = alkaline phosphatase.
imaging tests.
Bilious Vomiting Syndrome

B
OTHER LABORATORY TESTS metoclopramide (0.2–0.4 mg/kg PO q6–8h)
• Fecal examination to detect Giardia or and cisapride (0.5 mg/kg PO q8–12h);
other parasites. • Baseline cortisol to rule out cisapride only available through compound-
BASICS hypoadrenocorticism. • GI panel—pancreatic ing pharmacies. • Erythromycin (0.5–1 mg/
OVERVIEW lipase immunoreactivity (PLI), trypsin‐like‐ kg q8h) stimulates gastric motility by
• Bilious vomiting syndrome (BVS) is immunoreactivity (TLI), cobalamin, folate. activation of motilin receptors and may also
suspected to be secondary to alterations in IMAGING resolve signs.
normal gastrointestinal (GI) motility. BVS is • Barium contrast study may reveal delayed CONTRAINDICATIONS/POSSIBLE
associated with chronic intermittent vomiting gastric emptying, although finding must be INTERACTIONS
of bile, thought to be the result of reflux of interpreted with caution. • Barium given • Gastric prokinetic agents should not be
intestinal contents (bile) into the stomach. The with meals, radiopaque markers, or using administered in patients with GI obstruction.
normal aboral gastric and intestinal motility special motility capsule (Smartpill®) may also • Metoclopramide can cause nervousness,
and functional pylorus prevent the reflux of bile demonstrate delayed gastric motility. anxiety, or depression. • Cisapride at higher
back into the stomach. When bile is refluxed
DIAGNOSTIC PROCEDURES doses can cause vomiting, diarrhea, or
into the stomach it is normally rapidly removed
• Endoscopic findings frequently unremarkable abdominal cramping. • Erythromycin can
by subsequent peristaltic contractions. Bile
and help rule out underlying GI disease. • May cause vomiting.
remaining in the gastric lumen along with
gastric acid and pepsin can subsequently cause be evidence of bile in stomach or gastritis in
gastric mucosal damage. • Clinical signs often antral region of stomach. • Endoscopy useful
occur early in the morning, suggesting that to rule out structural or inflammatory disease,
prolonged fasting or gastric inactivity may since BVS is diagnosis of exclusion. FOLLOW‐UP
modify normal motility patterns, resulting in • Most patients respond to one of these
bile reflux. • System affected—GI. treatments and clinical response supports the
SIGNALMENT diagnosis. • Failure to respond suggests
• Commonly observed in dogs, rarely in cats. TREATMENT another underlying or causative factor.
• Most animals are young or middle‐aged. • Generally not serious debilitating disorder
• No breed or sex predisposition. if truly BVS, but important to rule out major
conditions such as gastritis, IBD, or GI
SIGNS neoplasia. • Idiopathic bilious vomiting cases
• Chronic intermittent vomiting of bile MISCELLANEOUS
generally treated symptomatically on an
associated with empty stomach. Signs outpatient basis and treatment response ASSOCIATED CONDITIONS
generally occur late at night or early in supports suspected diagnosis. • Feeding the Gastroesophageal reflux.
morning. Signs may occur daily, but usually animal small frequent meals, including late SEE ALSO
intermittent. Between episodes, animal evening meal, often resolves clinical signs; • Gastric Motility Disorders.
appears normal and most dogs appear healthy food possibly could act as buffer to refluxed • Gastroesophageal Reflux.
immediately after vomiting episodes. • Results bile or may in some way enhance GI motility.
of physical examination usually unremarkable. ABBREVIATIONS
• Trial with hypoallergenic diet (novel protein
• BVS = bilious vomiting syndrome.
CAUSES & RISK FACTORS or hydrolyzed protein) can also improve
• Cause unknown (idiopathic). • Primary clinical signs, which may actually suggest
• IBD = inflammatory bowel disease.
gastric hypomotility or abnormal intestinal underlying food‐responsive enteropathy. • If
• PLI = pancreatic lipase immunoreactivity.
peristaltic motility are suspected as probable diet modification fails, medical treatment
• TLI = trypsin‐like‐immunoreactivity.
underlying causes. • Conditions causing should be considered.
gastritis, duodenitis, or intestinal obstructive Suggested Reading
disease may be responsible for altered proximal Ferguson LE, Wennogle SA, Webb CB.
GI motility and can cause bile reflux; investi- Bilious vomiting in dogs: retrospective
gate for parasitism (e.g., Giardia), inflamma- study of 20 cases (2002–2012). J Am Anim
tory bowel disease (IBD), intestinal neoplasia,
MEDICATIONS Hosp Assoc 2016, 52:157–161.
or obstructions as possible etiologies. DRUG(S) OF CHOICE Washabau RJ. Gastrointestinal motility
• Previous pyloric opening or resection surgery • Choices include agents for gastric mucosal disorders and gastrointestinal prokinetic
can increase risk of enterogastric reflux. protection against refluxed bile or use of therapy. Vet Clin North Am Small Anim
gastric prokinetic agents to improve motility. Pract 2003, 33(5):1007–1028.
• Often single evening dose of medication Webb C, Twedt DC. Canine gastritis. Vet
may be all that is required to prevent clinical Clin North Am Small Anim Pract 2003,
signs if signs occur at night. • Drugs for 33(5):969–985.
DIAGNOSIS gastric mucosal protection include various Author Leah Ferguson
DIFFERENTIAL DIAGNOSIS antacids or sucralfate (1 g/25 kg q8h). Consulting Editor Mark P. Rondeau
• Any number of GI and non‐GI disorders • Drugs that block gastric acid production, Acknowledgment The author and book
can cause chronic vomiting. Giardia should including famotidine (0.5–1.0 mg/kg editors acknowledge the prior contribution
be excluded since signs of this disease may q12h–24h), ranitidine (1–2 mg/kg q8–12h), of David C. Twedt.
mimic those of BVS. • IBD can result in bile and omeprazole (0.7–1.5 mg/kg q12–24h)
reflux. • Intestinal obstruction or partial may be beneficial; ranitidine has mild gastric
obstructions should be ruled out. prokinetic effects in vitro and may be
CBC/BIOCHEMISTRY/URINALYSIS beneficial, but is less effective acid reducer.
• Specific gastric prokinetic agents include
Results usually unremarkable.
Blastomycosis
B
• Seizures or neurologic deficits with CNS IMAGING
involvement. Radiographs
• Syncope if cardiac involvement.
BASICS • Lungs—generalized interstitial to nodular
Physical Examination Findings infiltrate, may be nonuniform distribution.
DEFINITION • Tracheobronchial lymphadenopathy.
Dogs
A systemic, mycotic infection caused by the • Changes may resemble metastatic neoplasia.
• Fever up to 104 °F (40 °C) in ~50% of
dimorphic soil organism Blastomyces dermatitidis. • Pleural effusion has been reported in dogs.
patients.
PATHOPHYSIOLOGY • Harsh, dry lung sounds, increased • Focal bone lesions—lytic and proliferative;
• A small spore (conidia) shed from the respiratory effort. can be mistaken for osteosarcoma.
mycelial phase (Ajellomyces dermatitidis) of • Generalized or regional lymphadenopathy DIAGNOSTIC PROCEDURES
the organism growing in soil is inhaled, with or without skin lesions or subcutaneous • Cytology of lymph node aspirates, lung, or
entering the terminal airway. swellings. lytic bone aspirates, tracheal wash fluid, or
• At body temperature, spore transforms to its • Uveitis with or without secondary impression smears of skin lesions—best
yeast form, which may initiate infection in lungs. glaucoma and conjunctivitis, ocular exudates, method for diagnosis.
• From a focus of mycotic pneumonia, yeast and corneal edema. • Histopathology of bone biopsies or
may disseminate hematogenously throughout • Lameness—bone involvement in up to 30%. enucleated eyes.
the body. • Testicular enlargement and prostatomegaly— • Organisms—usually plentiful in tissues;
• Immune response produces pyogranulo occasional. may be scarce in tracheal washes if there is no
matous inflammation. • Murmur and atrioventricular (AV) productive cough.
SYSTEMS AFFECTED block—with endocarditis and myocarditis.
PATHOLOGIC FINDINGS
• Respiratory—85% of affected dogs. Cats • Lesions—pyogranulomatous with budding
• Eyes, skin, subcutaneous tissues, lymphatic, • Increased respiratory effort. 5–20 μm diameter yeast; thick, refractile,
and musculoskeletal—commonly affected. • Granulomatous skin lesions. double-contoured cell wall; occasionally very
• Reproductive, nasal cavity, and heart—less • Visual impairment. fibrous with few organisms found.
commonly affected. • Special fungal stains—facilitate organism
RISK FACTORS
• Subclinical infection is uncommon. detection.
• Wet environment—banks of rivers, streams,
INCIDENCE/PREVALENCE lakes or swamps; most affected dogs live
Depends on environmental and soil within 400 meters of water.
conditions that favor growth of Blastomyces. • Exposure to recently excavated areas.
Growth of organism requires sandy, acidic soil • Reported in indoor-only cats. TREATMENT
and proximity to water.
NURSING CARE
GEOGRAPHIC DISTRIBUTION Severely dyspneic dogs—require prolonged
Most common along the Mississippi, Ohio, oxygen support; about 25% of dogs have
and Tennessee river basins. Also reported in DIAGNOSIS worsening of respiratory disease during first
Great Lakes and St. Lawrence River areas, days of treatment, attributed to an inflamm
southern Canada, mid-Atlantic states; has DIFFERENTIAL DIAGNOSIS
• Respiratory signs—bacterial pneumonia, atory response.
been found outside endemic area in Colorado.
metastatic neoplasia, heart failure, pleural ACTIVITY
SIGNALMENT effusion, or other fungal infection. Patients with respiratory compromise must be
Species • Lymphadenopathy—similar to restricted.
• Predominantly dog. lymphoma.
• Combination of respiratory disease with DIET
• Occasionally cat. N/A
ocular, bony, or skin/subcutaneous involve
Breed Predilections ment in a young dog supports the diagnosis. CLIENT EDUCATION
Large-breed dogs weighing ≥25 kg, especially • Treatment is costly and long term.
sporting breeds; may reflect increased CBC/BIOCHEMISTRY/URINALYSIS
• CBC reflects inflammation; mild anemia in • Infected dogs are not contagious to other
exposure rather than susceptibility. animals or people.
chronic cases.
Mean Age and Range • High serum globulins, borderline hypoal SURGICAL CONSIDERATIONS
• Dogs—most common in those 1–5 years of buminemia with chronic infection. • Removal of abscessed lung lobe may be
age; uncommon after 7 years of age. • Hypercalcemia (generally mild) in some dogs. required if medical treatment ineffective.
• Cats—no age predilection noted. • Blastomyces yeasts may be found in urine of • Blind eyes should be enucleated to remove
Predominant Sex dogs with prostatic involvement; mild potential sites of residual infection.
• Dogs—males in most studies. proteinuria can be present.
• Cats—none noted. OTHER LABORATORY TESTS
SIGNS • Urine or serum antigen testing—sensitivity
Historical Findings
>90%; sensitivity greater with urine test; MEDICATIONS
• Weight loss, hyporexia.
cross-reacts with other fungal infections (e.g.,
DRUG(S) OF CHOICE
• Cough, dyspnea.
histoplasmosis).
• Agar gel immunodiffusion (AGID)—not Itraconazole
• Ocular inflammation/discharge.
sensitive early in disease, but very specific for • Dogs—5 mg/kg PO q12h with a fat-rich
• Draining skin lesions.
infection. meal (e.g., canned dog food) for the first 3
• Lymphadenitis.
days, then reduce to 5 mg/kg PO q24h.
• Lameness.
(continued) Blastomycosis
B
• Cats—5 mg/kg PO q12h; open the 100 mg Thoracic Radiographs • Warn clients that blastomycosis is acquired
capsules containing pellets and mix with • Considerable permanent pulmonary from an environmental source and that they
palatable food. changes (fibrosis/scarring) may occur after the may have been exposed to the source; the
• Avoid antacid drugs as absorption best in infection resolves, making determination of incidence in dogs is 10 times that in humans.
acidic environment. persistent active disease difficult. • Encourage clients with respiratory and skin
• Treat for minimum 90 days, or for 1 month • At 90 days of treatment—if active lesions to inform their physicians that they
after all signs of disease have resolved (which- pulmonary disease, continue treatment for may have been exposed to blastomycosis.
ever is longer). additional 30 days. PREGNANCY/FERTILITY/BREEDING
• Absorption of compounded itraconazole is • If lungs appear normal, stop treatment and
Azole drugs can have teratogenic effects
unreliable and use is not recommended. repeat radiographs again in 30 days. (embryotoxicity found at high doses) and
• At 120 days of treatment—if the lungs
Fluconazole should ideally be avoided during pregnancy
• Dogs—5 mg/kg PO q12h.
appear the same as day 90, changes are (but the risk of not treating the mother must
• Cats—5–10 mg/kg PO q12–24h; 50 mg/cat.
residual (fibrosis); if clearer than day 90, be balanced with the theoretical risk of azole
• Inexpensive, but may require longer
continue treatment for 30 more days. If therapy to the fetuses).
treatment duration. lesions are significantly worse than at 90 days,
consider a change in therapeutic agent. ABBREVIATIONS
Amphotericin B • Continue treatment as long as improvement is • AGID = agar gel immunodiffusion.
• For dogs with neurologic signs or life- noted in the lungs; if there is no further • ALT = alanine transaminase.
threatening disease. improvement and no indication of active disease, • AV = atrioventricular.
• 0.5–1.0 mg/kg IV q48h; use lipid complex the lesions are likely the result of scarring. INTERNET RESOURCES
for dogs with renal dysfunction. Information on antigen testing: www.
Urine Antigen Testing
CONTRAINDICATIONS • Positive test is generally related to active disease. miravistalabs.com
Corticosteroids—may allow continued • If other signs have resolved, a negative test Suggested Reading
proliferation of organisms; patients with supports treatment discontinuation. Crews LJ, Feeney DA, Jessen CR, et al.
previous steroid therapy require longer Radiographic findings in dogs with
treatment duration; for dogs with life- PREVENTION/AVOIDANCE
• Location of environmental growth of pulmonary blastomycosis: 125 cases
threatening dyspnea, dexamethasone (1989–2006). J Am Vet Med Assoc 2008,
(0.1–0.2 mg/kg/day IV) for 2–3 days may be Blastomyces organisms unknown, thus
difficult to avoid exposure; exposure to lakes 232:215–221.
given with itraconazole treatment; taper and Foy DS, Trepanier LA, Kirsch EJ, et al. Serum
discontinue corticosteroids as soon as possible. and streams may be restricted (but limited
practicality). and urine Blastomyces antigen
PRECAUTIONS • Dogs that recover from the infection may concentrations as markers of clinical
Itraconazole and Fluconazole Toxicity be immune to reinfection. remission in dogs treated for systemic
• Anorexia—most common sign; attributed
blastomycosis. J Vet Intern Med 2014,
EXPECTED COURSE AND PROGNOSIS 28:305–310.
to liver toxicity; monitor serum alanine • Death—25% of dogs die during first week
aminotransferase (ALT) activity monthly or Legendre AM, Rohrbach BW, Toal RL, et al.
of treatment; early diagnosis improves chance Treatment of blastomycosis with
when anorexia occurs; temporarily discontinue of survival.
drug for patients with anorexia and moderate itraconazole in 112 dogs. J Vet Intern Med
• Severe pulmonary disease and CNS
ALT activity elevation; after appetite improves, 1996, 10:365–371.
involvement decrease prognosis. Mazepa AS, Trepanir LA, Foy DS. Retrospective
restart at half the previous dose. • Recurrence—approximately 20% of dogs;
• Ulcerative dermatitis—in some dogs due to
comparison of the efficacy of fluconazole or
usually within 3–6 months after completion itraconazole for the treatment of systemic
vasculitis; dose related; temporarily of treatment; may occur >1 year after treat-
discontinue drug until ulcers resolve, then blastomycosis in dogs. J Vet Intern Med
ment; a second course of azole treatment 2011, 25:440–445.
restart at half the previous dose. cures most patients; drug resistance has not Spector D, Legendre AM, Wheat J, et al.
Amphotericin B Toxicity been observed. Antigen and antibody testing for the
• Only absolute contraindication to therapy • With early detection of blastomycosis, the
diagnosis of blastomycosis in dogs. J Vet
is anaphylaxis, but major limiting factor is prognosis in cats appears similar to dogs. Intern Med 2008, 22:839–843.
cumulative nephrotoxicity. Author Daniel S. Foy
• Monitor serum creatinine concentration Consulting Editor Amie Koenig
throughout therapy—elevation above normal or
20% greater than baseline considered significant. MISCELLANEOUS
ZOONOTIC POTENTIAL available online
• Yeast form is not spread from animals to
humans, except through bite wounds;
FOLLOW-UP inoculation of organisms from dog bites has
PATIENT MONITORING occurred.
Serum chemistry—monthly to monitor for • Avoid cuts during necropsy of infected dogs
hepatic toxicity, or if anorexia develops. and avoid needle sticks when aspirating lesions.
Blepharitis
B
erythematosus (SLE), SH, drug eruption.
• Type IV (cell mediated)—contact and flea
bite hypersensitivity; drug eruption.
BASICS DIAGNOSIS
Bacterial
DEFINITION • Hordeolum—localized abscess of eyelid DIFFERENTIAL DIAGNOSIS
Inflammation of outer (skin) and middle glands, usually staphylococcal; may be external Clinical signs are diagnostic.
(muscle, connective tissue, and glands) (sty in young dogs, glands of Zeis) or internal CBC/BIOCHEMISTRY/URINALYSIS
portions of eyelid, usually with secondary (in old dogs, meibomian glands). • Generalized Usually normal unless metabolic cause (e.g.,
inflammation of palpebral conjunctiva. bacterial blepharitis and meibomianitis—usually diabetic dermatosis).
PATHOPHYSIOLOGY Staphylococcus or Streptococcus. • Bartonella
• Inflammation—immune mediated, henselae—chronic blepharoconjunctivitis in cats.
Indicated for systemic disorders, including
infectious, endocrine mediated, self- and • Pyogranulomas. • SH—young and old dogs.
hypothyroidism.
external trauma, parasitic, radiation, Neoplastic
nutritional. Inflammatory response often DIAGNOSTIC PROCEDURES
• Sebaceous adenomas and
exaggerated because conjunctiva is rich in • Eye examination—inciting cause, corneal
adenocarcinomas—from meibomian gland.
mast cells and densely vascularized. ulcer, foreign body, distichia, ectopic cilia,
• Squamous cell carcinoma—white cats.
• Meibomian gland dysfunction—bacterial keratoconjunctivitis sicca (KCS). • Ancillary
• Mast cell—may appear as swollen, hyper-
lipases alter meibomian lipids and plug gland; ocular tests— fluorescein, Schirmer tear test.
emic lesion.
produce irritating fatty acids, enhance • Thorough history and dermatologic exam:
bacterial growth, and destabilize tear film. Other ◦ Cytology—deep skin scrape, conjunctival
• External trauma—eyelid lacerations, scrape, or exudate from glands and pustules.
SYSTEMS AFFECTED thermal or chemical burns. • Mycotic— ◦ Wood’s light evaluation, dermatophyte
Ophthalmic dermatophytosis; systemic fungal granulomas. culture. ◦ KOH preparation. ◦ Intradermal
SIGNALMENT • Parasitic—demodicosis; sarcoptic mange; skin testing, other testing for hypersensitivity-
See Causes. Cuterebra and Notoedres cati. Note: Demodex induced disease. ◦ Consider referral to a
injai has a propensity for sebaceous glands dermatologist for refractory cases. • Aerobic
SIGNS
and can be associated with meibomian gland bacterial culture and sensitivity—of exudate
• Serous, mucoid, or mucopurulent ocular
dysfunction in dogs, including chalazia and from skin, conjunctiva, expressed meibomian
discharge. • Blepharospasm. • Eyelid
granulomatous blepharitis. • Chalazia—ster- glands, or pustules; often will not recover
hyperemia, edema, and thickening.
ile, yellow-white, painless meibomian gland Staphylococcus from patients with chronic
• Pruritus. • Excoriation. • Depigmentation—
swellings caused by granulomatous inflamma- meibomianitis and suspected SH. • Immuno
skin, hair (in Siamese-type cats with color
tory response to meibum in surrounding fluorescent antibody assay or PCR for FHV-1
points, lightening of hair on affected lids due
eyelid tissue. • Nutritional—zinc-responsive and Chlamydia—in conjunctival scrapings from
to increased skin temperature). • Alopecia.
dermatosis (Siberian husky, Alaskan cats with primary conjunctivitis or keratitis.
• Swollen, cream-colored meibomian glands.
Malamute, puppies), fatty acid deficiency. • Full-thickness wedge biopsy of eyelid.
• Elevated, pinpoint meibomian gland
• Endocrine—hypothyroidism (dogs);
orifices. • Abscesses. • Scales, crusts, papules, PATHOLOGIC FINDINGS
hyperadrenocorticism (dogs); diabetic
or pustules. • Single or multiple nodular Routine histopathology often nondiagnostic
dermatosis. • Viral—chronic blepharitis in
hyperemic swellings. • Concurrent in chronic disease.
cats (feline herpesvirus type 1 [FHV-1]).
conjunctivitis and/or keratitis.
• Irritant—drug reaction (e.g., neomycin);
CAUSES smoke in environment; post-parotid duct
Congenital transposition. • Familial canine dermato
• Eyelid abnormalities—may promote myositis—collie and Shetland sheepdog. TREATMENT
self-trauma or moist dermatitis. • Prominent • Nodular granulomatous episclerokeratitis—
fibrous histiocytoma and collie granuloma; APPROPRIATE HEALTH CARE
nasal folds, medial trichiasis, and lower lid See Nursing Care.
entropion—shih tzu, Pekingese, English may affect eyelids, cornea, or conjunctiva.
bulldog, Lhasa apso, pug; Persian and • Eosinophilic granuloma—cats; may affect NURSING CARE
Himalayan cat. • Distichia—shih tzu, pug, eyelids, cornea, or conjunctiva. • Eyelid contact • Prevent self-trauma—Elizabethan collar.
golden retriever, Labrador retriever, poodle, with tear overflow and purulent exudate (tear • Cleanse eyelids—to remove crusts; warm
English bulldog. • Ectopic cilia. • Lateral lid burn). • Keratitis, conjunctivitis, dacryocysti- compresses applied for 5–15 minutes 3–4
entropion—Chinese Shar-Pei, chow chow, tis. • Dry eye. times daily, avoiding ocular surfaces. Use
Labrador retriever, Rottweiler. • Orbital disease. • Radiotherapy. • Idiopathic— saline, lactated Ringer’s solution, or a
• Lagophthalmos—brachycephalic dogs; especially Persians and Himalayans. commercial ocular cleansing agent (e.g., I-Lid
Persian, Himalayan, and Burmese cats. • Deep RISK FACTORS ’n Lash®); clip periocular hair short.
medial canthal pocket—dolichocephalic dogs. • Breed predisposition to eyelid abnormalities • Common underlying cause in cats is
• Dermoids—Rottweiler, dachshund, and (e.g., entropion, ectropion). FHV-1 infection; minimize stress.
others; Burmese cat. • Hypothyroidism—may promote chronic DIET
Allergic bacterial disease in dogs. • Canine seborrhea— Only if food allergy.
• Type I (immediate)—atopy, food, insect may promote chronic generalized
meibomianitis, with predisposition for CLIENT EDUCATION
bite, inhalant, Staphylococcus hypersensitivity In cats with FHV-1-related blepharitis,
(SH). • Type II (cytotoxic)—pemphigus, Demodex injai infection.
inform client that there is no cure and that
pemphigoid, drug eruption • Type III clinical signs often recur when animal is
(immune complex)—systemic lupus stressed.
(continued) Blepharitis
B
SURGICAL CONSIDERATIONS affected dogs might also require treatment for weeks; should notice improvement within 10
• Temporary everting eyelid sutures—spastic demodecosis. • Eyelid lesions associated with days. • Most common causes of treatment
entropion; or in puppies before permanent puppy strangles—treat generalized condition. failure—use of subinhibitory antibiotic
surgical correction. • Repair eyelid lacerations. • Atopy—see Atopic Dermatitis. dosages, failure to correct one or more
• Lancing—large abscesses only; lance and Bacterial predisposing factors, early discontinuation of
curette hordeola that resist medical treatment • Based on culture and sensitivity or serologic
medications.
and chalazia that have hardened and cause testing. • Pending results—topical polymyxin PREVENTION/AVOIDANCE
keratitis; manually express infected B and neomycin with 0.1% dexamethasone Depends on cause.
meibomian secretions. ointment (q4–6h) and systemic broad- POSSIBLE COMPLICATIONS
spectrum antibiotic. • Cicatricial lid contracture—results in
Mycotic trichiasis, ectropion, or lagophthalmos.
Microsporium canis infection—see • Spastic entropion—because of blepharo
MEDICATIONS Dermatophytosis. spasm and pain. • Qualitative tear film
DRUG(S) OF CHOICE Parasitic deficiency—loss of proper meibum secretion.
• Recurrence of bacterial infection or FHV-1
Antibiotics Demodicosis, Notoedres infection, sarcoptic
mange—see relevant chapters. blepharoconjunctivitis.
• Systemic—for bacterial eyelid infections
(e.g., cephalexin 20 mg/kg IV q8h). For Idiopathic EXPECTED COURSE AND PROGNOSIS
Bartonella henselae infection in cats, therapy Clinical signs often controlled with topical Depend on cause.
may include doxycycline (10 mg/kg PO q12h polymyxin B and neomycin with 0.1%
for 3 weeks), pradofloxacin (5–10 mg/kg PO dexamethasone (q8–24h or as needed);
q12–24h for 28–42 days), or azithromycin occasionally may need prednisolone (0.5 mg/
(10 mg/kg PO q24h for 3 weeks). • Topical— kg PO q12h for 3–5 days, then taper) and/or MISCELLANEOUS
neomycin, polymyxin B, and bacitracin systemic antibiotic.
combination or chloramphenicol. ZOONOTIC POTENTIAL
CONTRAINDICATIONS • Dermatophytosis.
Congenital • Topical corticosteroids—do not use with
• Sarcoptic mange.
• Topical antibiotic ointment—q6–12h to corneal ulceration. • Many cats with
prevent frictional rubbing of eyelid hairs or presumed idiopathic blepharoconjunctivitis SEE ALSO
cilia on ocular surface. • Regularly flush have FHV-1 infection; topical and systemic • Atopic Dermatitis.
debris from deep medial canthal pocket using corticosteroids may exacerbate infection. • Conjunctivitis—Cats.
saline, lactated Ringer’s solution, or ocular • Oral tetracycline and doxycycline—do not • Conjunctivitis—Dogs.
irrigant. use in puppies and kittens. • Neomycin— • Dermatophytosis.
avoid topical use if possible cause of • Epiphora.
External Trauma • Keratitis—Nonulcerative.
• Topical antibiotic ointment—q6–12h; in
blepharitis. • Neomycin, bacitracin, and
polymyxin—avoid topical ophthalmic use in • Keratitis—Ulcerative.
patients with spastic entropion and blepharo • Red Eye.
spasm until surgical correction. • Systemic cats due to rare but potentially fatal anaphy
antibiotics. lactic reaction. ABBREVIATIONS
PRECAUTIONS • FHV-1 = feline herpesvirus type 1.
Allergic • KCS = keratoconjunctivitis sicca.
• Ectoparasitism—wear gloves; do not
• SH blepharitis—systemic broad-spectrum • SH = Staphylococcus hypersensitivity.
antibiotics and systemic corticosteroids contact ocular surfaces with a drug topically
applied to skin; apply artificial tear ointment • SLE = systemic lupus erythematosus.
(prednisolone 0.5 mg/kg PO q12h for 3–5
days, then taper); many patients respond to to eyes for protection. • Topical gentamicin, Suggested Reading
systemic corticosteroids alone; systemic neomycin, terramycin, and most ointments— Bettany S, Mueller R, Maggs D. Diseases of
cyclosporine (5 mg/kg PO q24h until may cause irritant blepharoconjunctivitis the eyelids. In: Maggs DJ, Miller PE, Ofri
remission, then q48–72h) if refractory to (rare); withdrawal may resolve condition. R, eds., Slatter’s Fundamentals of Veterinary
corticosteroids; failure of treatment—consider POSSIBLE INTERACTIONS Ophthalmology, 6th ed. St. Louis, MO:
injections of Staphylococcus aureus bacterin Staphylococcal bacterin may cause anaphy Saunders, 2018, pp. 127–157.
(Staphage Lysate®). • Infected meibomian lactic reaction (rare). Author Terri L. McCalla
glands—oral tetracycline (15–20 mg/kg PO Consulting Editor Kathern E. Myrna
q8h), doxycycline (3–5 mg/kg PO q12h), or
cephalexin (22 mg/kg PO q8h) for 3 weeks
(the former two are lipophilic and cause Client Education Handout
decreased production of bacterial lipases and FOLLOW-UP available online
irritating fatty acids); topical polymyxin B PATIENT MONITORING
and neomycin with 0.1% dexamethasone • Depends on cause, therapy. • Bacterial—
(q6–8h) or topical 0.02% tacrolimus systemic and topical treatment for at least 3
compounded ointment (q8–12h). Some
Blind Quiet Eye

B
RISK FACTORS IMAGING
• Poorly regulated diabetes mellitus—cataracts. • Ocular ultrasound—may demonstrate
• Related animals with genetic cataracts or PRA. retinal detachment (especially if the ocular
BASICS • Systemic hypertension—retinal detachment. media are opaque) or optic nerve mass lesion.
DEFINITION • CNS hypoxia—blindness may become • Plain skull radiographs—seldom inform
Loss of vision in one or both eyes without apparent after excessively deep anesthesia or ative. • CT or MRI—often helpful with
ocular vascular injection or other externally revival from cardiac arrest. orbital or CNS lesions.
apparent signs of ocular inflammation. DIAGNOSTIC PROCEDURES
PATHOPHYSIOLOGY See Figure 1.
Results from abnormalities in focusing images • Ophthalmic examination with a penlight—
on the retina, the retina detecting an image, DIAGNOSIS usually permits diagnosis of cataracts or retinal
optic nerve transmission, or the brain not detachments severe enough to cause blindness.
interpreting images correctly. • Ophthalmoscopy—may show PRA, late
Signs SARDS, or optic nerve disease; normal exam
SYSTEMS AFFECTED • Anterior segment inflammation and suggests early SARDS, retrobulbar optic
• Nervous. • Ophthalmic. glaucoma—conjunctiva typically injected. neuritis, or a CNS lesion. • Systemic arterial
SIGNALMENT • Young patients—may lack menace responses, blood pressure—determine in patients with
• Dog and cat. • Any age, breed, or sex. but will successfully navigate a maze or visually retinal detachment. • Electroretinography—
• Many causes (e.g., cataracts and progressive track hand movements or cotton balls. differentiates retinal from optic nerve or CNS
retinal atrophy) have a genetic basis and are • Postictal period—transient vision loss. disease. • Cerebrospinal fluid (CSF) tap—
often highly breed and age specific. • Abnormal mentation—may be difficult to may be of value with a neurogenic cause of
• Sudden acquired retinal degeneration determine whether an animal is visual; other vision loss.
syndrome (SARDS)—tends to occur in neurologic abnormalities help localize the lesion.
older dogs. • Optic nerve hypoplasia— Causes
congenital. • Optic neuritis, retinal detachment, SARDS,
SIGNS or visual cortex hypoxia—sudden vision loss TREATMENT
Historical Findings
(over hours to weeks). • SARDS—often • Try to obtain a definitive diagnosis on an
• Vary with underlying cause. • Bumping
preceded by polyuria, polydipsia, polyphagia, outpatient basis before initiating treatment.
into objects. • Clumsy behavior. • Reluctance and weight gain. • PRA—gradual vision loss, • Consider referral before attempting
to move. • Impaired vision in dim light. especially in dim light; apparently acute empirical therapy. • Most causes are not
vision loss with sudden change in environ fatal, but must perform a workup to rule out
Physical Examination Findings ment. • Cataract—either gradual or rapidly potentially fatal diseases. • Reassure client
• Vary with underlying cause. • Decreased or increasing opacification and vision loss in a that most causes of a blind quiet eye are not
absent menace or dazzle response. • Impaired quiet eye. • Optic nerve hypoplasia— painful and that blind animals can lead
visual placing responses. congenital; may be unilateral or bilateral. relatively normal and functional lives.
CAUSES • Optic neuropathy or CNS disease—other • Warn client that the environment should
• Cataracts—entire lens must become opaque signs of neurologic abnormalities. • Pupillary be examined for potential hazards to a blind
to produce complete blindness; incomplete light responses—usually normal with animal. • Advise client that patients with
opacification may reduce performance of cataracts or visual cortex lesions; sluggish to PRA or genetic cataracts should not be bred
visually demanding tasks. • Loss of focusing absent with retinal or optic nerve diseases. and related animals should be examined.
power of the lens—rarely completely blinding; • Ophthalmoscopy—normal with early • Retinal detachment—restrict exercise until
substantial hyperopia (far-sightedness) occurs SARDS, retrobulbar optic neuritis, and higher the retina is firmly reattached. • Calorie-
when the optical power of the lens is not visual pathway lesions; abnormal with retinal restricted diet—to prevent obesity owing to
replaced after lens extraction or if the lens detachment and disorders of optic nerve head. reduced activity level. • Cats with nutritionally
luxates posteriorly out of the pupillary plane CBC/BIOCHEMISTRY/URINALYSIS induced retinopathy—ensure diet has
and into the vitreous. • Retina—SARDS, • Usually normal, unless underlying systemic adequate levels of taurine. • SARDS, PRA,
progressive retinal atrophy (PRA), retinal disease. • Hyperglycemia or glucosuria—may optic nerve atrophy, and optic nerve
detachment, taurine deficiency (cats), note with diabetic cataracts. • Elevated alkaline hypoplasia—no effective treatment.
enrofloxacin toxicity (cats), ivermectin phosphatase (ALP) enzyme activity and • Cataracts, luxated lenses, and some forms
toxicity (dogs, cats). • Optic nerve—optic changes consistent with hyperadrenocorticism of retinal detachment—best treated
neuritis, neoplasia of the optic nerve or (Cushing’s syndrome)—suggest SARDS. surgically.
adjacent tissues, trauma, optic nerve hypoplasia, • Retinal detachment secondary to systemic
lead toxicity, excessive traction on the optic hypertension (cats)—azotemia or changes
nerve during enucleation resulting in trauma consistent with hyperthyroidism.
to the contralateral optic nerve or optic
chiasm (especially cats and brachycephalic OTHER LABORATORY TESTS MEDICATIONS
• Blood lead and serology for deep fungal or DRUG(S) OF CHOICE
dogs). • CNS (amaurosis)—lesions of the
optic chiasm or tract, optic radiation, or viral infections—consider for suspected • Depend on cause. • If workup is declined,
visual cortex. CNS-associated vision loss that optic neuritis (see Optic Neuritis and infectious disease is unlikely, and the likely
occurs at a level higher than the optic chiasm Papilledema). diagnosis is either SARDS or retrobulbar
• Low-dose dexamethasone suppression optic neuritis—consider systemic prednisolone
often has vague visual disturbances in which
the patient has some vision, but clearly does test—may help rule out Cushing’s syndrome (1–2 mg/kg/day PO for 7–14 days, then
not have normal vision. with SARDS. • Sex hormone abnormalities taper); may concurrently administer oral
are common in patients with SARDS. broad-spectrum antibiotic.
(continued) Blind Quiet Eye

B
Blind Quiet Eye
History, physical examination
Ophthalmic examination
Opaque ocular media
Cataracts
Check blood glucose Is the ocular media opaque?
+/– lens extraction
CLEAR OCULAR MEDIA
Is the fundus normal?
NO YES
Pupillary light response

Retinal Detachment Retinal Degeneration Optic Neuropathy
Consider PRA Congenltal Hypoplasia Abnormal
• CBC • Examine related Optic Neuritis
NORMAL
• Chemistry profile animals Consider CNS blindness
Do not breed ERG
• Urinalysis • CBC Rule out hypoxia
• Deep fungal serology Late SARDS • Chemistry profile Consider
• Systemic blood pressure Postinflammatory • Urinalysis • CSF tap NORMAL ABNORMAL
• Chest radiographs • No Rx for any • Deep fungal serology • CT/MRI Optic Neuritls SARDS
• CSF tap Consider
• CT/MRI • CBC
• Blood lead • Chemistry profile
• Urinalysis
• LDDST
Figure 1.
CONTRAINDICATIONS neuritis; may occur weeks, months, or years SEE ALSO

Do not use systemic corticosteroids or other after initial presentation. Optic Neuritis and Papilledema.
immunosuppressive drugs with optic neuritis and POSSIBLE COMPLICATIONS ABBREVIATIONS
retinal detachments that are infectious in origin. • Death. • Permanent vision loss. • Loss of • ALP = alkaline phosphatase. • CSF =
PRECAUTIONS the eye. • Chronic ocular inflammation and cerebrospinal fluid. • PRA = progressive
Pretreatment with corticosteroids may mimic pain. • Obesity from inactivity or as a sequela retinal atrophy. • SARDS = sudden acquired
or mask liver enzyme changes in SARDS. of SARDS. retinal degeneration syndrome.
POSSIBLE INTERACTIONS INTERNET RESOURCES
N/A • https://muffinshalo.com •http://www.
ALTERNATIVE DRUG(S) pepedog.com •https://www.akc.org/expert-
Oral azathioprine 1–2 mg/kg/day PO for 3–7
MISCELLANEOUS advice/health/seven-ways-to-keep-the-light-in-
days, then taper; may be used to treat ASSOCIATED CONDITIONS your-blind-dogs-life
immune-mediated retinal detachments if • SARDS (dogs)—signs similar to those of Suggested Reading
systemic corticosteroids are not effective; hyperadrenocorticism. • Neurologic disease— Maggs DJ, Miller PE, Ofri R. Fundamentals
perform a CBC, platelet count, and liver may note seizures, behavior or personality of Veterinary Ophthalmology, 6th ed. St
enzyme every 1–2 weeks for the first 8 weeks, changes, circling or other CNS signs. Louis, MO: Elsevier, 2018.
then periodically. • Cardiomyopathy (cats)—taurine deficiency. Rubin LF. Inherited Eye Disease in Purebred
AGE-RELATED FACTORS Dogs. Baltimore, MD: Williams & Wilkins,
• PRA and many cataracts—breed-specific ages 1989.
of onset. • SARDS—tends to occur in older Author Paul E. Miller
Consulting Editor Kathern E. Myrna
FOLLOW-UP dogs. • Optic nerve hypoplasia—congenital.
PATIENT MONITORING ZOONOTIC POTENTIAL
• Repeat ophthalmic examinations—as N/A Client Education Handout
required to ensure that ocular inflammation is PREGNANCY/FERTILITY/BREEDING available online
controlled and, if possible, vision is maintained. Corticosteroids and immunosuppressive
• Recurrence of vision loss—common in optic drugs may complicate pregnancy.
Blood Transfusion Reactions

B
Delayed Hemolysis
Immune reaction to RBC antigens (5–14
days after transfusion).
BASICS FOLLOW‐UP
Delayed Nonhemolytic Reaction
OVERVIEW Transmission of blood‐borne disease. PATIENT MONITORING
• Reaction to donor blood cells can result in • Check attitude, rectal temperature, and vital
minor (fever, urticaria) or major (hemolysis, signs before, during, and after transfusion. • For
anaphylactic shock) reactions, usually acute acute hemolytic reactions or septicemia—
but can be delayed. • Can occur with admini- intensive monitoring and supportive care
stration of any blood‐derived product. DIAGNOSIS required. • Measure PCV or hematocrit 2 hours
SIGNALMENT DIFFERENTIAL DIAGNOSIS post transfusion, sooner if clinical signs warrant.
• Dogs and cats. • No sex predilection. • All • Hemolysis—other hemolytic disease PREVENTION/AVOIDANCE
ages affected. (e.g., immune‐mediated hemolytic anemia, • Record any transfusion reaction in the
Babesia, zinc toxicity). • Fever, hypotension— medical file. • Pretransfusion testing: ∘ Screen
SIGNS infectious/inflammatory disease, contamination donors for infectious disease. ∘ Blood type
Acute Nonhemolytic Reaction of IV catheter sites. • Urticaria/pruritis— donors and recipients (imperative in cats).
• Fever, urticaria, erythema, pruritus (in allergic reaction; avoid coadministration of ∘ Cross‐match patients receiving repeated
10–25% of transfusions). • Septic shock from medications during transfusion to distinguish transfusions. • Have standard transfusion
bacterial contamination of blood products. drug vs. transfusion reaction. • Pigmenturia— protocols, dedicated storage for blood products.
• Transfusion‐associated circulatory overload hematuria or myoglobinuria vs. hemoglobinuria. • Transfusion administration should start
(TACO)—dyspnea, cough, cyanosis (congestive CBC/BIOCHEMISTRY/URINALYSIS slowly but be completed within 4 hours.
heart failure). • Transfusion‐associated acute Hemoglobinemia, leukocytosis, thrombocyto- • Leukoreduction of RBC‐containing products
lung injury (TRALI)—dyspnea, cyanosis. penia possible, bilirubinemia, pigmenturia may decrease incidence of reactions. • Older
• Citrate toxicity—facial pruritis, weakness. (hemoglobin/bilirubinuria). stored blood more likely to result in reaction.
• Hyperammonemia—encephalopathy.
OTHER LABORATORY TESTS POSSIBLE COMPLICATIONS
Acute Hemolytic Reaction • Cross‐match to confirm incompatibility. Fulminant hemolysis may cause acute renal
• Occurs in 1–5% of transfusions. • Bacterial culture or microscopic exam failure, multiorgan dysfunction, coagulopa-
• Tachycardia, shock, anaphylaxis, death. ination of blood may reveal contamination. thies, and cardiac arrhythmias.
• Collapse, lethargy, weakness. • Vomiting, • Centrifugation of donor blood may show
diarrhea. • Pigmenturia, potential for EXPECTED COURSE AND PROGNOSIS
hemolysis. • Acute course in most animals;
pigmentary nephropathy. • Restlessness,
hypersalivation, urticaria, facial swelling. nonhemolytic reactions have good prognosis.
• Hemolysis of transfused red blood cells • Prognosis guarded in animals with severe
(RBCs). reactions or hemolysis.
TREATMENT
Delayed Hemolytic Reaction
• Acute, nonhemolytic reaction—stop
Clinical signs of anemia may recur. transfusion: if signs resolve, restart at slower
Delayed Nonhemolytic Reaction rate, if signs recur, discontinue transfusion; if MISCELLANEOUS
Signs of blood‐borne disease (e.g., Babesia, dyspnea, supplemental oxygen; if volume
Mycoplasma haemofelis, Ehrlichia). overload/congestive heart failure, furosemide; SEE ALSO
animals with TRALI may require mechanical Sepsis and Bacteremia.
Cats and previously transfused dogs have ventilation. • Acute, hemolytic reaction—stop ABBREVIATIONS
higher risk of transfusion reactions. transfusion and administer IV fluids to • ATP = adenosine triphosphate. • MHC =
maintain blood pressure and treat shock; in major histocompatibility complex. • RBC =
Acute Nonhemolytic Reaction hypotensive patients, administer isotonic red blood cells. • TACO = transfusion‐
• Anaphylaxis/immune reaction to donor crystalloids (20–30 mL/kg, repeat as associated circulatory overload. • TRALI =
cells, major histocompatibility complex necessary); epinephrine and vasopressor transfusion‐associated acute lung injury.
(MHC) or plasma antigens, release of therapy for severe anaphylaxis.
inflammatory mediators and pyrogens. • RBC Suggested Reading
membrane fragility (from depleted adenosine Hann L, Brown DC, King LG, Callan MB.
triphosphate [ATP]) can result in mechanical Effect of duration of packed red blood cell
destruction during transfusion; degradation of storage on morbidity and mortality in dogs
ATP causes hyperammonemia in stored blood. MEDICATIONS after transfusion: 3,095 cases (2001–2010).
• Contamination of blood can result from DRUG(S) OF CHOICE J Vet Intern Med 2014, 28(6):1830–1837.
lack of aseptic collection or poor storage • For anaphylaxis—IV crystalloid as above,
Maglaras CH, Koenig A, Bedard DL,
conditions. • TACO results from rapid epinephrine 0.01 mg/kg IV. • For urticaria, Brainard BM. Retrospective evaluation of
transfusion or excessive transfusion volume. fever—diphenhydramine (1–2 mg/kg IM); the effect of red blood cell product age on
• Citrate toxicity causes hypocalcemia. dexamethasone sodium phosphate (0.1 mg/kg occurrence of acute transfusion‐related
IV once). • If septic shock suspected—broad‐ complications in dogs: 210 cases (2010–
Acute Hemolysis 2012). JVECC 2017, 27(1):108–120.
• Type II hypersensitivity reaction caused by spectrum IV antibiotics, IV fluid therapy.
• Volume overload—furosemide 2–4 mg/kg
Wardrop KJ. Update on canine and feline blood
naturally occurring or acquired antibodies donor screening for blood‐borne pathogens. J
against donor RBCs (cats have existing IV, oxygen. • Hypocalcemia—calcium
gluconate 50–150 mg/kg IV slowly (monitor Vet Intern Med 2016, 30(1):15–35.
alloantibodies against other blood type, dogs Author Jörg Bucheler
require prior sensitization). • Transfusion of ECG).
damaged RBCs.
Blue‐Green Algae Toxicosis

B
Neurotoxic hemostatic test results. • Diazepam (2–5 mg/
• Strychnine, metaldehyde, avitrol, pyrethrins/ kg IV, repeat in 30 min if necessary) for seizure
pyrethroids, zinc phosphide, bromethalin. control. • Phenobarbital (2–5 mg/kg IV
BASICS • Organophosphorus, carbamate, and q6–12h) for seizure control. • Methocarbamol
OVERVIEW organochlorine insecticides. • Penitrem A, (55–220 mg/kg IV) for muscle relaxation.
• Cyanobacterial blooms can occur in fresh methylxanthines. • Poisonous plants (Brunfelsia Alternative Drugs
and brackish waters, and in backyard ponds spp., cyanide, oleander, poison hemlock). • S‐adenosylmethionine (SAMe)—antioxidant
where algal material is concentrated. • Illicit substances (amphetamine and
and hepatoprotectant; no data on efficacy in
• Nutrient‐rich runoff, increased water derivatives), ephedra‐containing compounds. hepatotoxic cyanotoxin toxicosis available;
temperatures, and stagnant water conditions • Neurotoxic mushrooms.
dose 20 mg/kg PO q24h. • Ascorbic acid and
favor toxic bloom formation. • Blue‐green Dermatotoxic cimetidine—hepatocyte protectors; no data
algae exposure can lead to acute hepato‐ or Other causes of pruritus—allergies, infec on efficacy in hepatotoxic cyanotoxin
neurotoxicosis in animals and humans. • Skin tious, parasitic, dietary, endocrine. poisoning available. • N‐acetylcysteine (NAC)—
irritation following exposure to cyanobacteria‐ antioxidant; no data on efficacy in hepatotoxic
contaminated water may occur. • Hepatotoxic CBC/BIOCHEMISTRY/URINALYSIS
cyanotoxin toxicosis available; glutathione
blue‐green algae poisonings are more Hepatotoxic precursor that can be included in treatment
frequently reported than neurotoxic algal • Elevated serum liver enzymes—alanine regimen for acute hepatic failure at 140 mg/kg
intoxication. • Toxin‐producing transaminase (ALT), aspartate transaminase IV load, followed by 70 mg/kg IV q6h for 7
cyanobacteria include Microcystis, Anabena, (AST), alkaline phosphatase (ALP), bilirubin. treatments.
Aphanizomenon, Oscillatoria, Lyngbya, and • Hypoalbuminemia. • Hypoglycemia.
Planktothrix spp. • Microcystins are hepatotoxic Neurotoxic and Dermatotoxic
blue‐green algae toxins that have been found No specific changes.
worldwide. • Anatoxins, which include
anatoxin‐a and anatoxin‐as, are neurotoxic DIAGNOSTIC PROCEDURES FOLLOW‐UP
blue‐green algae toxins. Morphologic algal ID in suspect water, algal PATIENT MONITORING
material, or stomach content. Positive ID • Hepatotoxic—liver enzymes/function,
SIGNALMENT confirms hazard but is not confirmatory for
• Dogs—no breed, sex, or age predilection.
coagulation status. • Neurotoxic—
the toxin because toxicity is strain specific. thermoregulation, respiratory function,
• Cats—no cases reported.
Hepatotoxic blood gases.
SIGNS • Detection of algal material on fur or in PREVENTION/AVOIDANCE
Hepatotoxic stomach contents. • Analysis of stomach • Deny access to water with visible algal
• Diarrhea, weakness, shock. • Rapid contents and water/algal source for microcystins. blooms. • Remove algal blooms from ponds
progression to depression, coma, and death. Neurotoxic immediately and discard material safely.
Neurotoxic • Detection of anatoxin‐a in gastric contents, EXPECTED COURSE AND PROGNOSIS
• Onset of rigidity and muscle tremors within urine, bile, and suspect source material. • Prognosis poor to guarded for hepatotoxic
minutes to a few hours after exposure. • Depressed blood cholinesterase activity and neurotoxic; good for dermatotoxic.
• Rapid progression to paralysis, cyanosis, with anatoxin‐as poisoning. • Rapid onset and progression; often lethal.
and death.
Dermatotoxic
• Pruritus, erythema, urticaria. • Secondary
skin infection. TREATMENT MISCELLANEOUS
• No antidote available. • Rapid onset typically
CAUSES & RISK FACTORS ABBREVIATIONS
prevents timely therapeutic intervention.
• Access to and ingestion of toxin‐ • ALP = alkaline phosphatase. • ALT =
• Gastrointestinal decontamination with
contaminated water and/or algal material. alanine transaminase. • AST = aspartate
activated charcoal can be attempted, but efficacy
• Exposure to dietary supplements containing transaminase. • NAC = N‐acetylcysteine.
not known. • Hepatotoxic—supportive care,
the blue‐green algae Spirulina platensis and • SAMe = S‐adenosylmethionine.
close monitoring, and case‐specific IV fluids to
Aphanizomenon flos aquae that are contam
correct electrolytes and hypoglycemia, vitamin INTERNET RESOURCES
inated with microcystins. • Blooms more
K1, and plasma transfusions. • Neurotoxic— http://www.cdc.gov/habs
common in nutrient‐rich water in warmer
supportive care and seizure control. Suggested Reading
months. • Blooms concentrated through
• Dermatotoxic—supportive care and Bautista AC, Moore CE, Lin Y, et al.
wind or by removal into containers. • Certain
treatment for secondary skin infections. Hepatopathy following consumption of a
algae reside in the benthic zone, e.g., in
sediment; dogs mouthing material such as commercially available blue‐green algae
rocks from sediment can be at risk. dietary supplement in a dog. BMC Vet Res
2015, 11:136.
MEDICATIONS Puschner B, Bautista AC, Wong C.
DRUG(S) OF CHOICE Debromoaplysiatoxin as the causative agent of
• Activated charcoal—1 g/kg PO q6-8h until dermatitis in a dog after exposure to freshwater
DIAGNOSIS in California. Front Vet Sci 2017, 4:50.
2–3 days post ingestion; mix activated charcoal
DIFFERENTIAL DIAGNOSIS in water at 1 g/5 mL of water. • IV fluids— Authors Birgit Puschner and Adrienne
Hepatotoxic maintain hydration, induce diuresis, correct C. Bautista
• Amanitins, xylitol, cycad palms, hypoglycemia. • Dextrose—50% dextrose Consulting Editor Lynn R. Hovda
acetaminophen, manganese, pennyroyal oil, 1 mL/kg IV slow bolus (1–3 min). • Vitamin
cocklebur. • Other causes of acute liver K1—0.5–1.5 mg/kg SC/IM q12h; 1–5 mg/kg
failure—infectious, metabolic, dietary. PO q24h. • Blood products—dependent on
available online
Botulism
B
• Definitive diagnosis is based on detection
of botulinum toxin in serum, feces, vomitus,
BASICS or ingested food sample; by neutralization FOLLOW-UP
OVERVIEW test in small rodents; or by in vitro test that PATIENT MONITORING
• Paralytic illness caused by preformed measures toxin antigenicity rather than Monitor patients for respiratory failure,
neurotoxin produced by bacterium toxicity. • Detection of anti-C botulinum aspiration pneumonia, progressive lower
Clostridium botulinum (Gram +, anaerobe) neurotoxin antibodies may help support motor neuron signs, urinary tract infection,
contained in uncooked food, carrion, and clinical diagnosis. and ocular complications.
contaminated or improperly stored silage. IMAGING PREVENTION/AVOIDANCE
• Most cases in dogs caused by Clostridium Thoracic radiographs—possible megaesophagus • Prevent access to carrion and feed dogs
botulinum neurotoxin serotype C; neurotoxin and/or signs of aspiration pneumonia. cooked food. • Avoid contact with spoiled
interferes with release of acetylcholine at raw meat. • Samples should be refrigerated
neuromuscular junction, resulting in diffuse DIAGNOSTIC PROCEDURES
(not frozen) and manipulated with caution,
lower motor neuron signs. • Heavy molecular • Electromyography may reveal fibrillation
since humans are also sensitive to the toxin.
weight of the toxin seems to preclude its potentials and positive sharp waves in affected
transfer to placenta. muscles. • Motor nerve conduction velocity POSSIBLE COMPLICATIONS
may be normal or decreased, with reduced • Respiratory failure and death in severe cases.
SIGNALMENT amplitude of evoked muscle action potentials; • Aspiration pneumonia from megaesophagus
Dogs (naturally infected) and cats (experiment compound muscle action potentials can be and regurgitations. • Keratoconjunctivitis
ally infected except for one case report of decreased after low-frequency repetitive nerve sicca and corneal ulceration. • Prolonged
natural Clostridium botulinum type C stimulations. recumbence—pulmonary atelectasia and
toxicosis). infection; decubital sores; urine scalding.
SIGNS EXPECTED COURSE AND PROGNOSIS
• Maximum severity of signs usually reached
Historical Findings
• Signs appear a few hours to 6 days after
within 12–24 hours. • Neurologic signs disappear
toxin ingestion. • Other dogs living in the TREATMENT in reverse order of appearance; complete recovery
same environment may be affected. • Acute, • If recent ingestion—gastric lavage, usually occurs within 1–3 weeks, and requires the
symmetric, progressive weakness develops, cathartics (avoid agents containing formation of new nerve terminals and functional
starting in the pelvic limbs and ascending to magnesium), or enemas may be useful. neuromuscular junctions.
the trunk, thoracic limbs, neck, and muscles • Mildly affected dogs recover over a period
innervated by the cranial nerves; severe of several days with supportive treatment
tetraparesis or tetraplegia ensues. including physical therapy, frequent
Physical Examination
turning, good bedding (to prevent decubital MISCELLANEOUS
sores), bladder care (catheterization),
• Possible increased or decreased heart rate. SEE ALSO
artificial tears (to prevent corneal ulceration),
• In severe cases—diaphragmatic respiration. • Coonhound Paralysis (Acute
and feeding from an elevated position
Neurologic Examination Findings (when megaesophagus present). • Dogs Polyradiculoneuritis). • Myasthenia Gravis.
• Mental status—normal. • Cranial nerves— with respiratory difficulties require • Snake Venom Toxicosis—Coral Snakes.
may reveal sluggish pupillary light reflexes intensive care monitoring with arterial • Tick Bite Paralysis.
(PLR), diminished palpebral reflexes, blood gas, intermittent esophageal suction, ABBREVIATIONS
decreased jaw tone, decreased gag reflex, alimentation by nasogastric or gastrotomy • PLR = pupillary light reflex.
salivation, and dysphonia. • Gait and tube, and eventually ventilatory support.
posture—a stiff, short-stride gait (no ataxia) is
Suggested Reading
Añor S. Acute lower motor neuron tetrapare
initially observed until recumbence develops
sis. Vet Clin North Am Small Anim Pract
(usually within 12–24 hours). • Spinal
2014, 44(6):1201–1222,
reflexes—decreased to absent with decreased
Barsanti J, Greene C, eds. Infectious Diseases
muscle tone (to atonia) and muscle atrophy.
• Autonomic signs—mydriasis with decreased
MEDICATIONS of the Dog and Cat, 4th ed. St. Louis, MO:
DRUG(S) OF CHOICE Saunders Elsevier, 2012, pp. 416–422.
PLR, decreased lacrimation, ileus, and urine
• Type C antitoxin may cause anaphylaxis; Elad D, Yas-Natan E, Aroch I, et al. Natural
retention or frequent voiding of small
not effective when the toxin is already fixed Clostridium type C toxicosis in a group of cats.
volumes. • No hyperesthesia.
at the nerve ending. • Antibiotics are not J Clin Microbiol 2004, 42(11):5406–5408.
recommended since they might increase the Lamoureux A, Pouzot-Nevoret C, Escriou C. A
release of toxins through bacterial lysis or case of type B botulism in a pregnant bitch. J
by promoting intestinal infection; to be Small Anim Pract 2015, 56(5):348–350.
DIAGNOSIS used only if secondary infections occur. Silva R, Martins R, Assis R, et al. Type C
botulism in domestic chickens, dogs and
DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS/POSSIBLE black-pencilled marmoset (Callithrix
• Acute canine polyradiculoneuritis penicillata) in Minas Gerais, Brazil.
INTERACTIONS
(coonhound paralysis). • Myasthenia gravis. Anaerobe 2018, 51:47–49.
Aminoglycosides, procaine penicillin,
• Tick bite paralysis. • Coral snake venom Uriarte A, Thibaud J, Blot S. Botulism in 2
tetracyclines, phenothiazines, antiarrhythmic
toxicity. • Dumb form of rabies. • Lasalocid urban dogs. Can Vet J 2010, 51:1139–1142.
agents, and magnesium should be avoided
(growth promoter in ruminants) toxicosis. Author Hélène L.M. Ruel
(neuromuscular transmission blockade).
CBC/BIOCHEMISTRY/URINALYSIS Acknowledgment The author and book
Usually normal. editors acknowledge the prior contribution of
Roberto Poma (deceased).
Brachial Plexus Avulsion

B
contusion (neurapraxia). • Brachial plexus motion, massage therapy. • Monitor
tumor—usually chronic, progressive onset. noncomplicated cases for 4–6 months before
• Brachial plexus neuritis or neuropathy— considering amputation.
BASICS rare, bilateral deficits, unknown etiology;
OVERVIEW acute onset; no trauma. • Fibrocartilaginous
• Trauma with traction and/or severe embolic myelopathy—deficits of ipsilateral
abduction of a forelimb causes avulsion of hind limb and mild deficits of contralateral
forelimb and hind limb are usually present.
MEDICATIONS
nerve rootlets from their spinal cord attach-
ment. • Ventral (motor) nerve roots are more • Migrating foreign body – slow onset and no DRUG(S) OF CHOICE
susceptible than dorsal (sensory) roots. • It is history of trauma. • Pure radial nerve Prednisolone (prednisone)—1-week anti-
important to rule out nerve root avulsions in paralysis caused by fracture of humerus or inflammatory course may decrease early
traumatized animals that are not able to bear first rib—no nerve root sign. • Lateralized edema and favor healing of reversible injuries.
weight on a forelimb, especially before intervertebral disc protrusion.
surgical repair of orthopedic injuries. IMAGING
SIGNALMENT CT or MRI—visualize lesion; rarely needed
• Dogs and cats. • No age, sex, or breed for diagnosis. FOLLOW-UP
predilection. DIAGNOSTIC PROCEDURES POSSIBLE COMPLICATIONS
SIGNS • Clinical—history of trauma with sudden • Skin excoriation and secondary infection—
• Depend on the extent and distribution of onset of typical neurologic deficits. • Define from trauma to unprotected paw. • Trophic
rootlet damage. • Motor signs—paresis/ involved spinal nerve roots—map motor and ulcers—thin, traumatized skin, especially over
weakness (partial damage) to paralysis sensory deficits; note signs of Horner’s arthrodesis sites. • Paresthesia may lead to
(complete ventral root avulsion). • Sensory syndrome; determine if cutaneous trunci self-mutilation.
signs—decreased to absent pain perception reflex is present. • Electromyography (EMG) EXPECTED COURSE AND PROGNOSIS
(dorsal root damage). • Muscle atrophy— and nerve conduction studies (NCS) may • Preserved pain sensation (dorsal roots
begins within a week of injury. • Complete help further define deficits and detect signs of intact)—suggests less severe injury to ventral
avulsion—spinal nerves C5 to T2; most recovery—from 5–7 days post injury, EMG nerve roots. • Cranial avulsion—better
common; combines cranial and caudal avulsion shows denervation in affected muscles. prognosis with preserved sensation to distal
deficits. • Cranial avulsion—C5 to C7 nerves: PATHOLOGIC FINDINGS limb and ability to bear weight. • Complete
supraspinatus and infraspinatus muscle atrophy, • Ventral and dorsal root avulsions— avulsion—poor prognosis for recovery,
loss of shoulder and elbow movement flexion intradurally at level of root–spinal cord amputation likely. • Rarely, mild cases may
(dropped elbow), analgesia of craniodorsal junction (most fragile area because it lacks resolve after 2–3 months.
scapula and medial forearm, possible diaphragm protective perineurium). • Neuroma
hemiplegia detected by fluoroscopy (phrenic formation may develop over time on pial
nerve roots C5 to C7); if roots C8 to T2 are surface of spinal cord.
preserved, weight bearing remains almost
normal. • Caudal avulsion—spinal nerves C7 MISCELLANEOUS
to T2: inability to bear weight with knuckling SEE ALSO
over dorsum of paw; if C5 to C7 are spared, the Polyneuropathies (Peripheral Neuropathies).
limb is held in a flexed position and there is TREATMENT
analgesia distal to the elbow (except for a small ABBREVIATIONS
Appropriate Health Care
area on the medial aspect of the forearm); T1 to • EMG = electromyography. • NCS = nerve
• No specific treatment. • Outcome depends
T2 involvement causes an ipsilateral partial conduction studies.
on initial damage. • Amputation of limb—
Horner’s syndrome (anisocoria only) and lack may be necessary for patients showing Suggested Reading
of ipsilateral cutaneous trunci reflex (reflex complications (infections/self-mutilation, Bailey CS. Patterns of cutaneous anesthesia
present contralaterally). • Bilateral avulsion— likely as a result of paresthesia) and no associated with brachial plexus avulsions in
rarely encountered, caused by a significant fall improvement. • Carpal fusion (arthrodesis) the dog. JAVMA 1984, 185:889–899.
with sternal landing and splaying of limbs. and transposition of biceps muscle tendon— Braund KG. Neuropathic disorders. In:
• Over time, complications of self-trauma may consider only with adequate function of Braund KG, ed., Clinical Neurology in
occur as a result of paresthesia in the most triceps and musculocutaneous muscles. Small Animals: Localization, Diagnosis and
severe cases. Treatment. Ithaca, NY: IVIS, 2003. http://
Nursing Care
CAUSES & RISK FACTORS www.ivis.org/advances/Vite/braund20b/
• Protective wrap or boot to protect distal
Trauma—road accident; hung by foot; chapter_frm.asp.
paw if patient walks a lot/walks on rough Walmsley G, Scurrell E, Summers B, et al.
dragged; fall. surfaces—increased skin fragility and lack of Foreign body induced neuritis masquerad-
protective reflexes due to sensory deficits can ing as a canine brachial plexus nerve sheath
result in severe excoriations when animal tumour. Vet Comp Orthop Traumatol
walks on affected limb. • Early and sustained 2009, 22(5):427–429.
DIAGNOSIS physical therapy—crucial to prevent severe Author Christine F. Berthelin-Baker
muscle atrophy and tendon contraction to
DIFFERENTIAL DIAGNOSIS keep joints and muscles mobile during
• Brachial plexus trauma without avulsion— recovery of reversible injuries; passive range of
rare; temporary deficit owing to root
Brachycephalic Airway Syndrome

B
concurrent disease or exacerbating circumstances. infection, nasopharyngeal abscess.
• Laryngeal collapse reported in brachycephalic • Neoplasia obstructing the nasopharynx,
breed puppies as young as 6–7 months. glottis, larynx, or trachea. • Laryngeal
BASICS paralysis. • Pharyngeal mucocoele.
Predominant Sex
DEFINITION • Nasopharyngeal polyp or cyst.
No sex predilection.
Partial upper airway obstruction in brachy CBC/BIOCHEMISTRY/URINALYSIS
cephalic dogs and cats caused by any of the SIGNS
CBC—usually normal, but polycythemia
following: stenotic nares, overlong soft palate, Historical Findings can occur with chronic hypoxia, and
everted laryngeal saccules, and laryngeal • Snoring, stridor, stertorous breathing. leukocytosis if concurrent infection or
collapse. Hypoplastic trachea can also be • Tachypnea, frequent panting. • Coughing severe stress.
present and worsen respiratory distress. and gagging. • Difficulty eating and
swallowing. • Ptyalism, regurgitation, and OTHER LABORATORY TESTS
PATHOPHYSIOLOGY • Arterial blood gas—to diagnose respiratory
• In normal dogs, the upper airway accounts vomiting. • Syncope or collapse.
acidosis and hypoxemia, and response to
for 50–70% of total airway resistance. Brachy- Physical Examination Findings oxygen supplementation. • Pulse oximetry—
cephalic breeds have increased upper airway • Stridor and stertorous breathing. to diagnose hypoxemia.
resistance due to stenosis of nares, aberrant • Stenotic nares—medial collapse of lateral
formation of nasal conchae, and presence of nasal cartilage. • Increased respiratory IMAGING
nasopharyngeal turbinates. Skull bones are effort—retraction of the commissures of Radiographic Findings
shortened in length but normal in width, and lips, open-mouth breathing or constant • If stable, cervical and thoracic radiographs
soft tissues are not proportionately reduced, panting, increased respiratory rate, abduction recommended. • Cervical radiographs may
resulting in redundant tissue and narrowed air of forelimbs, increased abdominal show thickened, elongated soft palate and
passages. • Increased airway resistance leads to component of respiration, recruitment of suggest tracheal hypoplasia. • Thoracic
more negative intra-airway pressures—may result secondary muscles of respiration. • In severe radiographs can reveal aspiration pneumonia,
in secondary eversion of laryngeal saccules, distress, may see paradoxical abdominal pulmonary edema, air in esophagus, and
further elongation of palate, and laryngeal movement, inward collapse of intercostal hypoplastic trachea (TD/TI = tracheal
collapse. • Recruitment of pharyngeal dilator muscles during inspiration, orthopnea, and diameter at the level of thoracic inlet/thoracic
muscles (sternohyoid) becomes necessary to cyanosis. Hyperthermia may be present. inlet distance, which is the distance from the
maintain airway patency; sleep apnea may occur sternum to the ventral surface of TI. A ratio
CAUSES
secondary to relaxation of these muscles. <0.13 in bulldogs and <0.16 in other brachy-
• Inherited or congenital defects in
SYSTEMS AFFECTED conformation. • Elongated soft palate—over cephalic breeds suggests hypoplastic trachea).
• Respiratory—respiratory distress, hypox 90% of surgical cases in dogs. • Stenotic Fluoroscopy
emia, hypercarbia, hyperthermia, aspiration nares—about 50% of dogs; most common Gives information about degree of dynamic
pneumonia, noncardiogenic pulmonary defect in cats. • Aberrant formation of rostral pharyngeal obstruction by palate and
edema from airway obstruction. and caudal nasal conchae. • Presence of concurrent disease such as collapsing
• Cardiovascular—cardiovascular collapse if nasopharyngeal turbinates (20% of dogs) trachea (uncommon in brachycephalic
complete airway obstruction or severe hyper- and 100% of English bulldogs. • Laryngeal dogs).
thermia occurs. • Gastrointestinal—may be disease—everted laryngeal saccules (>50% DIAGNOSTIC PROCEDURES
reluctant to eat or drink; increased airway of dogs) and/or laryngeal collapse (∼10%
resistance can exacerbate hiatal hernia, of dogs). Laryngoscopy/Pharyngoscopy
gastroesophageal reflux, and esophagitis. • Performed under general anesthesia. • Due
RISK FACTORS to risk of airway obstruction, owner should
GENETICS • Breed. • Obesity—worsens airway be prepared for surgical intervention if
Brachycephalic head shape—inherited defect obstruction, associated with poorer outcome deemed necessary. • Overlong soft palate
in development of skull bones perpetuated by postoperatively, and may contribute to gastro- extends more than just a few millimeters
selective breeding. esophageal reflux and aspiration pneumonia. beyond tip of epiglottis and hangs down
INCIDENCE/PREVALENCE • Excitement and/or warm, humid weather— into glottis. • Soft palate is often thickened
• Dogs—common in brachycephalic breeds. increased panting can lead to airway edema, and inflamed. • May have inflammation and
• Cats—less commonly severe enough to further compromise of the lumen, and edema of arytenoid cartilages. • Everted
require treatment. hyperthermia. • Exercise—dogs are often laryngeal saccules are diagnosed by visual
exercise intolerant due to airway compromise izing two smooth, round, glistening masses
GEOGRAPHIC DISTRIBUTION and hypoxia. • Sedation—relaxation of
Worldwide in ventral half of laryngeal opening—they
muscles of pharynx and palate can cause often obscure visualization of vocal folds.
SIGNALMENT complete airway obstruction. • Respiratory • Laryngeal collapse can also be seen.
infection or concurrent pulmonary disease— • Flexible endoscopy with retroflexed view
Species
will cause further respiratory compromise. of nasopharynx can detect nasopharyngeal
Dog and cat.
• Endocrine disease (hypothyroidism and turbinates.
Breed Predilections hyperadrenocorticism)—could worsen weight
• Dogs—brachycephalic breeds (English gain and panting. Tracheoscopy
bulldogs most common—up to 55% of • Can reveal hypoplastic trachea with overlap
breed, French bulldog, pug, Boston terrier); of dorsal tracheal rings and dorsal tracheal
Norwich terriers and Cavalier King Charles membrane. • Collapsing trachea can also be
spaniels affected by a variant of the syndrome. diagnosed.
• Cats—Persians and Himalayans.
DIAGNOSIS
CT Scan
Mean Age and Range
DIFFERENTIAL DIAGNOSIS Can identify and grade aberrant nasopharyngeal
• Foreign bodies of nasopharynx, larynx, or turbinates.
• Young adults, most diagnosed by 2–3 years.
• If diagnosed later than 4 years, look for
trachea. • Infection—upper respiratory
(continued) Brachycephalic Airway Syndrome

B
trimming all mucosal tissue with curved for dogs that have correction of both stenotic
scissors. • Severe laryngeal collapse might nares and elongated soft palate. • Without
require cricoarytenoid and thyroarytenoid surgery, prognosis poor due to continued
TREATMENT caudolateralization or permanent tracheostomy. progression of acquired components of
APPROPRIATE HEALTH CARE brachycephalic airway syndrome. • Lifelong
• Surgery recommended for patients with avoidance of risk factors recommended.
significant clinical signs or to prevent
progressive respiratory dysfunction. • Severe
respiratory distress requires rapid intervention MEDICATIONS
including O2 supplementation, cautious use of DRUG(S) OF CHOICE MISCELLANEOUS
antianxiety medication. • If hyperthermic, cool • Dexamethasone sodium phosphate for
via convective losses by wetting patient with 12–24h pre- or postoperatively at 0.1 mg/kg ASSOCIATED CONDITIONS
cool water and placing fan to blow over them; IV q12–24h to reduce edema and inflammation. • Aspiration pneumonia. • Heat stroke.
administer IV fluids, up to a shock rate if • Broad-spectrum antibiotics indicated if • Hiatal hernia. • Hypoplastic trachea.
extremely hyperthermic (T° >106 °F [41 °C]). aspiration pneumonia present until culture and AGE-RELATED FACTORS
• If complete airway obstruction, immediate sensitivity results obtained. • Omeprazole Older dogs may have a worse outcome
orotracheal intubation and/or temporary 0.7 mg/kg q24h or pantoprazole 1 mg/kg postoperatively, but most have some
tracheostomy is indicated. • Dexamethasone q24h, cisapride 0.2 mg/kg q8h, and sucralfate improvement.
sodium phosphate can be administered 0.5–1 g q12h for dogs with concurrent
(0.1 mg/kg IV) to reduce inflammation. PREGNANCY/FERTILITY/BREEDING
esophagitis, gastritis, and/or duodenitis.
Enlarged abdomen and pressure on the
NURSING CARE CONTRAINDICATIONS diaphragm in the pregnant bitch can further
• Patients require 24-hour monitoring Overuse of steroids can lead to panting, compromise respiratory function by
because of risk of acute airway obstruction weight gain, and gastrointestinal ulceration, decreasing tidal volume.
and death. • Monitor respiratory rate, effort, which can exacerbate signs of brachycephalic
heart rate, pulse quality, mucous membrane INTERNET RESOURCES
airway syndrome.
color, capillary refill time, temperature, and https://www.acvs.org/small-animal/
PRECAUTIONS brachycephalic-syndrome
other physical parameters before and after
Sedation should be used with caution because
surgery. • Pulse oximetry and arterial blood
of risk of upper airway obstruction with
Suggested Reading
gases, depending on severity of condition. Ginn JA, Kumar MSA, McKiernan BC,
muscle relaxation.
• Administer IV fluids at maintenance rate Powers BE. Nasopharyngeal turbinates in
and minimize handling and stress. • O2 brachycephalic dogs and cats. J Am Anim
therapy and cooling as necessary. Hosp Assoc 2008, 44(5):243–249.
ACTIVITY Monnet E. Brachycephalic airway syndrome.
Usually self-limited. FOLLOW-UP In: Slatter D, ed., Textbook of Small Animal
Surgery, 3rd ed. Philadelphia, PA: Saunders,
DIET PATIENT MONITORING 2003, pp. 808–813.
• Weight loss is recommended if overweight. Postoperatively, 24-hour monitoring to Poncet CM, Dupre GP, Freiche VG, Bouvy
• For obese, stable patients, weight loss is observe for airway swelling and obstruction BM. Long-term results of upper respiratory
recommended prior to surgery. that may require temporary tracheostomy. syndrome surgery and gastrointestinal tract
CLIENT EDUCATION PREVENTION/AVOIDANCE medical treatment in 51 brachycephalic
• Avoidance of risk factors is critical. • Inform • Selection by breeders for dogs without dogs. J Small Anim Pract 2006,
owners that dogs with brachycephalic airway severe conformational changes—difficult 47(3):137–142.
syndrome are at increased anesthetic risk, because breed standards encourage these. Poncet CM, Dupre GP, Freiche VG, et al.
especially if obese, or have cardiac disease or • Avoid risk factors, particularly weight gain. Prevalence of gastrointestinal tract lesions in
aspiration pneumonia. • Inform owners that brachycephalic dogs with upper respiratory
surgery often improves but does not normalize syndrome: clinical study in 73 cases (2000–
• Hyperthermia and heat stroke. • Aspiration
airway. 2003). J Small Anim Pract 2005, 46:273–279.
pneumonia. • Death in about 10% of
Riecks TW, Birchard SJ, Stephens JA. Surgical
SURGICAL CONSIDERATIONS patients from airway disease. • Most common
correction of brachycephalic syndrome in
• Evaluation for elongated soft palate postoperative complication is airway swelling
dogs: 62 cases (1991–2004). J Am Vet Med
performed under general anesthesia when and obstruction within first 24 hours, may
Assoc 2007, 230(9):1324–1328.
patient is stable. • Temporary tracheostomy necessitate temporary tracheostomy.
White RN. Surgical management of laryngeal
can be placed to facilitate exposure or to treat • Continued respiratory difficulty after
collapse associated with brachycephalic
airway obstruction. • Stenotic nares are corrective surgery. • Excessive resection of
airway obstruction syndrome in dogs.
corrected by resection of a wedge of the palate resulting in nasal aspiration of food
J Small Anim Pract 2012, 53:44–50.
dorsolateral nasal cartilage and planum; contents due to inability to close pharynx
Authors David A. Puerto and Lori S.
hemorrhage is controlled with pressure during swallowing. • Progressive laryngeal
Waddell
followed by closure of the surgical wound with collapse resulting in need for permanent
Consulting Editor Elizabeth Rozanski
3 or 4 sutures of 3-0 or 4-0 absorbable suture tracheostomy.
material. • Elongated soft palate is resected EXPECTED COURSE AND PROGNOSIS
using scissors, carbon dioxide laser, or bipolar • Prognosis good for improvement in Client Education Handout
sealing device; remove only enough to allow breathing (80% or more have good to excellent available online
contact of center of soft palate with tip of results), but airway still abnormal. • Prognosis
epiglottis. • Sacculectomy performed by better for dogs other than English bulldogs and
grasping tissue with Allis tissue forceps and
Brain Injury
B
implies progression from intracranial bleeding,
cerebral edema, ischemia. • Seizure activity—
cerebral or diencephalon involvement.
BASICS DIAGNOSIS
DEFINITION • Evidence of head trauma—open wounds, DIFFERENTIAL DIAGNOSIS
• Traumatic—external forces.• Nontraumatic— epistaxis, blood in ear canal. • Cardiac or Systemic causes of altered states of conscious-
hypoxia, metabolic disorders, vascular disruption, respiratory insufficiency—hypoxia, cyanosis, ness or central vestibular signs—metabolic
infection, toxicity, neoplasia. • Primary—direct hypoventilation. • Poor perfusion—weak pulse, disease; toxins; drugs; infection.
initial insult when tissue and vessels are pale mucous membranes. • Skull palpation— CBC/BIOCHEMISTRY/URINALYSIS
stretched, compressed, or torn. • Secondary— fracture, open fontanelle. • Sustained • Reflect systemic effects of neurologic signs.
alterations of brain vasculature and tissue bradycardia—midbrain, pontine, or medullary • Alterations in serum sodium suggest central
following primary injury. lesion. • Cushing reflex—bradycardia and ADH abnormalities.
PATHOPHYSIOLOGY hypertension. • Ecchymosis, petechiae, retinal
• Acceleration, deceleration, and rotational hemorrhages, or distended vessels—hypertension,
• Arterial blood gas. • Coagulation profile.
forces traumatize brain tissue. • The brain has coagulopathy. • Papilledema—cerebral edema.
• Infectious disease titers.
high oxygen and glucose requirements; • Retinal detachment—infectious, neoplastic,
reduced blood flow puts it at great risk for or hypertensive cause. IMAGING
hypoxia. • Oxygen delivery dependent on • Skull radiographs—detect fractures, lytic
Neurologic Examination Findings
cerebral blood flow (CBF) and cerebral lesion. • CT—detect acute hemorrhage,
perfusion pressure (CPP) (= mean arterial Mental Status infarcts, fractures, lytic lesion, penetrating
pressure [MAP] – intracranial pressure [ICP]). • Level of consciousness and cranial nerve foreign bodies, hydrocephalus, herniation.
• Intracranial bleeding, edema (vasogenic and deficits—cerebral cortex (better prognosis), • MRI—detect cerebral edema, hemorrhage,
cytotoxic), vasodilation, and/or vasospasms midbrain/brainstem, or multifocal. • Postural mass, hydrocephalus, infiltrative diseases,
increase ICP, causing low CBF, ischemia, brain changes—decerebrate rigidity with midbrain inflammation, herniation, fractures.
swelling, and herniation; slow, progressive lesion; decerebellate rigidity with cerebellar • Ultrasound optic disk—more than 3 mm
increase in ICP better tolerated than small, lesion. • Peracute focal deficits—vascular or diameter may be associated with brain edema.
acute rise. • Hypotension, hypoxia—major neoplastic causes.
contributors to secondary injury. Pupillary Light Reflexes • ECG—detects arrhythmias. • BP—assess
SYSTEMS AFFECTED • Miotic responsive pupils—cerebral or perfusion. • Cerebrospinal fluid (CSF)
• Nervous—altered mentation, cranial nerve diencephalic lesion (rule out traumatic analysis—if cause unknown and no contra-
deficit, seizures, twitching, postural changes. uveitis, Horner’s syndrome). • Pinpointed indications.
• Cardiovascular—arrhythmia. • Endocrine/ unresponsive pupils—diencephalic, pontine,
PATHOLOGIC FINDINGS
metabolic—alteration in antidiuretic hormone or medullary lesion. • Dilated unresponsive
• Brain edema, inflammation. • Herniation.
(ADH) release and sodium concentration; central pupil(s) or midpoint fixed unresponsive
• Hemorrhage. • Hydrocephalus. • Infarct.
temperature dysregulation; insulin resistance; pupils—midbrain lesion.
• Laceration, contusion. • Hematoma. • Skull
depletion of cortisol. • Ophthalmic—changes in Cranial Nerves fracture, lytic lesion. • Necrosis. • Apoptosis.
eye position, eye movements, pupillary light • Normal with altered mentation—
reflex, papilledema. • Respiratory—hyper‐ or cerebrum/diencephalic lesion. • CN II—loss
hypocapnea; abnormal breathing patterns; of menace and dazzle response with dilated
neurogenic pulmonary edema. unresponsive pupils; cranial forebrain. • Loss
of physiologic nystagmus—brainstem lesion. TREATMENT
• Head and neck injuries found in up to 34% • CN III—midbrain lesion. • CN V–XII— APPROPRIATE HEALTH CARE
of dogs and cats suffering blunt force trauma. pontine or medullary lesion. • Goals of therapy—support oxygenation and
• Head trauma reported in up to 25% of dogs Respiratory Patterns ventilation; maintain BP and CPP; decrease
with severe blunt force trauma and in 50% of • Cheyne‐Stokes—severe diffuse cerebral or ICP; decrease cerebral metabolic rate.
dogs and cats injured by motor vehicles and diencephalon lesion. • Hyperventilation— • Maintain systolic BP >90 mmHg and
crush injuries. • Additional causes— midbrain lesion. • Ataxic or apneustic— partial pressure of carbon dioxide (PCO2) at
penetrating injuries, fall from heights, human‐ pontine or medullary lesion. 35–40 mmHg; with suspected elevated ICP,
inflicted trauma. • Parenchymal and hyperventilation to 32–35 mmHg.
CAUSES • Maintain partial pressure of oxygen (PaO2)
extradural hematomas found in 10% of dogs
• Trauma. • Prolonged hypoxia or ischemia. >60 mmHg, arterial oxygen saturation (SaO2)
and cats with signs of mild head injury and in
• Prolonged shock. • Severe hypoglycemia. >90%, peripheral oxygen saturation (SpO2)
up to 80% with severe head injury.
• Prolonged seizures. • Severe hyper‐ or >94%. • Avoid cough or sneeze reflex during
SIGNALMENT hypothermia. • Alterations in serum osmolality. intubation or nasal oxygen supplementation;
Species • Toxins. • Neoplasia. • Hypertension. lidocaine (dogs: topical and 1–2 mg/kg IV)
Dog and cat. • Hemorrhage. • Inflammatory, infectious, before. • Do not compress jugular veins.
immune‐mediated diseases. • Thiamin • Orotracheal intubation if gag reflex lost.
SIGNS deficiency. • Hydrocephalus. • Parasitic
migration. NURSING CARE
Historical Findings
• Aggressive therapy for midbrain/brainstem
• Determine cause—trauma, cardiac arrest, RISK FACTORS lesion or declining neurologic signs. • Overzealous
heart failure, hypertension, toxins, vascular • Free‐roaming—trauma, toxins. fluid resuscitation can contribute to brain
event, coagulopathy, severe respiratory • Coexisting cardiac, respiratory, hematologic, edema. • Small‐volume fluid resuscitation
compromise, prolonged seizures, hypoglycemia, hepatic disease. • Diabetes mellitus— techniques to maintain systolic BP >90 mmHg
jaundice. • Decline in neurologic condition— insulin therapy. with normal heart rate. • Combination of
(continued) Brain Injury

B
isotonic crystalloids (10–20 mL/kg increments) • Levetiracetam—20–30 mg/kg IV/IM/PO/ • Arrhythmias. • Hypotension. • Hypernatremia.
with hydroxyethyl starch (5 mL/kg increments) rectal q8h if seizure activity. • Hypokalemia. • Respiratory failure. • Residual
over 5–8 minutes. • Avoid hypertension. Other neurologic deficits. • Death.
• Level head with body or elevate head and • Reducing cerebral metabolic rate with heavy EXPECTED COURSE AND PROGNOSIS
neck to 20° angle. • Keep airway unobstructed; sedation using dexmedetomidine (3 μg/kg slow • Young animals, minimal primary brain
use suction and humidify if intubated; bolus followed by 3–7 μg/kg/h CRI IV) with injury, secondary injury consisting of cerebral
hyperoxygenate, consider IV lidocaine prior to ketamine (1 μg/kg slow bolus followed by 1 μg/ edema—best prognosis. • No deterioration
suctioning. • Lubricate eyes. • Reposition every kg/h CRI IV) with uncontrolled seizures or for 48 hours—better prognosis. • Rapid
2–4 hours to avoid hypostatic pulmonary propofol (2–4 mg/kg IV then 0.1–0.4 mg/kg/ resuscitation of systolic BP to >90 mmHg
congestion, pressure sores. • Prevent fecal/urine min); must intubate and support blood pressure, and avoiding hypoxemia—better neurologic
soiling. • Maintain normal body temperature. oxygenation, and ventilation. • Cooling patient outcome. • Modified Glasgow Coma Score
• Maintain hydration with balanced crystalloid to 32–33 °C (89–91 °F) for 48h may provide may offer prognostic insight.
solution. • Rehabilitation exercises. cerebral protection when administered within 6
ACTIVITY hours of global ischemia or severe brain injury.
• Restricted. • Consult rehabilitation specialist • Glucose regulation. • Careful nasogastric tube
for appropriate exercises to maintain muscle tone. feeding for early trickle flow feeding; cisapride
(0.5 mg/kg PO q8–12h) and metoclopramide
MISCELLANEOUS
CLIENT EDUCATION
(1–2 mg/kg/day) may promote gastrointestinal SYNONYMS
• Neurologic signs may worsen before improving.
motility. • Desmopressin for refractory hyper- • Head trauma. • TBI.
• Neurologic recovery may not be evident for
several days; possibly >6 months for residual natremia; emergency dosage not established for SEE ALSO
neurologic deficits. • Serious systemic animals (dogs: 4 μg topical conjunctival q12h; Stupor and Coma.
abnormalities contribute to CNS instability. cats: 5 μg SC q12h).
ABBREVIATIONS
SURGICAL CONSIDERATIONS CONTRAINDICATIONS • ADH = antidiuretic hormone. • CBF =
Depressed skull fracture, penetrating foreign Drugs that cause hypertension, hypotension, cerebral blood flow. • CPP = cerebral perfusion
body, uncontrollable ICP elevation (insuf- hyperexcitability, or increase in metabolic rate. pressure. • CRI = continuous rate infusion
ficient CSF drainage, hematoma/mass PRECAUTIONS • CSF = cerebrospinal fluid. • ICP = intracranial
evacuation, herniation). • Avoid hypotension, hypoxemia, hyper pressure. • MAP = mean arterial pressure.
tension, hyperglycemia, hypoglycemia, • MEM = meningoencephalomyelitis. • PaO2 =
hypernatremia, hypo‐ or hypervolemia. partial pressure of oxygen. • PCO2 = partial
• Keep head and neck above plane of body. pressure of carbon dioxide. • SaO2 = arterial
• Do not compress jugular veins. oxygen saturation. • SpO2 = peripheral oxygen
MEDICATIONS • Furosemide, mannitol, and hypertonic saturation. • TBI = traumatic brain injury.
DRUG(S) OF CHOICE saline—can cause hypovolemia and hypo INTERNET RESOURCES
Elevated ICP tension. • Maintain PCO2 >32 mmHg; avoid http://www.traumaticbraininjury.com
• Ensure systolic BP >90 mmHg; lower ICP by hyperventilation in the first 24–8h and do
not perform therapeutic hyperventilation Suggested Reading
hyperventilation, drug therapy, drainage of CSF Dewey CW, Downs MO, Aron DN, et al.
from ventricles, or surgical decompression. (32–35 mmHg) for extended periods (>48h).
Acute traumatic intracranial haemorrhage
• 7% hypertonic saline—2–4 mL/kg IV. in dogs and cats. Vet Comp Orthop
• Furosemide—0.75 mg/kg IV; may decrease Traumatol 1993, 6:29–35.
CSF production. • Mannitol—0.5–1 g/kg IV Dewey CW, Fletcher DJ. Head trauma
bolus repeated at 2h intervals 3–4 times in FOLLOW‐UP management. In: Dewey CW, ed., A Practical
dogs, and 2–3 three times in cats; repeated Guide to Canine and Feline Neurology, 2nd
doses must be given on time; improves CBF PATIENT MONITORING
• Repeated neurologic examinations— ed. Ames, IA: Wiley, 2008, pp. 221–235.
and lowers ICP; may exacerbate hemorrhage. Fletcher D, Syring R. Traumatic brain injury.
• Glucocorticosteroids—no benefit in acute
deterioration warrants aggressive therapeutic
intervention. • BP—maintain systolic BP In: Silverstein D, Hopper K, eds., Small
management and long‐term outcome in Animal Critical Care Medicine. St. Louis,
human traumatic brain injury (TBI); anti‐ >90 mmHg. • Blood gases, pulse oximetry,
end‐tidal CO2—to assess need for oxygen MO: W.B. Saunders, 2014, pp. 723–727.
inflammatory doses (prednisone 1 mg/kg/day) Freeman C, Platt SR. Head trauma, In: Platt
may be of benefit with brain edema related to supplementation or ventilation. • Blood
glucose—avoid severe persistent hyperglycemia SR, Garosi LS, eds., Small Animal
intracranial neoplasia and infectious meningo Neurological Emergencies. London:
encephalomyelitis (MEM); immunosuppressive and hypoglycemia. • ECG—arrhythmias
may affect perfusion, oxygenation, and CBF. Manson, 2012, pp. 363–382.
doses (2 mg/kg/day) in combination with Sande A, West C. Traumatic brain injury: a
additional immunosuppressive drugs in • ICP—to detect elevations and monitor
response to therapy. review of pathophysiology and management.
immune‐mediated MEM. • Provide analgesia/ J Vet Emerg Crit Care 2010, 20:177–190.
sedatives (e.g., fentanyl 3–5 μg/kg IV, then PREVENTION/AVOIDANCE Author Elke Rudloff
3–5 μg/kg/h CRI ± lidocaine 3–5 mg/kg/h) as Keep pets in a confined area or leashed. Acknowledgment The author and book
indicated; avoid agents that can reduce CPP. POSSIBLE COMPLICATIONS editors acknowledge the prior contribution of
Avoid ketamine with obstructive intracranial • Seizures. • Brain herniation. • Intracranial Rebecca Kirby.
lesions. • Thrashing, seizures, or uncontrolled hemorrhage. • Progression from cerebral cortical
motor activity—diazepam CRI (0.5–1 mg/kg/h), to midbrain signs. • Malnutrition. • Aspiration
midazolam CRI (0.2–0.4 mg/kg IV), or propofol pneumonia. • Hypostatic pulmonary Client Education Handout
(3–6 mg/kg IV titrated to effect; 0.1–0.6 mg/ congestion. • Corneal desiccation. • Urine available online
kg/min CRI); monitor for hypotension; scalding. • Airway obstruction from mucus.
intubate if unable to protect airway.
Brain Tumors
B
100,000 animals, or 1–3% of all deaths where immunologic and metabolic disorders,
necropsy was done. • Primary nervous system toxicities, nutritional disorders, trauma,
tumors in dogs account for 60–80% of all vascular disorders, degeneration, and
BASICS such tumors reported in domestic animals idiopathic disorders.
DEFINITION (10–20% in cats; 10–20% in other species). CBC/BIOCHEMISTRY/URINALYSIS
• Brain tumors of cats and dogs may be • The most common sites for neoplasia to The major objective in the completion of
classified as either primary or secondary, occur in immature dogs (<6 months), in these tests is to eliminate extracranial causes
depending on the cell type of origin. decreasing order, are the hematopoietic for signs of cerebral dysfunction.
• Primary brain tumors originate from cells system, brain, and skin. • Reported incidence
normally found within the brain and meninges, in cats is 3.5/100000. OTHER LABORATORY TESTS
including the neuroepithelium, lymphoid N/A
SIGNALMENT
tissues, germ cells, endothelial cells, and IMAGING
malformed tissues. • Secondary tumors are Breed Predilections • Survey radiographs of the thorax and
either neoplasms that have reached the brain • Meningiomas occur most frequently in abdominal ultrasound—to rule out primary
by hematogenous metastasis from a primary dolichocephalic breeds of dog. • Glial cell malignancy elsewhere in body. • Skull
tumor outside the nervous system, or tumors and pituitary tumors occur commonly radiographs—of limited value; may detect
neoplasms that affect the brain by local in brachycephalic breeds of dog. • Canine neoplasms of skull or nasal cavity that involve
invasion, or extension, from adjacent breeds overrepresented include boxer, golden brain by local extension. • Occasionally, lysis
non-neural tissues such as bone. • Pituitary retriever, Doberman pinscher, Scottish terrier, or hyperostosis of skull may accompany
gland neoplasms (adenomas or carcinomas) and Old English sheepdog. • There does not primary brain tumor (e.g., meningioma of
and tumors arising from cranial nerves (e.g., appear to be a breed predisposition for cats), or there may be radiographically visible
nerve sheath tumor of trigeminal, oculomotor, development of brain tumors in cats. mineralization within a neoplasm. • CT—
or vestibulocochlear nerves) are considered Mean Age and Range provides accurate determination of presence,
secondary brain tumors. • Brain tumors occur in dogs and cats of any location, size, and anatomic relationships of
PATHOPHYSIOLOGY age. • Most frequent in older dogs, with many intracranial neoplasms. • MRI—
• Brain tumors result in cerebral dysfunction greatest incidence in dogs >5 years of age. considered superior to CT in localization and
by causing both primary effects, such as • Median age for diagnosis of meningiomas, characterization of most brain tumors.
infiltration of nervous tissue or compression gliomas, and choroid plexus tumors in dogs DIAGNOSTIC PROCEDURES
of adjacent anatomic structures, and has been reported as 10–11 years, 8 years, and
5–6 years, respectively. CSF Analysis
secondary effects, such as hydrocephalus.
• CSF—may help to rule out inflammatory
• Additional primary effects include Predominant Sex causes of cerebral dysfunction: in some cases
disruption of cerebral circulation and local Older male cats appear to be most susceptible may support diagnosis of brain tumor. • Care
necrosis, which may result in further damage to meningiomas. should be used in collection of CSF, because
to neural tissue. • The most important
SIGNS increased ICP may be present in association
secondary effects of a primary brain tumor
• Vary with tumor location. • The most with brain tumor, and pressure alterations
include disturbance of cerebrospinal fluid
frequently recognized clinical sign associated associated with CSF collection may lead to
(CSF) flow dynamics, elevated intracranial
with a brain tumor of a dog or cat is seizures, brain herniation. • CSF collection usually
pressure (ICP), cerebral edema, or brain
particularly should first seizure occur after 5 delayed until advanced imaging has been
herniation. • Secondary effects usually are
years of age. • Other clinical signs frequently completed to evaluate factors such as presence
more diffuse or generalized in their clinical
associated with brain tumor are abnormal of cerebral edema or hemorrhage. • In
manifestations and may mask the precise
behavior and mentation, visual deficits, general, increased CSF protein content and
location of a focal intracranial lesion.
circling, ataxia, head tilt, and cervical spinal normal to increased CSF white blood cell
SYSTEMS AFFECTED hyperesthesia. • Signs that result from disease count have been considered “typical” of a
Nervous (brain). in given location in nervous system are brain neoplasm.
GENETICS similar, regardless of precise cause. • On basis Biopsy
• An unusually high incidence of of signalment, history, and results of complete • Cytologic evaluation of smear preparations
meningiomas has been reported in cats with physical and neurologic examinations, it is from biopsy tissue, rapidly fixed in 95%
mucopolysaccharidosis type I. • Specific possible to localize a problem to the brain alcohol and stained with hematoxylin and
genetic factors associated with breed and, in some cases, to determine the approx- eosin, may be done within minutes of biopsy
predisposition have not been identified. imate location. collection. • Tissue biopsy remains sole
• Brachycephaly provisionally has been CAUSES method available for definitive diagnosis of
associated with the SMOC-2 and • Uncertain. • Dietary, environmental, brain tumor type in cats or dogs, and is
thrombospondin-2 genes on canine genetic, chemical, viral, traumatic, and essential consideration prior to any type of
chromosome 1, and a component of glioma immunologic factors may be considered. therapy. • Biopsy not always attempted
susceptibility provisionally has been mapped because of practical considerations, such as
to a region on canine chromosome 2. cost and morbidity. • CT-guided stereotactic
• Molecular and genetic classification of brain biopsy systems provide relatively rapid and
tumors may permit targeted therapies in the extremely accurate means of tumor biopsy,
future. DIAGNOSIS with low rate of complications.
INCIDENCE/PREVALENCE DIFFERENTIAL DIAGNOSIS
PATHOLOGIC FINDINGS
• Brain tumors appear to be more common
Categories of disease that may result in
• Classification of CNS tumors in dogs and
in dogs than in other domestic species. clinical signs similar to those of a brain tumor
cats primarily is based on the characteristics
• Reported incidence in dogs is 10–20 per
include congenital disorders, infections,
of their constituent cell type, pathologic
(continued) Brain Tumors

B
behavior, topographic pattern, and secondary available for use in dogs and cats: surgery, POSSIBLE COMPLICATIONS
changes present within and surrounding the irradiation, and chemotherapy. • Aspiration pneumonia due to depressed
tumor. • Meningioma is most common Surgery swallowing reflexes associated with increased
intracranial neoplasm of dogs and cats. • Neurosurgical intervention is an essential ICP. • Seizures.
• Classification of glial subset of neuroepi consideration in management of brain tumors EXPECTED COURSE AND PROGNOSIS
thelial tumors is based on predominant cell in cats or dogs, whether for complete excision, • Little information available concerning
type (e.g., astrocyte or oligodendrocyte). partial removal, or biopsy. • Meningiomas, survival times of dogs or cats with brain
Dogs particularly those located over cerebral tumor that have received only palliative
• Embryonal tumors have been consolidated convexities or in frontal lobes of cerebrum, therapy (i.e., therapy to control secondary
under single term “primitive neuroecto may be completely (or almost completely) effects of a tumor without an attempt to
dermal tumors” (or PNETs) to accommodate removed by surgery, especially in cats. eradicate the tumor). • Results of one study
their anaplastic nature. • Brain tumors • Primary calvarial tumors also may be indicate mean and median survival of 81 days
arising from lymphoreticular cells removed surgically prior to other types of and 56 days, respectively, following CT
traditionally have been grouped under a therapy. diagnosis of primary brain tumor in each of 8
heading of reticulosis or histiocytic lymphoma. Radiation Therapy dogs. • Results from several studies confirm
• Skull tumors that affect the brain by local that prognosis for a dog or cat with a primary
• Irradiation may be used either alone or in
extension include osteosarcoma, chondro combination with other treatments for either brain tumor may be significantly improved by
sarcoma, and multilobular osteochondro primary or secondary brain tumors. • Careful surgical removal and irradiation, either alone
sarcoma. • The most frequently seen treatment planning by qualified and or in combination.
secondary tumors of dogs include local experienced radiation therapist is essential to
extension of nasal adenocarcinoma; success of radiation therapy. • A major
metastases from mammary, prostatic, or development in radiation therapy is
pulmonary adenocarcinoma; metastases from
hemangiosarcoma; and extension of pituitary
emergence of more precise protocols that MISCELLANEOUS
spare tissues surrounding the brain tumor
adenoma or carcinoma. • Nerve sheath ASSOCIATED CONDITIONS
(e.g., stereotactic radiotherapy).
tumors arising from cranial nerves Dogs that have been treated for a brain tumor
(particularly oculomotor nerve and Chemotherapy may develop a second type of tumor
trigeminal nerve) may occur in dogs. Alkylating agents (e.g., carmustine [BCNU], elsewhere in the body.
lomustine [CCNU], and temozolomide),
Cats ABBREVIATIONS
antimetabolic agents (e.g., cytosine arabino-
• Meningiomas involving multiple • CSF = cerebrospinal fluid.
side), and ribonucleotide reductase inhibitors
intracranial sites (including third ventricle) • ICP = intracranial pressure.
(e.g., hydroxuurea) may result in reduction of
relatively common in cats. • Primary brain • PNET = primitive neuroectodermal tumor.
tumor size and improvement of clinical signs
tumors other than meningiomas occur in dogs with glial cell tumors; however, Suggested Reading
infrequently in cats. • Tumors that have been evidence of efficacy in animals is lacking. Dickinson PJ. Advances in diagnostic and
reported include astrocytoma, ependymoma, treatment modalities for intracranial
oligodendroglioma, choroid plexus papilloma, tumors. J Vet Intern Med 2014,
medulloblastoma, lymphoma, olfactory 28:1165–1185.
neuroblastoma, and gangliocytoma. Dickinson PJ. Intracranial tumors in dogs.
• Lymphoma of the brain may be primary or MEDICATIONS Vet Focus 2014, 24(2):2–10.
secondary, or may be an aspect of multicentric DRUG(S) OF CHOICE Hicks J, Platt S, Kent M, Haley A.
lymphoma of cats. • Secondary tumors that • Glucocorticoids may be used for edema Canine brain tumors: a model for
have been reported to occur in the brain of reduction and, in some cases (e.g., lymphoma), human disease? Vet Comp Oncol 2017,
cats include pituitary macroadenomas and for retardation of tumor growth. • Some 15(1):252–272.
macrocarcinomas, and metastatic carcinoma. animals with brain tumor demonstrate Kohler RJ, Arnold SA, Eck DJ, et al.
• Local extension may occur either from dramatic improvement in clinical signs for Incidence of and risk factors for major
tumors of middle ear cavity (e.g., squamous weeks or months with sustained gluco complications or death in dogs undergoing
cell carcinoma), nasal cavity (e.g., nasal corticoid therapy. • Antiepileptic drugs (e.g., cytoreductive surgery for treatment of
adenocarcinoma), or skull (e.g., phenobarbital, bromide, levetiracetam) may suspected primary intracranial masses.
osteosarcoma). be utilized for control of generalized seizures. J Am Vet Med Assoc 2018,
• Mannitol and hypertonic saline are agents 253(12):1594–1603.
best suited for effective reduction of increased Rossmeisl JH. New treatment modalities for
ICP. brain tumors in dogs and cats. Vet Clin
TREATMENT Small Anim 2014, 44:1013–1038.
Author Richard A. LeCouteur
• Beyond general efforts to maintain homeo-
stasis, major goals of therapy for brain tumor FOLLOW-UP Client Education Handout
are to control secondary effects, such as PATIENT MONITORING available online
increased ICP or cerebral edema, and to • Serial neurologic examinations. • Serial CT
eradicate the tumor or reduce its size. or MRI examinations.
• Beyond palliative care, three methods of
therapy for a brain tumor currently are
Breeding, Timing
B
continue during estrus and cease only at the CBC/BIOCHEMISTRY/URINALYSIS
onset of diestrus. • Physical signs alone— N/A
unreliable for precise determination of fertile OTHER LABORATORY TESTS
BASICS period. • Receptivity—may be detected by
DEFINITION touching the perineum near the vulva; if Dogs
Timing of insemination(s) to maximize receptive, female will “flag” by elevating the • Semi-quantitative progesterone ELISA—
pregnancy risk and litter size. tail to one side and lifting the vulva dorsally. adjunct to vaginal cytologic examination.
• Quantitative serum progesterone testing—
PATHOPHYSIOLOGY Cats preferred when breeding with frozen semen;
LH response to a single mating—may vary especially useful in animals with reduced
Dogs
substantially. fertility. Commercial labs or in-house
• Must determine ovulation day so that
breeding(s) occur(s) at proper time. • Fresh, Historical Findings machines available. ◦ Progesterone
chilled, or frozen semen—usually limited to Dogs concentration <1 ng/mL (3.18 nmol/L)
one or two inseminations; insemination must Sanguineous vulvar discharge during estrus. before LH peak, 1.5–4 ng/mL (4.8–
be timed relative to ovulation for maximum 12.7 nmol/L) at LH peak, 4–10 ng/mL
Cats (12.7–31.8 nmol/L) at ovulation; continues
fertility. • Ovulation may vary relative to
Return to estrus in <30 days may indicate to rise during diestrus/pregnancy.
onset of heat (proestrus), standing heat
failure to ovulate; interestrus usually 8–10 ◦ Commercial laboratories use various
(estrus), vaginal cytology. • Luteinizing
days, but highly variable even within queen; methods of progesterone concentration
hormone (LH)—controls ovulation; peaks on
some queens will breed while pregnant. measurement, so values indicative of LH and
same day or after full cornification is
observed; ovulation occurs approximately 2 Physical Examination Findings ovulation vary among labs. ◦ Documenting
days after peak; 2–3 days (54–72 hours) more Dogs rapid rise in progesterone concentration
required for oocyte maturation; mature • Interest shown by male. • Vulva less turgid. subsequent to initial rise is more reliable
oocytes viable for minimum 2–3 days; thus • Vaginal discharge—less color and amount. indicator of ovulation than single measure
fertile period is 4–8 days after LH peak, and • Flagging. • Females show mounting ment of LH peak or initial rise in
maximum fertility is 5–6 days after LH peak. behavior. • Fully cornified and crenulated progesterone. • LH testing—must sample
• Serum progesterone concentration— pale vaginal epithelium. • Digital palpation daily to observe LH peak; can use serum
increase closely associated with LH peak. of vagina may be resented by bitch in progesterone to signal when to start testing or
proestrus, improving throughout proestrus use the initial rise in progesterone concentration
Cats
until estrus. May feel edematous mass on as surrogate for LH peak.
• Ovulation—usually induced; timing of
breeding is not as critical as with dogs; depends floor of caudal vagina, just cranial to urethral Cats
on adequate gonadotropin-releasing hormone os, that should shrink as optimal breeding Serum progesterone testing to verify
(GnRH) and then LH release triggered by period approaches. ovulation.
vaginal stimulation. • Adequate stimulation— Cats IMAGING
characterized by copulatory cry and postcoital • Fully cornified vaginal epithelium. Ultrasonographic imaging of ovaries—may
reaction; frequency of coital stimuli important • Interest shown by male. • No changes in help determine ovulation; perform daily, best
in determining adequacy of coital contact. external genitalia. • Vocalizes, rubs objects. if using color flow Doppler.
• LH—peak concentration and duration of • Lordosis.
elevation determine number of follicles DIAGNOSTIC PROCEDURES
CAUSES
ovulating; higher concentration with multiple Dogs
copulations; response to copulation depends Dogs • Vaginal cytologic examination—imprecise
on day of estrus (greater release on estrus day 3 • Limited number of breedings. • Female indicator of fertile period; cornification of
than on estrus day 1); release partially depends unreceptive to male. • Artificial insemination vaginal epithelium with clear background
on duration of exposure to estrogen. (fresh, chilled, or frozen semen). usually coincides with sexual receptivity.
SYSTEMS AFFECTED Cats ◦ Proestrus (in breeder terms, “day 1,” first
Reproductive • Coitus—too early or too late in estrus; too sign of hemorrhagic vaginal discharge)—most
few times. • Artificial insemination. epithelial cells are noncornified. ◦ Percentage
GENETICS of cornified cells (cells with angular cytoplasm
N/A RISK FACTORS and pyknotic nuclei or nuclei that fail to take
N/A up stain) increases during proestrus.
N/A ◦ Estrus—90% or more cornified cells,
background of slide free of debris. ◦ Breeders
refer to estrus by day, usually occurs day
N/A
DIAGNOSIS 10–18 in breeder terms. ◦ Diestrus—abrupt
SIGNALMENT decline in percentage of cornified cells (20–50%)
Dog and cat. DIFFERENTIAL DIAGNOSIS in a single day: day 1 of diestrus (D1); normal
• Vaginal discharge—proestrus or estrus; to see neutrophils on days 1–4 of diestrus.
SIGNS
vaginitis; neoplasia, pyometra, urinary tract • Vaginoscopy—edematous vaginal folds
General Comments infection. • Refusal to allow intromission— until LH peak, then vagina pale with slight
Dogs anatomic abnormalities of Mullerian duct wrinkling (crenulation) as edema decreases
• Onset of estrus—usually associated with a development, vulvovestibular or vestibulo with estradiol decline; by optimum breeding
change in the vaginal discharge from vaginal junction, acquired abnormality from period crenulation is obvious, until diestrus
sanguineous to barely red and decreased dystocia or breeding trauma, vaginal when folds are flat and edema disappears.
vulvar edema; sanguineous discharge may hyperplasia, behavioral.
(continued) Breeding, Timing

B
CLIENT EDUCATION (chemiluminescence assay, fluorescence,
Client education on physical, behavioral, and ELISA) progesterone assay—more accurate
endocrinologic changes that occur during than semi-quantitative kits; several in-house
TREATMENT estrous cycle, and how variable timing of these analyzers available; turnaround times should
APPROPRIATE HEALTH CARE changes can be from animal to animal, can be less than 24 hours. • Serum separator tubes
improve owner compliance and satisfaction. cause false elevations in chemiluminescence
Dogs
SURGICAL CONSIDERATIONS progesterone assay; anticoagulant may affect
• Fresh semen, multiple breedings—
Surgical AI requires standard postoperative reported concentration (serum > heparin
inseminate q48h, starting 48–96h after
care. plasma > EDTA plasma).
initial rise in serum progesterone concen
tration is observed until D1. • Fresh
semen, two breedings—inseminate either
on days 3 and 5 or on days 4 and 6 after
LH peak or initial rise in serum progesterone MEDICATIONS MISCELLANEOUS
concentration; use standard artificial AGE-RELATED FACTORS
insemination (AI) pipettes or modified DRUG(S) OF CHOICE
Cats—hCG (100–500 IU/cat IM); GnRH Split heats in young bitches—period of
Foley catheters (several sizes available); proestrus (may be prolonged to 6 weeks or
vaginal insemination on or after day 5 may (25–50 μg/cat IM).
more), followed by cessation of signs, and
be associated with reduced pregnancy rates subsequent resumption of estrus cycle (1–3
and litter sizes due to beginning of cervical weeks later); no initial rise in progesterone or
closure. • Frozen or chilled semen—frozen LH concentration occurs with first proestrus/
semen is less viable than chilled, thus FOLLOW-UP estrus; subsequent estrus usually normal.
timing is more critical; one or two
intrauterine inseminations most common: PATIENT MONITORING PREGNANCY/FERTILITY/BREEDING
inseminate on day 5 or 6 after LH peak or • Dogs—serial vaginal cytology to determine Ultrasound—conceptuses can first be
initial rise in serum progesterone D1; ovulation is ~6 days before D1. • Dogs— detected 18–20 days after LH peak (requires
concentration (day 0) or 3 days after serum whelping is 65 ± 1 days from LH peak, 63 ± 1 high-resolution, high-frequency probe, easier
progesterone concentration ≥5 ng/mL days from ovulation, or 57 ± 1 days from D1; in toy breeds) or 2–3 days earlier in cats;
(16 nmol/L); for intrauterine insemination for fresh, chilled, or frozen semen: repeat commonly done 4 weeks post breeding;
via transcervical endoscopy (TCI) or quantitative serum progesterone measurement recommend earlier exam in bitches with
surgical insemination, serum progesterone after initial progesterone rise or LH peak to history of pregnancy loss or infertility.
concentration on day of insemination verify >10 ng/mL (32 nmol/L). • Cats—use
SEE ALSO
should be ≥12 ng/mL (38 nmol/L; value is serum progesterone assay 1 week post
• Infertility, Female—Dogs.
laboratory dependent). • Timing insemination to verify ovulation. • Cats—
• Ovulatory Failure.
insemination based on serum progesterone queening is 62–71 days from first breeding.
• Vaginal Discharge.
concentration improves chance of PREVENTION/AVOIDANCE • Vaginal Malformations and Acquired Lesions.
conception and increased litter size. N/A
• Blood collection and vaginal examination
ABBREVIATIONS
POSSIBLE COMPLICATIONS • AI = artificial insemination.
q48h are adequate in most cases.
Dogs • D1 = first day of diestrus.
Cats • GnRH = gonadotropin-releasing hormone.
• Vaginal cytologic examinations—compare
• Increase likelihood of ovulation and litter • hCG = human chorionic gonadotropin.
D1 with prospective estimation based on
size by maximizing number of matings; breed • LH = luteinizing hormone.
progesterone; if estimates differ, pregnancy
on successive days. • Breed at least 4 times • TCI = endoscopic transcervical insemination.
rates are reduced. • Semi-quantitative
daily at least 2–3 hours apart on days 2 and 3
of estrus to maximize LH release. • May
progesterone kits—must come to room Suggested Reading
temperature before use; concentrations falsely Johnston SD, Root Kustritz MV, Olson PN.
induce ovulation by administration of
elevated when using a cold kit. • Serum Breeding management, artificial insemina-
exogenous hormones—GnRH or human
progesterone concentration—allow blood to tion, in vitro fertilization, and embryo
chorionic gonadotropin (hCG) after mating.
clot at room temperature; separate cells from transfer in the queen. In: Johnston SD,
ACTIVITY serum 20 minutes after collection; falsely low Root Kustritz MV, Olson-Schultz P, eds.,
• No alteration in activity necessary except concentrations occur when using serum mixed Canine and Feline Theriogenology.
confinement—bitch will search for male. with red blood cells (progesterone binds to Philadelphia, PA: Saunders, 2001, pp.
• Keep strictly away from unintended erythrocytes). • Hemolyzed or lipemic 406–413.
sexually intact males. specimen—may give falsely low progesterone Author Cathy J. Gartley
concentration. • Quantitative Consulting Editor Erin E. Runcan
Bronchiectasis
B
• Foreign body pneumonia.
• Neoplasia.
BASICS CBC/BIOCHEMISTRY/URINALYSIS MEDICATIONS

• Neutrophilia and monocytosis.
OVERVIEW • Hyperglobulinemia. DRUG(S) OF CHOICE
• Clinical condition seen primarily in dogs; • Proteinuria—can be seen with secondary • Intravenous antibiotics—may be required
irreversible dilatation of the bronchi; caused amyloidosis, glomerulonephritis, or sepsis. initially; good choices: ampicillin (10–20 mg/
by chronic infectious or inflammatory airway kg IV q6–8h) and enrofloxacin (5–10 mg/kg
disease, foreign body pneumonia, or OTHER LABORATORY TESTS q24h).
associated with primary ciliary dyskinesia. Arterial blood gas analysis—hypoxemia; • Broad-spectrum agents with efficacy against
• Occurs in cats as a sequela to longstanding widened alveolar–arterial oxygen gradient. both aerobes and anaerobes and that offer
inflammatory lung disease or neoplasia. IMAGING good penetration of pulmonary tissue—
• Airways are pulled open by surrounding • Radiography—insensitive for the diagnosis. preferred; combination of enrofloxacin
lung tissue; pooling of secretions can occur, Abnormalities visible late in the course of (5–20 mg/kg PO q24h) and clindamycin
which perpetuates lung damage and allows disease include dilatation of the lobar bronchi (5–11 mg/kg PO q12h) or amoxicillin–
colonization by bacteria. with lack of normal tapering in the periphery; clavulanate often effective.
• Can be cylindrical or saccular, focal or diffuse thickening of bronchial walls; mixed • Azithromycin can be a good alternative
diffuse. bronchial, interstitial, and alveolar pattern. antibiotic for outpatient care.
• Changes can be focal or diffuse. • Long-term use of antibiotics (2 months to
SIGNALMENT
• Primarily dogs but radiographically • CT—bronchus >2 times the width of the lifelong)—based on bacterial culture and
detected in many cats. adjacent pulmonary artery in dogs, sensitivity testing; may be required even if
• Cocker spaniels and perhaps West abnormally dilated bronchi near the lung culture of airway specimens yields no growth.
Highland white terriers predisposed. periphery; thickened airways; cystic • Bronchodilators—may be beneficial,
• Young animals (<1 year) with primary dilatations of the bronchi with or without although animals usually have irreversible
ciliary dyskinesia. pulmonaray consolidation. airflow limitation; extended release theophylline
• Middle-aged to old dogs with chronic
advised.
pulmonary disease. • Eosinophilic lung disease requires treatment
• Bronchoscopy—saccular or tubular
with glucocorticoids.
SIGNS dilatation of the airways.
• Saline nebulization and coupage highly
• Chronic cough—usually moist and • Airway sampling—cytologic examination
beneficial in removing secretions.
productive; hemoptysis. of bronchoalveolar lavage fluid or tracheal
• Recurrent fever. wash specimens; culture for aerobic and CONTRAINDICATIONS/POSSIBLE
• Exercise intolerance. anaerobic bacteria and Mycoplasma; typically INTERACTIONS
• Tachypnea or respiratory distress. find suppurative inflammation with high • Theophylline derivatives and fluoro
• Chronic nasal discharge or sinusitis, numbers of neutrophils, or increased quinolones—concurrent use causes high and
particularly with primary ciliary dyskinesia. eosinophils indicating eosinophilic broncho possibly toxic plasma theophylline
• Moist, harsh inspiratory crackles; loud pneumopathy; may culture a mixed concentration.
expiratory lung sounds or wheezes on population of bacteria; some cases appear to • Furosemide—avoid; dries airway secretions.
physical exam. have sterile inflammation. • Cough suppressants—avoid; will trap
• Tracheal hypersensitivity. PATHOLOGIC FINDINGS secretions and bacteria in lower airway and
• Dilated bronchi. perpetuate damage.
• Primary ciliary dyskinesia. • Diffuse peribronchial and alveolar
• Inadequately treated infectious or inflammation and fibrosis.
inflammatory lung conditions (pneumonia, • Squamous metaplasia of bronchial
bronchitis, or eosinophilic lung disease). epithelium. FOLLOW-UP
• Smoke inhalation, chronic aspiration PATIENT MONITORING
pneumonia, radiation injury, and inhalation • Clinical response—outpatient.
of environmental toxins—predispose animal • Serial CBC, blood gas analysis, and thoracic
to airway injury and colonization by bacteria. TREATMENT radiographs.
• Chronic bronchial obstruction or foreign • Inpatient—severe condition: intravenous
body pneumonia—development of bronchiec PREVENTION/AVOIDANCE
fluids and antibiotics; oxygen administration.
tasis distal to the obstructed region common. • Antibiotics—complete a full course of
• Airway nebulization and coupage to
• Signs related to bronchiectasis may not be therapy in patients that appear to have
facilitate removal of viscid pulmonary
recognized until long after the primary injury. parenchymal involvement.
secretions, often lifelong.
• Early recognition and resolution of foreign
• Gentle activity enhances clearance of
body pneumonia.
secretions.
• Appropriate treatment of eosinophilic
• Long-term antibiotic administration.
pneumonia.
DIAGNOSIS • Stress to owner the importance of
appropriate follow-up care. POSSIBLE COMPLICATIONS
DIFFERENTIAL DIAGNOSIS • Single affected lung lobe or bronchial Chronic recurrent pulmonary infection likely.
• Recurrent bacterial bronchopneumonia. obstruction—lung lobectomy can be
• Fungal pneumonia. EXPECTED COURSE AND PROGNOSIS
curative. • Chronic and recurrent clinical signs
• Chronic bronchitis.
• Infectious or parasitic bronchitis. expected; some degree of coughing will always
be present.
(continued) Bronchiectasis
B
• Animals can live for years with bronchiec • Chronic bronchitis. (1988–2000). J Am Vet Med Assoc 2003,
tasis if managed properly. • Pneumonia—bacterial, eosinophilic 223(11):1628–1635.
• Some patients succumb to respiratory aspiration, foreign body. Johnson LR, Johnson EG, Vernau W, et al.
failure. • Smoke inhalation. Bronchoscopy, imaging, and concurrent
• Other organs may fail if bacteremia or Suggested Reading diseases in dogs with bronchiectasis
glomerulonephritis develops. Cannon MS, Johnson LR, Pesavento PA, (2003–2014). J Vet Int Med 2016,
et al. Quantitative and qualitative computed 30(1):247–254.
tomographic imaging features of Author Lynelle R. Johnson
bronchiectasis in dogs. Vet Rad US 2013, Consulting Editor Elizabeth Rozanski
MISCELLANEOUS 54(4):351–357.
Hawkins EC, Basseches J, Berry CR, et al.
Demographic, clinical, and radiographic
• Primary ciliary dyskinesia.
features of bronchiectasis in dogs: 316 cases
• Chronic sinusitis.
Bronchitis, Chronic
B
coughing because of increased tracheal hyperadrenocorticism could be responsible
sensitivity. • Small airway disease—assumed for obesity and/or enlarged liver/abdomen,
when expiratory abdominal push (during testing should be considered if clinically
BASICS quiet breathing) or end-expiratory wheezing is indicated.
DEFINITION detected. • Bronchovesicular lung sounds, IMAGING
• Chronic coughing for longer than 2 months end-inspiratory crackles, and wheezing (result
that is not attributable to another cause (e.g., of airflow into obstructed airways) may be Thoracic Radiography (High Resolution
neoplasia, congestive heart failure, heard. • Loud end-expiratory snap is Computed Topography)
eosinophilic pneumonia, or infectious suggestive of concurrent airway collapse. Common features (in descending order of
bronchitis). • Partly nonreversible and often • Cardiac auscultation—murmurs secondary frequency)—bronchial thickening; interstitial
slowly progressive condition owing to to valvular insufficiency common in dogs, but pattern; middle lung lobe consolidation
accompanying pathologic airway changes. not always associated with congestive heart (cats); atelectasis; hyperinflation and
failure; chronic bronchitis usually results in diaphragmatic flattening (primarily cats).
PATHOPHYSIOLOGY
normal or slower than normal resting heart Echocardiography
• Recurrent airway inflammation suspected,
rate and pronounced sinus arrhythmia; in cats, • May reveal right heart enlargement with
but a specific cause is rarely determined.
tachycardia is possible. • Obesity— common; pulmonary hypertension. • Helps rule out
• Persistent tracheobronchial irritation—
important complicating factor. • Severe dental cardiac disease as a cause of coughing.
causes chronic coughing; leads to changes in
disease may predispose to lower airway colon- • Check for pulmonary hypertension via
tracheobronchial epithelium and submucosa.
ization and possible infection (dogs). Doppler echocardiography.
• Airway inflammation, epithelial edema, and
thickening—prominent. • Excess production CAUSES DIAGNOSTIC PROCEDURES
of thickened mucus is a hallmark. • In severe, Chronic airway inflammation initiated by
very chronic cases—probable increased lung multiple causes, although specific cause rarely Bronchoscopy
resistance; decreased expiratory airflow, identified. Preferred test for assessing the lower airways.
especially in cats; in dogs, possible sequelae • Allows direct visualization of structural as
RISK FACTORS
such as broncholamacia and bronchiectasis. • Long-term exposure to inhaled irritants.
well as functional (dynamic) changes; allows
• Obesity. • Recurrent bacterial infection.
selected airway sampling (e.g., biopsy and
SYSTEMS AFFECTED
• Dental disease and laryngeal disease—result
lavage). • Gross changes—excess mucoid to
• Respiratory • Cardiovascular—pulmonary
in bacterial showering of lower airways. mucopurulent secretions; epithelial edema or
hypertension, cor pulmonale. • Nervous—
thickening with blunting of bronchial
syncope (infrequent).
bifurcations; irregular or granular mucosa;
INCIDENCE/PREVALENCE mucosal polypoid proliferations can indicate
Common in dogs and cats. chronic bronchitis or chronic eosinophilic
GEOGRAPHIC DISTRIBUTION DIAGNOSIS pneumonia. • Large airway caliber changes
Worldwide DIFFERENTIAL DIAGNOSIS (e.g., static or dynamic airway collapse and
• Bronchiectasis. • Eosinophilic broncho bronchiectasis)—may be detected as
SIGNALMENT complicating problems.
pneumopathy. • Foreign bodies. • Heartworm
Species disease. • Bacterial, pneumonia. • Neoplasia— Evaluation of Airway Secretions
Dogs and cats. metastatic more than primary. • Pulmonary • Must collect from lower airways—helps to
Breed Predilections parasites or parasitic larval migration. establish underlying cause if present or to
• Dogs—small and toy breeds common; also • Pulmonary fibrosis—cats and dogs. determine the severity of inflammation.
observed in large breeds. • Siamese cats and • Pulmonary granulomatosis. • Congestive • Throat swab cultures are not representative
domestic shorthairs affected. heart failure—typically associated with high of lower airway flora • Tracheal aspiration or
resting heart rate and left atrial enlargement, bronchoalveolar lavage—collect specimens for
Mean Age and Range which may lead to collapse of left principal cytologic examination and bacterial/
Most often affects middle-aged and old bronchus. mycoplasmal culture or qPRC assessment.
animals.
CBC/BIOCHEMISTRY/URINALYSIS • Quantitated aerobic bronchoalveolar lavage
Predominant Sex • Rarely diagnostic. • Neutrophilic (BAL) cultures help differentiate infection
N/A, although spayed females are often leukocytosis common. • Absolute eosinophilia— versus airway colonization; reported cutoff is
overrepresented (might be due to weight suggests but not diagnostic for allergic >1.7 × 103 colony-forming units (CFU) for
gain). bronchitis. • Polycythemia secondary to infection in dogs. Anaerobic and Mycoplasma
SIGNS chronic hypoxia—may be seen. • Liver cultures recommended as well. • Cytology—
enzymes and bile acids may be elevated due inflammation primary finding; most cells are
Historical Findings neutrophils, eosinophils, or macrophages;
• Coughing—hallmark of tracheobronchial
to passive congestion.
evaluate for bacteria, parasites, neoplastic cells,
irritation; usually harsh and dry; post-tussive OTHER LABORATORY TESTS and contamination with foreign material.
gagging common (owners often misinterpret • Fecal and heartworm tests—rule out • Recurrent infections—implicated in patho-
this as vomiting, especially in dogs). pulmonary parasites. • Pulse oximetry— genesis of bronchitis; however, positive cultures
• Exercise intolerance, difficult breathing, useful for detecting hemoglobin desaturation. are not frequently reported; Mycoplasma infection
wheezing (in cats). • Cyanosis and even • Arterial blood gas analysis—collect, ice, discussed but rarely confirmed as a cause.
syncope may be noted in severe cases. and have analyzed at a local hospital; mild to
moderately low partial pressure of oxygen PATHOLOGIC FINDINGS
Physical Examination Findings See Bronchoscopy under Diagnostic
• Patients usually bright, alert, and afebrile.
(PaO2) seen with severe condition; aids in
prognosis and monitoring treatment. • As Procedures.
• Tracheal palpation—typically results in
(continued) Bronchitis, Chronic

B
mask (e.g., AeroDawg); however, the most complications. • Bronchectasis and airway
adequate dose is not clearly established. remodeling.
TREATMENT Bronchodilators EXPECTED COURSE AND PROGNOSIS
Commonly prescribed, although limited • Progressive airway changes—syncopal
APPROPRIATE HEALTH CARE evidence of efficacy. episodes, chronic hypoxia, right ventricular
• Usually outpatient—oxygen can be given at hypertrophy, and pulmonary hypertension.
home in chronic cases. • Inpatient—if Antibiotics
• Acute exacerbations—common with
requires oxygen therapy, parenteral medication, • Select on basis of quantitated culture and
sensitivity test results. seasonal changes, air quality changes,
or aerosol therapy; patients that owners worsened inflammation, and potentially
cannot keep calm at home during initial Antitussives development of secondary infection.
stages of therapy. • Indicated for nonproductive, paroxysmal,
NURSING CARE continuous, or debilitating cough. • Dogs—
Consider saline nebulization followed by butorphanol (0.55 mg/kg PO q6–12h;
coupage and/or gentle exercise to encourage 0.055–0.11 mg/kg SC); hydrocodone
(0.1–0.3 mg/kg q6–8h PO). Over-the- MISCELLANEOUS
removal of airway secretions.
counter cough suppressants are rarely ASSOCIATED CONDITIONS
ACTIVITY effective; gabapentin 2–5mg.kg by mouth • Syncope—secondary to chronic coughing
• Exercise—moderate (not forced) useful in every eight hours (but unestablished efficacy). or development of pulmonary hypertension.
clearing secretions; assists with weight loss. • Increased susceptibility to airway infection,
• Limit if exertion causes excessive coughing. CONTRAINDICATIONS
Lasix and atropine—do not use because chronic hypoxia, pulmonary hypertension,
• Use a harness instead of a collar. and cor pulmonale.
of drying effects on tracheobronchial
DIET secretions. PREGNANCY/FERTILITY/BREEDING
Weight loss critical—improves PaO2, attitude, Safety in pregnant animals not established for
and exercise tolerance in obese patients; PRECAUTIONS
• Beta agonists (e.g., terbutaline and most of the recommended drugs.
reduces cough frequency.
albuterol)—may cause tachycardia, SYNONYMS
CLIENT EDUCATION nervousness, and muscle tremors; typically Chronic bronchitis.
• Warn client that chronic bronchitis is an transient. • Theophylline—may cause
incurable disease and complete suppression of SEE ALSO
tachycardia, restlessness, excitability,
all coughing is an unattainable goal. • Stress • Asthma, Bronchitis—Cats. • Bronchiectasis.
vomiting, and diarrhea; evaluate ethylene
that aggressive treatment (including weight • Cough. • Hypoxemia. • Tracheal Collapse.
diamine tetra-acetate (EDTA) plasma sample
control, avoiding risk factors, and medical for peak plasma concentration (ideally ABBREVIATIONS
treatment) minimizes the severity of the 5–20 μg/mL); toxicity may be more common • BAL = bronchoalveolar lavage. • CFU =
coughing and slows disease progression in with generic formulations. colony-forming unit. • EDTA = ethylene
most patients. diamine tetra-acetate. • PaO2 = partial
SURGICAL CONSIDERATIONS pressure of oxygen.
Fluoroquinolones decrease theophylline
Treat severe dental disease to minimize clearance in dogs and can result in Suggested Reading
secondary bacterial complications. theophylline toxicity. Grotheer M, Hirschberger J, Hartmann K, et
al., Comparison of signalment, clinical,
ALTERNATIVE DRUG(S)
laboratory and radiographic parameters in
Maropitant (some antitussive properties
cats with feline asthma and chronic bronchi-
suggested, but not advised yet).
MEDICATIONS tis. J Feline Med Surg. 2020, 22(7):649–655.
Reinero CR, Masseau I, Grobman M, et al.,
DRUG(S) OF CHOICE Perspectives in veterinary medicine:
Corticosteroids Description and classification of bronchi-
• Diminish airway inflammation and FOLLOW-UP olar disorders in cats. J Vet Intern Med.
coughing regardless of the underlying cause. PATIENT MONITORING 2019, 33(3):1201–1221.
• Indicated for noninfectious conditions. • Follow abnormalities revealed by physical
Rozanski E. Canine chronic bronchitis. An
• With allergic or hypersensitivity reactions— examination and selected diagnostic tests— update . Vet Clin N Am Small Anim Pract
require long-term administration; attempt to determine response to treatment. • Monitor 2020, 50:393–404.
wean off steroids or determine lowest effective weight; arterial blood gases usually improve Author Cécile Clercx
dosage. • Prednisolone preferred in cats. after significant weight loss. Consulting Editor Elizabeth Rozanski
• Prednisone or prednisolone usually initiated
at 0.5–1 mg/kg PO q12h for a variable time, PREVENTION/AVOIDANCE
with tapering of the dosage based on clinical Avoid and address risk factors (see Risk Client Education Handout
signs. • Inhaled agents (e.g., budenoside or Factors). available online
fluticasone 1–3 puffs using metered dose POSSIBLE COMPLICATIONS
inhalers [variable concentrations exist] a day) • Syncope—possible complication of
are often effective and can be used to reduce chronic coughing, particularly in toy-
systemic side effects of corticosteroids; they breed dogs. • Pulmonary hypertension
are delivered via a spacer chamber and face and cor pulmonale—most serious
Brucellosis
B
Physical Examination Findings positive RSAT and negative 2ME, retest in
• Peripheral lymphadenopathy. • Males— 2–4 weeks.
swollen scrotum with scrotal dermatitis, Agar Gel Immunodiffusion (AGID) Test
BASICS enlarged firm epididymides, orchitis, • Soluble antigen test—recommended;
DEFINITION prostatitis. • Chronic infection—unilateral or employs antigens highly specific for
• Contagious disease of dogs caused by bilateral testicular atrophy, spinal pain, antibodies against Brucella spp. (including B.
Brucella canis. • Rarely caused by B. suis, B. discospondylitis, posterior weakness, ataxia. canis, B. abortus, and B. suis); reactive
abortus, or B. mellitensis. • Characterized by • Chronic recurrent anterior uveitis without
antibodies appear 4–12 weeks after infection
abortion and infertility in females, epididymitis signs of systemic disease; also iris hyperpig and persist; may be positive after other tests
and testicular atrophy in males. mentation, vitreal infiltrates, multifocal become equivocal or negative.
chorioretinitis. • Vaginal discharge—may last • ELISA—using purified cytoplasmic
PATHOPHYSIOLOGY several weeks after abortion. • Fever (rare).
B. canis—a small, intracellular Gram-negative antigens; not yet commercially available.
bacterium; has propensity for growth in CAUSES • PCR—available at some diagnostic
lymphatic, placental, and male genital B. canis—Gram-negative coccobacillus; laboratories; high sensitivity and specificity.
(epididymis and prostate) tissues. morphologically indistinguishable from other • Cell wall antigen test—not recommended;
members of genus. highly sensitive but not standardized; frequent
SYSTEMS AFFECTED
RISK FACTORS false positives.
• Hemic/lymph/immune—lymph nodes,
spleen, bone marrow, mononuclear leukocytes. • Breeding kennels, pack hounds. • Contact IMAGING
• Reproductive—target tissues of gonadal with strays in endemic areas. Discospondylitis—radiographic changes slow
steroids (gravid uterus, fetus, testes to develop, may not be seen even when spinal
epididymides, prostate gland). • Other pain is present.
tissues—intervertebral discs, anterior uvea, DIAGNOSTIC PROCEDURES
meninges (uncommon). DIAGNOSIS Isolation of Organism
GENETICS DIFFERENTIAL DIAGNOSIS • Blood cultures—when clinical and serologic
No known genetic predisposition. • Abortions—maternal, fetal, or placental findings suggest diagnosis, can be isolated
INCIDENCE/PREVALENCE abnormalities. • Systemic infections—canine from blood of infected dogs if they have not
• Incidence unknown. • Seroprevalence—not distemper, canine herpesvirus, B. abortus, received antibiotics; onset of bacteremia 2–4
well defined; false-positive results common hemolytic streptococci, E. coli, leptospirosis, weeks after oral-nasal exposure, persists for 8
with agglutination tests. • Prevalence— toxoplasmosis. • Inguinal hernia. months to 5.5 years. Culture is preferred
1–18% in United States, Japan; higher in • Discospondylitis—fungal infections, method for diagnosis in endemic situations or
rural United States; 25–30% in stray dogs in actinomycosis, staphylococcal infections, with known exposure (1–8 weeks ago); must
Mexico, Peru. nocardiosis, streptococci, or Corynebacterium specifically request Brucella culture. • Culture
diphtheroids. or PCR of vaginal fluids or vaginal swab after
abortion. • Semen or urine—PCR more
United States, Mexico, Japan, South America; CBC/BIOCHEMISTRY/URINALYSIS
practical than culture. • Tissue samples—
Spain, Tunisia, China, Bulgaria; individual • Normal in uncomplicated cases. • Chronic
culture or PCR of prostate, testicle, epididymis,
outbreaks in Germany, Czech Republic. infection—hyperglobulinemia and hypo
lochia, or placenta. • Contaminated
albuminemia. • Cerebrospinal fluid—
SIGNALMENT samples—media that contain antibiotics (e.g.,
neutrophilic pleocytosis, elevated protein
Species Thayer–Martin medium) have proven useful.
(meningoencephalitis); normal in
Dogs discospondylitis. • Urinalysis usually Semen Quality
Breed Predilections normal. • Sperm motility, immature sperm, inflamm
• No evidence of breed susceptibility, atory cells (neutrophils) with epididymitis.
reportedly high prevalence in beagles. • Pure • Abnormalities usually evident by 5–8 weeks
Serologic testing—most common diagnostic
breeds in commercial kennels (“puppy mills”). post infection; conspicuous by 20 weeks.
method; subject to error due to false-positive
• Azoospermia without inflammatory cells
Mean Age and Range reactions to several species of bacteria
common with bilateral testicular atrophy.
• Any age. • Most common in sexually common with tube agglutination tests;
mature dogs. chronically infected dogs may test negative. Lymph Node Biopsy
• Tissues (lymph node, uterus, testes) should
Predominant Sex Rapid 2-Mercaptoethanol Slide
be sterilely obtained, cultured on appropriate
Most common in females. Agglutination Test (RSAT) media, and submitted for histopathology.
• Simple, inexpensive, rapid. • Detects • Lymphoid hyperplasia—large numbers of
SIGNS
infected dogs 3–4 weeks after infection; plasma cells. • Intracellular bacteria—may be
General Comments accurate in identifying noninfected dogs. observed in macrophages with special stains
Suspect with abortions, reproductive failures, • Screening test—sensitive, not specific; high (e.g., Brown–Brenn stain). • Histopathologic
or genital disease. rate (50%) of false-positive tests. • Confirm examination of testes—necrotizing vasculitis,
Historical Findings results with other tests. inflammatory cells, granulomatous lesions.
• Animals may appear healthy or have vague Mercaptoethanol Tube Agglutination PATHOLOGIC FINDINGS
signs of illness. • Lethargy. • Loss of libido. Test (2ME) • Gross findings—lymph node enlargement,
• Swollen lymph nodes. • Back or neck pain. • Semi-quantitative—similar information to splenomegaly, enlarged and firm epididymides,
• Abortion—commonly 6–8 weeks after RSAT, but inactivates immunoglobulin (Ig) M. scrotal edema, or atrophy of one or both testes;
conception, although pregnancy may • Good screening test (lacks specificity). • If chronic infection: anterior uveitis and
terminate at any stage.
discospondylitis. • Microscopic changes—
(continued) Brucellosis
B
diffuse lymphoreticular hyperplasia; chronic chlortetracycline, or minocycline: 25 mg/kg
infection: lymph node sinusoids with plasma PO q8h for 4 weeks) or doxycycline (10 mg/
cells and macrophages that contain bacteria, kg PO q12h for 4 weeks) and dihydrostrepto
diffuse lymphocytic infiltration and granulo mycin (10 mg/kg IM q8h during weeks 1 and MISCELLANEOUS
matous lesions in all genitourinary organs 4). • Enrofloxacin (10–20 mg/kg PO q24h ZOONOTIC POTENTIAL
(especially prostate, epididymis, uterus, and for 30 days)—not recommended: variable • Human infections possible; usually mild
scrotum); inflammatory cell infiltration and results. flu-like symptoms. • Severe infections,
necrosis of prostate parenchyma, seminiferous CONTRAINDICATIONS including hepatomegaly, splenomegaly,
tubules. • Ocular changes—granulomatous Tetracyclines—do not use in immature animals. meningitis, endocarditis reported in
iridocyclitis; exudative retinitis; leukocytic immunocompromised children and adults.
exudates in anterior chamber. ALTERNATIVE DRUG(S)
Gentamicin—6–15 mg/kg IM/SC q12h; PREGNANCY/FERTILITY/BREEDING
limited success; insufficient data on efficacy • Abortions at 45–60 days of gestation
combined with tetracycline. typical. • Pups from infected bitches may be
infected or normal.
TREATMENT SYNONYMS
APPROPRIATE HEALTH CARE Contagious canine abortion.
Outpatient FOLLOW-UP ABBREVIATIONS
ACTIVITY PATIENT MONITORING • 2-ME = mercaptoethanol tube agglutination test.
Restricted • Serologic tests—monthly at least 3 months • AGID = agar gel immunodiffusion.
CLIENT EDUCATION after completion of treatment; continuous, • Ig = immunoglobulin.
• Goal is eradication of B. canis from animal persistent decline in antibodies to negative • RSAT = rapid 2-mercaptoethanol slide
(seronegative, no bacteremia for at least 3 status indicates successful treatment. agglutination test.
months); sometimes result is persistent low • Recrudescent infections (rise in antibody Suggested Reading
antibody titers with no systemic infection. levels, recurrence of bacteremia after therapy)— Greene CE, Carmichael LE. Canine brucel-
• Antibiotic treatment is expensive, time retreat, neuter and retreat, or euthanize. losis. In: Greene CE, ed., Infectious Diseases
consuming, and controversial (because • Blood cultures—negative for at least 3 of the Dog and Cat, 3rd ed. St. Louis, MO:
outcomes are uncertain, and organism has months after completion of treatment. Saunders Elsevier, 2012, pp. 398–411.
potential to recrudesce). • Euthanasia is PREVENTION/AVOIDANCE Johnson CA, Carter TD, Dunn JR, et al.
strongly recommended for breeding or • Vaccine—none. • Testing—all females Investigation and characterization of
commercial kennels; treatment is only before estrus if breeding is planned; breeding Brucella canis infections in pet-quality dogs
recommended for spayed or castrated dogs if males at frequent intervals. • Quarantine and and associated human exposures during a
the owner is willing to accept the ongoing test all new dogs twice at monthly intervals 2007–2016 outbreak in Michigan. JAVMA
zoonotic risk. • Before treatment is attempted before entering breeding kennel; test all 2018, 253:322–336.
for an intact household pet or breeding dog, breeding animals yearly. Kauffman LK, Petersen CA. Canine
client must clearly agree that animal will be brucellosis old foe and reemerging scourge.
neutered and potentially euthanized if POSSIBLE COMPLICATIONS Vet Clin Small Anim 2019, 49:763–779.
treatment fails. • Zoonotic infection is a • Owner reluctance to neuter or euthanize Keid LB, Soares RM, Vasconcellos SA, et al.
possibility; discuss proper sanitation and valuable dogs, regardless of treatment failure. Comparison of agar gel immunodiffusion test,
prevention of exposure. • Remind owners of ethical considerations, rapid slide agglutination test, microbiological
obligation not to sell or distribute infected dogs. culture, and PCR for the diagnosis of canine
Neuter/spay plus treatment—when EXPECTED COURSE AND PROGNOSIS brucellosis. Res Vet Sci 2009, 86:22–26.
euthanasia is unacceptable to owner. • Prognosis guarded. • Infected for <3–4 Author Robyn Ellerbrock
months—likely to respond to treatment. Consulting Editor Amie Koenig
• Chronic infections—may not respond to Acknowledgment The author and book
therapy. • Discospondylitis—may need editors acknowledge the prior contribution of
repeated or long-term drug treatment, rarely Stephen C. Barr.
MEDICATIONS surgical intervention. • Combination therapy
DRUG(S) OF CHOICE with gentamicin or streptomycin, doxycycline,
• Several therapeutic regimens have been enrofloxacin, and rifampin has successfully
available online
evaluated, results have been equivocal; treat- treated ocular disease in dogs. • Successfully
ment duration longer than 30 days may be treated (seronegative) dogs are susceptible to
required. • Most successful—combination of reinfection.
a tetracycline (tetracycline hydrochloride,
Calcipotriene/Calcipotriol Toxicosis
CBC/CHEMISTRY/URINALYSIS rebound hypercalcemia may occur and repeat
C • Hyperphosphatemia. • Hypercalcemia. dosing necessary in 3–7 days. ◦ Prednisone
• Azotemia. • Hyposthenuria, isosthenuria. 1 mg/kg PO BID or dexamethasone 0.2 mg/
BASICS • Neutrophilia. kg IV BID; initially or at a later time; wean
OVERVIEW OTHER LABORATORY TESTS slowly. • Furosemide 1 mg/kg PO BID or
• Calcipotriene, also known as calcipotriol, is Ionized calcium preferred over serum 0.1–0.66mg/kg/h IV CRI- only in well-
a synthetic analogue of calcitriol, an active calcium. hydrated patients. • If hyperphosphatemic -
metabolite of Vitamin D3. • Calcitriol activity: aluminum hydroxide: 30–90 mg/kg/day
• Anti-psoriatic—increases epithelial cell IMAGING divided; with meals.
differentiation and decreases keratinocyte Thoracic and abdominal radiographs—
mineralization of soft tissue structure including CONTRAINDICATIONS/POSSIBLE
proliferation. • Promotes calcium retention—
kidneys, blood vessels, lungs, and intestine. INTERACTIONS
triggers intestinal absorption, renal reabsorption,
• Bisphosphonate use may result in hypo
and mobilization of bone resorption of PATHOLOGIC FINDINGS calcemia. • Long-term adverse effects from
calcium. • Toxic exposure leads to Coronary artery mineralization, gastrointestinal use of bisphosphonates in juvenile/growing
hypercalcemia with soft tissue mineralization hemorrhage and mineralization, renal tubular dog or cat unknown.
(hypercalcemic nephropathy), cardiac necrosis and renal cortical mineralization,
conduction disturbance, and gastrointestinal pulmonary mineralization.
ulceration. • Cream, ointment, foam, and
solution formulation for treatment of human
psoriasis; common tradenames—Calcitrene®, FOLLOW-UP
Dovonex®, Sorilux®, Taclonex®. • Very low PATIENT MONITORING
margin of safety—consider all exposures TREATMENT
• Therapy immediately post ingestion focuses • Baseline CBC, serum chemistry, urinalysis;
toxic. • Organ systems affected— monitor renal values, hydration parameters,
cardiovascular, endocrine/metabolic, on decontamination and serial monitoring; if
hypercalcemia occurs, weeks-long therapy is and calcium/phosphorous levels q12–24h × 4
gastrointestinal, musculoskeletal, nervous, days minimum; if hypercalcemia/hyperphospha
renal/urologic. necessary due to slow release of stored product
from fat/muscle tissue. • Oral irrigation with temia occurs continued monitoring of
SIGNALMENT water if patient has recently licked product. calcium/phosphorous, renal values, and
Dogs and cats, with small or young animals at • Early emesis or gastric lavage. • Activated hydration parameters advised until
increased risk for toxicity. charcoal (1–2 gm/kg) with a cathartic × 1, normalized—up to 3–4 weeks. • Urine
SIGNS followed by activated charcoal only q6–8h × 2 output. • Appetite. • Heart rate/blood
• Early (0–24 hours)—vomiting, anorexia, doses; monitor sodium concentration. • Fluid pressure.
diarrhea, depression, polyuria, polydipsia. therapy—if hypercalcemic: IV 0.9%NaCl PREVENTION/AVOIDANCE
• Late (18–72 hours)—hypercalcemia, rehydrate prn then 2× maintenance to • Do not allow pets to lick humans where
hyperphosphatemia, azotemia/acute renal encourage calciuresis; if normocalcemic: IV or calcipotriene was applied. • Keep medication
injury. • Other—bradycardia, arrhythmias, SC fluids PRN to maintain hydration. inaccessible to pets.
hematemesis, melena, abdominal pain, • Diet—if hypercalcemic: calcium-restricted
prescription diet or veterinary nutritionist- POSSIBLE COMPLICATIONS
oliguria. • End stage—anuria, acute renal Dystrophic mineralization of soft tissue, acute
failure/dystrophic calcification of soft tissue, guided homemade diet.
kidney failure, death.
coma, death.
CAUSES & RISK FACTORS Good prognosis if rapid, aggressive, and
Toxic exposure occurs when pets chew continuing therapy is provided and hypercalcemia/
product tube/bottle or lick skin of human MEDICATIONS hypophosphatemia minimized. Guarded to
where product has been applied. • Antiemetics PRN (e.g. maropitant 1mg/kg
poor prognosis if soft tissue mineralization
SC/IV, 2mg/kg PO q24h). • Proton pump
occurs.
inhibitor (e.g., omeprazole 1 mg/kg PO q24h)
or H2 blocker (e.g., famotidine 1mg/kg IM/
IV/PO/SC q 12-24h; slow IV administration
DIAGNOSIS advised for cats). • Sucralfate (0.25–1g PO
DIFFERENTIAL DIAGNOSIS q8h on empty stomach). • Cholestyramine MISCELLANEOUS
• Vitamin D toxicity—vitamin D (0.3–1 g/kg PO q8h × 4 days post ingestion); Suggested Reading
supplements, cholecalciferol rodenticide. may reduce enterohepatic recirculation of Gwaltney-Brant S, Calcipotriene/calcipotriol.
• Ethylene glycol toxicity. • Grape/raisin vitamin D by reducing reabsorption of vitamin In: Hovda LR, Brutlag A, Poppenga R,
toxicity. • Renal failure—acute or chronic. D–bound bile acids. • If hypercalcemic: Peterson K, eds., Blackwell’s Five-Minute
• Infectious disease—blastomycosis, ◦ Treatment goals—serum calcium <12.5 mg/ Veterinary Consult Clinical Companion:
heterobilharziasis, histomoniasis, bacterial dL or ionized calcium <1.33 mmol/L. Small Animal Toxicology, 2nd ed. Ames, IA:
osteomyelitis. • Hypoadrenocorticism. ◦ Bisphosphonate tx (e.g., pamidronate Wiley-Blackwell, 2016, pp. 172–177.
• Hypercalcemia of malignancy. sodium 1.3–2.0mg/kg diluted in 150cc saline Author Susan Holland
• Hyperparathyroidism, primary. IV CRI × 2–4 h or zoledronate 0.25 mg/kg in Consulting Editor Lynn R. Hovda
• Idiopathic hypercalcemia of cats. • Large- 50cc saline IV CRI x 15 min); bisphosphonates
volume ingestion of calcinogenic plants— block dissolution of calcium hydroxyapatite
Cestrum diurnum, Solanum malacoxylon. and inhibit osteoclastic bone resorption;
• Severe dehydration. reduction in calcium level seen in 1–3 days;
Calcium Channel Blocker Toxicosis

status and large number of pills ingested. CONTRAINDICATION/POSSIBLE
• Temporary cardiac pacing when medical INTERACTIONS C
therapy fails. • IV fluid bolus over 15–20 min Vasopressors/sympathomimetics may not be
BASICS for hypotension—cats, 10–20 mL/kg; dogs, as effective as other therapy and may make
OVERVIEW 20–30 mL/kg. patients less response to other therapy.
• Calcium channel blockers (CCBs): class IV
antidysrhythmics used to treat systemic
hypertension, cardiac disease, tachydys
rhythmias, and oliguric/anuric renal failure in MEDICATIONS
dogs and cats. • CCBs inhibit movement of FOLLOW-UP
Ca through L-type voltage-gated slow Ca DRUG(S) OF CHOICE PATIENT MONITORING
channels located on cardiac muscle, • Activated charcoal (1–2 g/kg) PO, repeat Monitor heart rate/ECG, BP, and BG for
atrioventricular (AV) and sinoatrial (SA) activated charcoal for extended-release (ER) 6–12h with immediate-release preparations
nodes, vasculature smooth muscle, and formulations. • Atropine (0.02–0.04 mg/kg and 12–24h for ER/sustained-release (SR)
pancreatic beta cells. • Three classes of IV) for sinus bradycardia. • Calcium preparations, depending on peak drug levels.
CCBs—phenylalkylamine, benzothiazepine, infusion—first-line therapy despite normo
calcemia to increase Ca availability for muscle EXPECTED COURSE AND PROGNOSIS
dihydropyridine; CCB class determines the • Ingestion of immediate-release preparations
effect on the body. function and improve contractility. ◦ Ca
gluconate 10% bolus 0.5–1.5 mL/kg IV over typically result in clinical signs in 8–12h.
SIGNS 5–10 min followed by CRI of 0.5–1.5 mL/ • SR or ER preparations may take 12–24h
Systems affected include: • Cardiovascular— kg/h, titrated to effect; monitor continuous for clinical signs to develop. • Prognosis
bradycardia, AV dissociation and AV block ECG and infusion should be slowed or depends on dose ingested and response to
(first, second, or third degree), hypotension. stopped if bradycardia or conduction therapy. • Toxicosis normally results in
• Gastrointestinal—vomiting, diarrhea, ileus. blockade worsens. ◦ Ca chloride 10% bolus bradycardia, hypotension, and in severe cases
• Respiratory—pulmonary edema. 0.15–0.5 mL/kg IV; central line decreased mental status, coma, and apnea.
• Nervous—decreased mentation, weakness, recommended due to risk of tissue injury
collapse, seizures. • Endocrine/metabolic— secondary to drug extravasation.
hyperglycemia, metabolic acidosis secondary • Intravenous fat emulsion (IFE)—may bind
to hypoperfusion. lipid-soluble drugs, increase Ca available for MISCELLANEOUS
muscle contraction, and provide an energy
ABBREVIATIONS
source for heart muscle. ◦ IFE 20% solution
dose—1.5 mL/kg IV bolus over 1 min; follow
• BG = blood glucose.
DIAGNOSIS with CRI of 0.25 mL/kg/min for 30–60 min;
• CCB = calcium channel blocker.
additional IV doses: 1.5 ml/kg every 4–6h or
DIFFERENTIAL DIAGNOSIS • ER = extended release.
CRI of 0.5 mL/kg/h; monitor serum for
• Beta blocker antagonist toxicosis. • Cardiac • HIE = high-dose insulin euglycemia.
lipemia every 2–4h to determine if additional
disease with bradyarrhythmias. • IFE = Intravenous fat emulsion.
dosing is needed. • High-dose insulin
• Cardiovascular drug overdose (e.g., • SA = sinoatrial.
euglycemia (HIE) treatment—may provide
clonidine, digoxin toxicosis). • Sedative • SR = sustained release.
energy for heart muscle and increase Ca
overdose (e.g., opioid or baclofen toxicosis). Suggested Reading
available for muscle contraction.
• Sick sinus syndrome. • Hyperkalemia. Hayes CL, Knight M. Calcium channel
Recommended treatment: ◦ Check blood
• Decompensated shock. blocker toxicity in dogs and cats. Vet Clin
glucose (BG) concentration and administer
CBC/CHEMISTRY/URINALYSIS dextrose if BG <100 mg/dL. ◦ Administer North Am Small Anim Pract 2012:
• Hyperglycemia. • Azotemia and elevated regular insulin at 1 unit/kg IV, followed by 42:263–277.
liver enzymes with prolonged hypo- CRI at 0.5–2 units/kg/h; may increase every Author Katherine L. Peterson
perfusion. 10 min up to maximum dose of 10 units/ Consulting Editor Lynn R. Hovda
OTHER LABORATORY TESTS kg/h; when signs resolve, decrease insulin by
Blood gas—metabolic acidosis. 1–2 units/kg/h. ◦ Monitor BG every 10 min
while titrating insulin dose; once stabilized, Client Education Handout
IMAGING check BG every 30–60 min; central line available online
Chest radiographs to evaluate for pulmonary placement recommended for frequent glucose
edema with respiratory signs. monitoring and dextrose administration
DIAGNOSTIC PROCEDURES during HIE treatment; dextrose supplemen
• ECG—first-, second-, and third-degree AV tation will be needed to maintain normal BG
block; prolonged PR, QRS, and QT intervals. concentrations and continued up to 24h after
• Echocardiogram—negative inotropy, discontinuation of insulin therapy. ◦ Monitor
decreased cardiac output. potassium concentration every hour during
titration, then every 6h; administer potassium
chloride to keep potassium concentrations
within normal range. • Glucagon—may not
be as effective as HIE or IFE; dose is
TREATMENT 0.05–0.2 mg/kg slowly IV bolus, followed by
• Emesis if asymptomatic and <2 hours after CRI of 0.05–0.1 mg/kg/h.
exposure. • Gastric lavage if decreased mental
Campylobacteriosis
C • Fecal leukocytes—in gastrointestinal tract
and stool. • Fecal culture—submit feces in
BASICS Amies transport medium with charcoal or FOLLOW-UP
OVERVIEW Cary-Blair medium kept refrigerated at 4 °C PATIENT MONITORING
• Campylobacter jejuni—fastidious, in transit. • Species-specific quantitative Repeat fecal culture after treatment.
microaerophilic, Gram-negative curved PCR—current methodology may be biased to
bacteria; often isolated from healthy dogs and detect C. jejuni and C. coli.
• Good hygiene (hand washing). • Routinely
cats; may cause superficial erosive entero Direct Examination of Feces clean and disinfect runs, food and water
colitis. • Infection—fecal–oral route from • Gram stain—make smear; leave Gram bowls. • Do not feed raw-meat diets to
contaminated food, water, raw meat safranin on for longer period. • Wet companion animals.
(especially chicken), environment; localized mount—large numbers of highly motile
in crypts of intestine; motile; produces EXPECTED COURSE AND PROGNOSIS
bacteria (characteristic darting motility).
multiple enterotoxins. • Invasion of gut • Adults—usually self-limiting. • Juveniles
mucosa—hematochezia, inflammation, PATHOLOGIC FINDINGS with severe or persistent enterocolitis—
ulceration, edema; bacteria shed in feces for • Gross—diffuse colon thickening, prognosis good with appropriate intervention.
weeks to months. • Up to 49% of dogs congestion/edema; hyperemia of small
without diarrhea and 45% of normal cats intestine; enlarged mesenteric lymph nodes.
carry C. jejuni and shed it in feces. • Thickening of intestinal smooth muscle in
cats.
SIGNALMENT MISCELLANEOUS
• Dogs; less commonly cats. • Prevalence— ASSOCIATED CONDITIONS
higher in puppies and kittens up to 6 months. Concurrent infection with other pathogenic
• Can cause chronic disease. bacteria, enteric parasites, viruses.
TREATMENT
SIGNS ZOONOTIC POTENTIAL
• Diarrhea—varies; mucoid and watery, Mild Enterocolitis
High (C. jejuni, C. coli, C. upsaliensis).
hemorrhagic; may be chronic. • Tenesmus. • Outpatient. • Usually self-limiting.
• Fever, anorexia, intermittent vomiting PREGNANCY/FERTILITY/BREEDING
Severe Enterocolitis
possible. • Adults—may be asymptomatic Erythromycin—safe in early pregnancy.
• Inpatient, especially if very young, fever,
carriers. • Abortion and perinatal death. hematochezia, melena. • Severe neonatal INTERNET RESOURCES
CAUSES & RISK FACTORS disease—isolate; aggressive therapy. • NPO http://www.cfsph.iastate.edu/DiseaseInfo/
• C. jejuni, C. coli, C. upsaliensis, C. for 24 hours; then bland diet. • Mild disease.php?name=campylobacteriosis&l
helviticus, C. lari, and more uncommon dehydration—oral fluid therapy with enteric ang=en
species. • Kennels/intensive housing, poor fluid replacement solution. • Severe Suggested Reading
sanitation/hygiene, fecal contamination in dehydration—intravenous fluid therapy with Acke E. Campylobacteriosis in dogs and cats:
environment. • Young animals—debilitated, balanced isotonic replacement solution. a review. N Z Vet J 2018, 66:221–228.
immunosuppressed, parasitized. • Plasma transfusion may be required. Marks SL, Rankin SC, Byrne BA, et al.
• Nosocomial infection in hospitalized • Locally acting intestinal adsorbents/ Enteropathogenic bacteria in dogs and cats:
patients. • Adults—concurrent intestinal protectants. diagnosis, epidemiology, treatment, and
infections (e.g., Salmonella, parvovirus, control. J Vet Intern Med 2011,
hookworms). • Feeding homemade or 25:1195–1208.
commercially available raw meat–based Montgomery MP, Robertson S, Koski L, et al.
diets. MEDICATIONS MDR Campylobacter jejuni outbreak
linked to puppy exposure. MMWR Morb
DRUG(S) OF CHOICE Mortal Wkly Rep. 2018, 67:1032–1035.
• Antibiotics—for systemic illness (e.g., high
Author Patrick L. McDonough
fever, dehydration), when diarrhea or Consulting Editor Amie Koenig
DIAGNOSIS abnormal clinical signs persist >7 days, in
DIFFERENTIAL DIAGNOSIS immune-suppressed patients. • Erythromycin
• Bacterial enterocolitis—Salmonella, Yersinia 10–20 mg/kg PO q8h for 5 days; drug of
enterocolitica, Clostridium difficile, Clostridium choice. • Enrofloxacin—dog, 10 mg/kg PO/
perfringens. • Parasitic—helminths (whipworms); IV/IM q24h; cat, 5 mg/kg PO/IM/IV q24h.
protozoa (Giardia, Isospora). • Viral— • Tylosin 11 mg/kg PO q8h for 7 days.
parvovirus; signs often more severe. • Dietary • Septicemia—parenteral broad-spectrum
indiscretion, intolerance. • Drugs, toxins. antibiotics indicated. • Multidrug resistance
• Pancreatitis. • Intussusception, other causes (vs. macrolides, quinolones) becoming more
of abdominal pain. • Distinguish from other common.
causes of chronic diarrhea. • Primary CONTRAINDICATIONS/POSSIBLE
intestinal disease. INTERACTIONS
CBC/BIOCHEMISTRY/URINALYSIS • Antidiarrheal drugs that reduce intestinal
• Leukocytosis—possible. • Biochemistry motility are contraindicated. • Enrofloxacin—
abnormalities—effects of diarrhea, may induce arthropathy in dogs <28 weeks of
dehydration (e.g., azotemia, electrolyte age; caution with use in cats.
disturbances).
Candidiasis
• Fluconazole—5 mg/kg PO q12h; very
effective and excreted unchanged in urine (high C
concentration in commonly infected sites).
BASICS DIAGNOSIS • Itraconazole—5–10 mg/kg PO q12h;
OVERVIEW DIFFERENTIAL DIAGNOSIS effective, can use if organism resistant to
• Candida—dimorphic fungus with the yeast Considered whenever the primary condition fluconazole; not recommended for urinary tract
phase (Candida spp.) being part of the normal does not respond as expected. infection (poor urinary excretion).
flora of the mouth, nose, ears, and gastrointestinal • In lower urinary tract Candida infections
(GI) and urogenital tracts of dogs and cats. resistant to fluconazole—infuse 10–30 mL of
• Reflect underlying inflammation and organ
• C. albicans and C. parapsilosis most 1% clotrimazole into the bladder every other
involvement (unless neutropenic).
commonly cultured from clinically healthy day for three treatments.
• Urinalysis—may show yeast or clumps of
dogs. • Candida may develop drug resistance—
mycelial elements (pseudohyphae) with
• Recovery from mucosal surfaces does not consider drug sensitivity testing if suspected.
inflammatory cells; concurrent bacterial
imply disease; organisms may cause oppor • Caspofungin—may be option for resistant
urinary tract infection common.
tunistic infection, colonize damaged tissues, or isolates.
invade normal tissues of immunosuppressed OTHER LABORATORY TESTS
animals. • Cytology—spherical to oval yeast cells
• Pathogenic role determined by infiltration 5–7 μm in diameter; pseudohyphae and
of organisms into tissues, or detection of septate hyphae 3–5 μm wide.
• Culture—grows well on blood agar and
FOLLOW-UP
organisms in presumed sterile sites (e.g.,
urinary bladder, peritoneal cavity). often is isolated from specimens submitted PATIENT MONITORING
• Organ systems most affected include GI, for bacterial culture; more easily isolated from • Fluconazole and itraconazole—hepatic
renal/urologic, skin, and respiratory. urine than blood. toxicity; monitor serum alanine aminotransferase
• Conditions that suppress the immune • PCR and antigen tests available. (ALT) activity monthly initially and check if
system (e.g., feline immunodeficiency virus DIAGNOSTIC PROCEDURES patient becomes anorexic.
[FIV] infection) increase the likelihood of • After signs have resolved—reculture sites of
• Lesions—to determine if Candida is truly a
isolation in asymptomatic animals. pathogen, requires demonstration of infection; continue treatment for 2 weeks
organisms penetrating the tissues. beyond negative culture; repeat cultures 2 weeks
SIGNALMENT after completion of treatment and again if signs
Cats and dogs—any age and breed. • Urine sample—cystocentesis; culture of
multiple colonies of Candida supports recur.
SIGNS diagnosis. EXPECTED COURSE AND PROGNOSIS
• Nonhealing ulcers in the oral, upper • Should resolve within 2–4 weeks of treatment
• Otitis (dogs)—culture of Candida spp. or
respiratory, GI, or urogenital mucosa—signs identification of yeast or mycelial elements on with correction of immunosuppression.
reflect location/extent of disease: ear cytology suggests diagnosis. • Control of the underlying disease is
◦ Cystitis—hematuria, stranguria, and necessary to prevent recurrence.
• In febrile patients, culture catheter tips.
pollakiuria. • May resolve spontaneously if the underlying
◦ Otitis—head shaking, scratching. PATHOLOGIC FINDINGS
• White caseous foci in the infected tissue.
condition is corrected.
◦ Oral cavity—drooling.
• Inflammation around IV catheters or • Large numbers of both yeast and pseudo-
gastrotomy tubes. hyphae in tissues surrounded by necrosis and
• Ulcerative, red skin lesions. suppurative inflammatory reaction.
• Systemic disease with fever, cardiac and/or • May be pyogranulomatous in more chronic MISCELLANEOUS
neurologic abnormalities can be seen. infections.
ZOONOTIC POTENTIAL
CAUSES & RISK FACTORS Genetic similarities between human and
• Infection—rare; associated with neutro animal isolates suggest a potential for transfer
penia, parvovirus or FIV infection, of C. albicans between species.
endocrinopathies, glucocorticoid therapy, TREATMENT ABBREVIATIONS
gastrotomy tubes, indwelling urinary • Treat underlying causes of • ALT = alanine aminotransferase.
catheters/urethrostomy, IV catheters, and immunosuppression. • FIV = feline immunodeficiency virus.
incomplete bladder emptying. • Remove indwelling catheters, if possible. • GI = gastrointestinal.
• Lower urinary tract disease may predispose
to candiduria. Suggested Reading
• Administration of antibiotics in prior 30 days. Reagan KL, Dear JD, Kass PH, et al. Risk
• Occasionally local or systemic infection is factors for Candida urinary tract infections
MEDICATIONS in dogs and cats. J Vet Intern Med 2019,
seen in animals without predisposing
conditions. DRUG(S) OF CHOICE 33:648–653.
• Skin damaged by burns, trauma, or • Topical therapy (mucosal lesions)—nystatin Author Daniel S. Foy
necrotizing dermatitis. or amphotericin B. Consulting Editor Amie Koenig
Canine Coronavirus Infections

• For CRCoV—respiratory secretions,
C fomites likely sources of infection.
BASICS FOLLOW-UP
OVERVIEW PREVENTION/AVOIDANCE
• Canine enteric coronavirus (CCoV)— DIAGNOSIS • CCoV vaccines—controversial; inactivated
sporadic outbreaks of enteritis in dogs; and live viral vaccines; appear safe; moderate
worldwide distribution. DIFFERENTIAL DIAGNOSIS efficacy may be due to variability of CCoV
• Canine pantropic coronavirus (CPCoV)— • Infections caused by enteric bacteria, strains; not recommended; do not cross-
variant of CCoV, fatal disease in dogs <6 protozoa, other viruses; canine kennel cough protect against CPCoV, CRCoV.
months, described principally in Europe. complex pathogens. • Strict quarantine, sanitation essential in
• CCoV, CPCoV—closely related to feline • Other mild to moderate upper respiratory kennels: susceptible to common disinfectants.
infectious peritonitis (FIP) virus, feline disease. • CCoV, CRCoV—highly contagious; spread
enteric coronavirus. • Food intoxication or intolerance. rapidly.
• Canine respiratory coronavirus (CRCoV)— CBC/BIOCHEMISTRY/URINALYSIS POSSIBLE COMPLICATIONS
associated with canine infectious respiratory Normal; lymphopenia with more virulent Diarrhea with CCoV—may persist 10–12
disease complex (kennel cough); worldwide CCoV isolates. days, may recur.
distribution; genetically and serologically
distinct from CCoV. OTHER LABORATORY TESTS EXPECTED COURSE AND PROGNOSIS
• Incubation period 1–3 days.
Serologic tests—available; not standardized, • Prognosis—good, except severe infections
• CCoV infection—usually inapparent; mild to
difficult to interpret due to frequent asympto- of young pups.
severe enteritis possible; death reported in young matic infection. • Majority recover after short illness.
pups; infects upper two-thirds of small intestine DIAGNOSTIC PROCEDURES
and associated lymph nodes; crypt cells spared. • Viral isolation for CCoV, CRCoV—
• Simultaneous infection with canine parvo- possible but not recommended.
virus (CPV)-2 possible; severe, often fatal. • Specific reverse transcriptase polymerase MISCELLANEOUS
• CPCoV—infects intestinal tract, after short chain reaction (RT-PCR)—using feces for
viremia distributes to organs like spleen, lungs, CCoV, respiratory swabs for CRCoV; ASSOCIATED CONDITIONS
brain. CPCoV defined by presence of virus in • Concurrent infection with CPV or other
• Coronaviruses undergo rapid evolution, are extraintestinal organs. agent.
highly variable; differences in virulence likely • Immunofluorescence of small intestine— • Infections with other respiratory pathogens
between isolates. fatal cases; may show viral antigen in cells with CRCoV.
SIGNALMENT lining villous epithelium. ABBREVIATIONS
• Dogs of all ages, breeds; disease more severe PATHOLOGIC FINDINGS • CCoV = canine enteric coronavirus.
in young. • Gross—dilated small intestine filled with • CPCoV= canine pantropic coronavirus.
• CRCoV infections more common in gas, watery green-yellow material. • CPV = canine parvovirus.
winter, in shelters. • Bowel loops congested, hemorrhagic; • CRCoV = canine respiratory coronavirus.
mesenteric lymph nodes enlarged, • FIP = feline infectious peritonitis.
SIGNS • RT-PCR = reverse transcriptase polymerase
• Vary greatly—CPCoV virulent isolates
edematous.
• Histopathology—atrophy and fusion chain reaction.
cause systemic disease.
• Adults—most infections inapparent.
of intestinal villi, deepening of crypts, Suggested Reading
• Puppies—mild to severe, occasionally fatal,
increased cellularity of lamina propria, Decaro N, Cordonnier N, Demeter Z, et al.
enteritis. epithelial cell flattening, increased goblet European surveillance for pantropic canine
• Diarrhea—may be explosive; yellow-green or
cells. coronavirus. J Clin Microbiol 2013,
• CPCoV—hemorrhagic lesions in various 51:83–88.
orange; loose or liquid; typically malodorous
(characteristic); may persist for days to >3 organs (lungs, small intestines, spleen, lymph Mitchell JA, Cardwell JM, Leach H. European
weeks; may recur; young dogs may suffer nodes). surveillance of emerging pathogens associated
severe, protracted diarrhea, dehydration. with canine infectious respiratory disease. Vet
• Vomiting. Microbiol 2017, 212:31–38.
• Coughing, dyspnea—CRCoV associated Author Sophie Le Poder
with kennel cough complex. TREATMENT Consulting Editor Amie Koenig
• Anorexia, lethargy. • Most dogs recover without treatment. Acknowledgment The author and book
• For CPCoV—pyrexia, anorexia, depression, • CCoV—fluid, electrolyte treatment if editors acknowledge the prior contribution of
vomiting, hemorrhagic enteritis, respiratory dehydration severe. John S. Parker.
distress, and leukopenia that persists >1 week; • CRCoV—as for canine kennel cough
ataxia, seizures, and death also possible. complex.
• Stress—greatest risk; sporadic outbreaks
have occurred in dogs attending shows, in
kennels where new dogs frequently intro MEDICATIONS
duced; crowding and unsanitary conditions
promote illness. DRUG(S) OF CHOICE
• For CCoV, CPCoV—feces primary source Antibiotics—not usually indicated, except
of infection; virus shed for 2 weeks. with enteritis, sepsis, severe respiratory illness.
Canine Degenerative Myelopathy

Worldwide C
BASICS SIGNALMENT DIAGNOSIS
Canine progressive adult-onset fatal neurode- So far the DM-associated SOD1:c.118A allele • Type II intervertebral disc herniation.
generative disease that has recently been is in >150 breeds or varieties; a second SOD1 • Intramedullary spinal cord neoplasia.
shown in many breeds to be a result of a mutation (c.52 A>T) was found only in • Degenerative lumbosacral stenosis.
mutation in the superoxide dismutase 1 gene Bernese mountain dogs. DM has been • Hip dysplasia.
(SOD1). Mutations in SOD1 are known to histopathologically confirmed in many • Other coexisting orthopedic disease.
cause some forms of amyotrophic lateral purebred and mixed-breed dogs.
sclerosis (ALS), also known as Lou Gehrig’s Mean Age and Range • Usually normal.
disease. Initial signs of progressive upper • Mean—9 years of age in large dogs; mean • Performed to rule out other underlying
motor neuron spastic paresis and general age at onset is 11 years in Pembroke Welsh metabolic disease.
proprioceptive ataxia in the pelvic limbs occur corgi. • Urinalysis may identify secondary urinary
in older dogs. If euthanasia is delayed, clinical • Range—between 8 and 14 years. tract infection.
signs progress to flaccid tetraparesis/plegia
Predominant Sex OTHER LABORATORY TESTS
and other lower motor neuron signs.
No known sex predilection. • Urine culture and sensitivity testing.
PATHOPHYSIOLOGY SIGNS • Thyroid function testing.
• A c.118 G>A transition in Exon 2 of SOD1 • Early: • Electrodiagnostic testing results are normal
that predicts an E40K missense mutation ◦ Upper motor neuron paraparesis. in early diagnosis of DM.
underlies most degenerative myelopathy (DM); ◦ Insidious, progressive, asymmetric • Genetic testing—test result of at-risk can
a second SOD1 missense mutation (c.52 A>T) general proprioceptive ataxia; gait shows support a presumptive diagnosis of DM in
has been seen only in Bernese mountain dogs. long-strided spastic paraparesis. light of typical clinical signs and normal
• Lesions may represent a multisystem ◦ Paw replacement deficits. findings on neuroimaging and cerebrospinal
central-peripheral axonopathy. ◦ Spinal reflexes usually present or fluid analysis.
• Predilection for lesion severity in mid- exaggerated (patellar reflex may be
thoracic spinal cord may be a result of lower IMAGING
reduced). • Survey spinal radiography.
percentages of radicular artery contributions ◦ Presence of crossed-extensor reflex is
and small-diameter vessels when compared to • Myelography evaluates for compressive
variable. spinal cord disease.
other spinal cord regions. ◦ Lack of paraspinal hyperesthesia is key
• Paucity of vascular supply in thoracic spinal • Myelography combined with CT—more
clinical feature. sensitive technique to evaluate suspicious
cord may predispose it to damage from • Later:
oxidative and metabolic disturbances. lesions.
◦ Pelvic limb paresis leading to plegia, • MRI—preferred technique to evaluate for
SYSTEMS AFFECTED eventually progressing to tetraparesis/ extramedullary compressive and intramedul-
• Central and peripheral nervous systems. plegia. lary lesions.
• Thoracolumbar spinal cord in early stage. ◦ Mild to moderate loss of muscle mass in
pelvic limbs due to neurogenic atrophy. DIAGNOSTIC PROCEDURES
• Progresses to involve the cervical and
◦ Reduced spinal reflexes in pelvic limbs. • CSF analysis evaluates for inflammatory
lumbar spinal cord and peripheral nervous
◦ ± Urinary and fecal incontinence. disease.
system later in the course of the disease.
• End stage: • Definitive diagnosis is determined by
• Neurons in the brainstem also may be affected.
◦ Flaccid tetraplegia. post-mortem histopathology of spinal cord.
• Disease also involves the sensory nerve roots
and dorsal root ganglia. ◦ Difficulty with swallowing and tongue PATHOLOGIC FINDINGS
movements. • Spinal cord axons and myelin affected most
GENETICS ◦ Absence of spinal reflexes in all limbs. severely in dorsal and dorsal portion of lateral
• Most commonly autosomal recessive ◦ Reduced to absent cutaneous trunci funiculi.
inheritance. reflex. • Vacuolated axon cylinders/myelin sheaths
• Due to preponderance of purebred dogs ◦ Profound generalized muscle wasting. most extensive in mid-thoracic spinal cord.
affected, a familial inheritance is currently ◦ Urinary and fecal incontinence. • Astroglial proliferation is prominent in
suspected. severely affected areas of lesion distribution.
• Mutations in SOD1 are causative for DM
CAUSES
• Hereditary disease and genetic predi- • Usually, lesion distribution is described as
but are incompletely penetrant. asymmetric and discontinuous; however,
• Dogs that are homozygous for the mutant
sposition.
• Other hypothesized causes include more recent evidence describes lesion distrib
allele are at highest risk for developing DM; not ution as symmetric and continuous in dogs
all dogs that test homozygous for the mutation immune-mediated, metabolic deficiencies,
toxic, and oxidative stress. that survive for long periods with DM.
will develop DM, but dogs that test normal • Neuronal cell body loss in ventral horn is
(clear) are highly unlikely to develop DM; dogs RISK FACTORS evident at terminal or end-stage disease.
that test carrier are less likely to develop DM, • Dogs homozygous for the mutant allele(s) • Nerve specimens show fiber loss resulting
but this has been documented in some breeds. are at highest risk. from axonal degeneration and secondary
• There may be other environmental factors demyelination.
Prevalence rate of DM reported for all dogs and modifying genes; studies underway. • Muscle specimens show large and small
collected from the Veterinary Medical groups of atrophic fibers typical of denervation.
Database (1990–1999) was 0.19%.
Canine Degenerative Myelopathy (continued)
• Intervertebral Disc Disease, Thoracolumbar.

C • Lumbosacral Stenosis and Cauda Equina
Syndrome.
TREATMENT FOLLOW-UP
ABBREVIATIONS
APPROPRIATE HEALTH CARE PATIENT MONITORING • ALS = amyotrophic lateral sclerosis.
• Supportive care. • Repeat neurologic examinations. • DM = degenerative myelopathy.
• Breeds of small size may survive longer with • Urine retention. • SOD1 = superoxide dismutase 1.
DM because the pet owner is able to more • Urinalysis and urine culture to monitor for
easily give the appropriate care. urinary tract infection. INTERNET RESOURCES
• www.caninegeneticdiseases.net/dm/
NURSING CARE PREVENTION/AVOIDANCE maindm.htm
• When dog becomes nonambulatory, keep • Decubitus ulceration. • www.ofa.org/diseases/dna-tested-diseases/dm
on a well-padded surface to prevent decubitus • Urine retention.
ulceration over bony prominences. • Dermatitis from urine scald. Suggested Reading
• Keep hair trimmed, and skin clean and • Weight gain. Awano T, Johnson GS, Wade C, et al.
dry to prevent urine scald secondary to Genome-wide association analysis reveals a
POSSIBLE COMPLICATIONS SOD1 missense mutation canine degenera-
incontinence. • Urine retention may predispose to urinary
• Urine should be monitored for odor and tive myelopathy that resembles amyotrophic
tract infections. lateral sclerosis. Proc Natl Acad Sci USA
color change, which may indicate urinary • Local skin infections from decubitus ulceration.
tract infection. 2009, 106:2794–2799.
• Physical therapy using range-of-motion and EXPECTED COURSE Coates JR, March PA, Ogelsbee M, et al.
active exercises may help maintain limb AND PROGNOSIS Clinical characterization of a familial
mobility and muscle strength. • Nonambulatory paraparesis occurs within degenerative myelopathy in Pembroke
9–12 months from time of onset of signs. Welsh Corgi dogs. J Vet Intern Med 2007,
ACTIVITY 21:1323–1331.
• Tetraparesis may be evident within 3 years
• Exercise is encouraged to slow disuse Coates JR, Wininger FA. Canine degenerative
atrophy of pelvic limbs, but fatigue should from time of onset of signs.
• Long-term prognosis is poor. myelopathy. Vet Clin North Am Small
be monitored and exercise intensity Anim Pract 2010, 40:929–950.
adjusted. March PA, Coates JR, Abyad R, et al.
• Hydrotherapy can involve use of an Degenerative myelopathy in 18 Pembroke
underwater treadmill setup. Welsh Corgi dogs. Vet Pathol 2009,
• A wheel cart may assist with patient MISCELLANEOUS 46:241–250.
mobility. Ogawa M, Uchida K, Yamato O, et al.
DIET • Other neurologic diseases associated with Neuronal loss and decreased GLT-1
• Maintain balanced diet. old-age onset. expression observed in the spinal cord of
• Prevent weight gain. • Spinal cord neoplasia. Pembroke Welsh Corgi Dogs with canine
• Intervertebral disc disease. degenerative myelopathy. Vet Pathol 2014,
CLIENT EDUCATION
• Orthopedic disease. 51:591–602.
• Long-term prognosis is poor.
Wininger FA, Zeng R, Johnson GS, et al.
• Meticulous nursing care is crucial to AGE-RELATED FACTORS Degenerative myelopathy in a Bernese
preventing secondary complications in a Older dogs commonly affected. Mountain Dog with a novel SOD1 missense
recumbent patient.
ZOONOTIC POTENTIAL mutation. J Vet Intern Med 2011,
SURGICAL CONSIDERATIONS None 25:1166–1170.
None Zeng R, Coates JR, Johnson GC, et al. Breed
distribution of SOD1 alleles previously
N/A
associated with canine degenerative myelopa-
SYNONYMS thy. J Vet Intern Med 2014, 28:515–521.
• Canine ALS. Author Joan R. Coates
MEDICATIONS • DM.
DRUG(S) OF CHOICE • Degenerative radiculomyelopathy.
Clinical trials are underway to determine • German Shepherd dog myelopathy. Client Education Handout
effectiveness in slowing or halting disease SEE ALSO available online
progression. • Intervertebral Disc Disease, Cervical.
Canine Distemper
◦ Gray matter disease—affects cerebral dog are suggestive of infection; may be useful
cortex, brainstem, and spinal cord and may for risk assessment of clinically healthy dogs C
cause a nonsuppurative meningitis, in shelter environment.
BASICS seizures, mentation change, and ataxia; • CDV antibody in cerebrospinal fluid
DEFINITION dogs may die in 2–3 weeks; some dogs (CSF)—indicative of distemper encephalitis,
• Acute to subacute, contagious, febrile, often recover (associated with prompt humoral false negatives possible.
fatal disease with respiratory, urogenital, and cell-mediated immunity), others IMAGING
gastrointestinal, ocular, and CNS manifest- develop white matter disease. • Radiographs—evaluate pulmonary disease.
ations. ◦ White matter disease—multifocal disease, • CT and MRI—may or may not show
• Caused by canine distemper virus (CDV), a commonly cerebellovestibular signs, paresis, lesions; MRI sensitive for demyelination.
Morbillivirus in the Paramyxoviridae family. ataxia, occasionally myoclonus; some dogs
• Affects many Carnivora species; mortality die 4–5 weeks after initial infection with DIAGNOSTIC PROCEDURES
rate varies greatly. noninflammatory, demyelinating disease; some • Immunohistochemical detection in haired
dogs may recover with minimal CNS injury. skin, nasal mucosa, and footpad epithelium.
PATHOPHYSIOLOGY
• Optic neuritis and retinal lesions may • Viral antigen or viral inclusions—in buffy
• Natural route of infection—airborne and
occur; anterior uveitis, keratoconjunctivitis coat cells, urine sediment, conjunctival or
droplet exposure; from nasal cavity, pharynx,
sicca possible. vaginal imprints, trans-tracheal wash
and lungs, virus replication occurs in local
• Hardening of footpads (hyperkeratosis) and (negative results do not rule out CDV).
lymph nodes; within 1 week, viral shedding
nose—some virus strains; uncommon. • Reverse transcriptase polymerase chain
occurs (mainly in respiratory exudates but also
• Enamel hypoplasia of teeth after neonatal reaction (RT-PCR)—on buffy coat, urine
urine) and virtually all lymphatic tissues
infection. sediment cells, respiratory secretions,
become infected; spreads via viremia to surface
epithelium of respiratory, gastrointestinal, and CAUSES conjunctival swabs, CSF; false negatives
urogenital tracts and to CNS. • CDV exposure. possible, false positives with recent
• Disease progression depends on virus strain • Incompletely attenuated vaccines (rare). vaccination (uncommon).
• CSF—moderate mononuclear pleocytosis,
and host immune response: RISK FACTORS
◦ Strong cellular and humoral immune
elevated concentrations of CDV-specific
Contact of nonimmunized animals with antibody, interferon, and viral antigen early in
response—subclinical infection. CDV-infected animals (dogs, wild carnivores).
◦ Weak immune response—subacute
disease course.
infection; longer survival. PATHOLOGIC FINDINGS
◦ Failed immune response—death within
2–4 weeks after infection; frequently due to Gross
CNS manifestations. DIAGNOSIS • Thymus—greatly reduced in size (young
• Viral excretion can occur for up to 2–3 months. animals); sometimes gelatinous.
• Lungs—patchy consolidation.
SYSTEMS AFFECTED • Diagnosis based on clinical suspicion;
• Footpads, nose—hyperkeratosis.
• Multisystemic—all lymphatic tissues, combination of respiratory and gastrointestinal,
• Mucopurulent discharges—from eyes and
surface epithelium in respiratory, alimentary, ± CNS disease, in unvaccinated dog.
nose, bronchopneumonia, catarrhal enteritis,
and urogenital tracts, skin, endocrine and • Respiratory signs—can mimic kennel cough.
skin pustules (secondary bacterial infection).
exocrine glands. • Enteric signs—differentiate from canine
• CNS—brain and/or spinal cord. parvovirus, coronavirus, parasitism (giardiasis), Histologic
bacterial infections, gastroenteritis from toxin • Intracytoplasmic eosinophilic inclusion
INCIDENCE/PREVALENCE ingestion, inflammatory bowel disease. bodies—in epithelium of bronchi, stomach,
• Dogs—sporadic outbreaks. • CNS form—differentiate from auto urinary bladder; also in reticulum cells and
• Wildlife (raccoons, skunks, fox, tigers)— immune meningoencephalitis (granulomatous leukocytes in lymphatic tissues.
fairly common. meningoencephalomyelitis, necrotizing • Inclusion bodies in glial cells and neurons—
GEOGRAPHIC DISTRIBUTION encephalitis, meningoencephalitis of frequently intranuclear; also in cytoplasm.
Worldwide unknown etiology), protozoal (e.g., • Immunofluorescence and/or immunocyto
toxoplasmosis, neosporosis), fungal (e.g., chemistry, virus isolation, and/or RT-PCR
SIGNALMENT
cryptococcosis), and rickettsial (e.g., performed on tissues from lungs, stomach,
Species ehrlichiosis, Rocky Mountain spotted fever) urinary bladder, lymph nodes, brain.
Most species of the order Carnivora; has been meningoencephalitis, rabies.
reported in large exotic cats.
Mean Age and Range Lymphopenia in early infection; rare
Young, especially unvaccinated animals are thrombocytopenia; intracytoplasmic TREATMENT
most susceptible. inclusions in white and red blood cells. APPROPRIATE HEALTH CARE
SIGNS OTHER LABORATORY TESTS Inpatient medical management to intensive
• Fever—intermittent peaks starting 3–6 days • Serology—positive antibody tests do not care as indicated; isolate patient to prevent
after infection. differentiate between vaccination and spread to other dogs.
• Gastrointestinal and/or respiratory signs— exposure to virulent virus; patient may die
nasal and ocular discharge, depression, NURSING CARE
from acute disease before neutralizing • Symptomatic.
anorexia, vomiting, diarrhea; often exacer antibody is produced. Immunoglobulin (Ig) • IV fluids—for hypovolemia, support.
bated by secondary bacterial infection. M responses may occur up to 3 months after • Oxygen therapy, nebulization, and
• CNS—common; generally after systemic exposure to virulent virus, up to 3 weeks after
disease (depends on virus strain). coupage—for pneumonia.
vaccination; rising IgG titers in unvaccinated • Clean ocular, nasal discharges.
Canine Distemper (continued)
ACTIVITY • Modified live vaccine for CDV (MLV-CD)— AGE-RELATED FACTORS

C Limited, to reduce spread. prevents infection and disease; two types • Young puppies—more susceptible;
DIET available: mortality rate is higher.
◦ Canine tissue culture-adapted vaccines • Nonimmunized old dogs—highly
Depends on extent of gastrointestinal
involvement. (e.g., Rockborn strain)—induce complete susceptible to infection and disease.
immunity in virtually 100% of susceptible ZOONOTIC POTENTIAL
CLIENT EDUCATION dogs; rarely, a postvaccinal fatal encephalitis
• Inform client that mortality rate is about 50%. Possible that humans may become subclini-
develops 7–14 days after vaccination, cally infected with CDV; immunization
• Inform client that dogs appearing to recover especially in immunosuppressed animals.
from early catarrhal signs may develop fatal against measles virus also protects against
◦ Chick embryo-adapted vaccines (e.g.,
CNS disease. CDV infection.
Lederle strain)—safer; postvaccinal
• Presenting neurologic abnormalities usually encephalitis does not occur; only about PREGNANCY/FERTILITY/BREEDING
not reversible. 80% of susceptible dogs seroconvert. In utero infection—occurs in antibody-nega-
◦ Other species—chick embryo can safely tive bitches; rare; may lead to abortion or to
be used in variety of wildlife species (e.g., persistent infection; infected neonates may
gray fox); Rockborn type fatal in these develop fatal disease by 4–6 weeks of age.
MEDICATIONS animals. SYNONYMS
• Killed vaccines—useful for species in which • Canine distemper.
DRUG(S) OF CHOICE either type of MLV-CD is fatal (e.g., red • Hard pad disease.
• Antiviral drugs—none known to be effective. panda, blackfooted ferret).
• Broad-spectrum antibiotics—for secondary • Canarypox recombinant CDV vaccine. SEE ALSO
bacterial infection (CDV is immuno Myoclonus
suppressive), beta-lactams or cephalosporins Maternal Antibody
• Important. ABBREVIATIONS
are good initial choices. • CDV = canine distemper virus.
• Anticonvulsant therapy—phenobarbital, • Most puppies lose protection from
maternal antibody at 6–12 weeks of age; 2–3 • CSF = cerebrospinal fluid.
potassium bromide, levetiracetam. • Ig = immunoglobulin.
• Myoclonus—no proven treatment; single vaccinations should be given during this
period. • MLV-CD = modified live virus of canine
case report describes use of botulinum toxin distemper.
type A. • Heterotypic (measles virus) vaccination—
recommended for puppies that have maternal • RT-PCR = reverse transcriptase polymerase
CONTRAINDICATIONS antibody; induces protection from disease but chain reaction.
Corticosteroids—use anti-inflammatory not from infection. INTERNET RESOURCES
dosages with caution; may provide short-term https://www.uwsheltermedicine.com/library/
control. Immunosuppressive dosages may POSSIBLE COMPLICATIONS
Possibility of CNS signs developing for 2–3 resources/canine-distemper-cdv
enhance viral dissemination.
months after catarrhal signs have subsided. Suggested Reading
PRECAUTIONS Greene CE, Vendevelde M. Canine distem-
Tetracycline, fluoroquinolones—avoid in EXPECTED COURSE
per. In: Greene CE, ed., Infectious Diseases
growing animals. AND PROGNOSIS of the Dog and Cat, 4th ed. St. Louis, MO:
• Depends on strain and individual host
response—subclinical, acute, subacute, fatal, Lempp C, Spitzbarth I, Puff C, et al. New
or nonfatal infection. aspects of pathogenesis of canine distemper
• Mild CNS signs—patient may recover;
FOLLOW-UP myoclonus may continue for several months
leukoencephalitis. Viruses 2014,
6:2571–2601.
PATIENT MONITORING or indefinitely. Loots AK, Mitchell E, Dalton DL, et al.
• Monitor for CNS abnormalities, partic • Death—2 weeks to 3 months after
Advances in canine distemper virus
ularly seizures. infection; mortality rate ~50%. pathogenesis research: a wildlife perspective.
• Monitor for respiratory distress or • Euthanasia—owner may elect if or when
J Gen Virol 2017, 98:311–321.
dehydration in acute phase. neurologic signs develop; indicated if Pesavento PA, Murphy BG. Common and
PREVENTION/AVOIDANCE uncontrollable seizures occur. emerging infectious disease in the animal
• Vaccination. shelter. Vet Pathol 2014, 51:478–491.
• Isolate puppies to prevent infection from Author Michelle C. Tensley
wildlife (e.g., raccoons, foxes, skunks), Consulting Editor Amie Koenig
CDV-infected dogs, ferrets. MISCELLANEOUS Acknowledgment The author and book
• Recovered dogs may shed virus for up to 4 editors acknowledge the prior contribution of
months; isolate for this time period or until Stephen C. Barr.
• Persistent or latent Toxoplasma gondii
multiple negative RT-PCR tests.
infections—may be reactivated due to
Vaccines immunosuppressive state. Client Education Handout
• Duration of immunity from most vaccines • Respiratory infections with Bordetella available online
is >3 years. bronchiseptica (kennel cough).
Canine Infectious Diarrhea

loss, hyporexia; no history of dietary indiscretion. • Hypoglycemia—parvoviral enteritis and
• Physical examination findings—depends on systemic salmonellosis. C
etiology and severity; may include dehydration, • Panhypoproteinemia and hypocholesterol
BASICS poor body condition, borborygmus, flatulence, emia if secondary protein-losing enteropathy
DEFINITION hematochezia, melena, visualization of worms or GI blood loss.
• Viral, enteropathogenic bacterial, protozoal, on rectal exam or peri-anal, signs of sepsis or IMAGING
or parasitic etiologies; small, large, or mixed- systemic inflammatory response syndrome • Abdominal radiographs if no response to
bowel diarrhea. (SIRS). symptomatic care to rule out other causes of
• Secondary systemic signs with canine CAUSES diarrhea.
parvovirus (CPV)-2 and salmonellosis. • Viral—coronavirus, CPV-2, circovirus. • Abdominal ultrasound recommended in
• Presence of organisms on diagnostic • Bacterial—Campylobacter spp., Clostridium nonpediatric patients with diarrhea that is
screening does not indicate causation; perfringens enterotoxin, Clostridium difficile nonresponsive to symptomatic care.
patient factors (clinical signs, age, toxins, Salmonella spp.
environmental exposure) should be DIAGNOSTIC PROCEDURES
• Parasitic—Toxocara spp., Ancylostoma
considered before treatment. • Fecal flotation—for intestinal parasitism;
spp.,Toxascaris leonine, Dipyldium caninum, false negatives possible (ova are intermittently
• Some dogs will have self-resolution; Trichuris vulpis.
diagnostic testing appropriate for more shed); dogs suspected to have intestinal
• Protozoal—Giardia spp. parasitism should have multiple fecal flotations
severely affected animals or if clinical signs are • Coccidial—Cryptosporidium spp.,
persistent having ruled out other causes of performed or be treated with anthelmintics.
Cystoisospora spp. • Fecal cytology—bacterial morphology
acute or chronic diarrhea.
• Puppies with acute diarrhea should be RISK FACTORS (frequent spirochetes, spores) or presence of
screened for CPV-2. • Pediatric and young adult dogs more fungal or protozoal organisms.
commonly affected, particularly for viral • Giardia ELISA.
PATHOPHYSIOLOGY enteritis, Cryptosporidium spp., roundworm • Infectious diarrhea PCR panels detect a
• Typically, fecal–oral route of infection. (Toxocara and Toxascaris), Cystoisospora spp., range of possible causes of diarrhea; however,
• Diarrhea from enterotoxins, osmotic and Campylobacter spp. caution should be used in interpretation of
diarrhea, or invasion of epithelium resulting • Administration of antimicrobials and these assays, as a positive result does not
in inflammation. immunosuppressive drugs increase risk for necessarily indicate causation and false-
• Up to 50% of dogs may have coinfections. hospital-associated colonization of C. difficile. negative results are possible.
• Crowding and poor sanitation. PATHOLOGIC FINDINGS
SYSTEMS AFFECTED
• Lack of regular parasiticide administration.
• Gastrointestinal (GI)—vomiting, diarrhea. • Gross examination of intestinal mucosa
• Dogs with environmental exposure to may demonstrate parasites attached to
• Cardiovascular—fluid balance.
livestock or wildlife for Cryptosporidium spp., intestinal mucosa with multifocal hemor-
INCIDENCE/PREVALENCE Campylobacter spp., Giardia spp. rhagic ulcerations, submucosal congestion or
• Prevalence of most pathogens similar in
hemorrhage, intestinal wall thickening.
dogs with or without diarrhea.
• Histopathology of intestine may show
◦ Coronavirus more common in dogs with
eosinophilic, neutrophilic, or lymphoplasmacytic
diarrhea.
◦ Dogs with diarrhea more likely to have
DIAGNOSIS enteritis with varying degrees of hemorrhage and
necrosis, depending on etiology.
>1 enteropathogen. DIFFERENTIAL DIAGNOSIS
• Specific prevalence in dogs in United States: • Acute diarrhea—dietary indiscretion, foreign
◦ 0–6%—CPV-2, Salmonella spp., body, pancreatitis, GI neoplasia; non-GI
Cystoisospora spp., Dipylidum caninum, diseases: hepatotoxicity, renal disease, other
Campylobacter spp., C. difficile toxin A systemic diseases (commonly other clinical TREATMENT
and B, ascarids. signs such as hyporexia, vomiting, icterus). APPROPRIATE HEALTH CARE
◦ 7–20%—whipworms, Giardia spp., • Chronic diarrhea—chronic enteropathy • Mildly affected dogs—outpatient basis.
Cryptosporidium, circovirus. (dietary responsive, antibiotic responsive, or • Moderate to severely affected dogs may
◦ 35–60%—C. perfringens enterotoxin A inflammatory bowel disease), chronic require IV administration of isotonic
or alpha toxin gene, hookworm. pancreatitis, primary GI neoplasia, and balanced electrolyte solution for dehydration.
GEOGRAPHIC DISTRIBUTION non-GI diseases of other organs. • Electrolyte and acid-base imbalances should
• Widespread. CBC/BIOCHEMISTRY/URINALYSIS be corrected with fluid therapy and moni-
• Prevalence of etiologies varies by location. • Eosinophilia—possible with intestinal tored closely.
SIGNALMENT parasitism. • Dextrose should be supplemented
• Anemia and/or microcytosis—GI hemor- parenterally in dogs with hypoglycemia.
• Species—dog.
• Breed predilections—none.
rhage or iron deficiency, particularly with • Packed red blood cell or plasma transfusions
• Mean age and range—largely pediatric and
high worm burden (e.g., T. vulpis) or GI should be given as needed for severe anemia or
young adult dogs; older animals if in high-risk mucosal shedding (e.g., CPV). coagulopathies from sepsis (rare).
• Leukopenia—parvoviral enteritis (bacterial
environments. DIET
translocation or bone marrow suppression) or • Easily digestible diets until clinical signs
SIGNS systemic salmonellosis.
• General comments—range from mild to
have resolved, followed by slow transition
• Hyponatremia and hyperkalemia with large (3–4 days) to maintenance diet.
severely affected. bowel diarrhea—T. vulpis. • In anorexic pediatric patients, nasogastric
• Historical findings—acute or chronic, small or • Azotemia and electrolyte derangements
large bowel diarrhea; possibly vomiting, weight tube feeding of liquid diet recommended if
with dehydration. anorexia persists ≥48 hours.
Canine Infectious Diarrhea (continued)
CLIENT EDUCATION POSSIBLE INTERACTIONS ZOONOTIC POTENTIAL

C • For most infectious organisms, environ- • Metronidazole given at higher doses for • Giardiasis—low risk of transmission.
mental decontamination prevents transmis- giardiasis or long-term use can lead to • Cryptosporidiosis.
sion to other pets/people and reinfection; vestibular signs. • Salmonellosis.
isolation during hospitalization may be • Some dogs may be sensitive to sulfa- • Campylobacter jejuni.
warranted depending on underlying cause. containing medications used for treatment of • Toxocara spp. (ascarids)—visceral larval
• Appropriate vaccination and deworming coccidiosis. migrans in humans, most common in
schedules should be followed. children.
• Dogs with identified infectious causes of • Ancylostoma (hookworms)—cutaneous
diarrhea should be isolated from other dogs if larval migrans in humans, most common in
possible until clinical signs resolve. children.
FOLLOW-UP
SURGICAL CONSIDERATIONS PREGNANCY/FERTILITY/BREEDING
PATIENT MONITORING
Viral and parasitic enterocolitis can result in If heavy endoparasite load, fenbendazole can
• Case-based, may include reassessment of
intussusceptions, especially in puppies. be administered to pregnant bitches from
anemia, leukopenia, or electrolyte derange-
14th day of gestation through to 14th day of
ments as appropriate.
lactation. If risk of infection is high, all
• Persistent clinical signs after appropriate
puppies (and mothers) should be treated with
treatment is suggestive for alternative cause of
appropriate anthelmintics at 2, 4, 6, and 8
MEDICATIONS diarrhea.
weeks of age.
• Patients with recurrent clinical signs should
DRUG(S) OF CHOICE
be retested, particularly if environmental SEE ALSO
• Many cases will self-resolve with supportive
reinfection is possible (e.g., giardiasis, • Acute Diarrhea.
care and time.
campylobacteriosis). • Campylobacteriosis.
• Empiric therapy pending diagnostics, if
• Canine Coronavirus Infections.
clinical signs persist—probiotics, or metroni- PREVENTION/AVOIDANCE
• Canine Parvovirus.
dazole (10 mg/kg PO q12h) and fenbenda- • Routine vaccination.
• Clostridial Enterotoxicosis.
zole (50 mg/kg PO q24h for 5 days). • Monthly flea/tick or heartworm preventa-
• Coccidiosis.
• Anthelmintics—fenbendazole (50 mg/kg tive with combination anthelmintic therapy.
• Diarrhea, Chronic—Dogs.
PO q24h for 5 days), pyrantel pamoate • Avoid subjecting poorly vaccinated or
• Giardiasis.
(5–10 mg/kg PO for 3 days). immunocompromised animals to high-traffic
• Hookworms (Ancylostomiasis).
• Coccidiostatic—sulfadimethoxine areas, including but not limited to pet supply
• Roundworms (Ascariasis).
(50–60 mg/kg PO q24h for 5–10 days), stores, dog parks, or newly introduced poorly
• Salmonellosis.
ponazuril (50 mg/kg PO once). vaccinated pets.
• Whipworms (Trichuriasis).
• Antiprotozoal drugs—fenbendazole POSSIBLE COMPLICATIONS
(50 mg/kg PO q24h for 5 days). ABBREVIATIONS
• Sepsis.
• Campylobacteriosis with persistent clinical • CPV-2 = canine parvovirus.
• Anemia.
signs—erythromycin (10–15 mg/kg PO q8h) • GI = gastrointestinal.
• Electrolyte disturbances.
or azithromycin (5–10 mg/kg PO q24h). • SIRS = systemic inflammatory response
• Aspiration pneumonia if concurrent
• Probiotics may be of benefit for dogs with syndrome.
vomiting (uncommon).
bacterial enteritis with acute or chronic signs; Suggested Reading
probiotics should be selected with evidence of EXPECTED COURSE AND PROGNOSIS
Gookin JL. Infection, large intestine. In:
efficacy (e.g., Visbiome®). • Usually good to excellent; underlying
Washabau RJ, Day MJ, eds., Canine &
• Patients with systemic illness, leukope- immunosuppressive conditions may increase
Feline Gastroenterology. St. Louis, MO:
nia, or suspected GI mucosal barrier susceptibility to infection and worsen prognosis.
breakdown (evidenced by blood in the • Parvoviral enteritis carries guarded to poor
Lappin MR. Infection, small intestine. In:
feces) should be treated with broad-spec- prognosis without treatment; appropriate
Washabau RJ, Day MJ, eds., Canine &
trum antimicrobial agents and as indicated supportive care provides full recovery rates of
Feline Gastroenterology. St. Louis, MO:
by specific etiology. 90% or more.
• Dogs with confirmed salmonella should Authors Kasey E. Mabry and Tracy Hill
not be treated with antibiotics unless Consulting Editor Amie Koenig
systemically ill.
PRECAUTIONS MISCELLANEOUS
Metronidazole dose should be reduced in AGE-RELATED FACTORS
animals with hepatic insufficiency. Puppies and young dogs affected.
Canine Infectious Respiratory Disease

Physical Examination Findings OTHER LABORATORY TESTS
• Uncomplicated—cough readily induced with Pulse oximetry and arterial blood gas analysis— C
minimal tracheal pressure; lung sounds often can reveal hypoxemia in pneumonia.
BASICS normal; systemically healthy. • Complicated— IMAGING
DEFINITION low-grade or intermittent fever (39.4–40.0 °C; • Uncomplicated disease—radiographs:
A multifaceted disease whereby infectious disease 103–104 °F); increased intensity of normal unremarkable; most useful for ruling out
and environment contribute to the genesis of lung sounds, crackles or wheezes possible. other differential diagnoses. • Complicated
cough and other respiratory signs in dogs. CAUSES disease—radiographs: interstitial and
PATHOPHYSIOLOGY • Viral—canine distemper virus (CDV); canine alveolar lung pattern with a cranioventral
Initiated by injury to the respiratory adenovirus (CAV-2); canine parainfluenza distribution typical of bacterial pneumonia;
epithelium by viral infection followed by (CPIV); canine respiratory coronavirus can see diffuse interstitial lung pattern
invasion of damaged tissue by bacterial, (CRCoV), canine reovirus; canine herpesvirus-1 typical of viral pneumonia; mixed lung
mycoplasmal, or other virulent organisms, (CHV-1); canine influenza virus (CIV; H3N8 pattern can be present.
resulting in further damage and clinical signs. or H3N2); canine bocavirus, canine hepacivirus; DIAGNOSTIC PROCEDURES
canine pneumovirus (CnPnV). • Most viral • In cases with severe disease—ideally
SYSTEMS AFFECTED pathogens (except CHV and CDV) primarily
Respiratory—upper and lower airways can be perform bronchoalveolar lavage via
infect epithelial and lymphoid tissue of the bronchoscopy for cytology and microbial
involved. Multisystemic—cases that develop upper and lower respiratory tract; in severe
sepsis. culture; tracheal wash sample acceptable, but
cases, causing desquamation of the epithelium increased likelihood for upper airway
GENETICS and aggregation of inflammatory cells in the contamination. • Antimicrobial sensitivity
None lungs, leading to secondary bacterial coloni pattern of cultured bacteria—identification
INCIDENCE/PREVALENCE zation and infection; CRCoV infection leads to aids markedly in providing an effective
Most common in areas of high density with loss of cilia associated with the respiratory treatment plan. • PCR from bronchoalveolar
immunologically naïve or immunosuppressed epithelium, increasing the severity and duration lavage, nasal, ocular, or pharyngeal secretions
patients (i.e., training kennels, shelters, of secondary infections. • Bacterial—Bordetella can be used to detect virus, though there is
veterinary hospitals). bronchiseptica, with no other respiratory difficulty in interpreting results as many
pathogens, produces clinical signs healthy animals shed virus in the absence of
GEOGRAPHIC DISTRIBUTION indistinguishable from those of other bacterial
Worldwide clinical signs.
causes; Streptococcus equi subsp. zooepidemicus is
SIGNALMENT associated with a particularly virulent course PATHOLOGIC FINDINGS
that can progress to death; Pseudomonas, • CPIV—causes few to no clinical signs;
Species Escherichia coli, Klebsiella, Pasteurella, lungs of infected dogs 6–10 days after
Dog Streptococcus, Mycoplasma, and other species exposure may contain petechial hemorrhages
Breed Predilections equally likely. that are evenly distributed over the surfaces;
None detected by immunofluorescence in
RISK FACTORS columnar epithelial cells of the bronchi and
Mean Age and Range • Substandard hygienic conditions and
bronchioles 6–10 days after aerosol
• Most severe in puppies 6 weeks–6 months overcrowding—encountered in some pet exposure. • CAV-2—lesions confined to the
old. • Can develop in dogs of all ages, partic- shops, shelters, research facilities, and respiratory system; large intranuclear
ularly with preexisting airway disease. boarding and training kennels. • Coexisting inclusion bodies found in bronchial
Predominant Sex subclinical airway disease—congenital epithelial cells and alveolar septal cells;
None anomalies; chronic bronchitis; bronchiectasis. clinical signs tend to be mild and short-
SIGNS lasting; lesions persist for at least a month
after infection. • CIV (H3N8, H3N2)—
General Comments fulminant disease characterized by secondary
• Related to the degree of respiratory tract DIAGNOSIS Mycoplasma or bacterial infection and
damage and age of the affected dog and virulence pulmonary hemorrhage. • CRCoV—
of infectious organism. • Can be subclinical, DIFFERENTIAL DIAGNOSIS
characterized by marked inflammation of
mild, or severe with pneumonia. • Most viral, • In systemically well dogs—parasitic
the trachea and nares with cilia loss in the
bacterial, and mycoplasmal agents spread rapidly bronchitis, irritant tracheobronchitis, airway
former; detected by immunohistochemistry
from seemingly healthy dogs to others in the foreign body, airway collapse. • In a dog with
of the trachea or bronchioles. • Streptococcus
same environment; signs usually begin about 3–7 systemic signs—fungal or bacterial (aspiration)
equi subsp. zooepidemicus infection—acute,
days after exposure to the infecting agent(s). pneumonia, primary or metastatic neoplasia,
fibrinosuppurative pneumonia with large
congestive heart failure, migrating foreign
Historical Findings numbers of cocci found within the pulmonary
body. • Provisional diagnosis of infectious
• Uncomplicated—acute-onset cough in an parenchyma and, often, septic thomboemboli.
tracheobronchitis is made in a dog with
otherwise healthy animal; dry and hacking, • Bordetellosis and severe bacterial
compelling clinical signs and a history of
soft and dry, moist and hacking, or paroxysmal, infection—evidence of purulent bronchitis,
exposure to the implicated organisms. • See
followed by gagging, retching, and expecto tracheitis, and rhinitis with hyperemia and
Cough.
ration of mucus; excitement, exercise, and enlargement of the bronchial, mediastinal,
pressure on the trachea induce coughing spells. CBC/BIOCHEMISTRY/URINALYSIS and retropharyngeal lymph nodes; may see
• Complicated (severe)—inappetence to • Early, mild leukopenia (5,000–6,000 cells/ large numbers of Gram-positive or Gram-
anorexia; cough is moist and productive; dL)—can be detected; suggests viral cause. negative organisms in the mucus of the
lethargy, difficulty breathing, hemoptysis, and • Neutrophilic leukocytosis with a toxic left tracheal and bronchial epithelium.
exercise intolerance can occur. shift—frequently found with severe pneumonia.
Canine Infectious Respiratory Disease (continued)
CONTRAINDICATIONS shortens the course. • Typical course of severe

C • Do not use cough suppressants in patients disease—2–6 weeks; patients that die often
with pneumonia. • Employ glucocorticoids only develop severe pneumonia that affects
TREATMENT in cases with significant inflammatory disease multiple lung lobes and multiple organ
APPROPRIATE HEALTH CARE refractory to conventional supportive care. dysfunction due to sepsis.
• Outpatient—strongly recommended for PRECAUTIONS
uncomplicated disease. • Inpatient—strongly None
recommended for complicated disease and/or
pneumonia. POSSIBLE INTERACTIONS
Fluoroquinolones and theophylline deriva- MISCELLANEOUS
NURSING CARE tives—concurrent use causes high and ASSOCIATED CONDITIONS
Fluid administration—indicated for possibly toxic plasma theophylline concentra- May accompany other respiratory tract
complicated disease and/or pneumonia. tion. Dose reduce theophylline while anomalies.
ACTIVITY concurrently administering fluoroquinolones.
AGE-RELATED FACTORS
Enforced rest—14–21 days with uncompli- ALTERNATIVE DRUG(S) Most severe in puppies 6 weeks–6 months old
cated disease; for at least the duration of None and in puppies from commercial pet shops
radiographic evidence of pneumonia in and humane society shelters.
severely affected dogs.
ZOONOTIC POTENTIAL
DIET Potential zoonotic risk of Streptococcus equi
Good-quality commercial food. FOLLOW-UP subsp. zooepidemicus and B. bronchispetica
CLIENT EDUCATION PATIENT MONITORING reported in single case reports.
• Isolate patient from other animals; infected • Uncomplicated disease—should resolve PREGNANCY/FERTILITY/BREEDING
dogs can transmit the agent(s) before onset of spontaneously or respond to treatment in 10–14 High risk in dogs on extensive medical
clinical signs and afterward until immunity days; if patient continues to cough 14 days or treatment; especially risky for dogs in
develops. • Dogs with uncomplicated disease more after establishment of an adequate treat- overcrowded breeding facilities.
should respond to treatment in 10–14 days. ment plan, question the diagnosis of uncompli-
• Once infection spreads in a kennel, it can be SYNONYMS
cated disease. • Complicated disease— • Kennel cough. • Infectious
controlled by evacuation for 1–2 weeks and repeat thoracic radiography until at least 7 days
disinfection with commonly used chemicals, tracheobronchitis—uncomplicated disease.
beyond resolution of all clinical signs.
such as sodium hypochlorite (1 : 30 dilution), ABBREVIATIONS
chlorhexidine, and benzalkonium. PREVENTION/AVOIDANCE • CAV-2 = canine adenovírus. • CDV =
Shedding of the causative agent(s) of infectious canine distemper vírus. • CHV-1 = canine
respiratory disease in airway secretions of dogs herpesvirus-1. • CIV = canine influenza
undoubtedly accounts for the persistence of virus. • CnPnV = canine pneumovirus.
this problem in kennels, animal shelters, • CPIV = canine parainfluenza. • CRCoV =
MEDICATIONS boarding facilities, and veterinary hospitals. canine respiratory coronavirus.
DRUG(S) OF CHOICE Viral and Bacterial Vaccines
• Amoxicillin/clavulanic acid (12.5–25 mg/kg INTERNET RESOURCES
• Modified live CDV and CAV-2 vaccines https://www.cdc.gov/flu/other/canine-flu
PO q12h) or doxycycline (5 mg/kg PO q12h or provide reliable protection and are considered
10 mg/kg PO q24h)—initial treatment of core vaccines for all puppies; can be admin Suggested Reading
uncomplicated disease. • Penicillin (ampicillin istered at 6 weeks of age, every 2–4 weeks. • B. Bemis DA. Bordetella and Mycoplasma
10–20 mg/kg IV q6–8h or ticarcillin 40–50 mg/ bronchiseptica and CPIV vaccine—can vaccinate respiratory infection in dogs. Vet Clin
kg IV q6–8h) with aminoglycoside (gentamicin puppies mucosally or intranasally as early as 2–4 North Am Small Anim Pract 1992,
2–4 mg/kg IV/IM/SC q6–8h or amikacin weeks of age without interference from maternal 22:1173–1186.
6.5 mg/kg IV/IM/SC q8h) or fluoroquinolone antibody and follow with annual revaccination; Buonavoglia C, Martella V. Canine respira-
(enrofloxacin 5–10 mg/kg PO/IM/IV q24h)— can vaccinate mature dogs with a one-dose tory viruses. Vet Res 2007, 38(2):355–373.
usually effective for severe disease. intranasal vaccination (at the same time as their Chalker VJ, Owen WM, Paterson C, et al.
• Antimicrobial therapy—continue for at least puppies or when they receive their annual Mycoplasmas associated with canine
10 days beyond radiographic resolution. • B. vaccinations). • Inactivated B. bronchiseptica infectious respiratory disease. Microbiology
bronchiseptica and other resistant species—some parenteral vaccine—administered as two doses, 2004, 150(Pt 10):3491–3497.
antimicrobials may not reach adequate 2–4 weeks apart; initial vaccination of puppies is Erles K, Dubovi E, Brooks HW, Brownlie J.
therapeutic concentrations in the lumen of the recommended at or about 6–8 weeks of age; Longitudinal study of viruses associated
lower respiratory tract, so oral or parenteral revaccinate at 4 months of age. • Inactivated with canine infectious respiratory disease. J
administration may have limited effectiveness; CIV vaccines (H3N2 and H3N8) available to Clin Micro 2004, 42:4524–4529.
nebulization with gentamicin (3–5 mg/kg) can reduce severity and duration of clinical signs but Priestnall SL, Mitchell JA, Walker CA, et al.
decrease bacterial numbers when administered considered noncore; can be administered New and emerging pathogens in canine
daily for 3–5 days; use in conjunction with starting at 6 weeks as two doses, 2–4 weeks infectious respiratory disease. Vet Path
systemic antibiotics in dogs with parenchymal apart; results in seroconversion. 2014, 51(2):492–504.
disease. • Butorphanol (0.55 mg/kg PO Author Jonathan D. Dear
q8–12h) or hydrocodone bitartrate (0.22 mg/kg POSSIBLE COMPLICATIONS Consulting Editor Elizabeth Rozanski
PO q6–8h)—effective suppression of dry, N/A
nonproductive cough not associated with EXPECTED COURSE AND PROGNOSIS
bacterial infection. • Bronchodilators (e.g., • Natural course of uncomplicated disease, if Client Education Handout
terbutaline 0.625–5 mg/dog q8–12h)—may be untreated—10–14 days; simple restriction of available online
used to control bronchospasm and wheeze. exercise and prevention of excitement
Canine Parvovirus
• Higher fatality rates are seen in hounds, • Severely affected dogs exhibit severe
gundogs, and nonsporting pedigree groups. neutropenia with onset of intestinal damage. C
• Leukocytosis during recovery.
BASICS Mean Age and Range
• Serum chemistry profiles help assess
• Illness occurs at any age.
DEFINITION • Most severe in dogs 6–24 weeks of age.
electrolyte disturbances (especially
• An acute systemic illness characterized by hypokalemia), presence of azotemia,
vomiting, hemorrhagic enteritis, and Predominant Sex panhypoproteinemia, hypoglycemia.
leukopenia. None
• Myocardial form was observed in puppies SIGNS • Virus antigen detection in stool at onset of
in late 1970s, now rare. disease and for 2–4 days afterward; many
General Comments
• Most puppies protected against neonatal commercial point-of-care ELISA assays
Suspect CPV-2 infection whenever puppies
infection by maternal antibodies. available, also PCR and quantitative PCR
have an enteric illness.
• Monoclonal antibodies have revealed methodologies.
antigenic changes in canine parvovirus Historical Findings • Serologic tests are not diagnostic because
(CPV)-2; CPV2a, b, and c strains have been • Sudden onset of bloody diarrhea, anorexia, dogs often have high titers from vaccination
identified. and vomiting. and/or maternal antibodies.
• Original virus now virtually extinct in • Some dogs may collapse in a shock-like
domestic dogs. state and die without enteric signs. IMAGING
• CPV2c viruses are more virulent, and • In breeding kennels, several littermates may • Abdominal radiographs—generalized small
mortality rates higher. become ill simultaneously or within a short intestinal ileus; exercise caution to prevent
• CPV-2 is closely related to feline panleuko period. misdiagnosis of intestinal obstruction, but
penia virus (FPV). • Occasionally, one or two puppies in a litter have intussusception may cause obstructive pattern.
minimal signs, followed by death of littermates, • Abdominal ultrasound—fluid-filled, atonic
PATHOPHYSIOLOGY small and large intestines, duodenal and
which may reflect degree of virus exposure.
• Parvoviruses require actively dividing cells jejunal mucosal layer thinning with or
for growth. Physical Examination Findings without indistinct wall layers and irregular
• After ingestion of virus there is a 2–4-day • Hypovolemic shock—weak pulse, tachy- luminal-mucosal surfaces, extensive duodenal
period of viremia. cardia, dull mentation. and/or jejunal hyperechoic mucosal speckling,
• Early lymphatic infection is accompanied • Severe hemorrhagic diarrhea. and duodenal and/or jejunal corrugations;
by lymphopenia and precedes intestinal • Fluid-filled intestinal loops may be palpated. intussusceptions can be identified.
infection and clinical signs. • Dehydration, weight loss, abdominal
• By postinfection (PI) day 3, rapidly dividing discomfort. DIAGNOSTIC PROCEDURES
crypt cells of small intestine are infected. • May have fever or hypothermia. • Electron microscopy detects fecal virus
• Viral shedding in feces starts ∼3–4 days PI, during early stages of infection.
CAUSES • Samples for virus detection should be
peaks with clinical signs.
CPV-2. submitted during acute phase of infection;
• Virus ceases to be shed in detectable
amounts by PI days 8–12. RISK FACTORS ship specimens refrigerated, not frozen.
• Absorption of bacterial endotoxins from • Unvaccinated dogs. PATHOLOGIC FINDINGS
damaged intestinal mucosa plays a role in • Dogs <4 months of age. • Gross changes include subserosal congestion
CPV-2 disease. • Co-pathogens such as parasites, viruses, and and hemorrhage or frank hemorrhage into
• Intensity of illness related to viral dose and certain bacterial species (e.g., Campylobacter small intestinal lumen, or intestines that are
antigenic type. spp., Clostridium spp.) may exacerbate illness. empty or contain yellow or blood-tinged fluid.
• Severe, often fatal parvoviral infections have • Mesenteric lymph nodes often enlarged and
SYSTEMS AFFECTED
been demonstrated in puppies exposed edematous, with hemorrhages in cortex.
• Cardiovascular—myocarditis (uncommon),
simultaneously to CPV-2 and canine coronavirus. • Thymic atrophy in young dogs.
hypovolemia.
• Crowding and poor sanitation. • Pulmonary edema and hydropericardium
• Hemic/lymphatic/immune. may be only gross change in dogs with
myocarditis and heart failure.
GENETICS • Histopathology reveals intestinal
Unknown inflammation and necrosis, with severe villus
DIAGNOSIS atrophy.
Common in breeding kennels, animal DIFFERENTIAL DIAGNOSIS
shelters, pet stores. • Canine coronavirus infection.
• Salmonellosis; colibacillosis; other enteric
GEOGRAPHIC DISTRIBUTION bacterial infections.
Worldwide • Gastrointestinal foreign bodies. TREATMENT
SIGNALMENT • Gastrointestinal parasites. APPROPRIATE HEALTH CARE
• Acute hemorrhagic diarrhea syndrome • Symptomatic and supportive (see Acute
Species (previously hemorrhagic gastroenteritis). Vomiting; Acute Diarrhea; Gastroenteritis,
Dog • Intussusception (may be concurrent). Acute Hemorrhagic Diarrhea Syndrome),
Breed Predilections • Toxin ingestion. including IV fluids, antibiotics, antiemetics,
• Certain breeds are at increased risk, CBC/BIOCHEMISTRY/URINALYSIS and analgesics.
including Rottweiler, Doberman pinscher, • Intensity depends on severity of signs;
• Lymphopenia—characteristic; commonly
American pit bull terrier, Labrador retriever, occurs PI days 4–6. both in- and outpatient treatment protocols
German shepherd dog, and Yorkshire terrier. exist.
Canine Parvovirus (continued)
• Goals are to provide intestinal nutrients, DRUG(S) OF CHOICE admission is associated with 96% survival,
C restore and maintain fluid and electrolyte Additional recommended drugs include and a serum thyroxine concentration
balance, and resolve shock, sepsis, and parenteral antibiotics (ampicillin and >0.2 μg/dL at 24 hours after admission is
endotoxemia. gentamicin) and antiemetics (e.g., ondanse- associated with 100% survival. An HDL-
• Fecal microbiota transplant may speed tron, maropitant). cholesterol concentration >50.2 mg/dL at
resolution of diarrhea. PRECAUTIONS admission is associated with 100% survival.
• Prompt, intensive inpatient care leads to
Gentamicin may cause renal toxicity in
treatment success. dehydrated puppies.
• Proper, strict isolation procedures are
essential.
• Exercise care to prevent spread of CPV-2, a
MISCELLANEOUS
very stable virus. ASSOCIATED CONDITIONS
• Antiviral drugs have not yet been shown to FOLLOW-UP Coinfection with intestinal helminths and
be a critical part of treatment. PATIENT MONITORING Giardia are indicative of unhygienic housing
There is an increased incidence of discospondy- conditions and can worsen clinical signs and
NURSING CARE
litis in puppies that had parvovirus infection. contribute to morbidity.
• Hospitalize patients and monitor for
dehydration and electrolyte imbalance. PREVENTION/AVOIDANCE AGE-RELATED FACTORS
• Fluids are usually supplemented with • Inactivated and live vaccines are available
Infection less likely in dogs >1 year of age,
potassium chloride, 5% dextrose, and for prophylaxis, and vaccines differ in their but can still occur, especially if unvaccinated.
possibly sodium bicarbonate (if severe capacity to immunize puppies with maternal ZOONOTIC POTENTIAL
metabolic acidosis due to bicarbonate loss). antibodies. Parvovirus per se is not zoonotic, but these
ACTIVITY • Vaccination with a modified live vaccine at puppies may harbor coinfections with Giardia,
Restrict until symptoms abate. 4 weeks of age in puppies with high maternally which can be zoonotic.
derived antibody concentrations resulted in PREGNANCY/FERTILITY/BREEDING
DIET
seroconversion rates of up to 80%; this may Pregnant animals are likely to abort.
Puppies receiving early enteral nutrition via a
lead to a decreased window of susceptibility
nasoesophageal tube (compared to puppies SEE ALSO
to CPV infection and might be an adjunct
that received nothing enterally until cessation • Acute Diarrhea.
control method in contaminated
of vomiting) showed earlier clinical improve- • Acute Vomiting.
environments.
ment, significant weight gain, and improved • Canine Coronavirus Infections.
• Control of CPV-2 requires efficacious
gut barrier function, which could limit • Gastroenteritis, Acute Hemorrhagic
vaccines, isolation of puppies, and stringent
bacterial or endotoxin translocation. Diarrhea Syndrome.
hygiene.
CLIENT EDUCATION • Sepsis and Bacteremia.
POSSIBLE COMPLICATIONS • Shock, Septic.
• Inform about need for thorough disin
• Septicemia/endotoxemia.
fection, especially if other dogs are on ABBREVIATIONS
• Bacterial pneumonia.
premises; strict sanitation is essential; a 1 : 30 • CPV = canine parvovirus.
• Intussusception.
dilution of bleach (5% sodium hypochlorite) • FPV = feline panleukopenia virus.
• Discospondylitis.
destroys CPV-2 in a few minutes. • PI = postinfection.
• If possible, isolate puppies until they reach EXPECTED COURSE AND PROGNOSIS
3 months of age and vaccinate repeatedly; • Prognosis is guarded in severely affected Suggested Reading
typical protocols involve vaccination at 6, 9, puppies. Mohr AJ, Leisewitz AL, Jacobson LS, et al.
and 12 weeks of age. • Prognosis is good for dogs that receive Effect of early enteral nutrition on intestinal
• Puppies can be infected with virulent virus prompt initial treatment and survive initial permeability, intestinal protein loss, and
before any vaccine will confer immunity. crisis—approximately 80% survival rate. outcome in dogs with severe parvoviral
• CPV-2 is shed for less than 2 weeks after • Poor prognosis if a patient is purebred, has enteritis. J Vet Intern Med 2003,
infection; no carrier state has been substan- a low bodyweight, and if the following 17:791–798.
tiated. biomarker levels are present after 24 hours of Schoeman JP, Goddard A, Herrtage ME.
intensive therapy: severe persistent leuko- and Serum cortisol and thyroxine concentra-
SURGICAL CONSIDERATIONS tions as predictors of death in critically ill
• Exercise caution to prevent misdiagnosis of lymphopenia, persistently elevated or rising
serum cortisol concentration (>8.1 μg/dL), puppies with parvoviral diarrhea. J Am Vet
intestinal obstruction, especially if vomiting is Med Assoc 2007, 231:1534–1539.
only clinical sign. severe hypothyroxinemia (<0.2 μg/dL),
hypocholesterolemia (<100 mg/dL), and Venn EC, Preisner K, Boscan PL, et al.
• Intussusceptions can occur. Evaluation of an outpatient protocol in the
persistently elevated serum C-reactive protein
(>97.3 mg/L). treatment of canine parvoviral enteritis.
• Conversely, puppies with a good prognosis J Vet Emerg Crit Care 2017, 27:52–65.
are of mixed breed, >6 months old, and show Author Johan P. Schoeman
MEDICATIONS the following biomarker values: total leukocyte Consulting Editor Amie Koenig
See Acute Vomiting; Acute Diarrhea; count >4.5 × 103/μL, lymphocyte count >1 ×
Gastroenteritis, Acute Hemorrhagic Diarrhea 103/μL, and mature neutrophil count >3 ×
Syndrome. 103/μL. Additionally, a serum cortisol
available online
concentration <8.1 μg/dL at 48 hours after
Canine Schistosomiasis (Heterobilharziasis)

OTHER LABORATORY TESTS ZOONOTIC POTENTIAL
• Elevated parathyroid hormone-related Stages in the dog pose no threat to people; C
protein (PTH-rp) reported in dogs with with shared waterway exposure, cercariae can
BASICS hypercalcemia. cause skin lesions in people.
OVERVIEW • PCR on feces (Texas A&M Gastrointestinal SYNONYMS
• Heterobilharzia americanum is a trematode Laboratory). • Schistosomiasis.
of the genus Schistosoma that has fresh water IMAGING • Swimmer’s itch (human, skin penetration of
lymnaeid snails as intermediate hosts and Contrast radiographs and ultrasound may cercariae).
raccoons as the natural definitive host. reveal thickened bowel walls; calcified eggs
• Eggs passed in the feces of raccoons hatch ABBREVIATIONS
disseminated into tissues may give the false • PTH-rp = parathyroid hormone-related
to release miracidia that penetrate freshwater impression of soft tissue mineralization.
snail hosts. After a period of development and protein.
asexual multiplication, the snails release DIAGNOSTIC PROCEDURES Suggested Reading
cercariae that infect the next host by skin • Eggs with miracidia can be identified in Fabrick C, Bugbee A, Fosgate G. Clinical
penetration. After penetrating skin, larvae feces, but feces must be kept in saline (not features and outcome of Heterobilharzia
undergo a migration to the lung and then water) or miracidia will spontaneously hatch, americana infection in dogs. J Vet Intern
make their way to mesenteric veins, where making diagnosis impossible. Med 2010, 24:140–144.
separate males and females form pairs. Eggs • Fecal direct or sedimentation methods are Flowers JR, Hammerberg B, Wood SL, et al.
laid by female worms are carried to the preferred to fecal flotation; routine fecal Heterobilharzia americana infection in a
intestinal wall, where they erode their way flotation will not detect these heavy eggs; if dog. J Am Vet Med Assoc 2002,
through to the lumen to be passed in the used, requires flotation with sugar solution 220:193–196.
feces. Other eggs are carried to the liver or with specific gravity of 1.3. Stone RH, Frontera-Acevedo K, Saba CF,
other organs by the bloodstream, where they • Histopathology—trematode eggs in et al. Lymphosarcoma associated with
lodge and cause granulomatous disease. multiple organs (especially liver, intestine, Heterobilharzia americana infection in a
• Dogs become infected in contact with pancreas, lymph nodes); lymphoplasmacytic, dog. J Vet Diag Invest 2011,
freshwater containing cercariae. histiocytic, and eosinophilic to granuloma 23:1065–1070.
• Endemic in raccoons in southeastern United tous enteritis, hepatitis with possible Author Dwight D. Bowman
States; canine cases reported from Arkansas, peri-portal fibrosis, dystrophic mineralization Consulting Editor Amie Koenig
Indiana, Florida, Georgia, Kansas, Louisiana, of multiple tissues.
North Carolina, Oklahoma, and Texas.
SIGNALMENT
Dogs, typically adult, that have access to
swampy areas or bayous. TREATMENT
Inpatient care for the first few days of treat-
SIGNS ment may be warranted, as the response to
• Lethargy (most common sign), weight loss, worm kill may require supportive care.
and decreased appetite.
• Other signs include vomiting, diarrhea,
anorexia, polyuria/polydipsia; more rarely
melena, borborygmus, ascites.
MEDICATIONS
Swimming in freshwater in areas DRUG(S) OF CHOICE
contaminated with cercariae from miracidia. • Praziquantel—25 mg/kg PO q8h for 2–3 days.
• Fenbendazole—50 mg/kg PO q24h for
10 days; clinical improvement without
parasite elimination has been reported with
fenbendazole.
DIAGNOSIS
• Coccidiosis.
• Bacterial diarrhea.
• Viral enteritis.
FOLLOW-UP
• Check feces after treatment to ensure that it
• Hepatopathies.
does not contain eggs.
CBC/BIOCHEMISTRY/URINALYSIS • Reinfection from environment is possible.
• CBC—anemia, lymphopenia, eosinopenia
or eosinophilia, thrombocytopenia.
• Biochemistry—elevated liver enzyme
activities, azotemia, hypercalcemia, hyper
natremia, hyperglobulinemia, MISCELLANEOUS
hypoalbuminemia. In Japan and other countries with endemic
• Urinalysis—proteinuria. Schistosoma japonicum, dogs can be infected
with this human and zoonotic species.
Car Ride Anxiety—Dogs and Cats

CAUSES & RISK FACTORS • Anticipate and avoid evoking the pet’s fears
C • Behavioral causes include unruliness, to prevent exacerbating established fears; for
inadequate or poor prior experience traveling; example, when carrying a pet in a carrier,
BASICS insufficient adaptation to carriers, leashes, or consider their viewpoint and the unsettling
DEFINITION restraint devices; fear and reactivity to visual motion that may be experienced.
Excessive or disruptive distress, fear, or panic stimuli such as people, animals, bikes, or cars; • Avoid reprimands or scolding.
associated with vehicle travel. Anxiety and generalized anxiety. • Avoid forcing pets that are unfamiliar or do
exhibited during travel can be mistaken for • Prior stressful or uncomfortable experiences not get along to be in close proximity.
excitement. following car rides such as veterinary visits, Management and Safety
boarding, or shelter relinquishment. • Provide stable footing and secure resting
PATHOPHYSIOLOGY
• Traumatic events such as sudden stops or locations.
Unknown or not definitively determined.
car accidents. • Consider crating if pet acclimated to crate
Lack of car ride experience, generalized
• Medical conditions may exacerbate or confinement; pet seat belts, barriers, and seat
anxiety disorder, nausea, previous negative
manifest as anxiety—motion sickness, slings can also be beneficial.
experience with car rides; fear, anxiety, or
musculoskeletal pain or discomfort, dental • A nondriver should accompany highly
arousal related to visual or auditory stimuli.
disease or pain, gastrointestinal upset, sensory distressed pets.
SYSTEMS AFFECTED hypersensitivity.
• Behavioral. Anxiety Reduction
• Gastrointestinal. • Multimodal comforting and anxiolytic
• Neuromuscular. support provides the best outcome.
• Window shades, covered crates, solid wall
GENETICS DIAGNOSIS carriers, or products for dogs such as Doggles®
May be genetic component, but experiential
DIFFERENTIAL DIAGNOSIS or Thundercap® may alleviate anxiety related
learning may be more significant.
• Fear and anxiety-related behavior. to visual stimuli.
INCIDENCE/PREVALENCE • Manifestation of pain, nausea, or physical • Classical music or psychoacoustically
Reported in over 50% of cats and over 20% discomfort. designed music for dogs or cats may help to
of dogs. • Acute onset or abrupt change in car ride calm; music or white noise may mute
anxiety warrants ruling out contributory perception of fear-evoking sounds.
SIGNALMENT medical conditions. • Comforting pressure wraps may alleviate
Dog and cat. anxiety.
Breed Predilections • Synthetic pheromone analogues (Adaptil®,
If indicated by clinical signs and prior to drug
None Feliway®) sprayed into carriers, onto bedding,
therapy.
or on a bandana (for dogs) may reduce anxiety.
Mean Age and Range OTHER LABORATORY TESTS • Anxiety-reducing supplements or
Any. Young or ill animals may be predisposed If indicated by clinical signs. medications should be considered.
to motion sickness.
IMAGING Behavior Modification
Predominant Sex If indicated by clinical signs. • Rehearse settle and relax positions when not
None
traveling.
SIGNS • Teach the dog to get in and out of the car
by positive reinforcement (e.g., food or toy
Historical Findings
TREATMENT reward).
• May include pacing, restlessness,
• Teach cats and small dogs to go in and out
inappetence, vigilance, excitability, and ACTIVITY of carriers willingly; they should be acclimated
vocalization including whining or high- Normal. Recommend adequate exercise and to the motion of being in a carrier that is
pitched barking in dogs and growling, play before car ride. being carried.
hissing, meowing, or yowling in cats.
DIET • Practice training when travel is not imminent;
• Locomotion varies between individuals—
• Normal. use positive reinforcement training and avoid
some may pace while others remain
• Providing highly palatable food during car reprimand or intimidation training; animals
immobile; fear that manifests as freezing or
travel may distract, reduce stress, and promote should never receive corrections from shock,
hiding may be underrecognized and
a positive association with car travel. prong, or choke collars.
underreported.
• If the pet has experienced nausea or • During travel, provide comforting activities
• Pet-related panic, vocalization, and pacing
vomiting in association with car travel, fasting such as toys, food chews, or feeding puzzles
may impair owner’s ability to drive safely.
is recommended. that may distract the pet, reduce anxiety, or
• Travel-related anxiety may prevent owners
counter-condition the pet to car rides.
from taking pets to destinations (e.g., CLIENT EDUCATION
veterinary visits, grooming, social events, A complete behavior program includes
training). empathy, environmental management, and
Physiologic and Physical Signs behavior modification together with supple-
May include panting, rapid heart rate, ments or medication where indicated. MEDICATIONS
drooling, urination, vomiting, defecation. Compassion DRUG(S) OF CHOICE
Physical Examination • Give thoughtful preparation and consid General Comments
Normal unless underlying medical problems. eration for the pet’s perspective before • Psychotropic medication, supplements, or
traveling; allow time for travel and be pheromones may be beneficial or necessary
patient.
(continued) Car Ride Anxiety—Dogs and Cats

Table 1
C
Benzodiazepine doses
Canine Feline
Alprazolam 0.02–0.1 mg/kg PO q6–12h 0.025–0.1 mg/kg PO q8–24h
Clonazepam 0.1–1.0 mg/kg PO q8–12h 0.02–0.2 mg/kg PO q12–24h
Diazepam 0.5–2 mg/kg PO PRN (e.g., q6h)
Lorazepam 0.025–0.2 mg/kg PO q24h to PRN 0.025–0.05 mg/kg PO 12–24h
Oxazepam 0.2–1 mg/kg PO q12–24h 0.2–0.5 mg/kg PO 12–24h
as an adjunct to the behavior program; • Cat—25–50 mg/cat for car travel. • Lavender essential oils may have a calming
short-acting anxiolytics are appropriate for • Side effects—sedation, lethargy, effect in dogs, but avoid in cats since floral
pets traveling occasionally; administer incoordination, cardiac conduction scents may be aversive.
anxiolytics so that optimal effect precedes disturbances, agitation. CONTRAINDICATIONS
onset of anxiety; the effect of anxiolytics Gabapentin Avoid use or use with caution in combination
may be overcome by severe anxiety or • Cat—20 mg/kg (50–150 mg/cat) 2–3h with any drug that enhances serotonin
distress; high or repeated doses, extreme before travel. transmission (e.g., trazodone, SSRIs, TCAs)
anxiety, and other medical conditions • Dog—10–30 mg/kg PRN to BID; may be and that may pose an increased risk for
increase the risk for profound sedation and started twice daily 12–48h in advance. serotonin syndrome.
drug reactions. • Side effects—sedation, ataxia.
• Drugs should be trial dosed in advance to PRECAUTIONS
determine effects, side effects, optimal dose, Clonidine All listed medications are extra-label or off-label
and duration. • Dog—0.01–0.05 mg/kg PO; begin at low (except maropitant). Use with informed consent.
• Address concurrent behavioral conditions dose and titrate to most effective dose;
(e.g., separation anxiety, fears, phobias, maximum effect may take up to 2h with
anxiety, reactivity) that may warrant faster absorption on an empty stomach; may
ongoing anxiolytics (e.g., tricyclic anti be started twice daily 12–48h in advance.
• Side effects—transient hyperglycemia,
FOLLOW-UP
depressants [TCAs] or selective serotonin
reuptake inhibitors [SSRIs]) in conjunction anticholinergic, hypotension, collapse, PATIENT MONITORING
with the treatment of travel-related anxiety. bradycardia, agitation; use with caution in Ask about travel-related distress as part of
cardiac disease or compromised renal or liver wellness assessment, and recommend early
Benzodiazepines function. intervention and prevention. Travel-related
• Anxiolytic; see Table 1 for drug options and difficulties pose a barrier for bringing pets to
dosing information. Dexmedetomidine Oromucosal Gel
the veterinary hospital.
• Give 30–60 minutes prior to travel. • Dogs—125 μg/m2 onto oral mucosa 30–60
• Side effects—incoordination, hyperphagia, min prior to travel; can be repeated in 2h. PREVENTION/AVOIDANCE
paradoxical excitability, muscle relaxation, • Licensed for use in dogs with noise aversion. • Provide preventive guidance on making
possible amnesic effect that might interfere • Side effects—sedation, paradoxical excite travel positive and carrier training at first
with learning. ment, pale mucous membranes, emesis. puppy or kitten visit.
• Hyperphagia may be advantageous for pets • Avoid travel for severely affected pets.
Acepromazine
with stress anorexia. • Use appropriate medication when travel
• Dog and cat—0.5–2.2 mg/kg PO.
• Oxazepam and lorazepam have no active required.
• Not for sole use; may be combined with
intermediate metabolites and may be safer anxiolytic medication for added sedation. EXPECTED COURSE
if hepatic function compromised; injectable • Side effects—ataxia, inhibits thermoregulation, AND PROGNOSIS
midazolam may be useful if administered peripheral vasodilation, muscle tremor or Likely to worsen if untreated.
in the veterinary hospital before home travel. spasm, altered noise reactivity.
Maropitant Pheromone
• May be indicated for nausea related to F3 cheek gland pheromone or dog-appeasing
travel and prior to opioid sedation. pheromone given 30–60 min before travel. MISCELLANEOUS
• Dog—1–2 mg/kg PO 2h before travel; for
motion sickness 8 mg/kg given with a small Natural Supplements ASSOCIATED CONDITIONS
amount of food 1–2h before travel. • For mild to moderate anxiety or adjunctive • Generalized anxiety disorder, noise-related
• Cat—1 mg/kg SC daily.
therapy—alpha-casosopene alone or in a diet fears and phobias, separation anxiety; hyper-
in combination with l-tryptophan; l-theanine attachment.
Trazodone alone or in combination products containing • Dental disease or pain.
• Dog—2–5 mg/kg; titrate up to 5–10 mg/kg whey protein, Phellodendron amurense, and
based on effect; higher doses may be utilized Magnolia officinalis; melatonin; Souroubea AGE-RELATED FACTORS
by experienced clinicians; may be started and Plantanus; or a calming probiotic Cognitive decline may exacerbate anxiety.
twice daily 12–48h in advance. supplement.
Car Ride Anxiety—Dogs and Cats (continued)
ZOONOTIC POTENTIAL • Fears, Phobias, and Anxieties—Cats. Horwitz D, ed. Blackwell’s 5 Minute Consult
C A distressed pet may cause distraction and put • Fears, Phobias, and Anxieties—Dogs. Clinical Companion: Canine and Feline
drivers at risk for accidents. ABBREVIATIONS Behavior, 2nd ed. Hoboken, NJ: Wiley,
PREGNANCY/FERTILITY/BREEDING • SSRI = selective serotonin reuptake inhibitor.
2018, pp. 873–884.
Drug use in breeding, pregnant, or lactating • TCA = tricyclic antidepressant.
Author Theresa L. DePorter
animals should be avoided. Consulting Editor Gary M. Landsberg
INTERNET RESOURCES
SEE ALSO www.catalystcouncil.org/resources/video
• Fear and Aggression in Veterinary Suggested Reading
Visits—Cats. Crowell-Davis SL, Murray T, Dantas L.
• Fear and Aggression in Veterinary Veterinary Psychopharmacology, 2nd ed.
Visits—Dogs. Hoboken, NJ: Wiley, 2019.
Carbon Monoxide Toxicosis

• Smoke inhalation, primary neurologic
disease, and severe metabolic disease. C
BASICS CBC/BIOCHEMISTRY/URINALYSIS FOLLOW-UP
Biochemistry—may see liver and kidney value • Patient monitoring—neurologic status, BP
OVERVIEW elevations secondary to hypoxia.
• Carbon monoxide (CO)—odorless,
and ECG during hospitalization; frequency
colorless, nonirritating gas produced by OTHER LABORATORY TESTS depends on stability of patient.
inefficient combustion of carbon fuels. • Carboxyhemoglobin can be measured via • Possible complications—delayed neurologic
• Common sources are fires, automotive co-oximetry; may return to normal within signs within days to weeks of initial improvement;
exhaust, leaking coal, oil, or natural gas/ hours after removal from CO source. deafness may occur/persist in survivors.
propane furnaces, gas appliances or fireplaces, Available at human hospital or veterinary • Expected course and prognosis—respond
and some paint strippers and sprays. specialty/diagnostic lab. and improve rapidly to oxygen therapy
• CO is absorbed into the blood, forming • Blood gas—metabolic acidosis due to lactic (within 30–60 minutes); prognosis guarded
carboxyhemoglobin (COHb). acidosis; arterial blood gas may have normal to poor with persistent or worsening respira-
• Affinity of CO for hemoglobin is approx partial pressure of oxygen (PaO2). tory and neurologic signs.
imately 240 times that of oxygen. • Prevention—use adequate ventilation with
IMAGING use of kerosene heaters in kennels and use
• COHb cannot bind oxygen and impairs Thoracic radiographs—evaluate for
oxyhemoglobin from releasing oxygen to the CO detectors.
pulmonary injury and rule out other causes of
tissues. respiratory signs.
• Major effect is acute cellular hypoxia,
leading to death. DIAGNOSTIC PROCEDURES
• Survivors may have cardiac damage, acute • Pulse oximetry may overestimate hemo MISCELLANEOUS
and delayed neurotoxicity. globin saturation (SpO2); COHb and
oxyhemoglobin absorb light at the same ASSOCIATED CONDITIONS
• Lethal concentration is approximately
wavelength. Animals in house fires may have dermal burns,
1,000 ppm (0.1%) for 1 hour.
• ECG—sinus tachycardia or cardiac thermal and smoke inhalation injury to the
SIGNALMENT dysrhythmia, ST-T depression with myocardial airways, corneal ulcerations, or other injuries.
Dogs and cats equally affected. hypoxia/anoxia. ZOONOTIC POTENTIAL
SIGNS • Blood pressure—hypotension common in People and other pets in the same
shock. CO-contaminated environment are at risk.
Acute Exposure
• Acute signs progress within minutes to hours. PREGNANCY/FERTILITY/BREEDING
• Neurologic signs—lethargy or agitation, CO reduces oxygen-carrying ability of
weakness, ataxia, depressed mentation, maternal blood, producing fetal hypoxia,
deafness, coma, seizures. TREATMENT abortion, or neurologic impairment of the
• Respiratory—tachypnea and dyspnea. • Supplemental oxygen (flow-by, mask, nasal, fetus, often with minimal effects on the dam.
• Cardiovascular—tachycardia, dysrhythmias, oxygen cage, or intubation ± mechanical ABBREVIATIONS
hypotension. ventilation)—improves oxygen delivery to • COHb = carboxyhemoglobin.
• Hyperemic skin and mucous membranes vital organs, especially brain and heart; • PaO2 = partial pressure of oxygen.
are rarely apparent in animals. decreases half-life of COHb. • SpO2 = oxygen saturation.
• Hyperbaric oxygen therapy use is
Chronic Exposure controversial and not readily available in Suggested Reading
• Nausea, vomiting, decreased activity, and veterinary medicine, but will further reduce Berent AC, Todd J, Sergeeff J, et al. Carbon
cough; may mimic other diseases. half-life of COHb. monoxide toxicity: a case series. J Vet Emerg
• Disturbance of postural and position • IV fluid therapy for hydration and Crit Care 2005, 15(2):128–135.
reflexes and gait. perfusion and to correct metabolic acidosis. Fitzgerald KT. Carbon monoxide. In:
Peterson ME, Talcott PA, eds. Small Animal
CAUSES & RISK FACTORS Toxicology, 3rd ed. St. Louis, MO: Elsevier
• Housed in areas with blocked exhaust vents,
Saunders, 2013, pp. 479–487.
furnaces, appliances, or chimneys; exposure to Vaughn L, Beckel N. Severe burn injury, burn
automobile exhaust or kerosene heaters in shock, and smoke inhalation injury in small
closed spaces with poor ventilation. MEDICATIONS animals. Part 1: Burn classification and
• Trapped in house or kennel fires. DRUG(S) OF CHOICE pathophysiology. J Vet Emerg Crit Care
• Animals with impaired cardiac or • Sedatives and anxiolytics may be needed to 2012, 22(2):179–186.
pulmonary function. allow oxygen supplementation—diazepam Vaughn L, Beckel N, Walters P. Severe burn
0.1–0.5 mg/kg IV q6–8h. injury, burn shock, and smoke inhalation
• Short-acting opioids such as fentanyl injury in small animals. Part 2: Diagnosis,
(2–5 μg/kg IV followed by CRI 2–5 μg/kg/h) therapy, complications, and prognosis. J Vet
can be used for pain and sedation. Emerg Crit Care 2012, 22(2):187–200.
DIAGNOSIS Author Katherine L. Peterson
DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS/POSSIBLE Consulting Editor Lynn R. Hovda
• Sedatives, ethanol, ethylene glycol, INTERACTIONS Acknowledgment The author and book
petroleum hydrocarbons, lead poisoning; Limit 100% oxygen to <24 hours to avoid editors acknowledge the prior contribution of
cyanide or hydrogen sulfide gas toxicosis. oxygen toxicosis. Gary D. Osweiler.
Carcinoid and Carcinoid Syndrome

OTHER LABORATORY TESTS • Adjuvant carboplatin therapy has been
C • Serum serotonin, serum chromogranin A, reported in a dog with a completely excised
and urinary 5-hydroxyindoleacetic acid are nonmetastatic jejunal carcinoid.
BASICS measured in humans suspected of carcinoid
OVERVIEW tumors; these tests are more diagnostic than
• Carcinoid tumors are neuroendocrine direct measurement of serum amine and
tumors arising from amine precursor uptake peptides.
• Serum serotonin levels were found to be
FOLLOW-UP
and decarboxylation (APUD) cells. Abdominal ultrasound and thoracic radio-
• Carcinoids originate from enterochromaffin increased tenfold in a dog with an intestinal
graphs should be performed regularly to
and enterochromaffin-like cells of the gastro- carcinoid; other testing has not been docu-
identify metastasis.
intestinal tract, but can be found in the liver, mented in animals with carcinoid tumors.
gall bladder, pancreas, tracheobronchial tree EXPECTED COURSE AND PROGNOSIS
IMAGING
and genitourinary system due to embryologic • Limited survival data exists (few reported
• Radiography and ultrasound can identify
origins. cases).
primary tumors and metastases.
• Carcinoids may secrete amines such as • Survival of 18 months seen in dog with
• CT scan and MRI may also be useful.
histamine, serotonin, prostaglandin, and intestinal carcinoid treated with surgery and
• In humans, more sensitive molecular
peptides such as bradykinins and tachykinins. carboplatin.
imaging includes radiolabeled somatostatin
• In humans, secretion causes “carcinoid • Survival of 12 months reported in cats with
receptor scintigraphy (OctreoScan); radioio-
syndrome.” This occurs in approximately extrahepatic carcinoids.
dinated metaiodobenzylguanidine (MIBG)
5–10% of patients with metastatic carcinoid imaging; and PET scans.
tumors. Hepatic degradation of excess
amines, notably seratonin, is bypassed, DIAGNOSTIC PROCEDURES
causing clinical signs. Human carcinoid • Biopsy often confirms diagnosis.
• If histopathologic results are equivocal, MISCELLANEOUS
syndrome is characterized by flushing,
abdominal pain, diarrhea, bronchospasm, and electron microscopy and/or immunohisto- ABBREVIATIONS
cyanosis. This syndrome has not been chemistry (looking for chromogranin A and/ • APUD = amine precursor uptake and
reported in small animals, although a recent or synaptophysin expression) may be used to decarboxylation.
report describes a dog with episodic collapse confirm a carcinoid tumor. • MIBG = metaiodobenzylguanidine.
and melena and an ileocecal carcinoid. PATHOLOGIC FINDINGS INTERNET RESOURCES
• Morbidity and mortality are more often a Tumors have a fine fibrovascular stroma with https://www.carcinoid.com
function of tumor size and gastrointestinal minimal to moderate cellular pleomorphism. Suggested Reading
blockage. Cytoplasm is eosinophilic and usually contains Corrigan A, Bechtel S. APUDomas:
• Primary carcinoid tumors in dogs have been secretory granules that stain argyrophilic and/ diagnosis, supportive care, and definitive
reported in the stomach, small intestine, or argentaffin-positive (silver stains). treatment. Proceedings of the American
colon, lung, gallbladder, and liver. In cats,
College of Veterinary Internal Medicine
carcinoids have been found in the stomach,
Forum, Indianapolis, Indiana, 2015.
small intestine, liver, and heart.
Rossmeisl JH Jr., Forrester SD, Robertson JL,
SIGNALMENT TREATMENT Cook WT. Chronic vomiting associated
• Dog—rare, generally >8–9 years of age. In some cases, surgical excision can be with a gastric carcinoid in a cat. J Am Anim
• Cat—rare, generally >7–8 years of age. curative, especially if no metastasis. Debulking Hosp Assoc 2002, 38(1):61–66.
SIGNS can decrease hormone secretion in humans, Author Virginia L. Gill
Clinical signs depend on the location of the and it may relieve tumor-related gastrointesti- Consulting Editor Patty A. Lathan
primary tumor or metastases and may include nal obstruction.
anorexia, vomiting, dyschezia, melena,
collapse, ascites, weight loss, and signs of
hepatic failure or gall bladder obstruction.
MEDICATIONS
DRUG(S) OF CHOICE
• Octreotide, a somatostatin analogue that
DIAGNOSIS inhibits hormone secretion from the tumor
DIFFERENTIAL DIAGNOSIS cells, is used in humans for palliative therapy;
Differentials include primary gastrointestinal as carcinoid syndrome has not been reliably
diseases—neoplasia, infection, inflammation, reported in animals with carcinoid tumors,
parasites, foreign body, dietary indiscretion, octreotide may be of little benefit.
or hepatic/biliary disease. • High-dose radioiodinated MIBG is used in
humans with nonresectable or metastatic
CBC/BIOCHEMISTRY/URINALYSIS carcinoid.
• Normal, possible mild nonregenerative • Interferons have demonstrated limited
anemia. success in humans with carcinoid tumors.
• Electrolyte abnormalities, elevated liver • Chemotherapy and radiotherapy have
enzyme activities, and hyperbilirubinemia can minimal efficacy in humans with carcinoid
be present. tumors.
Cardiac Glycoside Plant Toxicosis

Serum chemistry—hyperkalemia early and C
severe, may switch to hypokalemia.
BASICS FOLLOW-UP
OVERVIEW Serum digoxin levels may be useful in some PATIENT MONITORING
• Same toxic profile as digoxin, in particular ingestions. • ECG and blood pressure monitoring for
cardiovascular (CV) and gastrointestinal (GI) first 24 hours, then PRN.
signs. DIAGNOSTIC PROCEDURES • Strict attention to serum electrolytes.
• All plant parts, fresh or dry, are considered • Presence of plant pieces in vomit or stool.
• ECG monitoring for cardiac arrhythmias. PREVENTION/AVOIDANCE
toxic, but the concentration varies depending • Identify and recognize plants.
on specific plant and plant part. PATHOLOGIC FINDINGS • Oleander grows seemingly everywhere in
• Plants are best identified by scientific name. Sudden death is common. Plant pieces are parts of the SW United States and off-leash
• Common plants include Adenium obesum often found in the stomach and small dogs and cats should be monitored closely.
(desert rose); Apocynum cannabinum (dogbane); intestine. Clotted blood may be present in the
Asclepias spp. (milkweed); Calatropis spp. ventricles with a mottled appearance to the POSSIBLE COMPLICATIONS
(giant milkweed); Convallaria majalis (lily of epicardium. Histopathology findings are Sudden death.
the valley); Digitalis lanata (wooly foxglove); similar to digoxin toxicosis. EXPECTED COURSE AND PROGNOSIS
Digitalis purpurea (common or purple • Good nursing care for 5–7 days.
foxglove); Kalanchoe spp. (mother of millions); • Prognosis is good with early and
Nerium oleander (oleander); Ornithogalum appropriate care.
umbellatum (star of Bethlehem); Thevetia • Cardiac arrhythmias prolong treatment and
peruviana (yellow oleander). TREATMENT
• Emesis quickly after ingestion. hospitalization.
SIGNALMENT • Activated charcoal (1–2 g/kg) with a
• Cats are more sensitive to some of the plant cathartic × 1, followed by activated charcoal
toxins than dogs. without a cathartic every 6–8 hours × 2 doses.
• Dogs with the ABCB1-1Δ gene mutation • Asymptomatic animals—hospitalize and MISCELLANEOUS
may be more sensitive to toxins. monitor for 12 hours.
ABBREVIATIONS
SIGNS • Symptomatic animals—hospitalize and
• CV—bradycardia (rarely tachycardia), monitor with an ECG for 24 hours; administer
• CV = cardiovascular.
atrioventricular (AV) block, all forms of appropriate IV fluids (dependent on serum
• Fab = fragment antigen binding.
arrhythmias, death from asystole. potassium) to maintain blood pressure but not
• GI (most frequent)—hypersalivation, overload the CV system; monitor blood pressure
vomiting ± blood, diarrhea ± blood. closely, as hypotension may be persistent. INTERNET RESOURCES
• Neuromuscular—coma, tremors, seizures • http://www.petpoisonhelpline.com/poisons
(rarely); may be related to decreased cardiac • http://www.aspca.org/pet-care/animal-
output. poison-control/toxic-and-non-toxic-plants
CAUSES & RISK FACTORS MEDICATIONS Suggested Reading
• Cardiac glycoside–containing plants inhibit Eucher J. Cardiac glycosides. In: Hovda LR,
the ATPase sodium/potassium pump, DRUG(S) OF CHOICE Brutlag A, Poppenga RH, Peterson K, eds.
• Digoxin-specific fragment antigen binding Blackwell’s Five-Minute Veterinary Consult
resulting in an increase in intracellular sodium
and a decrease in intracellular potassium; (Fab; Digibind®) may be useful in some cases, Clinical Companion: Small Animal
increased intracellular (myocyte) calcium especially oleander toxicosis. Toxicology. Ames, IA: Wiley-Blackwell,
• Antiemetics if vomiting is severe or persistent— 2016, pp. 760–769.
results in increased cardiac contractions.
• Animals with a prior history of cardiac or
maropitant 1 mg/kg SC/IV/PO q24h in dogs Author Lynn R. Hovda
renal disease and receiving digoxin or other and cats; ondansetron 0.5–1 mg/kg IV, SC, PO Consulting Editor Lynn R. Hovda
cardiac glycoside drugs are at risk. q8–12h in dogs and cats.
• Bradycardia—atropine 0.02–0.04 mg/kg
IV/IM/SC in dogs and cats; repeat q4–6h as Client Education Handout
needed. available online
• Antiarrhythmics may be necessary in
DIAGNOSIS patients with ventricular dysrhythmias,
DIFFERENTIAL DIAGNOSIS evidence of poor perfusion, or who remain
• Beta blocker or calcium channel blocker tachycardic despite IV fluid therapy—
toxicosis. lidocaine: dogs, 2–4 mg/kg IV to effect.
• Cardiac disease in general. • GI protectants as needed—H2 blockers
• Digoxin/digitoxin toxicosis. such as famotidine (0.5–1 mg/kg PO/SC/IM/
• Ingestion of medications with known IV q12h); omeprazole (0.5 mg/kg PO daily);
cardiac effects. or sucralfate (0.25–1 g PO q8h).
• Ingestion of other plants with known CONTRAINDICATIONS/POSSIBLE
cardiac effects such as Taxus spp. (yew), INTERACTIONS
Rhododendron spp. (azalea, rhododendron), Beta blockers and calcium channel blockers
Kalmia spp. (mountain laurel, lambkill), and may have an additive effect on AV conduc-
Pieris japonica (Japanese pieris). tion and cause complete heart block.
Cardiomyopathy, Arrhythmogenic Right Ventricular—Cats

absence of myocardium in the RV free wall. • Focal or multifocal myocarditis.
C Histopathology is required to distinguish • Apoptotic cardiomyocytes.
this from ARVC and demonstrates
BASICS apposing endocardial and epicardial
OVERVIEW surfaces, without any interposed adipose
Arrhythmogenic right ventricular cardiomyopathy tissue or any evidence of inflammation or
necrosis.
TREATMENT
(ARVC) is a rare primary cardiomyopathy • Medical management of right-sided CHF is
characterized by progressive atrophy of the right CBC/BIOCHEMISTRY/URINALYSIS the mainstay of treatment for clinically
ventricular (RV) and/or right atrial (RA) Alanine aminotransferase may be elevated affected cats with ARVC.
myocardium, with replacement by fatty or secondary to hepatic congestion. • Anti-arrhythmic therapy is not routinely
fibrofatty tissue that may act as an arrhythmogenic required, but in cases with hemodynamically
substrate. The condition in cats typically manifests IMAGING
significant arrhythmias, anti-arrhythmic drugs
as signs of right-sided congestive heart failure Radiographic Findings should be selected based on the suspected
(CHF) due to progressive RV dysfunction. A • Cardiomegaly, typically in regions of right underlying mechanism of the arrhythmia.
variety of arrhythmias have been observed in cats atrium and right ventricle; left atrial enlarge-
with ARVC; however, sudden death does not ment may also be noted.
appear to be well recognized in this species. • Pleural effusion.
SIGNALMENT • Ascites.
• Cats. • Pericardial effusion. MEDICATIONS
• Caudal vena caval dilation. See Congestive Heart Failure, Right-Sided.
• One study reported mean age at present
ation of 7.3 years (range: 1–20 years). Echocardiographic Findings
• Breed or sex predilections unknown. • Severe RA and RV dilation.
SIGNS • RV systolic dysfunction/hypoknesis.
• Tricuspid regurgitation. FOLLOW-UP
General Comments • Paradoxical septal motion.
Compared to dogs and humans, sudden death PATIENT MONITORING
• Focal aneurysms may be observed in the Recheck when decompensation or other
does not appear to be as well recognized in cats RV wall, often toward the apex.
with ARVC, despite the wide variety of clinical signs develop.
• Left atrial enlargement sometimes seen.
arrhythmias documented with this condition. EXPECTED COURSE
Historical Findings AND PROGNOSIS
• Lethargy. ECG Prognosis appears to be very poor in cats
• Anorexia. • A variety of various arrhythmias have been identified with ARVC. Reported median
• Dyspnea. observed in cats with ARVC. survival time after development of clinical
• Tachypnea. • Ventricular premature complexes (right- signs of approximately 1 month (range:
• Abdominal distention may be noted. sided or left-sided in origin). 2 days to 4 months). Most cats die or are
• Ventricular tachycardia. euthanized due to signs of right-sided
Physical Examination Findings • Atrial fibrillation. CHF or thromboembolic complications.
• Signs consistent with right-sided CHF. • Supraventricular tachycardia.
• Dyspnea. • Ventricular premature complexes.
• Tachypnea. • Right bundle branch block.
• Jugular venous distention. • First-degree atrioventricular block.
• Ascites. • Third-degree atrioventricular block. MISCELLANEOUS
• Heart and/or lung sounds may be muffled. • RA and RV enlargement (tall P wave, deep SEE ALSO
• Weak femoral pulses. S waves in lead II), right axis deviation. • Cardiomyopathy, Arrhythmogenic Right
• Hepatosplenomegaly. Ventricular—Dogs.
• Thoracic percussion may reveal presence of Paracentesis and Fluid Analysis
Fluid analysis of pleural or abdominal • Congestive Heart Failure, Right-Sided.
pleural effusion.
• May auscult arrhythmia. effusions typically reveals modified transudate ABBREVIATIONS
consistent with right-sided CHF. • ARVC = arrhythmogenic right ventricular
CAUSES & RISK FACTORS cardiomyopathy.
• Unknown. PATHOLOGIC FINDINGS
• CHF = congestive heart failure.
• A genetic mutation in the striatin (desmosomal Gross Pathology • RA = right atrial.
protein) gene is associated with ARVC in some • Moderate-to-severe RA and RV dilation. • RV = right ventricular.
dogs. Genetic mutations are identified in approx- • Severe thinning of RA and RV walls, which
imately 60% of humans with ARVC, with are easily trans-illuminated. Suggested Reading
mutations identified in at least 13 genes. Genetic • Left atrial dilation and rarely left ventricular Fox P, Maron B, Basso C, et al.
studies in feline ARVC are lacking. dilation may be seen in some cats. Spontaneously occurring arrhythmogenic
• Thrombi sometimes identified. right ventricular cardiomyopathy in the
domestic cat: a new animal model similar
Histopathology to the human disease. Circulation 2000,
• RV myocardial atrophy with replacement 102(15):1863–1870.
DIAGNOSIS by fatty or fibrofatty tissue. Author Michael Aherne
DIFFERENTIAL DIAGNOSIS • Fibrosis may also be observed in right Consulting Editor Michael Aherne
Uhl’s anomaly—a congenital abnormality atrium, left ventricular free wall, and
characterized by partial or complete interventricular septum.
Cardiomyopathy, Arrhythmogenic Right Ventricular—Dogs

• Uncommon forms of acquired cardiac
disease (neoplasia, endocarditis). C
• Abdominal disease (especially splenic
BASICS disease) can be associated with VPCs. TREATMENT
• Echocardiography and abdominal • The goals of therapy include reduction of
OVERVIEW
A myocardial disease commonly character ultrasonography can be used to differentiate the number of VPCs, reduction of clinical
ized by ventricular tachyarrhythmias that can other causes of cardiac and abdominal disease. signs, and reduction of the risk of sudden
be accompanied by syncope or sudden death. cardiac death. Unfortunately, there is no
OTHER LABORATORY TESTS evidence that therapy can reduce the risk of
A small percentage (<5%) develop congestive • Genetic testing can now be performed to
heart failure with systolic dysfunction, sudden death. The decision to start therapy in
screen for the genetic mutation (https://cvm. the asymptomatic boxer with VPCs is
comparable to the dilated cardiomyopathy ncsu.edu/genetics) associated with arrhythmo
observed in other breeds. controversial, since all antiarrhythmics have
genic right ventricular cardiomyopathy. the potential to make the arrhythmia worse.
SIGNALMENT Submission samples can be either a blood However, dogs with as few as 300 VPCs/24
• Dog. sample in an EDTA tube or a buccal swab of hours have been observed to die suddenly. In
• Specific to the boxer, although a similar the oral mucosal surface. general, initiate antiarrhythmic drugs if there
presentation is infrequently observed in the • Plasma l-carnitine levels may be evaluated are >1,000 VPCs/24 hours and/or significant
English bulldog. in boxers with ventricular dilation and systolic runs of ventricular tachycardia or other signs
• Usually observed in mature dogs between dysfunction. However, plasma levels are not of arrhythmia complexity (e.g., bigeminy,
5 and 8 years of age. Dogs as young as 6 months always reflective of myocardial levels. If couplets), or clinical signs (syncope, exercise
have been reported and some affected dogs may plasma levels are not low, it is still possible to intolerance) related to the VPCs.
not develop clinical signs until >10 years of age. have low myocardial levels, and • Syncope and sudden cardiac death may be
supplementation with l-carnitine might be more frequently associated with stress and
SIGNS considered. excitement. Reduce stress and effort when
• Usually one of three presentations: possible. There is no direct relationship
◦ Asymptomatic dog with ventricular
IMAGING
between exercise restriction and survivability.
premature complexes (VPCs) detected on Thoracic Radiography Some dogs die while asleep. Thus, strict
routine examination. • Normal in most affected dogs. exercise restriction is not recommended.
◦ Syncope with VPCs detected on ECG or • Dogs with ventricular dilation and systolic
Holter monitor. dysfunction may have cardiac enlargement
◦ Signs of left heart failure (e.g., tachypnea, and evidence of heart failure (e.g., pulmonary
coughing) or biventricular failure (e.g., edema).
ascites, tachypnea, coughing) with VPCs; Echocardiography
MEDICATIONS
this presentation is least common. • Normal in most affected dogs. DRUG(S) OF CHOICE
• Sudden death may occur before develop • A small percentage of dogs have ventricular • The two best choices for treating the
ment of obvious clinical signs. dilation and systolic dysfunction, particularly ventricular arrhythmia are sotalol (1.5–
CAUSES & RISK FACTORS if they are homozygous for the deletion 2.0 mg/kg PO q12h) or mexiletine (5–6 mg/kg
• Adult onset, inherited (autosomal dominant). mutation. PO q8h). Some cases continue to have
• A genetic mutation (deletion) in a cardiac significant ventricular ectopy after treatment
DIAGNOSTIC PROCEDURES with one of these; such cases seem to respond
desmosomal gene (striatin) is associated with the
development of the disease. Dogs that are ECG well to the combination of sotalol and
homozygous for the striatin deletion appear to be • Many dogs will not have VPCs on an ECG mexiletine. These drugs have different
more likely to be more severely affected with a of brief duration since the arrhythmia can be mechanisms and appear to work in a safe and
higher number of VPCs, and are more likely to intermittent. However, some dogs will have complementary fashion.
have cardiac dilation and myocardial dysfunction. one or more upright VPCs on a brief lead • In dogs with systolic dysfunction and heart
Sudden death is more common. It is not yet II ECG. failure, consider treatment with furosemide,
known if this is the only genetic cause or if • In either case, if suspicion of disease is enalapril, pimobendan, spironolactone, and
additional genetic mutations will be identified. present, Holter monitoring is recommended l-carnitine.
• At least one family of boxers with VPCs, to determine the severity and complexity of CONTRAINDICATIONS/POSSIBLE
ventricular dilation, and systolic dysfunction the arrhythmia and to have a baseline for
INTERACTIONS
was found to have decreased myocardial comparison once treatment is started. If
Any antiarrhythmic drug has the potential to
l-carnitine levels and demonstrated some Holter monitoring is not available and the
make an arrhythmia worse.
clinical improvement when supplemented dog is symptomatic with upright VPCs on an
with l-carnitine. The cause and effect of this ECG, therapy should be considered.
relationship is unclear, and response to this PATHOLOGIC FINDINGS
supplementation does not occur in all dogs • Gross pathology is nonspecific in most
with myocardial dysfunction. cases. In a small percentage of cases, left FOLLOW-UP
• If possible, repeat the Holter monitor 2–3
and right ventricular dilation may be
observed. weeks after starting therapy to evaluate for a
• Histopathologic abnormalities include
response. Affected dogs can have an 85%
a fatty and fibrous infiltrate into the day-to-day variability in VPC number before
DIAGNOSIS medications; therefore, a good response to
right ventricular (and sometimes interven
DIFFERENTIAL DIAGNOSIS tricular and left ventricular) free wall. therapy would be an 85% reduction in VPC
• Aortic stenosis—moderate and severe forms number. It is also anticipated that the
can be associated with VPCs. complexity of the arrhythmia (bigeminy,
Cardiomyopathy, Arrhythmogenic Right Ventricular—Dogs (continued)

trigeminy, couplets, triplets, runs of thmics for years with good quality of life. SEE ALSO
C ventricular tachycardia) will be reduced once Dogs with systolic dysfunction and dilation • Ventricular Premature Complexes.
on therapy. It may not always be possible to have the worst prognosis, although some of • Ventricular Tachycardia.
achieve an 85% reduction in VPC number; these dogs do show improvement and a ABBREVIATIONS
in those cases an improvement in arrhythmia decreased rate of progression on l-carnitine • VPC = ventricular premature complex.
complexity and clinical signs would be supplementation. Author Kathryn M. Meurs
reasonable goals. Consulting Editor Michael Aherne
• Annual Holter monitoring and echocardio
graphy are suggested, since in some cases the
disease can be progressive.
• Advise owners that dogs are always at risk
MISCELLANEOUS
of sudden death. However, the majority of SYNONYMS
affected dogs can be maintained on antiarrhy Boxer cardiomyopathy.
Cardiomyopathy, Dilated—Cats
in this series. In the author’s experience, the taurine deficiency until shown to be
prevalence of feline idiopathic DCM may be unresponsive to taurine. C
less than 10%. • Myocardial failure secondary to long
BASICS standing congenital or acquired left
SIGNALMENT
DEFINITION ventricular volume overload diseases.
• Dilated cardiomyopathy (DCM) is a disease Species • End-staged remodeled hypertrophic
of the heart muscle characterized by systolic Cat cardiomyopathy may manifest with a dilated
myocardial failure and a dilated, volume- Breed Predilections hypocontractile heart.
overloaded heart that leads to signs of congestive Because the prevalence is low, breed predilections • Arrhythmogenic right ventricular
heart failure (CHF) or low cardiac output. are not clearly defined. That said, the Burmese cardiomyopathy.
• Before 1987, DCM was the second most cat may have an increased incidence. CBC/BIOCHEMISTRY/URINALYSIS
commonly diagnosed heart disease in cats. Many cats will have prerenal azotemia related
Mean Age and Range
Most cats had a secondary DCM as a result of to low cardiac output.
9 years (5–13 years).
taurine deficiency. Primary idiopathic DCM
is now an uncommon cause of heart disease Predominant Sex OTHER LABORATORY TESTS
in cats. None. (One study cites a male predisposition, • Ensure that thyroid concentrations are normal.
while another states a female overrepresentation.) • Plasma taurine concentrations less than
PATHOPHYSIOLOGY 40 nmol/L or whole blood taurine
• Histopathologically, the myocardium of SIGNS concentrations less than 250 nmol/L, are
cats with idiopathic DCM has evidence of General Comments subnormal and suggestive of taurine
myocytolysis, fibrosis, myofibril fragmen • Cats with idiopathic DCM usually present deficiency DCM. Taurine assays are
tation, and vacuolization. Gross examination for signs of CHF. performed at a limited number of institutions
reveals global eccentric enlargement of all • They are rarely diagnosed prior to onset of and require special handling.
four cardiac chambers. clinical signs. • Cardiac biomarkers such as plasma amine
• These anatomic changes are associated with terminal B-type natriuretic peptide (NT-proBNP)
progressive myocardial systolic failure, decreased Historical Findings
• Signs related to low cardiac output—
and cardiac troponin I (cTnI) concentrations
contractility, decreased compliance, and would be elevated in a cat with CHF due to
secondary mitral valve regurgitation due to anorexia, weakness, depression.
• Signs related to CHF—dyspnea, tachypnea.
idiopathic DCM.
mitral valve annular dilation. These changes are
typically identified by echocardiography. • Signs related to ATE—sudden-onset pain IMAGING
• Eventually, the chronic myocardial and paraparesis.
Radiography
dysfunction leads to CHF and clinical signs. Physical Examination Findings • Radiography often shows pleural effusion
SYSTEMS AFFECTED • Heart rate can be fast, normal, or slow. or pulmonary edema.
• Cardiovascular—DCM is a primary • Soft systolic heart murmur. • Generalized cardiomegaly.
myocardial disease and primarily affects the • Weak left cardiac impulse.
• Gallop sound. Echocardiography
heart and its ability to maintain an adequate • Diagnostic modality of choice.
cardiac output to maintain the body’s needs. • Possible arrhythmia.
• Hypothermia. • Characteristic findings include thin ventricular
• Musculoskeletal—cats with DCM can walls, enlarged left ventricular end-systolic and
present with aortic thromboembolism (ATE), • Prolonged capillary refill time.
• Tachypnea. end-diastolic dimensions, left atrial enlargement,
which causes acute paraparesis or monoparesis. and low fractional shortening.
• Renal/urologic—cats with DCM and CHF • Quiet lung sounds (pleural effusion).
• Crackles (pulmonary edema). • Pleural and pericardial effusion may be
often have poor renal perfusion and visualized.
commonly have prerenal azotemia. • Ascites.
• Hypokinetic femoral pulses. • Spontaneous echocardiographic contrast or
• Respiratory—cats usually present with a thrombus may be visualized.
tachypnea or dyspnea due to CHF with • Possibly, posterior paresis and pain as a
DCM. These cats can develop both result of ATE.
pulmonary edema and pleural effusion. CAUSES
ECG
GENETICS The underlying etiology of idiopathic DCM
• ECG may be normal or may show left atrial
Because of the human experience with DCM, remains unknown, although a genetic
or ventricular enlargement patterns.
it is likely that feline DCM also has a genetic predisposition has been identified in some
• Both ventricular and supraventricular
basis, either inherited or de novo, as the cause families of cats. Taurine deficiency was a
arrhythmias can be seen.
of the disease. No definitive mutation has common cause of secondary myocardial
failure before 1987. Pleural Effusion Analysis
been identified in the cat to date; however, a
• Pleural effusion typically is a modified
quantitative genetic evaluation of a large
cattery suggested an inherited factor in the transudate with total protein <4 g/dL and
development of DCM. nucleated cell counts of less than 2,500/mL;
chylous effusion may also be present.
INCIDENCE/PREVALENCE DIAGNOSIS • Analysis of the pleural effusion is important
Idiopathic feline DCM is relatively uncommon DIFFERENTIAL DIAGNOSIS to rule out other causes of pleural effusion
now that taurine is adequately supplemented • Taurine deficiency DCM; because primary such as pyothorax, infectious peritonitis, or
in cat foods. A retrospective survey of 106 cats idiopathic DCM and taurine deficiency have lymphosarcoma.
with feline myocardial disease from 1994 to similar clinical presentations, cats with PATHOLOGIC FINDINGS
2001 from Europe revealed that DCM was myocardial failure should be assumed to have • Heart : body ratio is increased.
diagnosed in approximately 10% of the cases • All four cardiac chambers are dilated;
Cardiomyopathy, Dilated—Cats (continued)
ventricular walls are thin and left ventricular q12h, until it is demonstrated that the patient supraventricular and ventricular arrhythmias.
C lumen is enlarged. is unresponsive to taurine or is not taurine Beta blockers are used in the long-term
• Valve anatomy is normal. deficient based on diagnostic testing. management of DCM in humans because of
• Histopathology shows myocytolysis and • Nitroglycerin (2% ointment) one-fourth to their positive myocardial effects and survival
myocardial fibrosis. one-half inch applied topically can be used in benefit. Clinical experience is limited in feline
conjunction with diuretics in the acute DCM and they must be used cautiously, as
management of severe CHF to further reduce they acutely decrease contractility and could
preload. Nitroglycerin will lower the dose of worsen CHF. Recommended dose ranges
furosemide and is particularly useful in from 3.125 to 6.25 mg PO q12–24h. Start
TREATMENT patients with hypothermia or dehydration. low and titrate up based on heart rate and
APPROPRIATE HEALTH CARE • Enalapril or benazepril, at a dose of clinical signs.
These cats usually present in CHF and should 0.25–0.5 mg/kg PO q24h, is recommended PRECAUTIONS
be treated as inpatients, typically in an to reduce afterload and preload as soon as the • Unless needed for acute cardiac rhythm
intensive care setting until more stable. cat is able to take oral medications and is control, drugs such as calcium channel
NURSING CARE clinically stable. Use with caution and blockers (diltiazem) or beta-adrenergic
• Thoracocentesis is often utilized for both possibly avoid if creatinine >2.5 mg/dL. blockers may reduce contractility and lower
therapeutic and diagnostic purposes. • Digoxin is optionally recommended to cardiac output. Use cautiously.
• Supplemental oxygen therapy is beneficial strengthen contractility and for its positive • Overzealous diuretic and vasodilation
for cats in CHF to decrease the work of neurohumoral effects at a dose of 0.03 mg/ therapy may cause azotemia and electrolyte
breathing. cat (one-fourth of a 0.125 mg tablet) or disturbances.
• If hypothermic, cautious external heat 0.01 mg/kg PO q48h. Digoxin can be given • Digoxin should not be used if renal
(incubator or heating water pad) is concurrently with pimobendan. However, insufficiency is documented or suspected.
recommended. digoxin is often omitted when pimobendan • Enalapril or benazepril should be used with
is given because of the difficulties in giving a caution and possibly withheld if serum
ACTIVITY cat several pills and digoxin’s side-effect
Indoors only after hospital discharge to creatinine is >2.5 mg/dL.
profile. • Dobutamine may cause seizures and cardiac
reduce stress. Let cat dictate its own activity. • Dobutamine at extremely low dosages can tachyarrhythmias.
DIET be given to a patient with severe signs of CHF
These cats typically are anorexic, thus and low cardiac output that cannot take oral
tempting their appetite with many types of medications. Dose varies 0.25–5 μg/kg/
food may be necessary. Eventually, a minute IV CRI. ECG monitoring is
low-sodium diet is recommended. recommended. FOLLOW-UP
• Because ATE is a concern, an antithrom
CLIENT EDUCATION PATIENT MONITORING
botic agent is also recommended. Clopidogrel
Some cats will need chronic intermittent • Repeat examination with ideally blood
given at a dose of 18.75 mg (one-fourth of a
thoracocentesis to manage significant pressure, diagnostic imaging (either a
75 mg tablet) PO q24h is generally the
accumulations of pleural effusion despite thoracic radiograph or focused thoracic
author’s preferred antithrombotic agent.
medical therapy. ultrasound for fluid assessment), and
Other options include aspirin 81 mg PO
q72h (with food) or low molecular weight chemistry panel within 1 week to determine
heparin (e.g., dalteparin 100–150 units/kg response of therapy.
SC q8–24h or enoxaparin 1 mg/kg SC • Home resting respiratory rate monitoring is
MEDICATIONS q12–24h). helpful to determine need for diuretic dose
• Antiarrhythmic drugs may also be needed adjustment or thoracocentesis.
DRUG(S) OF CHOICE • Periodically monitor electrolyte and renal
• Furosemide is recommended to manage
to control supraventricular or ventricular
arrhythmias. If hemodynamically significant parameters. Periodically monitor for CHF
pulmonary edema and pleural effusion. fluid accumulation with diagnostic imaging.
Recommended dose range is 1–4 mg/kg supraventricular tachycardia or rapid atrial
fibrillation is present, diltiazem is recomm • If using digoxin, serum blood concen
q8–12h. Initially, administer parenterally trations should be measured approximately
then switch to oral. Chronically the lowest ended. Usually, diltiazem is given orally in
either a non-sustained-release formulation 10–14 days after initiating therapy. Therapeutic
effective dose of furosemide is recommended. range is 0.5–1.5 ng/dL 8–12 hours post-pill.
• Pimobendan, an inodilator, is also recomm
(7.5 mg/cat PO q8h) or a sustained-release
oral formulation (Cardizem CD® at 10 mg/kg • Repeat diagnostic echocardiogram in 2–3
ended to strengthen contractility and provide months after initiating taurine supplemen
some vasodilation. Recommended dose range is PO q24h or Dilacor XR® 30 mg/cat [or 1/2
of an inner 60 mg tablet] PO q12h). tation to determine echocardiographic
0.1–0.3 mg/kg PO q12h. Although response to therapy. Although echocardio
pimobendan is not currently licensed for use in Diltiazem is also available in an injectable
formulation for urgent control of a graphic response may take 2–3 months to
cats, several recent publications have demonstrated assess, one should see dramatic clinical
its safety in cats and possibly a beneficial effect, supraventricular arrhythmia in a cat that
cannot take oral medications (0.05–0.1 mg/kg response within 2 weeks of initiating taurine
albeit in retrospective studies. One study in cats therapy if cat has taurine-responsive DCM.
with non-taurine-responsive DCM that were slow IV, repeated PRN up to 0.25 mg/kg).
treated with pimobendan had a median survival If rapid and sustained ventricular tachycardia, PREVENTION/AVOIDANCE
time that was four times longer than the cats lidocaine slow IV 0.2–0.5 mg/kg (repeat once Ensure that cats eat a high-protein diet with
not treated with pimobendan (49 vs. 12 days). or twice max) or sotalol PO 2 mg/kg q12h is sufficient dietary taurine. No vegetarian diets.
• Taurine supplementation is recommended
recommended.
• Beta blockers, such as atenolol, may be
initially in all cats with DCM at 250 mg PO
useful in the chronic management of both
(continued) Cardiomyopathy, Dilated—Cats

POSSIBLE COMPLICATIONS SYNONYMS Kittleson MD. Feline myocardial disease. In:
ATE is the most feared complication of any Cardiomyopathy Ettinger SJ, Feldman EC, eds. Textbook of C
feline myocardial disease. Veterinary Internal Medicine, 6th ed. St.
SEE ALSO Louis, MO: Elsevier, 2005, pp. 1082–1103.
EXPECTED COURSE • Aortic Thromboembolism. Lawler DF, Templeton AJ, Monti KL. Evidence of
AND PROGNOSIS • Congestive Heart Failure, Left-Sided. genetic involvement in feline dilated cardio
• These cats have a poor prognosis despite • Congestive Heart Failure, Right-Sided. myopathy. J Vet Intern Med 1993; 7:383–387.
intensive therapy. If cat is not taurine Pion PD, Kittleson MD, Rogers QR, et al.
responsive, survival is usually weeks to ABBREVIATIONS
Myocardial failure in cats associated with low
months. • ATE = aortic thromboembolism.
plasma taurine: a reversible cardiomyopathy.
• CHF can be medically refractory and • CHF = congestive heart failure.
Science 1987; 237:764–768.
recurrent despite appropriate medical therapy. • cTnI = cardiac troponin I.
Author Teresa C. DeFrancesco
• Repeated thoracocentesis may be necessary. • DCM = dilated cardiomyopathy.
Consulting Editor Michael Aherne
Suggested Reading
Ferasin L, Sturgess CP, Cannon MJ, et al.
Feline idiopathic cardiomyopathy: a
MISCELLANEOUS retrospective study of 106 cats (1994–2001).
J Feline Med Surg 2003; 5:151–159.
ASSOCIATED CONDITIONS Hambrook LE, Bennett PF. Effect of pimobendan
• CHF. on the clinical outcome and survival of cats with
• ATE. non-taurine responsive dilated cardiomyopathy.
• Pleural effusion. J Feline Med Surg 2012; 14:233–239.
• Cardiac arrhythmias.
Cardiomyopathy, Dilated—Dogs
SIGNALMENT Newfoundland, and cocker spaniel; diet-
C Species associated DCM, which may be associated
Dog with taurine deficiency, commonly secondary
BASICS to boutique, exotic-ingredient, or grain free
DEFINITION Breed Predilections (BEG) diets, is increasing recognized and
Dilated cardiomyopathy (DCM) character • Doberman pinscher, boxer. potentially reversible.
ized by left- and right-sided dilation, normal • Giant breeds—Scottish deerhound, Irish • Viral, protozoal, and immune-mediated
coronary arteries, anatomically normal wolfhound, Great Dane, St. Bernard, mechanisms have been proposed but not proven.
although commonly insufficient Newfoundland. • Doxorubicin toxicity.
atrioventricular valves, significantly decreased • Cocker spaniel, Portuguese water dog • Hypothyroidism and persistent tachy
inotropic state, and myocardial dysfunction (juvenile). arrhythmias (sometimes associated with
occurring primarily during systole; however, Mean Age and Range congenital tricuspid valve malformation) may
progressive diastolic dysfunction with restrictive 4–10 years. cause reversible myocardial failure.
physiology may also be present and is a
Predominant Sex
negative predictor of survival.
Males > females in most but not all breeds
PATHOPHYSIOLOGY (minor predisposition).
• Myocardial failure leads to reduced cardiac
SIGNS
DIAGNOSIS
output and congestive heart failure (CHF). DIFFERENTIAL DIAGNOSIS
• Atrioventricular (AV) annulus dilation and Historical Findings
• Myxomatous valvular degeneration.
altered papillary muscle function promote • Respiratory—tachypnea, dyspnea,
• Congenital heart disease.
valvular insufficiency. coughing.
• Heartworm disease.
• Although left-sided signs commonly • Weight loss, typically of lean muscle mass.
• Bacterial endocarditis.
predominate, evidence of severe right-sided • Weakness, lethargy, anorexia.
• Cardiac tumors and pericardial effusion.
disease can occur and infrequently is the • Abdominal distention.
• Airway obstruction—foreign body,
dominant clinical scenario. • Syncope, usually associated with
neoplasm, laryngeal paralysis.
arrhythmias (atrial fibrillation; ventricular
SYSTEMS AFFECTED • Primary pulmonary disease—bronchial
tachycardia).
• Cardiovascular. disease, pneumonia, neoplasia, aspiration,
• Some dogs are asymptomatic, having what
• Renal/urologic—prerenal azotemia. vascular disease (e.g., heartworms).
is termed preclinical DCM, the diagnosis of
• Respiratory—pulmonary edema, • Noncardiogenic pleural effusions
which in specific breeds is well described.
infrequently pulmonary hypertension. (e.g., pyothorax, hemothorax, chylothorax).
• Breed-specific echocardiographic parameters
• All organ systems are affected by reductions • Trauma resulting in diaphragmatic hernia,
coupled with cardiac biomarkers (NT-proBNP;
in cardiac output. pulmonary hemorrhage, hemothorax,
cardiac troponin I [cTnI]) may help identify
GENETICS pneumothorax.
dogs with preclinical DCM.
• Genetic cause or heritable susceptibility CBC/BIOCHEMISTRY/URINALYSIS
strongly suspected in most breeds and Routine hematologic tests and urinalysis are
• May be completely normal with preclinical
documented in some (Portuguese water dog, usually normal unless altered by severe
DCM.
boxer, and Doberman pinscher) with variable reductions in cardiac output or severe
• Weakness, possibly cardiogenic shock.
forms of inheritance. elevations in venous pressures (e.g., prerenal
• Hypokinetic femoral pulse from low cardiac
• A genetic test is commercially available for azotemia, high alanine aminotransferase,
output.
causative mutations in boxer dogs (striatin) hyponatremia), therapy for heart failure
• Pulse deficits with atrial fibrillation,
and Doberman pinscher (NCSU DCM 1— (e.g., hyponatremia, hypokalemia, hypo
ventricular or supraventricular premature
pyruvate dehydrogenase kinase; NCSU DCM chloremia, azotemia, and metabolic alkalosis
contractions, and paroxysmal ventricular
2—titin). from diuresis), or concurrent disease.
tachycardia.
• These mutations are not causative in other OTHER LABORATORY TESTS
• Jugular pulses from tricuspid regurgitation,
predisposed breeds in which they have been Cardiac biomarkers including NT-proBNP
arrhythmias, or right-sided CHF.
evaluated. and cTnI are elevated in both the preclinical
• Breath sounds—muffled with pleural
• Correlations between genotype and and clinical stages of the disease. Clinical
effusion; crackles with pulmonary edema.
phenotype have shown that Doberman studies investigating use of these markers for
• S3 or summation gallop sounds.
pinschers with both mutations have, on diagnosis, prognosis, and optimization of
• Mitral and/or tricuspid regurgitation murmurs
average, an earlier onset of clinical disease therapy are ongoing.
are common but usually focal and soft.
with a predisposition to sudden death; boxers
• Auscultatory evidence of cardiac arrhythmia IMAGING
homozygous for the mutation are more likely
is common.
to develop the DCM phenotype. Radiography
• Slow capillary refill time, infrequent cyanosis.
INCIDENCE/PREVALENCE • Hepatomegaly with or without ascites. • Typically normal in the preclinical phase.
Estimated at 0.5–1.1% in predisposed breeds • Generalized cardiomegaly and signs of
CAUSES CHF are common.
and perhaps higher in specific geographic
• Majority of cases represent familial • Left ventricular (LV) enlargement and left
regions.
abnormalities of structural, energetic, or atrial enlargement may be most evident in
GEOGRAPHIC DISTRIBUTION contractile cardiac proteins, some of which early cases.
None with the exception of Chagas’ cardio have been identified. • In some cases, the degree of cardiomegaly
myopathy, which is limited to the southern • Nutritional deficiencies (taurine and/or may be less than expected for the severity of
United States (Gulf Coast) and both Central carnitine) have been documented in several clinical signs; it is also often substantially less
and South America. breeds including golden retriever, boxer, than would be expected in a dog with
(continued) Cardiomyopathy, Dilated—Dogs

primary valvular heart disease and comparable DIET • If paroxysmal ventricular tachycardia is
clinical signs. • During initial therapy for clinical signs, present—administer lidocaine slowly in C
• Pleural effusion, hepatomegaly, ascites. simply maintaining adequate caloric intake is 2 mg/kg boluses (up to 8 mg/kg total over
Echocardiography paramount. 30 min) to convert to sinus rhythm; follow
• Gold standard for diagnosis. • Goal—reduce dietary sodium intake to with lidocaine infusion (50–100 μg/kg/min).
<12–15 mg/kg/day. • If lidocaine is ineffective—administer
• LV dilation often precedes overt reductions
in indices of systolic function. • Severe sodium restriction is typically not procainamide slowly at dose of 2–5 mg/kg
• Ventricular and atrial dilation. necessary when using potent cardioactive (up to 15 mg/kg) IV to convert to sinus
• Indices of myocardial systolic function therapy and may adversely affect appetite. rhythm; follow with 25–50 μg/kg/min CRI
(fractional shortening [FS%]), ejection • Best to use commercially prepared diets. (beware of proarrhythmia and infrequently
fraction, area shortening, and mitral annular CLIENT EDUCATION hypotension).
motion by tissue Doppler imaging may be • Emphasize potential signs associated with Maintenance Therapy
reduced. progression of disease and adverse side effects • ACE inhibitors (enalapril, benazepril,
• Spectral Doppler studies may confirm of medication. lisinopril) are considered cornerstone of
decreased velocity and/or acceleration of • Monitoring sleeping respiratory rate often therapy for DCM.
trans-aortic flow as well as mitral regurgitation gives insight into impending decompensation. • Enalapril (0.25–0.5 mg/kg PO q12h),
and/or tricuspid regurgitation. benazepril (0.5 mg/kg PO q12–24h), or
• Doppler evidence of restrictive LV filling is lisinopril (0.5 mg/kg PO q 12–24h) should
associated with decreased survival. be initiated early in the therapeutic regimen.
• Furosemide (1–4 mg/kg PO q8–12h) is
DIAGNOSTIC TESTS
MEDICATIONS used to control signs of congestion.
ECG • Torsemide (0.1–0.4 mg/kg PO q8–12h) is
• Sinus rhythm or sinus tachycardia with isolated DRUG(S) OF CHOICE
commonly employed as an alternative to
atrial or ventricular premature complexes. First identify patient problems—CHF (left or
furosemide, particularly in later-stage disease.
• Atrial fibrillation and ventricular tachycardia right-sided), arrhythmia, hypothermia, renal
• Spironolactone (1–2 mg/kg PO q12h) may
(paroxysmal or sustained) are very common failure, shock.
impart an independent survival benefit by
in Doberman pinschers. Preclinical Disease blocking aldosterone; higher doses can be
• Boxers commonly have isolated ventricular • There is clinical evidence (PROTECT Trial) used for refractory heart failure (2–4 mg/kg
arrhythmias without evidence of functional or that early intervention with pimobendan PO q12h).
anatomic heart disease. monotherapy substantially changes the course • Hydrochlorthiazide (1–2 mg/kg PO q12h)
• Prolonged QRS (>0.06 second), possible of preclinical disease in Doberman pinschers. may be beneficial as a third diuretic.
increased voltages (R >3 mV lead II), • These results are routinely extrapolated to • Beta blockers can be used cautiously once
suggesting LV enlargement. other breeds, but have not been proven. heart failure is controlled with other drugs
• May have “sloppy” R wave descent with • Critical evaluation suggests that early (see Precautions); if tolerated, they may
ST-T coving, suggesting myocardial disease or intervention with monotherapy using an improve myocardial function with chronic
LV ischemia. angiotensin-converting enzyme (ACE) use; carvedilol (0.25–1.25 mg/kg PO q12h) is
• May have low voltages (pleural or pericardial inhibitor is of minimal or no survival benefit an alpha and beta blocker with antioxidant
effusion, concurrent hypothyroidism). in preclinical disease. activity: start at the low end of the dose range
PATHOLOGIC FINDINGS Initial Stabilization and gradually up-titrate over a 6-week period
• Dilation of all chambers with or without • Treat hypoxemia with oxygen adminis if tolerated; consult with a cardiologist before
thinning of chamber walls. tration; prevent heat loss if hypothermic using beta blockers in clinical DCM patients
• Slightly thickened endocardium with pale (warm environment). as can result in rapid and profound clinical
areas within myocardium (necrosis, fibrosis). • If pulmonary edema—furosemide deterioration.
• Two histologically distinct forms—fatty (1–4 mg/kg IM/IV, then 1–2 mg/kg q6–12h • Pimobendan (0.25–0.3 mg/kg PO q12h) is
infiltration: degenerative type seen in boxers for first 1–3 days), or CRI 1–2 mg/kg/h a calcium-sensitizing drug and a vasodilating,
and Doberman pinschers; and attenuated (author’s preference). positive inotrope (inodilator) that, when
wavy fiber type: seen in many giant-, large-, • 2% topical nitroglycerin for first 24–48h added to furosemide, ACE inhibitors, and
and medium-sized breeds, including some for severe pulmonary edema—apply 1 inch–2 spironolactone improves functional heart
boxers and Doberman pinschers. inches q8h (beware of hypotension in both failure class and in Doberman pinschers
patients and staff ). increases survival time; the author has
• If significant pleural effusion—drain each administered pimobendan 0.5 mg/kg PO q8h
hemithorax. in refractory cases with perceived clinical
• If severe heart failure and cardiogenic benefit.
TREATMENT • The role of carnitine and taurine in therapy
shock—dobutamine may be indicated; this
APPROPRIATE HEALTH CARE drug may exacerbate arrhythmias, particularly of DCM remains controversial; however,
With the exception of severely affected dogs in hypoxic dogs; oral pimobendan (see dosing American cocker spaniels with DCM
(life-threatening arrhythmias, severe below) may have important acute (2–4h) generally respond favorably to taurine and
pulmonary edema, cardiogenic shock), most hemodynamic benefit as well; IV pimobendan l-carnitine supplementation, but still require
therapy can be administered on an outpatient (0.15 mg/kg) is available in select countries. additional cardiac medications.
basis. • Dobutamine 5–15 μg/kg/min infused for Arrhythmias
ACTIVITY 24–72h with care (start low and gradually • In atrial fibrillation, slowing of ventricular
Allow the dog to choose its own level of up-titrate based on response). rate response typically achieved with chronic
activity. administration of extended-release diltiazem
Cardiomyopathy, Dilated—Dogs (continued)
(Dilacor®) 2–7 mg/kg PO q12h, or atenolol POSSIBLE INTERACTIONS survival following identification in preclinical
C 0.75–1.5 mg/kg PO q12h (never start in • Quinidine, amiodarone, and diltiazem may phase averages over 700 days.
patient with active CHF), occasionally increase serum digoxin levels and predispose • Atrial fibrillation, paroxysmal ventricular
combined with digitalis at dose of 0.005 mg/ to digitalis intoxication. tachycardia, Doppler evidence of restrictive
kg PO q12h; therapeutic drug monitoring • Renal dysfunction, hypothyroidism, and LV filling, markedly decreased FS%, homo
recommended when administering digoxin. hypokalemia predispose to digitalis intoxication. zygosity for known mutations (boxer), or
• Therapeutic goal is obtaining resting presence of multiple mutations (Doberman
ALTERNATIVE DRUG(S)
ventricular rate of 100–140 bpm. • Other vasodilators, including hydralazine
pinschers) are believed to be markers for
• At-home monitoring with AliveCor Kardia shortened survival and increased risk for
and amlodipine, may be used instead of or in
device. addition to ACE inhibitors (beware of hypo- sudden arrhythmogenic death.
• This therapy merely controls ventricular rate,
tension).
by depressing atrioventricular nodal conduction; • Role of co-enzyme Q10, fish oil, and
generally does not convert rhythm from atrial arginine remains to be determined.
fibrillation to sinus rhythm.
• Amiodarone (10–15 mg/kg PO q24h for MISCELLANEOUS
7–10 days followed by 5–10 mg/kg PO ASSOCIATED CONDITIONS
q24h) may either control ventricular response Prevalence increases with age.
rate or in some cases result in conversion to FOLLOW-UP
SYNONYMS
normal sinus rhythm. PATIENT MONITORING • Congestive cardiomyopathy.
• Chronic oral therapy for ventricular • Serial clinical examinations, thoracic • Giant-breed cardiomyopathy.
tachycardia includes sotalol (1–2 mg/kg PO radiographs, blood pressure measurements,
q12h), mexiletine (5–10 mg/kg PO q8h), or routine serum biochemical evaluations SEE ALSO
amiodarone (5–10 mg/kg PO q24h). • Atrial Fibrillation and Atrial Flutter.
(including electrolytes), and electrocardio
• Mexiletine can be combined with sotalol if • Ventricular Tachycardia.
graphy are most helpful.
necessary. • Repeat echocardiography is rarely informative ABBREVIATIONS
CONTRAINDICATIONS or indicated. • ACE = angiotensin-converting enzyme.
Digoxin should be avoided in severe uncontrolled • Serial evaluation of serum digoxin levels • AV = atrioventricular.
paroxysmal ventricular tachycardia, in animals (therapeutic range: 0.5–1 ng/mL) taken 6–8 • BEG = boutique, exotic-ingredient, or grain
with compromised renal function, and in hours post-pill and serum biochemistries may free.
animals with important hypokalemia. help prevent iatrogenic problems. • CHF = congestive heart failure.
• cTnI = cardiac troponin I.
PRECAUTIONS POSSIBLE COMPLICATIONS • DCM = dilated cardiomyopathy.
• Calcium channel blockers and notably beta • Sudden death due most commonly to • FS% = percent fractional shortening.
blockers are negative inotropes and may have arrhythmias. • LV = left ventricular.
acute adverse effect on myocardial function; • Iatrogenic problems associated with medical
numerous human studies, however, have management (see above). INTERNET RESOURCES
suggested that chronic administration of beta https://cardiaceducationgroup.org
blockers may be of benefit in DCM. EXPECTED COURSE AND PROGNOSIS Author Matthew W. Miller
• Combination of diuretics and ACE • Always fatal unless associated with Consulting Editor Michael Aherne
inhibitors may result in azotemia, especially nutritional deficiencies.
in patients with severe heart failure or • Death usually occurs 6–24 months
preexisting renal dysfunction, and must be following diagnosis. Client Education Handout
closely monitored. • Dobermans typically have worst prognosis; available online
however, with addition of pimobendan,
Cardiomyopathy, Hypertrophic—Cats
Breed Predilections
Maine coon cats, ragdolls, Sphynx, British C
and American shorthairs, and Persians.
BASICS DIAGNOSIS
Mean Age and Range
DEFINITION • 5–7 years, with reported ages of 3 months– DIFFERENTIAL DIAGNOSIS
Inappropriate concentric hypertrophy of the 17 years. Some breeds of cats including • Other forms of cardiomyopathy.
ventricular free wall and/or the interventricular ragdolls and Sphynx may develop the disease • Hyperthyroidism.
septum of the nondilated left ventricle. The at a younger age (average of 2 years). • Aortic stenosis.
disease occurs independently of other cardiac • HCM is most often a disease of young to • Systemic hypertension.
or systemic disorders. middle-aged cats; unexplained murmurs in • Acromegaly.
PATHOPHYSIOLOGY geriatric cats are more likely associated with • Noncardiac causes of pleural effusion.
• Diastolic dysfunction results from a hyperthyroidism or hypertension. CBC/BIOCHEMISTRY/URINALYSIS
thickened, less compliant left ventricle. Predominant Sex • Results usually normal.
• High left ventricular filling pressure Male • Prerenal azotemia in some animals.
develops, causing left atrial (LA) enlarge- OTHER LABORATORY TESTS
ment. SIGNS
• MyBPC assay; mutation differs for Maine
• Pulmonary venous hypertension causes Historical Findings coon cats and ragdoll cats.
pulmonary edema. Some cats develop • Dyspnea, tachypnea. • In cats >6 years old, check thyroid hormone
biventricular failure (i.e., pulmonary edema, • Anorexia. concentration; hyperthyroidism causes
pleural effusion, small volume pericardial • Exercise intolerance. myocardial hypertrophy that might be
effusion without tamponade, and infrequently • Vomiting. confused with HCM.
ascites). • Collapse. • Serum NT-proBNP concentrations higher in
• Stasis of blood in the large left atrium • Sudden death. cats with HCM than in normal cats, and
predisposes the patient to aortic thrombo • Coughing is uncommon in cats with HCM higher still in cats with symptomatic HCM.
embolism (ATE). and suggests primary pulmonary disease. SNAP NT-proBNP point-of-care testing is also
• Dynamic aortic outflow obstruction and available to help differentiate symptomatic
systolic anterior mitral motion (SAM) with • Gallop rhythm (S3 or S4). cats with HCM from those that are sympto-
secondary mitral insufficiency may occur, but • Systolic murmur in approximately half of matic from other causes. Send-out serum
unlike in humans, appears not to affect prognosis. affected cats. NT-proBNP testing is useful in identifying cats
• Recent evidence suggests that some cats with suspicion of HCM from asymptomatic cats
• Apex heartbeat may be exaggerated.
with apparent hypertrophic cardiomyopathy • Muffled heart sounds, lack of chest with abnormal physical exam findings (e.g.,
(HCM) and congestive heart failure (CHF) compliance, and dyspnea characterized by murmur). Follow-up echocardiography
actually have transient myocardial thickening, rapid shallow respirations may be associated indicated in cats with serum NT-proBNP
often associated with high serum troponin I with pleural effusion. concentrations in “equivocal” or “high” range,
concentrations. These cats are younger than • Dyspnea and crackles if pulmonary edema or positive SNAP results.
average for HCM, with on average less severe is present.
left ventricular (LV) hypertrophy, and they • Weak femoral pulse. IMAGING
can experience resolution of both CHF and • Acute pelvic limb paralysis with cyanotic
LV hypertrophy. Radiography
pads and nailbeds, cold limbs, and absence of • Dorsoventral radiographs often reveal a
SYSTEMS AFFECTED femoral pulse in animals with ATE; emboli valentine-appearing heart because of atrial
• Cardiovascular—CHF, ATE, and rarely affect thoracic limbs. enlargement and a left ventricle that comes to
arrhythmias. • Arrhythmia in some animals. a point.
• Pulmonary—dyspnea if CHF develops. • May have no clinical signs. • Pulmonary edema, pleural effusion, or both
• Renal/urologic—prerenal azotemia. in some animals.
CAUSES
GENETICS • Radiographs may be normal in asymptomatic
• Usually unknown—multiple causes exist.
Some families of cats have been identified • MyBPC mutations in some cats with HCM.
cats.
with a high prevalence of the disease, and • Different forms of cardiomyopathy cannot
the disease appears to be an autosomal Possible Causes be reliably differentiated by radiography.
dominant trait in Maine coon cats and • Abnormalities of contractile protein myosin
or other sarcomeric proteins (e.g., troponin, Echocardiography
ragdoll cats, due to a mutation in the • Hypertrophy of interventricular septum
myosin-binding protein C (MyBPC) gene. myosin-binding proteins, tropomyosin).
• Abnormality affecting catecholamine-
(IVS) or LV posterior wall (diastolic wall
The genetics have not been definitively thickness >6 mm).
determined in other breeds; however, the influenced excitation contraction coupling.
• Hypertrophy may be symmetric (affecting
Maine coon and ragdoll mutations have not • Abnormal myocardial calcium metabolism.
• Collagen or other intercellular matrix
IVS and posterior wall) or asymmetric (affecting
been identified in affected Sphynx, Norwegian IVS or posterior wall, but not both).
forest cats, Bengals, Siberians, or British abnormality.
• Hypertrophy of papillary muscles.
shorthair cats. • Growth hormone excess.
• Normal or high fractional shortening.
• Dynamic LV outflow obstruction may
INCIDENCE/PREVALENCE • Normal or reduced LV lumen.
contribute to secondary LV hypertrophy.
Unknown, but relatively common. May be as • LA enlargement.
high as 15% of the population. RISK FACTORS • Systolic anterior motion of mitral valve
Offspring of animals with familial mutations (some animals).
SIGNALMENT of MyBPC. • LV outflow obstruction (some animals);
Species specialized Doppler studies performed by
Cat
Cardiomyopathy, Hypertrophic—Cats (continued)
experienced sonographers often reveal LV clopidogrel and any of those medications, • Depresses platelet aggregation, hopefully
C relaxation abnormalities (e.g., mitral inflow minimize potential for trauma and minimizing risk of thromboembolism.
E : A wave reversal). subsequent hemorrhage. • Warn owners that thrombi can still
• Thrombus in left atrium (rare). develop despite aspirin administration;
• Note: there is some overlap between normal aspirin appears to be not as effective as
cats (especially ketaminized or dehydrated) clopidogrel (1/4 of 75 mg tablet PO q24h)
and cats with mild HCM. Correlate echo in prevention of ATE, at least in cats with
findings with physical findings. Presence of MEDICATIONS previous embolic episode.
LA enlargement favors HCM. DRUG(S) OF CHOICE Nitroglycerin Ointment
DIAGNOSTIC PROCEDURES Furosemide • Dosage—one-fourth inch/cat topically
ECG • Dosage—1–2 mg/kg PO/IM/IV q8–24h. applied q6–8h or 2.5 mg/24h patch.
• Critically dyspneic animals often require • Often used in acute stabilization of cats with
• Sinus tachycardia (heart rate >240) common
with heart failure; however, some cats with severe high dosage (4 mg/kg IV); this dose can be severe pulmonary edema or pleural effusion.
heart failure and hypothermia are bradycardic. repeated in 1 hour if cat still severely • When used intermittently, may be useful
• Atrial and ventricular premature complexes dyspneic; indicated to treat pulmonary for long-term management of refractory cases.
seen more often in cats with cardiomyopathy, edema, pleural effusion, and ascites. CONTRAINDICATIONS
but also occasionally seen in normal cats. • Cats are sensitive to furosemide and prone Avoid beta blockers in cats with emboli; these
• Atrial fibrillation seen in some advanced cases. to dehydration, prerenal azotemia, and agents cause peripheral vasoconstriction. If
• Left axis deviation often seen. hypokalemia. beta blockers must be used in this setting for
• Prolongation of QT interval and QTc (QT • Once pulmonary edema resolves, taper to arrhythmia control, choose beta-1 selective
interval corrected for heart rate) often seen lowest effective dose. blocker such as atenolol.
with LV hypertrophy. Pimobendan
• Cannot differentiate different forms of PRECAUTIONS
• Dosage—0.25–0.3 mg/kg PO q12h. Use ACE inhibitors cautiously in azotemic
cardiomyopathy; may be normal. • Appears to be useful in management of animals.
Systemic Blood Pressure CHF (e.g., pulmonary edema or pleural
• Normotensive or hypotensive. effusion) in cats with HCM, possibly by ALTERNATIVE DRUG(S)
• Evaluate blood pressure in all patients with enhancing diastolic function and LA fractional Torsemide
myocardial hypertrophy to rule out systemic shortening; not used in management of • Dosage—0.1–0.5 mg/kg q24h, sometimes
hypertension as cause of hypertrophy. asymptomatic HCM at this time. with dose escalation to q12h.
• Not currently licensed for use in cats. • Used as substitute for furosemide in
PATHOLOGIC FINDINGS
• Nondilated left ventricle with hypertrophy Angiotensin-Converting Enzyme (ACE) refractory pulmonary edema or pleural
of IVS or LV free wall. Inhibitors effusion in cats with apparently normal (or at
• Hypertrophy of papillary muscles. • Dosage—enalapril or benazepril 0.25– least stable) renal function.
• LA enlargement. 0.5 mg/kg PO q24h. • Monitor renal function closely in first days
• Mitral valve thickening. • Indications in cats with HCM not well after switching to torsemide.
• Myocardial hypertrophy with disorganized defined—authors currently use for CHF. Spironolactone
alignment of myocytes (myofiber disarray). Beta Blockers • Dosage—1 mg/kg q12–24h.
• Interstitial fibrosis. • Used in conjunction with furosemide in
• Dosage—atenolol (6.25–12.5 mg/cat PO
• Myocardial scarring. cats with CHF, especially refractory effusions.
q12h).
• Hypertrophy and luminal narrowing of • May cause facial pruritis.
• Beneficial effects may include slowing of
intramural coronary arteries. sinus rate, correcting atrial and ventricular Warfarin and Low Molecular Weight
arrhythmias, platelet inhibition. Heparin
• More effective than diltiazem in controlling • Used sometimes in cats at high risk for
dynamic outflow tract obstruction. thromboembolism.
TREATMENT • Role in asymptomatic patients • See Aortic Thromboembolism.
unresolved, but many clinicians use if
APPROPRIATE HEALTH CARE Clopidogrel
dynamic outflow obstruction and hyper
Cats with CHF should be hospitalized. • Dosage—18.75 mg/cat/day.
trophy present.
NURSING CARE • Contraindicated in presence of CHF. • Platelet function inhibitor, superior to
• Minimize stress. aspirin in cats with previous ATE.
Diltiazem
• Oxygen if dyspneic. Beta Blocker plus Diltiazem
• Dosage—7.5–15 mg/cat PO q8h or 10 mg/kg
• Warm environment if hypothermic. • Cats that remain tachycardic on a single
PO q24h (Cardizem® CD) or 30 mg/cat q12h
ACTIVITY (Dilacor XR®). agent can be treated cautiously with a
Restricted with CHF. • Beneficial effects may include slower sinus combination of a beta blocker and diltiazem.
rate, resolution of supraventricular arrhythmias, • Monitor for bradycardia and hypotension.
DIET
Modest to moderate sodium restriction in improved diastolic relaxation, coronary and
animals with CHF. peripheral vasodilation, platelet inhibition.
• May reduce hypertrophy and LA
CLIENT EDUCATION dimensions in some cats.
• Many cats diagnosed while asymptomatic FOLLOW-UP
• Role in asymptomatic patients unresolved.
eventually develop CHF and may develop PATIENT MONITORING
ATE and die suddenly. Aspirin • Observe closely for dyspnea, lethargy,
• If cat is receiving warfarin, dalteparin, • Dosage—81 mg/cat q2–3 days if severe weakness, anorexia, and painful posterior
enoxaparin (Lovenox®), or combination of atrial enlargement. paralysis or paresis.
(continued) Cardiomyopathy, Hypertrophic—Cats

• If treating with warfarin, monitor prothrom- ∘∘ Asymptomatic cats—median survival • LA = left atrial.
bin time. 563 days (range: 2–3,778 days). • LV = left ventricular. C
• If treating with ACE inhibitor or spirono ∘∘ Cats with syncope—median survival • MyBPC = myosin-binding protein C.
lactone, monitor renal function and 654 days (range: 28–1,505 days). • QTc = QT interval corrected for heart rate.
electrolytes. ∘∘ Cats with CHF—median survival • SAM = systolic anterior mitral motion.
• Repeat echocardiogram in 6 months to 563 days (range: 2–4,418 days). Suggested Reading
assess efficacy of treatment for hypertrophy. If ∘∘ Cats with ATE—median survival Fox PR, Keene BW, Lamb K, et al.
beta blocker or diltiazem was prescribed in 184 days (range: 2–2,278 days). International collaborative study to assess
asymptomatic animal and there is evidence of ∘∘ Older age and larger left atria predicted cardiovascular risk and evaluate long-term
progressive hypertrophy/LA enlargement, shorter survival. health in cats with preclinical hypertrophic
consider switching to another class of cardiomyopathy and apparently healthy
medications (or adding an ACE inhibitor) cats: the REVEAL study. J Vet Intern Med
and recheck 4–6 months later. 2018, 32(3):930–943.
• Echocardiographic evaluations that reveal
LA diameters >2 cm or loss of LV systolic
MISCELLANEOUS McDonald K. Feline cardiomyopathy. In:
Smith FWK, Tilley LP, Oyama MA, Sleeper
function should prompt more aggressive ASSOCIATED CONDITIONS
MM, eds. Manual of Canine and Feline
prophylaxis against ATE (e.g., clopidogrel Aortic thromboembolism.
Cardiology, 5th ed. St. Louis, MO:
with low molecular weight heparin). PREGNANCY/FERTILITY/BREEDING Saunders Elsevier, 2016, pp. 153–180.
PREVENTION/AVOIDANCE • High risk of complications. Novo Matos J, Pereira N, Glaus T, et al.
Avoid stressful situations that might • Avoid aspirin. Transient myocardial thickening in cats
precipitate CHF. SEE ALSO associated with heart failure. J Vet Intern
POSSIBLE COMPLICATIONS • Aortic Thromboembolism. Med 2018, 32(1):48–56.
• Heart failure. • Congestive Heart Failure, Left-Sided. Romito G, Guglielmini C, Mazzarella MO,
• ATE and paralysis. • Hypersomatotropism/Acromegaly in Cats. et al. Diagnostic and prognostic utility of
• Cardiac arrhythmias/sudden death. • Hypertension, Systemic Arterial. surface electrocardiography in cats with left
• Hyperthyroidism. ventricular hypertrophy. J Vet Cardiol 2018,
EXPECTED COURSE AND PROGNOSIS 20(5):364–375.
• Murmurs, Heart.
• Animals homozygous for MyBPC mutations Authors Francis W.K. Smith, Jr., Bruce W.
more likely to develop severe HCM and at ABBREVIATIONS Keene, and Kathryn M. Meurs
earlier age than heterozygous animals. • ACE = angiotensin-converting enzyme. Consulting Editor Michael Aherne
• Prognosis varies considerably, probably • ATE = aortic thromboembolism.
because there are multiple causes. In one • CHF = congestive heart failure.
study of cats with HCM living at least • HCM = hypertrophic cardiomyopathy. Client Education Handout
24 hours following presentation: • IVS = interventricular septum. available online
Cardiomyopathy, Hypertrophic—Dogs
• Thyrotoxicosis. channel blockers has been advocated;
C • Mitral dysplasia. however, benefit has not been proven.
• Beta blockers or calcium channel blockers
BASICS IMAGING
may also improve myocardial oxygenation,
OVERVIEW Radiography reduce heart rate, improve LV diastolic
Hypertrophic cardiomyopathy (HCM) is • May be normal or may show LA or LV function, and control arrhythmias, and
defined as inappropriate myocardial hypertrophy enlargement. therefore may be useful in dogs with left CHF;
of a nondilated left ventricle, occurring in the • Pulmonary edema present with left CHF. however, benefit has also not been proven.
absence of an identifiable stimulus. HCM is rare Echocardiography CONTRAINDICATIONS/POSSIBLE
in dogs, and is characterized by left ventricular • Severe cases usually have marked LV and INTERACTIONS
(LV) concentric hypertrophy (increased wall papillary muscle hypertrophy, and LA • Positive inotropes may worsen dynamic
thickness). The primary disease process is enlargement. Hypertrophy is usually global, LVOTO.
confined to the heart and only affects other but can be more regional or segmental • Avoid calcium channel blockers in
organ systems when congestive heart failure (asymmetric). Milder forms may have subtle combination with beta blockers, as clinically
(CHF) is present. Increased LV wall thickness LV hypertrophy. significant bradyarrhythmias can develop.
leads to impaired ventricular filling (due to lack • Systolic anterior motion of the mitral valve, • Avoid potent arteriolar dilators in cases
of compliance and abnormal relaxation), with suggesting dynamic LV outflow tract with dynamic LVOTO. The use of milder
resultant increases in LV end-diastolic pressure obstruction (LVOTO), is common in dogs vasodilators such as ACE inhibitors in dogs
and left atrial (LA) pressure. LA enlargement is with HCM. with CHF is generally well tolerated.
usually in response to increased LV end-diastolic
pressure. Mitral insufficiency and/or dynamic LV
outflow tract obstruction commonly occur ECG
secondary to structural and/or functional • May be normal.
changes of the mitral valve apparatus caused by • ST segment and T wave abnormalities have FOLLOW-UP
papillary muscle malalignment due to hyper- been reported. • Depends on clinical severity. Serial
trophy. • Atrial or ventricular ectopic arrhythmias radiography and/or echocardiography may
may rarely occur. help characterize disease progression and
SIGNALMENT
• The incidence of HCM in dogs is very low, Blood Pressure guide medication adjustments.
Usually normal. Should be evaluated to rule • Due to the rarity of canine HCM,
thus accurate accounts of signalment are lacking.
• Young (<3 years) male dogs. out systemic hypertension as the cause of LV prognostic information is lacking. In dogs
• Rottweiler, Dalmatian, German shepherd, hypertrophy. with severe CHF or other complications,
pointer breeds and Boston terriers have been prognosis is generally guarded.
PATHOLOGIC FINDINGS
reported. • Abnormal heart : body weight ratio.
SIGNS • LV concentric hypertrophy.
• The interventricular septum may have an
Historical Findings MISCELLANEOUS
impact lesion, varying from a small opaque
• Most are asymptomatic.
lesion to a thickened plaque. ABBREVIATIONS
• Signs of left CHF predominate in sympto-
• The mitral valve is often thickened and • ACE = angiotensin-converting enzyme.
matic dogs.
elongated. • CHF = congestive heart failure.
• Syncope, generally during activity or exercise.
• Varying degrees of LA enlargement may be • HCM = hypertrophic cardiomyopathy.
• Sudden death is the most commonly
present. • LA = left atrial.
reported clinical sign.
• LV = left ventricular.
Physical Examination Findings • LVOTO = left ventricular outflow tract
• ± Systolic heart murmur. obstruction.
• ± Gallop heart sound.
• ± Signs of left CHF (e.g., dyspnea, cyanosis,
TREATMENT Suggested Reading
exercise intolerance, cough). Treatment is generally only pursued if there is Oyama MA. Canine cardiomyopathy. In:
evidence of CHF, severe arrhythmias, or Smith FWK, Tilley LP, Oyama MA, Sleeper
CAUSES & RISK FACTORS frequent syncope. Exercise restriction and MM, eds., Manual of Canine and Feline
The cause of canine HCM is unknown. sodium restriction are beneficial. Cardiology, 5th ed. St. Louis, MO:
Genetic abnormalities in genes coding for Saunders Elsevier, 2016, pp. 141–152.
myocardial contractile proteins have been Ware WA. Myocardial diseases of the dog. In:
documented in humans and cats. Ware WA, Cardiovascular Disease in Small
MEDICATIONS Animal Medicine. London: Manson/
Veterinary Press, 2011, pp. 280–299.
DRUG(S) OF CHOICE Author Michael Aherne
• In patients with left CHF, diuretics and Consulting Editors Michael Aherne
DIAGNOSIS angiotensin-converting enzyme (ACE) Acknowledgment The author and book
DIFFERENTIAL DIAGNOSIS inhibitor therapy are advocated. editors acknowledge the prior contribution of
• Systemic hypertension. • In dogs with severe dynamic LVOTO, Larry P. Tilley.
• Infiltrative cardiac disorders. administration of beta blockers or calcium
Cardiomyopathy, Nutritional
The underlying cause has not yet (as of toxic levels within the mitochondria (e.g.,
writing) been identified, and causation has multiple Co-A dehydrogenase defects), free C
not been proven. Nutritional management, L-carnitine is used to “scavenge” potentially
BASICS involving diet change and in some cases toxic excess metabolites, which appear
OVERVIEW taurine supplementation, has resulted in harmlessly in the plasma and eventually the
• Nutritional imbalances, such as taurine and improvement or resolution of cardiomyopathy urine as carnitine esters; in these cases, the
L-carnitine deficiency, can lead to the over a period of 3–12 months. Investigations total amount of carnitine (free carnitine plus
development of dilated cardiomyopathy are ongoing. that esterified to other molecules) in the
(DCM) in some dogs and cats. Deficiencies SIGNALMENT plasma or muscle may be normal or even
of other nutrients (e.g., selenium, zinc, high, but the ratio of free to esterified
vitamin E, thiamine, copper, iron) or nutrient Dogs carnitine is decreased; this situation is known
toxicities (e.g., iron, cobalt) also have the • Golden retrievers, American cocker spaniels, as carnitine insufficiency (since although the
potential to alter myocardial function, Newfoundlands, English setters, St. Bernards, concentration of free carnitine may be within
resulting in clinical manifestations of heart and Irish wolfhounds are reported to be the normal range, it is insufficient to meet the
disease. Additionally, relative nutritional predisposed to taurine-deficient DCM. body’s pathologically increased need for free
deficiencies or toxicities may interact with • L-carnitine deficiency has been reported in carnitine).
other toxic, infectious, or genetic insults in a family of boxers. • Certain families of boxers appear to be at
certain individuals to produce DCM. • Dogs eating BEG diets that are affected especially high risk of developing symptomatic
• Taurine is the most abundant free amino acid with suspected nutritional DCM have been DCM in association with, and probably
found in cardiac muscle, playing an important of varied ages and breeds. caused by, carnitine deficiency; a known
role in myocardial calcium regulation. Taurine Cats first-degree relative with cardiomyopathy
deficiency was first reported as a cause of Taurine deficiency is rare in cats fed should increase the index of suspicion.
reversible DCM in cats in 1987, prompting an commercial, nutritionally balanced diets. • The cause of the apparent, although unproven,
increase in the dietary taurine requirement for Taurine-deficient DCM can occur in cats fed link between BEG diets and canine DCM is
commercial cat foods, and since then DCM in vegetarian or home-prepared diets. unknown; however, the commonality of
cats is uncommon. Unlike cats, dogs should be ingredients in these diets has drawn the
SIGNS attention of veterinary nutritionists; the high
able to endogenously synthesize taurine;
• Clinical signs of taurine-deficient DCM are legume content of these foods (e.g., lentils
however, several breeds (e.g., American cocker
related to poor myocardial contractility, and peas), less studied protein sources (e.g.,
spaniel, Newfoundland, Irish wolfhound,
which can lead to congestive heart failure in kangaroo, alligator, bison), and other unusual
golden retriever) have reported predispositions
some cases; these signs include lethargy, ingredients (e.g., flaxseed) raise the possibility
to taurine deficiency and resultant DCM.
weakness, syncope, dyspnea and tachypnea. of a nutrient deficiency, toxicity, or nutrient–
Additionally, some commercial dog foods such
• Cats may also present for reproductive nutrient interaction that may predispose to
as grain-free, high-legume, lamb and rice
failure, poor growth, or blindness due to the development of DCM in some dogs.
formulations and high-fiber foods, have been
central retinal degeneration.
associated with taurine deficiency. Oral
• Clinical signs of carnitine deficiency can be
taurine supplementation can effect disease
diverse, ranging from clinical manifestations
reversal in deficient cats and significant
of DCM to skeletal muscle pain and exercise
improvement in dogs. DIAGNOSIS
intolerance.
• L-carnitine, a quaternary amine, is an
• See Cardiomyopathy, Dilated—Dogs. CBC/BIOCHEMISTRY/URINALYSIS
important part of enzyme systems that
transport fatty acids into mitochondria for CAUSES & RISK FACTORS Normal
oxidization to make energy. It also has other • Vegetarian and home-prepared diets OTHER LABORATORY TESTS
important cellular metabolic and scavenging increase the risk of taurine-deficient DCM in • Ideally, both whole blood and plasma
functions. Carnitine deficiency complicates cats if taurine is not exogenously supplemented taurine concentrations should be evaluated to
some cases of DCM in dogs. Plasma adequately. assess for taurine deficiency in any dog with
L-carnitine deficiency in association with • Factors predisposing to taurine deficiency DCM; if only one blood sample can be
cardiomyopathy does not mean that the in dogs include breed (possible genetic causes) analyzed, whole blood is considered a better
deficiency is the sole cause of the myopathy, and dietary components; high-fiber diets, indicator of long-term taurine status. Blood for
although correcting the deficiency, if possible, low-protein diets, lamb and rice diets, and taurine concentrations should be drawn into
makes medical and physiologic sense. In the beet pulp ingredients have been associated lithium heparin tubes and frozen immediately.
dog, dietary carnitine intake influences with taurine deficiency; dietary predisposition The normal whole blood taurine concentration
plasma concentrations significantly, and oral to taurine deficiency with these factors could range for dogs (200–350 nmol/mL) has been
carnitine supplementation is usually an be a result of inadequate taurine precursors questioned recently, especially in golden
effective means of raising plasma and (methionine and cysteine), low bioavailability retrievers, where normal has been proposed to
subsequently muscle carnitine levels. of taurine and/or precursors, reduced entero- be 213–377 nmol/mL. Historically, taurine-
• A perceived increase in recognition of hepatic bile acid recycling due to high dietary deficient DCM is diagnosed when whole
DCM in dogs eating boutique, exotic- fiber, excessive urinary taurine wasting, or blood concentrations are <150 nmol/mL in
ingredient, or grain-free (BEG) dog foods in gastrointestinal microbial interaction with dogs and <200 nmol/mL in cats, or when
2018 prompted an FDA investigation into a taurine. plasma taurine concentrations are <40 nmol/mL
possible relationship between BEG diets and • Some dogs with DCM have been in both species; values ≤213 nmol/mL
canine DCM. The majority of affected dogs documented to have carnitine transport (whole blood) and ≤63 nmol/mL (plasma)
eating BEG diets do not appear to be taurine defects, in which muscle carnitine is low have been proposed for DCM diagnosis in
or L-carnitine deficient; however, golden despite adequate plasma concentrations. In golden retrievers.
retrievers appear to be more susceptible to cases in which a mitochondrial enzyme defect • Plasma carnitine concentrations appear to
taurine deficiency when eating these foods. causes the accumulation of a metabolite to be a specific but insensitive indicator of
Cardiomyopathy, Nutritional (continued)
myocardial or skeletal muscle carnitine reasonable to trial with supplementation and • American cocker spaniels—(in combination
C deficiency. Plasma free carnitine concen assess response to treatment; taurine deficiency with taurine) 1 g (approximately 0.5 tsp
trations of less than 8 μmol/L are considered associated with DCM in American cocker L-carnitine powder) q8–12h.
diagnostic of systemic carnitine deficiency; spaniels is reported to respond to both taurine
plasma concentrations in the normal or and L-carnitine supplementation.
supernormal range do not rule out myocardial • Treatment with L-carnitine is indicated in
carnitine deficiency or insufficiency. addition to conventional treatment for DCM;
• There is no confirmatory laboratory test however, some dogs, including some families
FOLLOW-UP
Repeat echocardiogram 3–6 months after
currently available to diagnose nutritional of carnitine-deficient boxers, fail to respond
nutritional manipulation, including amino
DCM associated with BEG diets; dogs should clinically to supplementation. While supple-
acid supplementation and/or diet change.
be assessed for taurine and carnitine deficiency, mentation dramatically improves a small
Improvement in myocardial function may
and the diagnosis is solidified by response to percentage of dogs with DCM, the overall
take up to a year for dogs with nutritional
nutritional management. efficacy of L-carnitine supplementation for
cardiomyopathy.
IMAGING treatment of DCM is untested. If a trial of
Echocardiography is used to diagnose DCM. metabolic supplementation is desired in the
absence of known L-carnitine deficiency, the
DIAGNOSTIC PROCEDURES combination of L-carnitine with taurine and
• Endomyocardial biopsy is the gold standard to CoQ10 (100 mg as ubiquinol q8–12h) seems MISCELLANEOUS
assess myocardial carnitine levels, since plasma prudent.
carnitine concentrations are an insensitive ASSOCIATED CONDITIONS
• Transition to a high-quality, scientifically
indicator of muscle carnitine deficiency. N/A
backed, grain-based food with a well-studied
• Myocardial free carnitine concentrations protein source is critical to the recovery of AGE-RELATED FACTORS
<3.5 nmol/mg of noncollagenous protein are nutritional DCM associated with BEG diets. N/A
considered diagnostic of myocardial carnitine The role of taurine supplementation in the ZOONOTIC POTENTIAL
deficiency. absence of deficiency is uncertain; however, None
• Ratio of esterified to free carnitine >0.4 is there is no known detriment to empiric
considered diagnostic of carnitine supplementation, and taurine may have PREGNANCY/FERTILITY/BREEDING
insufficiency. therapeutic benefits apart from correction of Taurine deficiency may cause reproductive
deficiency. failure in cats.
SEE ALSO
• Cardiomyopathy, Dilated—Cats.
TREATMENT • Cardiomyopathy, Dilated—Dogs.
• Response to nutritional manipulation and MEDICATIONS ABBREVIATIONS
supplementation can take months, so patients • BEG = boutique, exotic-ingredient,
will require medications to support myocardial DRUG(S) OF CHOICE
grain-free.
function (e.g., pimobendan), antagonize Taurine • DCM = dilated cardiomyopathy.
neurohormonal activation (e.g., angiotensin- • Dogs—250 mg PO q12h if <10 kg;
converting enzyme inhibitors and 500 mg PO q12h if 10–25 kg; 1000 mg PO
Suggested Reading
Adin D, DeFrancesco T, Keene B, et al.
spironolactone), and diuretic therapy if q12h if >25 kg.
Echocardiographic phenotype of DCM
congestive heart failure is present (e.g., • Cats—250 mg PO q12h.
differs based on diet type. J Vet Cardiol
furosemide). L-Carnitine 2019, 21:1–9.
• Taurine supplementation if taurine
• Large-breed dogs—2 g (approximately 1 tsp Authors Darcy B. Adin and Bruce W. Keene
deficiency is diagnosed; if blood L-carnitine powder) q8–12h. Consulting Editor Michael Aherne
concentrations are not measured, it is
Cardiomyopathy, Restrictive—Cats
crackles. ◦ Muffled cardiac or respiratory • Functional findings (echocardiographic):
sounds if pleural effusion. ◦ Paralysis or paresis ◦ Severe LV diastolic dysfunction on Doppler C
with loss of femoral pulses; one or more echocardiography—restrictive LV filling with a
BASICS extremities cold and painful (ATE). peak velocity of early : late transmitral flow
DEFINITION CAUSES (E : A) ratio >2.0, short isovolumic relaxation
A rare, primary heart muscle disease character- • Primary RCM—currently unknown;
time (<37 msec), shortened deceleration time of
ized functionally by severe diastolic dysfunc- genetic cause documented in humans. E (<45 msec), low peak velocity of mitral annular
tion with restrictive left ventricular (LV) • Secondary RCM—late or end stage of
motion (E′), and E : E′ ≫15. ◦ Normal to low
filling and normal to near normal systolic underlying disease (e.g., hypertrophic normal LV systolic function (in some cases LV
function, morphologically by a nondilated, cardiomyopathy); link between prior systolic dysfunction is present). ◦ Regional wall
nonhypertrophied left ventricle with interstitial pneumonia and feline endomyo- motion abnormalities possible. ◦ Left atrial
increased endocardial and/or myocardial carditis leading to RCM suspected in one dysfunction. ◦ Severe left atrial appendage
fibrosis and severe atrial enlargement, and study. enlargement with evidence of blood stasis.
clinically by congestive heart failure (CHF), ◦ Midventricular obstruction with flow
thromboembolic disease, and cardiac death. turbulence in cats with bridging endomyocar-
dial fibrosis. ◦ In cats with other causes of
PATHOPHYSIOLOGY
restrictive physiology, characteristics of the
• Increased cardiomyofilament Ca2+ sensitivity DIAGNOSIS underlying disease can predominate; however,
leading to severely impaired myocardial
DIFFERENTIAL DIAGNOSIS severe atrial enlargement and restrictive LV
relaxation, high myocardial stiffness due to
• Advanced stages of other feline cardiomyo- filling will be present in nearly all cats.
endomyocardial fibrosis (endomyocardial type)
and/or interstitial fibrosis (myocardial type), and pathies: ◦ Hypertrophic, dilated, arrhythmo- DIAGNOSTIC PROCEDURES
disorganized myofiber architecture (disarray) are genic right ventricular, non-specific phenotype,
ECG
main characteristics of primary restricted and tachycardia-induced cardiomyopathy.
• Note: ECG findings are neither sensitive nor
cardiomyopathy (RCM); RCM-like myocardial ◦ Myocardial infarct. ◦ CHF secondary to
specific. • Sinus tachycardia is common, but
changes and clinical syndromes can result from thyrotoxicosis or hypertensive heart disease.
cats with severe CHF and hypothermia may
myocardial remodeling and dysfunction CBC/BIOCHEMISTRY/URINALYSIS be bradycardic. • Ventricular or supraven-
secondary to other causes (e.g., endomyocardi- Routine chemistry panel and urinalysis tricular ectopic beats, paroxysmal or sustained
tis, immune-mediated disease, or end-stage helpful to document concurrent or compli- supraventricular or ventricular tachycardia, or
hypertrophic cardiomyopathy). • Diastolic cating conditions (e.g., renal failure and atrial fibrillation. • Atrial or ventricular
heart failure and cardiogenic arterial thrombo- potassium depletion). enlargement patterns. • ST segment changes.
embolism (ATE) lead to high mortality.
OTHER LABORATORY TESTS Pathology
SYSTEMS AFFECTED • Plasma T4 concentration in cats ≥6 years • Note: histopathologic confirmation is
• Cardiovascular. • Respiratory. old. • Plasma cardiac troponin I concentra- needed to diagnose RCM. • Increased heart
GENETICS tion (more specific if ischemic heart disease or weight (>19 g). • Severe biatrial dilatation.
Primary RCM can be a spontaneous or myocarditis suspected). • Locally or diffusely thickened opaque
familial disease, but is generally considered of IMAGING endocardium. • False tendons (“moderator
genetic cause in humans with an autosomal bands”) present in some cats. • Normal
Thoracic Radiography luminal size of the left and right ventricles.
dominant pattern of inheritance; several genes
• Cardiomegaly with severe biatrial enlarge- • Diffuse or focal cardiomyocyte disarray.
encoding sarcomeric and nonsarcomeric
proteins can be affected; RCM-causing ment (“valentine” heart on v/d projections). • Increased interstitial and replacement
• Interstitial or alveolar infiltrates or pleural fibrosis. • Abnormal intramural coronary
mutations have not been identified in cats.
effusion with pulmonary venous distention if arterioles with medial hypertrophy and
INCIDENCE/PREVALENCE in CHF. narrowed lumen. • Increased number of
Primary feline RCM is rare—prevalence
Echocardiography inflammatory cells seen only in cats with acute
ranging from 1% to 5% of all myocardial
• Note: definitive diagnostic criteria are poorly endomyocarditis—this finding is commonly
diseases in cats.
defined and remain controversial. Early absent in cats with endocardial fibrosis.
SIGNALMENT (noncongestive) RCM has rarely been
• Cats. • Higher prevalence in Siamese and documented in cats. • Anatomic findings
oriental cats. • Middle-aged to older cats. characterizing the RCM phenotype include:
• Male predisposition. ◦ Severe biatrial enlargement. TREATMENT
SIGNS ◦ Nonhypertrophied, nondilated left ventricle
(normal chamber dimension, normal wall APPROPRIATE HEALTH CARE
Historical Findings thickness). ◦ Severe enlargement of the left • Patients with severe CHF are hospitalized
• Lethargy. • Weight loss. • Paresis or atrium with spontaneous echocardiographic for emergency care. • Mildly symptomatic
paralysis (i.e., signs of ATE). • Labored contrast or thrombi frequently seen. animals can be treated with outpatient
breathing. • Tachypnea. • Ascites. • Jugular ◦ Prominent, often diffuse echogenic scar medical management.
venous distension. • Cyanosis. (“moderator bands,” false tendons) leading to a NURSING CARE
Physical Examination Findings small LV lumen and narrowing at the mid- • Cats with respiratory distress should receive
• If not in CHF—arrhythmias. ◦ Prominent ventricle (endomyocardial fibrosis or “bridging” oxygen. • Sedation is usually beneficial.
gallop sounds are a hallmark. ◦ Heart murmur fibrosis). ◦ Focal areas of highly echogenic and • Thoracocentesis if relevant pleural effusion.
uncommon. • If in CHF—above signs plus the often thin myocardium indicative of ischemia or • Maintain a low-stress environment (e.g., cage
following: ◦ Tachypnea. ◦ Labored breathing. scarring. ◦ Myocardium can appear normal rest, minimize handling). • Heating pad for
◦ Cyanosis. ◦ Hepatomegaly or ascites with with pure myocardial form of RCM. ◦ Pleural hypothermic patients. • Respiratory rate should
jugular venous distention. ◦ Pulmonary effusion and pericardial effusion may be present. be used to monitor immediate treatment success.
Cardiomyopathy, Restrictive—Cats (continued)
ACTIVITY q48h) may allow better control of ventricular hours to monitor pulmonary infiltrate
C Cage rest for CHF patients. response rate in cats with atrial fibrillation; resolution. • Repeat physical examination
DIET cats with hemodynamically important and analysis of blood biochemistries after 3–7
In acute heart failure, maintain intake with ventricular and supraventricular ectopy can days’ treatment of acute CHF. • Stable
hand feeding if necessary. also benefit from sotalol (1.0–2.0 mg/kg PO patients reevaluated every 2–4 months or
q12h). • Pimobendan (0.25 mg/cat PO more frequently if problems occur.
CLIENT EDUCATION q12h) may be helpful in the management of
Owner should be counseled regarding PREVENTION/AVOIDANCE
chronic heart failure; note: pimobendan is not No known preventative measures for RCM.
technique of pill administration in cats, approved for clinical use in cats. • Treat
possible adverse effects of medications, associated conditions (e.g., dehydration, POSSIBLE COMPLICATIONS
importance of maintaining stable food and hypothermia, hypokalemia). • Clopidogrel Tissue necrosis or loss of function in limbs
water intake, and monitoring their cat’s (one-fourth of a 75 mg tablet PO q24h) to affected by thromboembolic complications,
resting respiratory rate at home. inhibit platelets chronically; aspirin (25 mg/ adverse effects of medications, sudden death,
kg PO q72h) may also be considered, but and euthanasia due to refractory heart failure.
efficacy is questionable; in cases of echogenic EXPECTED COURSE AND PROGNOSIS
smoke or prior ATE, dual platelet inhibition Variable, but most cats have a grave
MEDICATIONS (clopidogrel and aspirin) may be used. prognosis.
• Addition of low molecular weight heparin
DRUG(S) OF CHOICE (enoxaparin [Lovenox®] at 1–2 mg/kg q12h
Acute CHF SC) may be considered in cats at high risk for
• Parenteral administration of furosemide thromboembolic disease; apixaban (Eliquis®)
(1–2 mg/kg IV/IM/SC q2–6h); CRI may be at 0.625 mg/cat q12h in cats <5 kg body- MISCELLANEOUS
considered. • Dermal application of nitroglyc- weight and 1.25 mg/cat q12h in cats ≥5 kg ASSOCIATED CONDITIONS
erin ointment (2%, one-fourth inch q12h). has been recommended, but published Aortic thromboembolism and CHF.
• Oxygen delivered by cage, mask, nasal evidence is not available. • Treatment of cats
AGE-RELATED FACTORS
prongs, or flow-by. • Thoracocentesis if with preclinical RCM has rarely been
Hyperthyroidism should be ruled out with
relevant pleural effusion. • Dobutamine only if reported, but includes ACE inhibitors and
appropriate testing in feline patients with
cats are hypotensive (systolic blood pressure antiplatelet drugs; there is currently no
heart disease ≥6 years of age.
<90 mmHg); 1–5 μg/kg/minute as CRI, start specific drug for LV diastolic dysfunction.
a lower dose and increase over 0.5–1h. SYNONYMS
CONTRAINDICATIONS
• Severe supraventricular tachyarrhythmias can • Intermediate cardiomyopathy. • Unclassified
• Beta blockers should never be administered
be treated with diltiazem CRI (2–6 μg/kg/min cardiomyopathy.
in cats with RCM. • For diltiazem—brady-
IV). • Ventricular tachycardia may resolve with cardia, atrioventricular block, myocardial SEE ALSO
resolution of CHF. • Acute therapy of failure, and hypotension. • For furosemide— • Aortic Thromboembolism. • Congestive
ventricular tachycardia may include lidocaine severe dehydration, severe hypokalemia, and Heart Failure, Left-Sided. • Congestive Heart
(0.25–0.5 mg/kg IV slowly); monitor closely moderate to severe azotemia. • For ACE Failure, Right-Sided.
for neurologic signs of toxicity. • Pimobendan inhibitors—moderate to severe azotemia,
(0.25 mg/kg PO q12h) may be helpful to ABBREVIATIONS
hypotension, and hyperkalemia. • A = peak velocity of late transmitral flow.
increase cardiac performance in acute heart
POSSIBLE INTERACTIONS • ACE = angiotensin-converting enzyme.
failure, but is only used in animals that cannot
• Combination of ACE inhibitors and • ATE = arterial thromboembolism. • CHF
be stabilized and systemic hypotension cannot
be corrected. Note: pimobendan is not furosemide—hypotension and renal failure. = congestive heart failure. • E = peak velocity
approved for clinical use in cats and clinical • Chronic aspirin therapy may increase risk of early transmitral flow. • E′ = peak velocity
safety and efficacy data are limited. of renal side effects of ACE inhibitors and of mitral annular motion. • LV = left
• Antiplatelet medication (clopidogrel bisulfate may lead to inappetence and gastrointestinal ventricular. • RCM = restrictive
18.75 mg PO q24h) or anticoagulants (e.g., upset. • Combining antiplatelets and anti- cardiomyopathy.
unfractionated heparin 150–250 IU/kg SC coagulants may increase risk of bleeding. Suggested Reading
q6h) may be administered, in particular in cats Charles PY, Li YJ, Nan CL, Huang XP.
with severe left atrial enlargement and Insights into restrictive cardiomyopathy
spontaneous echocardiographic contrast. from clinical and animal studies. J Geriatr
Chronic Therapy FOLLOW-UP Cardiol 2011, 8:168–183.
• Furosemide is gradually decreased to lowest
Fox PR. Endomyocardial fibrosis and
PATIENT MONITORING restrictive cardiomyopathy: pathologic and
effective dose. • Angiotensin-converting • Frequent physical reexaminations to assess
enzyme (ACE) inhibitors may reduce fluid clinical features. J Vet Cardiol 2004,
response to treatment. • Frequent reevalua- 6:25–31.
retention, decrease the need for diuretics, and tion of hydration status and renal function,
counterbalance adverse effects of diuretics Author Karsten E. Schober
particularly in first few days of therapy to Consulting Editor Michael Aherne
(e.g., enalapril 0.25–0.5 mg/kg PO q12– avoid dehydration, hypokalemia, and
24h). • Diltiazem (1.5–2.5 mg/kg regular azotemia. • Repeated thoracocentesis if
diltiazem or 10 mg/kg q24h extended-release necessary. • “Hands-off ” hourly assessment of Client Education Handout
diltiazem) decreases heart rate and improves respiratory rate in first 12–24 hours can be available online
supraventricular arrhythmias in affected cats; used to monitor efficacy of CHF therapy.
the addition of digoxin (0.007 mg/kg PO • Radiographs may be repeated in 12–24
Cardiopulmonary Arrest
RISK FACTORS should not interfere with resuscitative
• Cardiovascular disease. procedures. C
• Respiratory disease. DIAGNOSTIC PROCEDURES
BASICS • Trauma. Once CPA has developed, continuous ECG
DEFINITION • Anesthesia. monitoring, blood pressure monitoring, pulse
• Cessation of effective perfusion and • Septicemia. oximetry, and capnography are useful in
ventilation because of loss of coordinated • Endotoxemia. monitoring effectiveness of resuscitative
cardiac and respiratory function. • Ventricular arrhythmias—ventricular procedures.
• Cardiac arrest invariably follows respiratory tachycardia, R on T phenomenon, multiform
arrest if not recognized and corrected. ventricular complexes.
• Increased parasympathetic tone—
PATHOPHYSIOLOGY
gastrointestinal disease, respiratory disease,
• Generalized or cellular hypoxia may be TREATMENT
manipulation of eyes, larynx, or abdominal
cause or effect of sudden death. Institute CPR immediately upon diagnosing
viscera.
• After 1–4 minutes of airway obstruction, CPA; CPR in veterinary patients should
• Prolonged seizing.
breathing efforts stop while circulation follow Reassessment Campaign on Veterinary
• Invasive cardiovascular manipulation—
remains intact. Resuscitation (RECOVER) evidence-based
pericardiocentesis, surgery, angiography.
• If obstruction continues for 6–9 minutes, guidelines, published in 2012 and divided
severe hypotension and bradycardia lead to into five domains. It is recommended the
dilated pupils, absence of heart sounds, and reader read the original publication.
lack of palpable peripheral pulse.
• After 6–9 minutes, myocardial contractions DIAGNOSIS Basic Life Support (Domain 2)
cease even though ECG may look normal— • Sudden cardiovascular collapse associated Immediate Recognition of CPA
pulseless electrical activity (formerly electrical with inadequate cardiac output leading to If patient is identified as being nonresponsive
mechanical dissociation). severe consequences. and apneic, start CPR immediately, do not
• Ventricular fibrillation, ventricular asystole, • Quick assessment and diagnosis are critical. take time to confirm via palpation of pulse
and pulseless electrical activity are rhythms • Assess the ABCs—airway, breathing, circu- or ECG.
indicating cessation of myocardial contractility. lation. Chest Compressions
SYSTEMS AFFECTED DIFFERENTIAL DIAGNOSIS • Perform CPR in continuous, uninterrupted,
• All systems are affected, but those requiring • Severe hypovolemia and absence of palpable 2-minute cycles when possible.
greatest supply of oxygen and nutrients pulses. • Use the cardiac pump in patients weighing
affected first. • Pericardial effusion with cardiac tamponade, <10 kg bodyweight; with the patient in right
• Cardiovascular. decreased cardiac output, and muffled heart lateral recumbency, perform compressions
• Renal/urologic. sounds. directly over the heart (intercostal spaces
• Neurologic. • Pleural effusion with respiratory arrest. 3–5); this can be performed using one or
SIGNALMENT • Respiratory arrest can be confused with two hands.
cardiopulmonary arrest (CPA). • Use the thoracic pump for patients
• Dog and cat.
• Any age, breed, or sex.
• Upper airway obstruction can rapidly weighing >10 kg bodyweight; with the
progress to CPA. patient in right lateral recumbency, apply
SIGNS thoracic compressions at the widest portion
• Lack of response to stimulation. CBC/BIOCHEMISTRY/URINALYSIS of the thorax.
• Loss of consciousness. May help identify underlying cause for CPA, • Different compression and ventilation
• Dilated pupils. but should not be part of initial triage. regimes have been reported.
• Cyanosis. OTHER LABORATORY TESTS • Providing appropriate compressions
• Agonal gasping or absence of ventilation. • Arterial blood gas evaluation may be useful (100–120 per minute) and appropriate
• Absence of peripheral pulses. during or after resuscitative procedures, but is ventilations (10 per minute) without stopping
• Hypothermia. not part of initial emergency management. compressions for ventilations and without
• Absence of audible heart sounds. • Venous blood gas evaluation may be more trying to synchronize ventilations with
CAUSES useful during cardiopulmonary resuscitation compressions is the goal; the chest should be
• Hypoxemia caused by ventilation–perfusion (CPR) than arterial blood gas and provides displaced ∼30–50%.
mismatch, diffusion barrier impairment, hypo- electrolyte and lactate concentrations. • Try to minimize discontinuing compressions
ventilation, or shunting. to interpret ECG.
• Poor oxygen delivery due to anemia or
IMAGING • Avoid leaning on the patient during chest
• Thoracic/abdominal focused assessment with compressions and allow full chest wall recoil.
vasoconstriction.
• Myocardial disease—infectious, inflammatory,
sonography for trauma (TFAST®/AFAST®) • Interposing abdominal compressions
infiltrative, traumatic, neoplastic, or embolic. may be useful in identifying underlying between chest compressions enhances
• Acid-base abnormalities.
disease; additional terminology being cerebral and coronary blood flow by
• Electrolyte derangements—hyperkalemia,
introduced, such as POCUS (point of care increasing aortic diastolic pressure; this
hypocalcemia, and hypomagnesemia. ultrasound) and eFAST (extended FAST). technique has not been shown to improve
• Thoracic or abdominal radiographs or survival, but should be considered if
• Hypovolemia.
• Shock.
abdominal ultrasound may help identify adequate personnel are available.
• Anesthetic agents.
underlying disease processes, but only
consider after patient has been stabilized. Airway and Ventilation
• Sepsis/septic shock. • Visualize the airway by extending the
• Echocardiography may confirm pericardial
• CNS trauma. patient’s head and neck and pulling the tongue
• Electrical shock.
effusion or underlying myocardial disease, but
forward; clear any debris (e.g., secretions,
Cardiopulmonary Arrest (continued)
blood, or vomitus) manually or with suction; Vasopressin • Diagnose and correct factors that led to
C use of a laryngoscope is advised. May be used as alternative to epinephrine initial CPA.
• Establish an airway by either oral endo 0.8 U/kg IV (20 U/ml; ~0.5 ml/10 kg PREVENTION/AVOIDANCE
tracheal intubation or, if complete patient); may be used in combination with Careful monitoring of all critically ill patients.
obstruction, emergency tracheostomy. epinephrine, especially if protracted CPR.
• Correct endotracheal tube placement POSSIBLE COMPLICATIONS
Atropine • Vomiting.
should be confirmed visually, by auscultation
• Atropine—0.04 mg/kg IV (0.4 mg/mL) • Aspiration pneumonia.
and/or capnography.
1 mL/10 kg patient. • Fractured ribs or sternebrae.
• 10 breaths per minute with a tidal volume
• Limited data to suggest benefit unless arrest • Pulmonary contusions and edema.
of 10 mL/kg and an inspiratory time of
is due to increased vagal tone. • Pneumothorax.
1 second; peak airway pressures should not
exceed 20 cm H2O. Fluids • Acute renal failure.
• Techniques for ventilation include mouth Administer fluids cautiously unless known • Neurologic deficits.
to mouth, mouth to nose, or mouth to hypovolemia has led to CPA. Crystalloids, • Cardiac arrhythmias.
endotracheal tube; these techniques provide colloids, or blood products may be consid- EXPECTED COURSE AND PROGNOSIS
∼16% oxygen; use of a mechanical ered, including Oxyglobin®. • Prognosis depends on underlying disease
resuscitator (Ambu® bag) and room air process.
provides 21% oxygen. • Rapid return to spontaneous cardiac and
• The preferred technique is endotracheal respiratory function improves the prognosis.
intubation and ventilation with 100% MEDICATIONS • Overall prognosis is poor; <10% of patients
oxygen using an Ambu bag or an anesthesia are discharged.
machine. DRUG(S) OF CHOICE
• The suggested rate of oxygen administration • See Advanced Life Support.
is 150 mL/kg/minute. • Administer drugs via intravenous, intra-
osseous, or intratracheal routes in descending
Circulation order of preference; volumes should be MISCELLANEOUS
• Assessment—palpate peripheral pulses and doubled if administering via the intratracheal
auscultate heart to confirm CPA. ZOONOTIC POTENTIAL
route and diluted in saline. None
• External thoracic compression provides at • Intracardiac administration should not be
best ∼30% of normal cardiac output; internal used unless open-chest CPR is being performed; SYNONYMS
cardiac compression is two to three times administration of epinephrine into the left • For CPA—cardiac arrest, heart attack.
more effective in improving cerebral and ventricle with concurrent digital or mechanical • For CPR—cardiopulmonary cerebral
coronary perfusion. compression of descending aorta is optimal. resuscitation (CPCR).
Open-Chest CPR PRECAUTIONS SEE ALSO
• Indicated if closed-chest CPR is ineffective Fluid administration should be used cautiously • Ventricular Fibrillation.
or preexisting conditions such as flail chest, and only if there is a known history of hypo- • Ventricular Standstill (Asystole).
obesity, diaphragmatic hernia, pericardial volemia; excessive fluid administration may ABBREVIATIONS
effusion, or other significant intrathoracic lead to decreased coronary perfusion. • CPA = cardiopulmonary arrest.
disease preclude closed-chest techniques.
• CPCR = cardiopulmonary cerebral
• Perform through a left thoracotomy at the
resuscitation.
fifth or sixth intercostal space.
• CPR = cardiopulmonary resuscitation.
• Perform a pericardectomy.
FOLLOW-UP • FAST = focused assessment with
• The palmar surface of the fingers and
sonography for trauma.
thumb is used to push the ventricular blood PATIENT MONITORING • POCUS = point of care ultrasound.
toward the great vessel; digital compression of • Maintain normal heart rate and blood • RECOVER = Reassessment Campaign on
the descending aorta may help improve pressure with fluids and inotropic agents. Veterinary Resuscitation.
coronary and cerebral perfusion. • Arterial blood pressure.
Advanced Life Support (Domain 4) • Central venous pressure. Suggested Reading
• Blood gas analysis. Fletcher DJ, Boller M, Brainard BM, et al.
This includes drug therapy and additional
• Support respiration with artificial RECOVER evidence and knowledge gap
resuscitation techniques. Drugs should be
ventilation and supplemental oxygen. analysis on veterinary CPR. Part 7: Clinical
administered every other CPR cycle
• Neurologic status—if signs of increased guidelines. J Vet Emerg Crit Care 2012,
(~q4 minutes).
intracranial pressure develop, consider 22(S1):102–131.
Epinephrine McIntyre RL, Hopper K, Epstein SE, et al.
mannitol, corticosteroids, and furosemide.
• Epinephrine low dose—0.01 mg/kg IV Assessment of cardiopulmonary resuscita-
• ECG—continuously.
(1 : 10,000) 1 mL/10 kg patient. tion in 121 dogs and 30 cats at a university
• Urine output.
• Epinephrine high dose—0.1 mg/kg IV teaching hospital (2009–2012). J Vet Emerg
• Body temperature.
(1 : 1000) can be used in protracted CPR. Crit Care 2014, 24(6):693–704.
• Radiograph thorax to assess resuscitative
injury. Author Steven L. Marks
Consulting Editor Michael Aherne
Cataracts
SIGNS • Hypocalcemia—can cause bilateral, diffuse
Historical Findings punctate or incipient cataracts. C
• Nutritional—use of unbalanced milk
BASICS • Cloudy/white appearance of the lens.
• Vision loss when the cataracts are bilateral
replacers in bottle-fed puppies and kittens.
DEFINITION • Electrical shock—chewing electrical cords
and diabetic cataracts with a rapid, bilateral
Opacification of the lens (focal or diffuse). onset. or lightning strike.
PATHOPHYSIOLOGY • Polyuria/polydipsia is noticed prior to RISK FACTORS
• The normal lens is composed of perfectly cataract development in diabetic dogs. • Diabetes mellitus (dogs).
aligned lens fibers that create a transparent • Chronic anterior uveitis.
structure. A clear capsule surrounds the cortex • Progressive retinal atrophy.
• General physical examination findings—
and nucleus. New lens fibers are continually unremarkable unless the dog is an
produced at the equator of the lens cortex undiagnosed diabetic.
throughout life. The aqueous humor provides • Ophthalmic examination findings—
nutrition to the lens. opacification in one or both lenses. DIAGNOSIS
• A cataract occurs when there is derange ∘∘ Incipient stage—small, focal opacity/
ment of lens fibers due to changes in lens DIFFERENTIAL DIAGNOSIS
opacities in the lens that does not interfere
nutrition, energy metabolism, protein Lenticular nuclear sclerosis—normal aging
with the view of the fundus; no vision
synthesis or metabolism, or osmotic balance. change in the lens of dogs and cats starting
deficits.
• Anterior uveitis is a common cause of at 6 years of age due to compression of
∘∘ Immature stage—diffusely cloudy
altered lens nutrition. older lens fibers in the center of the lens;
appearance to the lens with the tapetal
• Genetics can result in altered protein and gradually becomes more visible with age
reflection still visible and some portions of
energy metabolism, or protein synthesis, in and can be mistaken for a cataract in
the fundus visible through a dilated pupil;
the lens. geriatric patients; definitive diagnosis can
the menace reflex is positive.
• Diabetes mellitus affects the osmotic be made using mydriasis (1% tropicamide)
∘∘ Mature stage—completely opaque lens
balance in the lens. Hyperglycemia increases and the observation of a perfectly round,
with no tapetal reflection visible; blind.
glucose in the aqueous and lens overwhelming bilaterally symmetric, homogeneous nucleus
∘∘ Hypermature stage—wrinkled lens
the glycolysis pathway; glucose is shunted to in the center of each lens, and the ability to
capsule, areas of dense white mineraliz
the sorbitol pathway; sorbitol creates an view the fundus through the lens; vision is
ation, may have portions of liquefied cortex
osmotic gradient that draws water into the rarely affected and treatment is not indicated.
(white, sparkly to clear); deep anterior
lens and rapid cataract formation. The chamber; blind unless there is a large area CBC/BIOCHEMISTRY/URINALYSIS
sorbitol pathway requires aldose reductase of clear liquefied cortex. Dogs with diabetic cataracts may have
enzyme and dogs have more aldose reductase ∘∘ Intumescent mature cataract—opaque, hyperglycemia and glucosuria.
than cats, making cats more resistant to swollen lens usually due to the hyper
developing diabetic cataracts. The enzyme IMAGING
osmotic effect of diabetes; shallow anterior Ocular ultrasound can be used to evaluate the
levels vary between individuals, which may chamber.
explain dogs that are resistant to cataract posterior lens capsule for any sign of rupture
development. CAUSES and can evaluate for retinal detachment prior
• Hereditary—most common cause in dogs. to cataract surgery.
SYSTEMS AFFECTED
• Diabetes mellitus. DIAGNOSTIC PROCEDURES
Ophthalmic
• Anterior uveitis—either by altered nutrition of ERG is performed prior to cataract surgery to
GENETICS the lens from the abnormal aqueous, or by evaluate for retinal degeneration when the
• Inheritance has been established for many posterior synechia and inflammatory debris fundus is not visible due to the cataract.
dog breeds; the most common mode of causing opacification of the anterior lens capsule.
inheritance is autosomal recessive. • Trauma—perforating injury that disrupts the
• Inheritance has been established in the anterior lens capsule, most commonly a cat
Himalayan cat (autosomal recessive). claw injury, especially in puppies and kittens.
INCIDENCE/PREVALENCE • Senile—slowly progressive cataract in TREATMENT
• One of the leading causes of blindness in geriatric animals, usually beginning as dense ACTIVITY
dogs. nuclear sclerosis followed by gradual For safety, blind animals should not be
• The prevalence of genetic cataracts varies spoke-like opacities extending into the cortex. allowed access to an in-ground swimming
significantly; up to 10% in some breeds. • Congenital—due to heredity, in utero
pool or elevated decks with open railings; use
• Most diabetic dogs will develop cataracts insult, or associated with other congenital caution near stairs; restrict outside activity to
regardless of their diabetic control. ocular anomalies such as persistent pupillary fenced yards or leash walks.
• Cataracts are rare in cats. membranes, persistent hyperplastic primary
vitreous/persistent tunica vasculosa lentis, or a CLIENT EDUCATION
SIGNALMENT hyaloid artery attachment. • Cataract surgery is routinely performed,
Species • Surgery—transpupillary laser energy, with an overall 80–90% success rate.
Dogs and cats. intraocular instrument trauma. • Once the cataracts are removed they cannot
• Toxic—long-term ketoconazole therapy; return.
Breed Predilections • Artificial lens implants will restore essentially
suspected secondary to toxic by-products of
Over 135 dog breeds are suspected as being normal vision.
degenerating photoreceptors in dogs with
predisposed to hereditary cataracts. • Evaluation for surgery should be done early
progressive retinal atrophy.
Mean Age and Range • Radiation—when the eye is in the radiation in the course of cataract development to avoid
Cataracts can develop at any age; genetic treatment field for neoplasia of the mouth or complications that may result in the cataract
cataracts can develop as early as 6 months of age. head. becoming inoperable, to allow time to plan
Cataracts (continued)
for the surgery, and in some cases to eliminate been no published data conclusively showing causing the zonules to stretch and break,
C the need and extra cost for an ocular ultra- a significant reversal, or delay in progression; resulting in a lens subluxation or luxation.
sound and ERG. time spent trying medical therapy will delay EXPECTED COURSE AND PROGNOSIS
SURGICAL CONSIDERATIONS evaluation for surgery, resulting in surgery • Most cataracts are progressive, although the
• Phacoemulsification (removal of the
being performed at a suboptimal stage, or rate of progression can vary widely depending
cataract through a corneal incision using complications from the cataract making it on age, breed, and location of the cataract.
ultrasonic waves to emulsify and aspirate the inoperable. • Long-term prognosis following cataract
lens) is the most common technique for • A topical aldose reductase inhibitor, surgery is very good; however, some patients
cataract removal. Kinostat®, is in the final stage of FDA have increased risk for postoperative
• The ideal time for cataract surgery is the
approval. When made available, it may prove complications.
immature/early mature stage. helpful in delaying the onset of diabetic • Those that do not pursue surgery should be
• Inherited, diabetic, and senile cataracts are
cataracts in dogs. monitored for uveitis and glaucoma.
potentially good candidates for surgery;
cataracts secondary to anterior uveitis are
normally poor surgical candidates.
• Artificial intraocular lenses are routinely FOLLOW-UP MISCELLANEOUS
placed inside the patient’s lens capsule; lens
PATIENT MONITORING ASSOCIATED CONDITIONS
implants restore normal focus and help
• Incipient or early immature cataracts
minimize posterior capsular fibrosis; if a lens • Retinal detachment.
should be monitored regularly for progression • Lens-induced uveitis.
cannot be implanted (e.g., due to an unstable
in order to select the ideal time for surgery • Congenital ocular anomalies.
lens capsule or luxated lens), the dog or cat
and to avoid complications associated with
will still have functional vision. AGE-RELATED FACTORS
cataracts.
• Traumatic lens perforation with release of • Immediate referral for cataracts in young
• Postoperative monitoring by the surgeon is
lens cortex into the anterior chamber may dogs (<2 years of age) is recommended
critical for the success of surgery and should
require surgery to remove the lens, depending because the cataract can progress very rapidly,
be clearly discussed with the owner prior to
on the size of the capsular tear. with partial cortical liquefaction followed by
surgery.
retinal detachment.
PREVENTION/AVOIDANCE • Nuclear sclerosis is prominent in geriatric
Do not breed animals with cataracts. animals; a dilated exam may be necessary to
MEDICATIONS POSSIBLE COMPLICATIONS definitively distinguish nuclear sclerosis from
• Lens-induced uveitis—associated with cataract.
DRUG(S) OF CHOICE hypermature cataracts and cataracts that
• Topical anti-inflammatory medication is SEE ALSO
progress rapidly; caused by antigenic lens • Anterior Uveitis—Cats.
recommended q6–24h to help prevent or proteins leaking through the lens capsule.
treat lens-induced uveitis with immature, • Anterior Uveitis—Dogs.
Clinical signs can be subtle (e.g., low • Diabetes Mellitus Without Complication—
mature, and hypermature cataracts; this intraocular pressure) to extreme (granulo
can be a topical nonsteroidal anti- Cats.
matous uveitis with aqueous flare, miosis, • Diabetes Mellitus Without Complication—
inflammatory drug (NSAID) such as synechia, keratic precipitates); preoperative
flurbiprofen, diclofenac, or ketorolac, or a Dogs
uveitis increases postoperative complications.
topical steroid such as prednisolone acetate • Secondary glaucoma—impaired aqueous ABBREVIATION
1% or dexamethasone 0.1%; topical outflow from intraocular changes associated • NSAID = nonsteroidal anti-inflammatory
NSAIDs may be preferable in diabetic with lens-induced uveitis, or from an drug.
patients. intumescent cataract causing a forward Author Margi A. Gilmour
• Topical atropine q8–24h is indicated for displacement of the iris, narrowing the Consulting Editor Kathern E. Myrna
lens-induced uveitis; contraindicated with iridocorneal angle.
glaucoma. • Retinal detachment—associated with hyper-
• Oral NSAIDs (carprofen, meloxicam, mature cataracts and cataracts in young dogs Client Education Handout
deracoxib) are also used to treat lens-induced with a rapid onset and cortical liquefaction. available online
uveitis. • Lens luxation—associated with hypermature
• Topical antioxidants are advertised as able cataracts in which the lens and capsule shrink,
to reverse cataract changes; to date there have
Cerebellar Degeneration
hyperreflectivity on funduscopic exam.
• Decerebellate posture—opisthotonos with C
extensor rigidity of the forelimbs and flexed
BASICS hind limbs. • Cerebellar degeneration is not TREATMENT
characterized by altered mentation, proprio • Restrict to supervised activity in safe areas;
OVERVIEW
• Progressive and non-progressive etiologies. ceptive deficits, or paresis. • Progression of leash-walks only; avoid stairs, furniture,
Progressive - premature aging and neuronal signs varies. • Use caution in interpreting proximity to swimming pools, etc.
death; may be due to failure of neuronal progression of clinical signs—cerebellar • Amantadine has potentiating effects on
energy supply, ion regulation, excitotoxicity, ataxia in a puppy or kitten with cerebellar dopaminergic neurotransmission in CNS and
autoimmunity/inflammation, or inappropriate degeneration caused by in utero or neonatal anticholinergic activity; buspirone is serotonin
apoptosis; neonatal, postnatal, and adult onset infection may appear to worsen as the animal agonist; research models demonstrate some
(rare). • Nonprogressive - due to abnormal grows and becomes more active; the potential benefit for progressive cerebellar
cerebellar development following in utero or underlying disease process itself is degeneration; guidelines and clinical evidence
neonatal viral infection in cats (feline panleuko- nonprogressive. are lacking. • Neuroprotective agents (such as
penia) and dogs (canine herpesvirus, canine coenzyme Q10 and acetyl-L-carnitine) may
CAUSES & RISK FACTORS have promising effects.
parvovirus). • Causal mutations associated with progressive
SIGNALMENT cerebellar degeneration have been identified
in several breeds. • In utero or neonatal
Progressive
exposure to feline panleukopenia or canine
• Dog and cat. • Described in over 40 dog MEDICATIONS
herpesvirus infection. • Poor vaccination
breeds, often affecting a single family or
history or exposure to modified live virus DRUG(S) OF CHOICE
individual. • Eight causal mutations, all with
during gestation. • A syndrome of hepato- N/A
autosomal recessive mode of inheritance, have
cerebellar degeneration has been described in
been identified. Beagle (onset of clinical signs
a litter of Bernese mountain dogs.
before 1 month); Finnish hound (2 months),
• Paraneoplastic cerebellar degeneration has
Parson Russell terrier (2 months), Jack Russell
been reported in humans.
terrier (2–12 months) Hungarian Vizsla (3 FOLLOW-UP
months); Kerry blue terrier and Chinese • Neurologic status—examine at weekly-to-
crested (3–4 months); Old English sheepdog monthly intervals if progression of signs is
and Gordon setter (6 months – 3 years). uncertain; consider videotaping patient to
• Immune-mediated disorder described in DIAGNOSIS determine progression objectively.
Coton de Tulear (2 months). • Sporadic DIFFERENTIAL DIAGNOSIS • Progression of signs—rate varies depending
reports in miniature poodle (neonatal), • Lysosomal storage diseases—diffuse diseases on etiology; ranges from days to years.
papillon (5 months); Scottish terrier, Border of the CNS; differentiate by presence of • Nonprogressive disease—patient may show
Collie, Lagotto Romagnolo, Australian signs of involvement of parts of the CNS improvements as they learn to compensate for
Kelpie, Labrador Retriever, Bavarian outside of the cerebellum. • Toxicity (e.g., deficits. • Do not vaccinate pregnant animals
mountain dogs, Italian hound (2 months – hexachlorophene)—differentiate by history of with modified live virus. • Do not breed
1 year); English bulldog (5–8 months); exposure. • Inflammatory diseases—infectious animals with familial history of cerebellar
American Staffordshire terrier (2–9 years). (e.g., canine distemper and feline infectious disease.
• Late onset disorder described in Labrador peritonitis [FIP]) and immune-mediated
Retriever, Bern running dog, Irish setter, and (dogs). Differentiate from cerebellar
Brittany spaniel (signs at 5–13 years). degeneration by MRI and cerebrospinal fluid
• Cerebellar degeneration and coat color (CSF) analysis. Infectious diseases are
dilution reported in one family of Rhodesian MISCELLANEOUS
frequently accompanied or preceded by
ridgebacks. • X-linked mode of inheritance systemic signs of illness. • Cerebellar cyst— ABBREVIATIONS
suspected in English pointer (only males differentiate by advanced imaging (MRI). • CSF = cerebrospinal fluid.
affected). • Both early- (days to weeks) and • Medulloblastoma (cerebellar tumor)— • FIP = feline infectious peritonitis.
late- (years) onset in domestic shorthair cat. reported in dogs and cats <1 year old;
• Described in two Havana brown kittens
Suggested Reading
differentiate by advanced imaging (MRI) and de Lahunta A, Glass E, Kent M. Cerebellum.
from the same litter. Signs observed at one CSF analysis. • Other primary and metastatic In: de Lahunta A, Glass E, eds., Veterinary
month. Heritable nature suspected. tumors in adult dogs. Neuroanatomy and Clinical Neurology, 4th
Nonprogressive IMAGING ed. St. Louis, MO: W.B. Saunders, 2015,
• Two causal mutations identified in two dog • MRI is preferred imaging modality— pp. 368–408.
breeds. • Non-inflammatory disorder with cerebellum may be smaller than normal. Dewey CW, da Costa RC. A Practical Guide
autosomal recessive mode of inheritance • CT can aid in diagnosis of other conditions to Canine and Feline Neurology, 3rd ed.
reported in six litters of Coton de Tulear (signs (e.g., cyst); if MRI is not accessible, CT may Ames, IA: Wiley-Blackwell, 2016,
by 2 weeks). • Eurasier dog (2 months). have some value. pp. 183–191.
SIGNS Urkasemsin, G, Nielsen DM, Singleton A,
DIAGNOSTIC PROCEDURES et al. Genetics of hereditary ataxia in
• Cerebellar ataxia- hypermetria; broad-based • CSF analysis—normal with nonprogressive
stance; swaying of body, intention tremors. Scottish Terriers. J Vet Intern Med, 2017,
disease; normal-to-high protein concentration 31(4):1132–1139.
• Lack of menace responses with normal and normal cell counts with progressive disease.
vision and pupillary light reflexes. • Head tilt Authors Richard J. Joseph and Anne
• Cerebellar biopsy—may be only definitive E. Buglione
and episodes of vestibular ataxia with resting means of antemortem diagnosis.
or positional nystagmus. • Diffuse tapetal
Cerebellar Hypoplasia
• Final diagnosis possible only at necropsy. Care
C CBC/BIOCHEMISTRY/URINALYSIS • Restrict environment to prevent injuries
Usually normal. and road accidents—no climbing, falling, or
BASICS escaping.
OVERVIEW IMAGING • Nutritional support as needed.
Caused by incomplete development of parts MRI—cerebellar atrophy or malformation • Euthanasia—severely affected animals that
of the cerebellum owing to intrinsic (inherited) (incomplete or asymmetric filling of the are unable to feed, groom, or be housetrained.
or extrinsic (infectious, toxic, or nutritional) caudal cranial fossa by the cerebellum); rule
factors. out other malformations.
SIGNALMENT PATHOLOGIC FINDINGS
• Symptoms may not be visible until puppies • Cerebellum—normally very small in MISCELLANEOUS
and kittens begin to stand/walk (usually by newborn kitten or puppy (cerebellar
development continues for up to 10 weeks Suggested Reading
6 weeks old). de Lahunta A, Glass E, Kent M. Veterinary
• Hereditary in Airedale, chow chow, Boston postnatal); subtle to marked atrophy; as
necropsy is performed weeks to months after Neuroanatomy and Clinical Neurology,
terrier, Labrador retriever, Weimaraner, shih 4th ed. St. Louis, MO: W.B. Saunders,
tzu, miniature schnauzer, and bull terrier. birth, there is no sign of active inflammation.
• Transverse fibers of the pons—decreased 2015, pp. 389–390.
SIGNS size associated with marked cortical cerebellar Author Christine F. Berthelin-Baker
• Symmetric, nonprogressive cerebellar atrophy.
disorder—head bobbing; limb tremors; • Hydrocephalus—may be concomitant,
aggravated by movement or eating and resulting from multifocal inflammation or
disappear during sleep (intention tremors). multiple malformations (e.g., Dandy–Walker
• Cerebellar ataxia, wide-base stance. syndrome).
• Dysmetria and disequilibrium—falling, • Microscopic—depletion of cerebellar cortex
flipping over. cellular layers.
• Cats—usually transplacental or perinatal
infection with panleukopenia virus (wild or
from modified live virus used in some TREATMENT
vaccines), which selectively attacks rapidly None
dividing cells, e.g., external germinal layer of
the cerebellum at birth and for 2 weeks
postnatal.
• Dogs—hereditary in some breeds (autosomal
recessive). MEDICATIONS
DRUG(S) OF CHOICE
N/A
DIAGNOSIS INTERACTIONS
DIFFERENTIAL DIAGNOSIS N/A
• Age, breed, history, typical symmetric and
nonprogressive symptoms—usually sufficient
for tentative diagnosis.
• Early cerebellar abiotrophy—postnatal
degeneration after normal development; slow
FOLLOW-UP
progression of signs over weeks to months; PATIENT MONITORING
neonatal onset (beagle, Samoyed, Rhodesian Helps confirm the diagnosis (as necessary).
ridgeback, Irish setter, Jack Russell terrier, PREVENTION/AVOIDANCE
miniature poodle) or postnatal onset Avoid using modified live panleukopenia
(Australian kelpie at 5–6 weeks; Kerry blue vaccines in reproducing female cats and keep
terrier at 8–16 weeks; rough-coated collie at cats vaccinated against panleukopenia.
4–8 weeks; bullmastiff at 4–9 weeks).
• Neuroaxonal dystrophy—slowly progressive POSSIBLE COMPLICATIONS
cerebellar signs starting around 5 weeks of age N/A
in cats and 7 weeks in Chihuahuas. EXPECTED COURSE AND PROGNOSIS
• Cerebellar sequels of systemic canine herpes- • Slight improvement may occur as patient
virus infection—follow systemic illness. compensates for deficits.
• Concomitant seizures or other cerebral • Deficits—permanent; do not progress;
signs—suggest other malformations, such as compatible with a normal lifespan.
lissencephaly (wirehaired fox terrier and Irish • Some patients may be acceptable indoor
setter) or hydrocephalus. pets.
Cerebrovascular Accidents
CAUSES OTHER LABORATORY TESTS
Ischemic Stroke • Cerebrospinal fluid—unlikely to confirm C
CVA, may help rule out inflammatory CNS
BASICS Dogs disease. Variable findings; either normal, or mild
• Unknown in 50% of cases. • Endocrine mononuclear or neutrophilic pleocytosis; protein
DEFINITION
diseases—hyperadrenocorticism, hypothyroidism, concentration occasionally elevated.
• Sudden onset of nonprogressive focal brain
diabetes. • Embolism, thromboembolism— • Prothrombin time—screening test for extrinsic
signs. • Signs must remain for >24 hours for
neoplastic (hemangiosarcoma, lymphoma), mechanism defects. • Activated partial thrombo-
a diagnosis of cerebrovascular accident (CVA).
infectious (associated with bacterial plastin time—screening test for intrinsic
• Permanent brain damage usually ensues.
endocarditis or other sources of infection), mechanism defects. • Bleeding time—prolonged
• Called transient ischemic attack or TIA if
and aortic or cardiac. • Systemic in patients with von Willebrand’s disease; normal
clinical signs resolve within 24 hours.
hypertension—chronic kidney disease, protein with most other coagulation defects, except
PATHOPHYSIOLOGY losing enteropathy. • Fibrocartilaginous disseminated intravascular coagulation.
• Cerebrovascular diseases are the underlying embolism. • Intravascular lymphoma. • Thromboelastography, D-dimer assay, and
cause of CVA. • Brain abnormality resulting • Parasite migration (Cuterebra) or embolism antithrombin III—screening tests for hypercoag
from a pathologic process that compromises (Dirofilaria immitis). ulability syndrome as possible cause of ischemic
the blood supply to the brain. • Lesions
Cats stroke. • Endocrine testing—hyperadreno
affecting the cerebral blood vessels are divided
• High likelihood of concurrent disease. corticism, thyroid disease, and pheochro
into two broad categories: ◦ Hemorrhagic
• Parasite migration (Cuterebra or mocytoma. • Renal disease—urine protein/
stroke—ruptured blood vessel with hemor
heartworms). • Systemic hypertension— creatinine ratio.
rhage into or around the brain. ◦ Ischemic
hyperthyroidism, chronic kidney disease, IMAGING
stroke—abrupt disruption of blood flow from
heart disease. • Neoplastic embolism.
blockage of an artery depriving the brain Ischemic Stroke
• Intracranial telangiectasia. • Hypertropic
tissue of oxygen and glucose. • CT—often normal during acute phase.
cardiomyopathy. • Hyperthyroidism.
SYSTEMS AFFECTED • Pulmonary disease. • Liver disease. • MRI—within 12–24 hours of onset to
• Nervous. • Multisystemic—if underlying • Neoplasia elsewhere in the body. distinguish hemorrhage from infarction;
cause present. T2-weighted and fluid-attenuated inversion
Hemorrhagic Stroke recovery (FLAIR) images particularly useful;
INCIDENCE/PREVALENCE Dogs T2*-weighted (gradient echo) images to show
Unknown; supposed low compared to human. • Ruptured congenital vascular anomalies. presence of or exclude intracranial hemorrhage;
SIGNALMENT • Primary and secondary brain tumors. diffusion-weighted imaging (DWI) sequence:
• Inflammatory disease of arteries and veins ideal for identification of hyperacute stroke,
Species
(vasculitis). • Intravascular lymphoma. excluding stroke mimics; perfusion-weighted
Dog and cat.
• Brain hemorrhagic infarction. • Impaired MRI can be used to depict brain regions of
Breed Predilections coagulation. hypoperfusion and derive the tissue at risk by
• Ischemic stroke—cavalier King Charles comparing the results with the findings on
Cats
spaniel and greyhound seem predisposed; DWI. • Time of flight magnetic resonance
• Primary and secondary brain tumors.
small breed (≤15 kg) more likely to have angiography (MRA) and contrast-enhanced
• Inflammatory disease of arteries and veins
cerebellar infarct; large breed (>15 kg) more MRA can be used to assess intracranial
(vasculitis). • Brain hemorrhagic infarction.
likely to have midbrain or thalamic infarct. vascular status of stroke patients.
• Impaired coagulation—cerebral amyloid
• Hemorrhagic stroke—unknown.
angiopathy. • Systemic hypertension. Hemorrhagic Stroke
SIGNS • CT—very sensitive for detection of
RISK FACTORS
Historical Findings • Ischemic stroke—systemic hypertension, acute hemorrhage; hyperdensity due to
• Ischemic stroke—peracute to acute systemic conditions associated with hyper- hyperattenuation of X-ray beam by the globin
nonprogressive focal brain signs. • Hemorrhagic coagulability syndrome. • Hemorrhagic portion of blood; attenuation decreases until
stroke—acute to subacute focal or multifocal stroke—systemic hypertension, the hematoma is isodense at about 1 month
brain signs that can progress over a short coagulopathy. from onset; periphery of hematoma contrast-
period of time. enhances from 6 days to 6 weeks after onset
due to revascularization. • MRI—signal
intensity of intracranial hemorrhage is
• Fundus examination—may reveal tortuous
influenced by several intrinsic (time from ictus,
vessels (systemic hypertension), hemorrhage DIAGNOSIS source, size and location of hemorrhage) and
(coagulopathy or systemic hypertension), or
DIFFERENTIAL DIAGNOSIS extrinsic (pulse sequence and field strength)
papilledema (elevated intracranial pressure
• Head trauma—history and physical factors; as hematoma ages, oxyhemoglobin in
[ICP]). • Coagulation defects—may underlie
findings suggestive of trauma. blood breaks down sequentially into several
hemorrhagic stroke and cause hemorrhage in
• Decompensation from primary or meta- paramagnetic products (deoxyhemoglobin,
any tissue or organ and anemia.
static brain tumor—signs are progressive. methemoglobin, hemosiderin), each with
Neurologic Examination Findings • Infectious and noninfectious encephalitis— different MRI signal intensities; compared to
• Ischemic stroke—signs depend on the acute to subacute clinical signs that gradually other conventional sequences, T2*-weighted
localization of the vascular insult (prosence worsen. • Neurotoxicity—bilateral, symmetric (gradient echo) images demonstrate readily
phalon, midbrain, pons, medulla, cerebellum). neurologic deficits. detectable hypointensity regardless of time
• Hemorrhagic stroke—signs relate to from ictus, source and location of hemorrhage,
increased ICP with nonspecific forebrain and/ CBC/BIOCHEMISTRY/URINALYSIS
or field strength. • Multiple hemorrhagic
or brainstem disturbance. Most often normal; may show changes
lesions <5 mm—most often associated with
reflecting underlying cause.
hyperadrenocorticism, hypertension, chronic
Cerebrovascular Accidents (continued)
kidney disease, or hypothyroidism. • Single the hemorrhage spreads between planes of clopidogrel (2–4 mg/kg PO q24h) and low
C hemorrhagic lesion—most often associated white matter cleavage with minimal molecular weight heparin can be used
with Angiostrongylus vasorum. • Multiple destruction, leaving nests of intact neural prophylactically; low molecular weight heparin
hemorrhagic lesions ≥5 mm—most often tissue within and surrounding the hematoma. 80–150 IU/kg SC can be used in suspected or
associated with Angiostrongylus vasorum, confirmed case of hypercoagulable state;
primary extracranial neoplasia with metastases anti-factor Xa activity should be monitored,
(haemangiosarcoma). although this may not be practical.
DIAGNOSTIC PROCEDURES TREATMENT Hemorrhagic Stroke
Diagnosis of potential underlying causes. Mannitol—if suspected elevated ICP unrespon
NURSING CARE
Ischemic Stroke sive to extracranial stabilization measures
Ischemic Stroke (0.25–2 g/kg IV over 10–20 min up to q4-8h).
Evaluate for hypertension (and potential
• Monitoring and correction of basic physiologic
underlying causes), endocrine disease
variables (e.g., oxygen level, fluid balance, blood
(hyperadrenocorticism, hypothyroidism,
pressure, body temperature). • Maintenance of
hyperthyroidism, diabetes mellitus), chronic
systemic arterial blood pressure within physiologic
kidney disease (especially protein-losing
range; aggressive lowering of blood pressure FOLLOW-UP
nephropathy), protein-losing enteropathy,
should be avoided during acute stages unless the PATIENT MONITORING
heart disease, and metastatic diseases
patient is at high risk of end-stage organ damage Frequent neurologic evaluations in the first
(particularly hemangiosarcoma).
(systolic blood pressures >180 mmHg); 48–72 hours to monitor progress.
Hemorrhagic Stroke hypertension can develop as a physiologic EXPECTED COURSE AND PROGNOSIS
Evaluate for coagulopathy (and potential response to a stroke to ensure adequate cerebral • Maximum severity of signs usually reached
underlying causes), hypertension (and perfusion pressure; elevated blood pressure can within 24h for ischemic stroke. • Resolution
potential underlying causes), and metastatic persist for up to 72 hours after the onset of injury. of signs—gradual within 2–10 weeks; some
diseases (particularly hemangiosarcoma). • No evidence that glucocorticoid provides dogs/cats may be left with permanent
PATHOLOGIC FINDINGS beneficial neuroprotection; most neuroprotective neurologic signs due to irreversible brain
agents tested have either failed to prove their damage. • Dogs with causal medical condition
Ischemic Stroke efficacy in clinical trials or are awaiting further
• Ischemic necrosis centered on gray matter significantly more likely to relapse and have
investigation. significant shorter survival time than dogs with
due to selective vulnerability. • Lesions limited
to brain area vascularized by the affected vessel Hemorrhagic Stroke no identifiable medical condition. • Despite
with sharply demarcated borders; normal • Patient stabilization (airway protection, having a high likelihood of concurrent disease,
surrounding brain tissue; minimal to no mass monitoring and correction of vital signs). cat with ischemic stroke have been reported to
effect. • Global brain ischemia usually affects a • Assessment and monitoring of neurologic have a favorable short-term outcome, if neither
dense area of selectively vulnerable neurons; status. • Determination and treatment of clinical presentation nor concurrent disease
specific anatomic areas including cerebral potential underlying causes of hemorrhage. was severe. • Prognosis for global brain
cortex, hippocampus, certain basal nuclei (e.g., • Assessment for the need of specific treatment ischemia difficult to predict as there are no
caudate nuclei), thalamus, and cerebellar measures including management of raised ICP, controlled studies.
Purkinje cell layers are more susceptible to which revolves around reducing cerebral
hypoxic injury. • Early ischemic cell changes edema, optimizing cerebral blood volume, and
occur rapidly and are a result of energy eliminating space-occupying mass. • Risk of
neurologic deterioration and cardiovascular
deprivation with swelling of the mitochondria
instability highest during the first 24 hours
MISCELLANEOUS
and endoplasmic reticulum, which causes
cytoplasmic microvacuolation; more chronic after onset of intracranial hemorrhage, as the SYNONYMS
lesions are characterized by postnecrotic space-occupying lesion slowly expands and Stroke
atrophy of the brain parenchyma, endothelial cerebral vasogenic edema develops. ABBREVIATIONS
proliferation in viable capillaries, and • ACE = angiotensin-converting enzyme.
accumulation of Gitter cells. • CVA = cerebrovascular accident. • DWI =
Hemorrhagic Stroke diffusion-weighted imaging. • FLAIR =
• Parenchymal bleeding results from rupture MEDICATIONS fluid-attenuated inversion recovery. • ICP =
of the small penetrating brain arteries; most intracranial pressure. • MRA = magnetic
DRUG(S) OF CHOICE resonance angiography. • TIA = transient
acute cases reveal fresh hemorrhage and acute
neuronal necrosis that is slowly removed by Ischemic Stroke ischemic attack.
macrophages, leaving over time a cystic cavity • Antihypertensive—consider if systemic BP Suggested Reading
lined by fibrillary astrocytes. • Histology is >180 mmHg on serial evaluation and/or severe Lowrie M., De Risio L, Dennis R, et al.
characterized by presence of edema, neuronal ocular manifestations of hypertension. Concurrent medical conditions and
damage, macrophages, and neutrophils in the • Angiotensin-converting enzyme (ACE) long-term outcome in dogs with nontrau
region surrounding the hematoma. • While inhibitor—enalapril (0.25–0.5 mg/kg q12h) or matic intracranial hemorrhage. Vet Radiol
some cerebral hemorrhages stop quickly as a benazepril (0.25–0.5 mg/kg q12h) and/or Ultrasound, 2012, 53:381–388.
result of clotting and tamponade by the calcium channel blockers such as amlodipine Whittaker DE, Drees R, Beltran E. MRI and
surrounding regions, others tend to expand (0.1–0.25 mg/kg q24h); amlodipine is more clinical characteristics of suspected
over time; the latter is a result of continued effective in severe hypertension. • Prevention cerebrovascular accident in nine cats. J
bleeding from the primary source and to the of clot formation—consider in proven cardiac Feline Med Surg, 2017, 20:674–684.
mechanical disruption of surrounding vessels; sources of embolism; antiplatelet therapy with Author Laurent Garosi
low-dose aspirin (0.5 mg/kg PO q24h) or
Ceruminous Gland Adenocarcinoma, Ear
difficult to interpret due to superimposition therapy (every 3–4 months) is recommended
of bones in the skull. for the first year postoperatively. C
• Thoracic radiography to evaluate for • Serial CT or MRI to monitor for local
BASICS pulmonary metastasis. tumor regrowth may be recommended.
OVERVIEW • CT or MRI is most useful for loco-regional
• Most common primary malignant tumor of staging and before surgery and radiation • Permanent or transient Horner’s syndrome
the external ear canal, arising from modified therapy, providing greater detail than with secondary to surgery.
apocrine sweat glands (ceruminous glands). radiographs. • Permanent or transient facial paralysis
• Often locally invasive, but associated with a DIAGNOSTIC PROCEDURES following surgery (more frequent in cats).
low metastatic rate. • Cytologic examination of aspirate from
SIGNALMENT regional lymph nodes. • Median survival after lateral ear resection is
• Uncommon overall, but the most common • Cytologic examination of fine-needle around 10 months for both dogs and cats.
malignant tumor of the ear canal in both dogs aspirate from mass. • Median survival after TECABO is >3 years
and cats, followed by carcinoma of undeter- • Biopsy and histopathology. in both dogs and cats.
mined origin and squamous cell carcinoma. PATHOLOGIC FINDINGS • Median survival after radiation therapy is
• Cocker spaniels and German shepherd dogs • Cytology from fine-needle aspirate—round >3 years, but published information is on
are overrepresented. to polygonal epithelial cells arranged both small numbers only.
• Mean age—dogs, 10 years; cats, 11 years. singly and in large clusters with deep blue to • Poor prognosis associated with extensive
• No known sex predisposition. lavender-gray cytoplasm and a variable tumor involvement (advanced stage), preoper-
SIGNS quantity of black, intracytoplasmic granular ative neurologic signs, and conservative
• Progressive hearing loss. material; unable to differentiate adenocarci- therapy (e.g., lateral ear canal ablation alone).
• Similar to chronic, recurrent otitis externa— noma from adenoma consistently with
discharge, odor, pruritus, inflammation. cytology.
• Early appearance—pale pink, friable, • Histopathologic characteristics—apocrine
ulcerative, bleeding nodular mass(es) within type differentiation from ceruminous glands
and local invasion into stroma; neoplastic
MISCELLANEOUS
the external ear canal.
• Late appearance—large mass(es) filling the cells show moderate to marked nuclear atypia ASSOCIATED CONDITIONS
canal and invading through canal wall into with frequent mitotic figures. • Otitis externa.
surrounding structures. • Peripheral vestibular disease, Horner’s
• Regional lymph node enlargement. syndrome.
• Neurologic signs (vestibular signs, Horner’s • Chronic pain.
syndrome) may be present secondary to TREATMENT ABBREVIATIONS
middle ear involvement. • Total ear canal ablation and lateral bulla • NSAID = nonsteroidal anti-inflammatory
• Signs of pain and discomfort; pain upon osteotomy (TECABO) is the preferred drug.
opening the mouth. surgical approach over lateral ear resection. • TECABO = total ear canal ablation and
CAUSES & RISK FACTORS • Radiation therapy may be considered for bulla osteotomy.
Chronic inflammation and ceruminous gland either large (palliative intent) or incompletely Suggested Reading
hyperplasia/dysplasia appear to play a role in excised masses (curative intent). Bacon NJ, Gilbert RL, Bostock DE, White
tumor development. RA. Total ear canal ablation in the cat:
indications, morbidity and long-term
survival. J Small Anim Pract 2003,
MEDICATIONS 44:430–434.
DIAGNOSIS De Lorenzi D, Bonfanti U, Masserdotti C,
DRUG(S) OF CHOICE Tranquillo M. Fine-needle biopsy of
DIFFERENTIAL DIAGNOSIS • Chemotherapy not evaluated, but external ear canal masses in the cat:
• Proliferative chronic otitis externa with occasionally considered based on histologic cytologic results and histologic correlations
ceruminous gland hyperplasia. information and clinical staging results. in 27 cases. Vet Clin Pathol 2005,
• Inflammatory polyps. • Multimodal therapy incorporating 34:100–105.
• Other tumors including squamous cell corticosteroids or nonsteroidal anti-inflam- Moisan PG, Watson GL. Ceruminous gland
carcinoma, basal cell tumor, mast cell tumor, matory drugs (NSAIDs) and other analgesics. tumors in dogs and cats: a review of 124
papilloma, sebaceous gland tumor, ceruminous CONTRAINDICATIONS/POSSIBLE cases. J Am Anim Hosp Assoc 1996,
gland adenoma. 32:448–452.
INTERACTIONS
CBC/BIOCHEMISTRY/URINALYSIS N/A Théon AP, Barthez PY, Madewell BR, Griffey
Usually normal. SM. Radiation therapy of ceruminous gland
carcinomas in dogs and cats. J Am Vet Med
Assoc 1994, 205:566–569.
• Ear swab cytology for bacteria and yeast.
Author Jason Pieper
• Bacterial culture and sensitivity as needed. FOLLOW-UP Consulting Editor Timothy M. Fan
IMAGING PATIENT MONITORING Acknowledgment The author and book
• Skull radiography to assess potential • Physical examination and thoracic editors acknowledge the prior contribution of
involvement of the tympanic bulla, but this is radiography at regular intervals following Louis-Philippe de Lorimier.
Cervical Spondylomyelopathy (Wobbler Syndrome)
Mean Age and Range found no correlation between body
C • Doberman pinschers and other large-breed dimensions and incidence of CSM.
dogs are usually presented >3 years of age, • Fast growth rate has been proposed, but not
BASICS with a mean age of 6 years. confirmed by other studies.
DEFINITION • Giant-breed dogs are usually presented
• Cervical spondylomyelopathy (CSM) or <3 years of age, although late presentations
wobbler syndrome is a disease of the cervical can be seen.
spine of large- and giant-breed dogs. Predominant Sex DIAGNOSIS
• CSM is characterized by compression of the Males overrepresented, primarily in giant-
spinal cord and/or nerve roots associated with breed dogs. DIFFERENTIAL DIAGNOSIS
neurologic deficits and/or cervical pain. • Orthopedic conditions such as hip dysplasia
SIGNS and cruciate ligament rupture; differentiated
PATHOPHYSIOLOGY by neurologic examination (absence of ataxia).
• Compressive lesion caused by intervertebral General Comments
The classic clinical presentation is a slowly • Spinal neoplasia, spinal subarachnoid
disc herniation, osseous malformation, diverticulum, spinal synovial cysts, discospon-
thickened ligaments, or a combination, in a progressive pelvic limb ataxia with less severe
thoracic limb involvement. dylitis, osteomyelitis, meningomyelitis, trauma;
stenotic vertebral canal. differentiated by results of survey radiographs,
• Disc-associated compression—dogs >3 years; Historical Findings cerebrospinal fluid (CSF), myelography, CT,
intervertebral disc degeneration and subsequent • Chronic, slowly progressive gait dysfunc- CT myelography, or MRI findings.
protrusion might be secondary to abnormal tion is characteristic; acute presentations are
articular facet articulation in Doberman usually associated with neck pain; occasion- CBC/BIOCHEMISTRY/URINALYSIS
pinschers, which predisposes to increased ally, acute worsening of a dog with chronic N/A
rotational strain in the intervertebral discs. history is observed. IMAGING
• Vertebral malformation (bony-associated • Neck pain or cervical hyperesthesia is a
Survey Cervical Radiographs
compression)—most commonly seen in giant common historical finding; it occurs in
• Survey radiographs serve as a screening tool
breeds of dogs, usually in young adult dogs (<4 approximately 65–70% of Dobermans, and
years); the osseous malformation can compress 40–50% of other breeds. to rule out bony disorders; although
the spinal cord dorsoventrally (vertebral arch intervertebral disc narrowing or vertebral
Neurologic Examination Findings tipping can be seen, these findings are not
malformation), dorsolaterally (articular process • Cervical pain is the primary complaint in
malformation/osteoarthritic lesions), or laterally specific for CSM since they can be observed
only approximately 5% of patients. in clinically normal large-breed dogs.
(pedicular malformation/osteoarthritic lesions). • Gait changes are characterized by proprio- • Osteoarthritic changes of the articular
• Dynamic spinal cord compression (one that
ceptive ataxia and paresis (weakness); the processes can be seen in giant breeds.
changes with movements of the cervical ataxia and paresis are more obvious in the
spine) is always a component of the patho- Myelography
pelvic limbs, with lesions in the caudal
physiology with any type of compression. • Myelography can define the location(s) and
cervical spine (C5–6, C6–7); compressive
• Current evidence does not suggest that
lesions in the mid-cervical spine tend to cause direction (ventral, dorsal, lateral) of the spinal
instability has a primary role in the patho ataxia in all four limbs. cord compression.
genesis of CSM. • Stressed views (flexion or extension) may
• The thoracic limb gait can appear short-
SYSTEMS AFFECTED strided, spastic with a floating appearance, or cause significant risk of neurologic deterior-
Nervous very weak. ation.
• Linear traction myelography is a safer
GENETICS • Proprioceptive positioning deficits are
usually present, but dogs with chronic ataxia procedure and can distinguish a static from a
• Heritable basis proposed for borzoi and dynamic lesion.
basset hound. may not display them; the gait exam (presence
of ataxia) provides a more sensitive indication Advanced Imaging
• Recent evidence suggests that the disease is
of myelopathy than proprioceptive position- • CT myelography—cross-sectional visualiz-
inherited as an autosomal dominant trait
(with incomplete penetrance) in Doberman ing deficits. ation of the spinal cord compression and
pinscher. • Dogs can present nonambulatory. determination of sites with spinal cord
• Supraspinatus muscle atrophy and worn atrophy.
INCIDENCE/PREVALENCE toenails can be seen in some cases. • MRI—visualization of the spinal cord
CSM is probably the most common • Extensor muscle tone is commonly parenchyma, intervertebral disc, soft tissues,
neurologic disorder of the cervical spine of increased in all four limbs. and nerve roots; images can be obtained in
large- and giant-breed dogs. • Patellar reflexes are normal or increased; sagittal, transverse, and dorsal planes; spinal
GEOGRAPHIC DISTRIBUTION flexor reflex may be difficult to elicit in the cord signal changes allow more precise
N/A thoracic limbs due to increased extensor tone. identification of the main site of compression
CAUSES than CT and myelography; kinematic MRI is
SIGNALMENT a novel procedure that allows more precise
• Nutrition—excess protein, calcium, and
Breed Predilections caloric intake were proposed in Great Danes; identification of dorsal and ventral lesions,
• Doberman pinscher and Great Dane are the
nutrition does not appear to play a role in the primarily when the vertebral column is placed
most commonly affected breeds, with approxi- development of CSM in large-breed dogs. in extension.
mately 60–70% of cases seen in these breeds. • The cause of CSM is likely multifactorial. DIAGNOSTIC PROCEDURES
• Other breeds with a high incidence include CSF analysis—usually normal; mild mixed or
Rottweiler, German shepherd, Weimaraner, RISK FACTORS
• Body conformation—large head and long
neutrophilic pleocytosis can be seen in dogs with
Labrador, and Dalmatian. acute presentations; elevated protein concentra-
• CSM can be seen in any breed, including neck have been proposed, but later studies
tions can be observed with chronic presentations.
small-breed dogs.
(continued) Cervical Spondylomyelopathy (Wobbler Syndrome)

PATHOLOGIC FINDINGS affect diagnostic and treatment options.
• Spinal cord white matter tract demyelina- Doberman pinschers suspected of having C
tion at the site of spinal cord compression; CSM should be routinely evaluated for these
axonal damage can lead to Wallerian degener- MEDICATIONS conditions.
ation in the ascending and descending white DRUG(S) OF CHOICE AGE-RELATED FACTORS
matter tracts. • Corticosteroids—prednisone 1 mg/kg q24h • Young giant- or large-breed dogs—vertebral
• Neuronal loss, gliosis, and necrosis can be or 0.5 mg/kg q12h, progressively decreasing malformation and compression.
observed in the gray matter. dosage and frequency; most dogs can have • Older dogs—disc-associated compression.
• Chronic severe focal spinal cord compression prednisone discontinued after 4–8 weeks of
can lead to focal myelomalacia. treatment; dexamethasone 0.1–0.25 mg/kg ZOONOTIC POTENTIAL
q24h can be used as an alternative to N/A
prednisone in dogs severely affected; cortico- PREGNANCY/FERTILITY/BREEDING
steroids act by reducing the vasogenic edema N/A
TREATMENT often present in chronic compressive spinal
SYNONYMS
cord lesions.
APPROPRIATE HEALTH CARE • Cervical malformation-malarticulation.
• Gabapentin—10 mg/kg q8–12h can be
• Inpatient if surgical treatment is elected. • Cervical spondylopathy.
used for analgesia in cases of more severe
• Outpatient if medical management is chosen. • Cervical vertebral instability.
cervical pain.
NURSING CARE SEE ALSO
CONTRAINDICATIONS
• Nonambulatory dogs—keep patients on Intervertebral Disc Disease—Cats.
N/A
soft bedding and alternate recumbence side ABBREVIATIONS
every 4 hours to avoid bed sores. PRECAUTIONS
• CSF = cerebrospinal fluid.
• Bladder catheterization. Monitor for signs of gastroenteritis, gastric
• CSM = cervical spondylomyelopathy.
• Physical therapy is essential to avoid muscle hemorrhage, and cystitis. A proton pump
• NSAID = nonsteroidal anti-inflammatory drug.
atrophy and ankylosis, and to hasten recovery. inhibitor may be used to minimize the risk of
gastrointestinal bleeding. Suggested Reading
ACTIVITY da Costa RC. Cervical spondylomyelopathy
• Medically treated dogs should have POSSIBLE INTERACTIONS
(wobbler syndrome). Vet Clin North Am
restricted activity for at least 2 months. Do not use corticosteroids in combination
Small Anim Pract 2010, 40:881–913.
• Restriction of activity is also important for with nonsteroidal anti-inflammatory drugs
da Costa RC, Parent JM. Outcome of
the first 2 or 3 months postoperatively to allow (NSAIDs).
medical and surgical treatment in dogs
bone fusion and prevent implant displacement. ALTERNATIVE DRUG(S) with cervical spondylomyelopathy: 104
DIET NSAIDs (all kinds) can be used in dogs with cases. J Am Vet Med Assoc 2008,
Avoid excess of protein, calcium, or caloric only cervical hyperesthesia or mild ataxia. 233:1284–1290.
intake in giant-breed dogs with osseous De Decker SD, da Costa RC, Volk HA, et al.
compression. Current insights and controversies in the
pathogenesis and diagnosis of disc-associated
CLIENT EDUCATION cervical spondylomyelopathy in dogs. Vet
Inform that surgery offers the best chance of FOLLOW-UP
Rec 2012, 171:531–537.
improvement (approximately 80%), but there PATIENT MONITORING Jeffery ND, McKee WM. Surgery for
is a 1–5% risk of significant complications Repeat neurologic evaluation as often as disc-associated wobbler syndrome in the
associated with cervical surgical procedures. needed to monitor response to treatment. dog—an examination of the controversy.
SURGICAL CONSIDERATIONS PREVENTION/AVOIDANCE J Small Anim Pract 2001, 42:574–581.
• Ventral slot—commonly used and • Excessive activity, jumping, and running Martin-Vaquero P, da Costa RC, Drost WT.
recommended for single ventral compressions; should be avoided. Comparison of noncontrast computed
could also be used for two ventral compressions. • Avoid use of neck collars; use a body tomography and high field magnetic
• Dorsal laminectomy—primary indication harness instead. resonance imaging in the evaluation of Great
for dorsal or dorsolateral compressions; can Danes with cervical spondylomyelopathy.
POSSIBLE COMPLICATIONS Vet Radiol Ultrasound 2014, 55:4.
also be used for multiple ventral compres- Recurrence of clinical signs can occur in dogs
sions; hemilaminectomy is an alternative for Provencher M, Habing A, Moore SA, et al.
treated medically or surgically. Evaluation of osseous-associated cervical
lateralized osseous compressions.
• Distraction/stabilization/fusion techniques EXPECTED COURSE AND PROGNOSIS spondylomyelopathy in dogs using
are recommended primarily for single • About 80% of patients improve with surgery. kinematic magnetic resonance imaging. Vet
dynamic ventral compressions, but could be • Approximately 50% of patients improve Radiol Ultrasound 2017, 58:4.
used for multiple compressions. with medical treatment (restricted activity ± Provencher M, Habing A, Moore SA, et al.
• Cervical disc arthroplasty—novel technique corticosteroids) and 25% remain stable. Kinematic magnetic resonance imaging for
that appears safe and as effective as the evaluation of disc-associated cervical
traditional procedures; it can be used for spondylomyelopathy in Doberman
multiple compressions. Pinschers. J Vet Intern Med, 2016 30:4.
• Recurrence rate is approximately 20% with MISCELLANEOUS Author Ronaldo Casimiro da Costa
any surgical technique.
• Fenestration provides a very low success rate ASSOCIATED CONDITIONS
and is not recommended. Dilated cardiomyopathy, hypothyroidism, Client Education Handout
and von Willebrand’s disease are common in available online
Doberman pinscher dogs; these diseases can
Chagas Disease (American Trypanosomiasis)

Client Education
C • Test housemates/littermates of infected
dogs.
BASICS DIAGNOSIS • Take measures to eliminate the insect
OVERVIEW DIFFERENTIAL DIAGNOSIS vector—remove brush, pyrethroid insecticide.
• Caused by hemoflagellate protozoan • Cardiomyopathy. • Alert owner to possible zoonotic risk and
Trypanosoma cruzi. • Congenital heart defect (tricuspid valve potential for sudden death.
• Transmission through contact with infected dysplasia). • Infected female can transfer infection to
feces of the Reduviid (“kissing”) bug, • Myocarditis. offspring.
ingestion of bug vector, through blood • Distemper, other causes of meningo- • Cardiology tests (ECG, echocardiography)
transfusion, or vertical transmission to encephalitis. can identify dogs at risk of developing clinical
offspring. signs or sudden death.
• After multiplication at entry site (5 days
Generally normal.
postinfection [PI]), hematogenous spread to
heart, brain, and other organs. OTHER LABORATORY TESTS
• Maximal parasitemia at 14 days PI; • Cardiac troponin I—elevation indicates
associated with acute myocarditis and (less myocardial damage. MEDICATIONS
commonly) encephalitis. • Serology—presence of T. cruzi serum DRUG(S) OF CHOICE
• Infection becomes subpatent 30 days PI. antibodies (present by 16 days PI) confirms Limited therapeutic options for treating
• Dogs then enter long asymptomatic period infection, but not necessarily clinical disease. infection. Variable clinical response to
(months to years); subset develop cardio- • Tests can cross-react with Leishmania. Benznidazole; treated dogs still develop
myopathy. • Cytology—trypomastigote (blood form) myocardial damage. Other drug protocols
• South and Central America—endemic in occasionally on blood smear, lymph node under investigation.
humans and pets; infected animals are aspirate, abdominal effusion, or buffy coat
sentinels for human risk. during period of high parasitemia.
• United States—in southern states with • Cytology—amastigote (intracellular form)
infected vectors and reservoir hosts (raccoons, identified on lymph node aspirate or impression.
opossums, armadillos, mice, rats, squirrels). • PCR—detect parasite DNA in blood or FOLLOW-UP
tissue with high specificity; low sensitivity in • Monitor positive dogs for clinical disease.
SIGNALMENT • Prognosis unknown for asymptomatic,
chronic stage if parasite levels low.
• Dogs of any age, breed: positive dogs.
∘∘ Acute infection—more severe in dogs IMAGING • Dogs with clinical signs or arrhythmias
<2 years old. • Thoracic radiography—cardiomegaly, have guarded prognosis.
∘∘ Chronic infection—adults. pulmonary edema, pleural effusion.
∘∘ Sporting breeds and outdoor-housed dogs • Echocardiography—dilation of heart
more likely to be in contact with vectors or chambers, systolic dysfunction.
reservoir host.
• Cats—more recent evidence of infection MISCELLANEOUS
and organ pathology. ECG
ZOONOTIC POTENTIAL
• Supraventricular and ventricular arrhythmias,
SIGNS • Public health concern with limited treat-
atrioventricular block (any degree), bundle
General Comments
ment options.
branch block.
• Risk of human acquiring infection directly
Two syndromes can be difficult to distin- • Ambulatory ECG (Holter) to document
guish—acute myocarditis/encephalitis and from infected dog is low, but infected animal
abnormalities.
chronic arrhythmias and myocardial indicates presence of infected vectors or
dysfunction. PATHOLOGIC FINDINGS reservoir hosts.
• Acute—diffuse granulomatous myocarditis,
Historical Findings ABBREVIATIONS
myocardial necrosis, parasitic pseudocysts
• Lethargy, weakness. • PI = postinfection.
with intracellular amastigotes.
• Anorexia. • Chronic—lymphoplasmacytic inflamma- Internet Resources
• Abdominal distension (ascites). tion, loss of myocardial fibers, severe https://www.cdc.gov/parasites/chagas
• Cough, dyspnea. interstitial fibrosis.
• Syncope, sudden death.
Suggested Reading
• T. cruzi amastigotes in heart, lymph nodes, Barr SC, Saunders AB, Sykes J. Trypanosomiasis.
• Ataxia, seizures. liver, spleen, brain. In: Sykes J, ed., Canine and Feline
Physical Examination Findings Infectious Diseases. Philadelphia, PA:
• Tachy- or bradyarrhythmia. Saunders Elsevier, 2013, p. 760.
• Heart murmur. Meyers AC, Hamer SA, Matthews D, et al.
• Congestive heart failure (tachypnea, Risk factors and select cardiac characteristics
TREATMENT
dyspnea, ascites). • No currently approved treatment for in dogs naturally infected with Trypanosoma
• Hepatomegaly. cruzi. J Vet Int Med 2019, 33:1695–1706.
T. cruzi.
• Generalized lymphadenopathy (acute). Author Ashley B. Saunders
• Manage heart failure (see Congestive Heart
• Neurologic—weakness, ataxia, seizures Consulting Editor Amie Koenig
Failure, Left-Sided; Congestive Heart Failure,
(acute). Right-Sided). Acknowledgment The author and book
CAUSES & RISK FACTORS • Tachyarrhythmias—anti-arrhythmic drugs. editors acknowledges the prior contribution
Lives in or travels to endemic area. • Bradyarrhythmias—pacemaker of Stephen C. Barr.
implantation.
Chediak-Higashi Syndrome
IMAGING ABBREVIATIONS
N/A • ADP = adenosine diphosphate. C
• ATP = adenosine triphosphate.
BASICS DIAGNOSTIC PROCEDURES
Advanced platelet function testing or electron • cGMP = cyclic guanosine monophosphate.
OVERVIEW microscopy of platelets may provide Suggested Reading
• Autosomal recessive inherited disorder of additional evidence for diagnosis. August JR. Consultations in Feline Internal
Persian cats characterized by abnormalities in Medicine, 2nd ed. Philadelphia, PA:
cellular morphology and pigment formation. Saunders, 1994.
• Large intracytoplasmic granules in Colgan SP, Hull-Thrall MA, Gasper PW,
circulating leukocytes and melanocytes et al. Restoration of neutrophil and platelet
formed by fusion of preexisting granules. TREATMENT function in feline Chediak-Higashi
• Storage pool deficiency of adenosine • Provide ascorbic acid (vitamin C) to increase
syndrome by bone marrow transplantation.
diphosphate (ADP), adenosine triphosphate cyclic guanosine monophosphate (cGMP)
Bone Marrow Transplant 1991, 7:365–374.
(ATP), magnesium, and serotonin results concentration and to improve cell and platelet
Cowles BE, Meyers KM, Wardrop KJ, et al.
from lack of platelet-dense granules. function (no controlled studies in cats).
Prolonged bleeding time of Chediak-
• Prolonged bleeding from trauma, venipunc- • Transfusion of platelet-rich plasma or fresh
Higashi cats corrected by platelet transfu-
ture, or minor surgery occurs because of whole blood from healthy cats will temporarily
sion. Throm Haemost 1992, 67:708–712.
impaired platelet aggregation and release normalize bleeding time in affected indivi-
Author Kenneth S. Latimer
reaction. duals.
• Normal coagulation times. • Experimentally, bone marrow transplanta-
• Depressed chemotaxis. tion has restored neutrophil and platelet
• No change in rates of infection. function in cats, but is impractical for general
• Mildly depressed neutrophil count, but clinical use.
within reference interval.
• In humans, it is associated with one of eight
mutations in the LYST gene.
SIGNALMENT MEDICATIONS
• Persian cats with dilute smoke-blue coat DRUG(S) OF CHOICE
color and yellow-green irises (and white tigers). Ascorbic acid (100 mg PO q8h).
• Not reported in dogs.
SIGNS
INTERACTIONS
Historical Findings None
Prolonged bleeding from trauma, venipuncture,
or minor surgery.
• Red fundic reflex (lack of choroidal FOLLOW-UP
pigment).
• Dilute smoke-blue coat color and yellow- PATIENT MONITORING
green irises. None
• Photophobia (blepharospasm and epiphora) PREVENTION/AVOIDANCE
in bright light. Advise owner of potential for prolonged
CAUSES & RISK FACTORS bleeding after trauma, venipuncture, or minor
Genetic disease. surgery.
Prolonged bleeding time.
DIAGNOSIS Normal lifespan, with avoidance of trauma or
other situations that may predispose to
bleeding.
Lysosomal storage diseases (e.g., mucopoly-
saccharoidoses), therapy with antiplatelet
agents (e.g., aspirin, clopidogrel), other
inherited platelet function defect.
CBC/BIOCHEMISTRY/URINALYSIS MISCELLANEOUS
Romanowsky-stained blood smear— PREGNANCY/FERTILITY/BREEDING
leukocytes, especially neutrophils, contain • Provide genetic counseling to eliminate
pink to magenta cytoplasmic inclusions Chediak-Higashi syndrome from animals
approximately 2 μm in diameter. used for breeding.
OTHER LABORATORY TESTS • Neuter affected and carrier animals or
None advise owner not to breed.
Chemodectoma
OTHER LABORATORY TESTS • Aortic body tumors—animals treated with
C N/A pericardectomy MST 730 days vs. animals
IMAGING that did not have pericardectomy MST 42
BASICS days. Larger tumors (as determined by tumor
• Thoracic radiography—to evaluate for mass
OVERVIEW in the region of the heart base, pericardial weight to body weight ratio) more likely
• Chemodectomas are tumors arising from effusion, metastatic lesions in the lungs. associated with metastasis.
the chemoreceptor cells (such as in the aortic • Conformal radiation therapy in 1 dog—
• Cervical ultrasound, CT, or MRI—to
body and the carotid body). evaluate for masses arising in the neck. survival >42 months.
• Other names—aortic body tumors, cardiac • Stereotactic body radiation therapy in 6
• Echocardiography—to image mass and
paraganglioma, APUDoma (amine precursor aorta/pulmonary arteries/veins. dogs—tumor reduction by 30–76% in 4
uptake decarboxylase), and glomus body tumor. dogs, 3 dogs alive 408–751 days post
• Aortic body tumors more common (80–90%) DIAGNOSTIC PROCEDURES radiation therapy, 2 dogs died suddenly at
in dogs than carotid body tumors (10–20%). • Biopsy of mass. 150 days and 294 days post radiation therapy,
• ECG—if evidence of arrhythmia, may see and 1 dog died of unrelated causes 1228 days
SIGNALMENT low-amplitude QRS complexes with post radiation.
• Rare in cats. pericardial or pleural effusion, or electrical
• Dogs—age 6–15 years. alternans with pericardial effusion.
• Any breeds—but brachycephalic breeds
predisposed, especially boxers, Boston terriers,
English bulldogs, and German shepherd dogs. MISCELLANEOUS
• Males predisposed for aortic body tumors; PREGNANCY/FERTILITY/BREEDING
no sex predilection for carotid body tumors. TREATMENT
It is not recommended to breed animals with
SIGNS Aortic Body Tumors cancer. Chemotherapy is teratogenic—do not
• Nonspecific and dependent upon tumor • Surgical removal of mass—if possible. give to pregnant animals.
size and anatomic localization, and can • Subphrenic pericardectomy has been shown
to prolong survival. SEE ALSO
include lethargy, anorexia, weakness, collapse, Pericardial Disease.
coughing, respiratory distress, exercise • Symptomatic pericardiocentesis or thoraco-
intolerance, distended abdomen, vomiting, centesis. ABBREVIATIONS
sudden death. • Conformal radiation therapy or stereotactic • APUD = amine precursor uptake
• Carotid body tumor—may notice neck body radiation therapy—discuss with owners decarboxylase.
mass, regurgitation, dyspnea, Horner’s possible complications including cough, tachy- • MST = median survival time.
syndrome, head tilt, facial nerve paralysis, or arrhythmias, and congestive heart failure. Suggested Reading
laryngeal paralysis. • Palliative thoracoscopic-guided pericardial Kisseberth WC. Neoplasia of the heart. In:
• May be associated with pericardial effusion window. Withrow SJ, Vail DE, Page RL, eds., Small
and cardiac tamponade—muffled heart Carotid Body Tumors Animal Clinical Oncology, 5th ed. Philadelphia,
sounds, poor pulses, tachycardia, tachypnea, Surgical removal if possible—discuss with PA: Saunders, 2013, pp. 700–706.
weak pulses, slow capillary refill time, ascites. owners possibility of postoperative Horner’s Author Rebecca G. Newman
• May be associated with cranial vena cava syndrome and laryngeal paralysis. Consulting Editor Timothy M. Fan
syndrome (edema of head, neck, and forelimbs).
• May be associated with ascites secondary to
Both
right heart failure. Possible role of chemotherapy (doxorubicin)—
• May be associated with pleural effusion—
however, definitive studies are lacking.
decreased lung sounds ventrally, cyanosis.
• Cardiac arrhythmias with pulse deficits.
Chronic hypoxia may play a role in the MEDICATIONS
development of this disease in brachycephalic DRUG(S) OF CHOICE
breeds. • The role of chemotherapy in this disease
has not been published.
• Pharmacologic intervention for cardiac
insufficiency.
DIAGNOSIS
• Other masses located at the heart base (i.e.,
hemangiosarcoma, thymoma, ectopic thyroid FOLLOW-UP
carcinoma, mesothelioma, abscess, and PATIENT MONITORING
granuloma). Serial thoracic radiography or advanced
• Idiopathic pericardial effusion. imaging for monitoring tumor progression
• Pericarditis. and metastasis.
• Cardiomyopathy.
EXPECTED COURSE AND
• Valvular insufficiency.
PROGNOSIS
CBC/BIOCHEMISTRY/URINALYSIS • Carotid body tumors treated with surgery—
Typically normal, but 36% of patients can median survival time (MST) 25.5 months.
have nucleated red blood cells without anemia.
Cheyletiellosis
• Sarcoptes and Notoedres spp. mite infesta- • Milbemycin oxime—2 mg/kg PO once
tion; other fur mites. weekly for 4 weeks. C
• Endocrinopathy. • Moxidectin—subcutaneous injection every
BASICS • Dermatophytosis. 2 weeks for 3 treatments (non-FDA-approved
OVERVIEW • Pediculosis. usage: dogs).
• Contagious parasitic skin disease caused by • Doramectin—subcutaneous injection every
surface-living mites. Usually normal. week for three treatments (non-FDA-approved
• Signs of mild pruritus and scaling resemble usage: dogs).
other more common dermatoses. DIAGNOSTIC PROCEDURES
• Examination of epidermal debris—Cheyle- CONTRAINDICATIONS/POSSIBLE
• Potential zoonosis.
tiella mites are large and can be visualized with INTERACTIONS
• System affected—skin/exocrine.
a hand lens or microscope (10× objective); Prevent ingestion/avoid use of avermectins in
SIGNALMENT scales and hair may be examined under low sensitive dogs (MDR1/ABCB1 gene muta-
• Dogs and cats. magnification; finding mite eggs is diagnostic. tion, collie, sheltie, Australian shepherd, Old
• More severe in young animals. • Mite numbers may be low—concentration English sheepdog)—selamectin may be used
• Cocker spaniels, poodles, and longhaired of debris for examination increases the in these dog breeds.
cats may be inapparent carriers. likelihood of diagnosis; collection of debris:
SIGNS flea combing (most effective), skin scraping,
hair plucking, acetate tape preparation, scale
Historical Findings
collection, and fecal flotation. FOLLOW-UP
• Referred to as “walking dandruff,” because
• Response to insecticide treatment may be • Treatment failure requires a thorough
of the large mite size and excessive scaling.
required to definitively diagnose suspicious reevaluation for other causes of pruritus and
• Prevalence varies by geographic region
cases in which mites cannot be identified. scaling.
owing to mite susceptibility to common
flea-control insecticides and differences in • Reinfestation may indicate contact with an
climate. asymptomatic carrier or the presence of an
• Pruritus—usually absent to mild, but can unidentified source of mites
be severe: hypersensitivity to mite allergens TREATMENT
may develop, producing clinical signs similar • All animals in the same household must be
to infestations with Sarcoptes or Notoedres treated.
mites. • Clip long coats to facilitate treatment. MISCELLANEOUS
• Infestation often suspected only after • Weekly baths to remove scale, followed by
lesions in human beings develop (pseudo- rinses with an insecticide. ZOONOTIC POTENTIAL
scabies). • Lime-sulfur rinses—cats, kittens, dogs, and Pruritic papular rash may develop in human
puppies. beings.
• Routine flea sprays—not always effective: Suggested Reading
• Scaling— diffuse or plaque like; more
severe in chronically infested or debilitated treat all animals in the home before introduc- Hnilica KA, Paterson A. Small Animal
animals. ing a new pet. Dermatology: A Color Atlas and
• Environmental treatment with frequent Therapeutic Guide, 4th ed. St. Louis, MO:
• Lesions—dorsal orientation commonly
noted; head can be affected in cats. cleanings and insecticide sprays—reduces Elsevier, 2017.
• Underlying skin irritation may be
possibility of reinfestation. Saari S, Näreaho A, Nikander S. Canine
• Continue treatment for at least 6–8 weeks Parasites and Parasitic Diseases. London:
minimal.
• Cats may exhibit bilaterally symmetric
to prevent reinfestation from shed eggs. Academic Press, 2019.
• Combs, brushes, and grooming tools— Taylor MA, Coop RL, Wall RL. Veterinary
alopecia, bizarre behavior, head shaking, or
excessive grooming. discard or thoroughly disinfect before reuse. Parasitology. Ames, IA: Wiley-Blackwell, 2016.
Author Guillermina Manigot
CAUSES & RISK FACTORS Consulting Editor Alexander H. Werner
• Partial host specificity—dogs: C. yasguri. Resnick
Cats: C. blakei. Rabbits: C. parasitovorax.
• Cheyletiellosis should be considered in MEDICATIONS
every animal that shows scaling, with or DRUG(S) OF CHOICE
without pruritus. • Amitraz rinses—dogs only; 2-week intervals
• Contagion by direct contact or by fomites. for 4 applications.
• Common sources of infestation—animal • Fipronil—2-week intervals for 1–4 applications.
shelters, breeders, and grooming facilities. • Ivermectin—300 μg/kg PO/SC 3 times at
• Adult female mites may survive in the 2-week intervals; dogs and cats >3 months
environment up to 10 days. old; pour-on forms have shown efficacy in
• Eggs can be found on shed hair. cats (500 μg/kg 2 times at 2-week intervals;
non-FDA-approved usage; see Contraindications/
Possible Interactions).
• Selamectin—apply every 2–4 weeks for
DIAGNOSIS 3 applications (non-FDA-approved usage).
• Imidacloprid/moxidectin—apply every
DIFFERENTIAL DIAGNOSIS 2 weeks for 3 applications (non-FDA-
• Keratinization disorders. approved usage); imidacloprid alone: not
• Cutaneous hypersensitivity. effective.
Chlamydiosis—Cats
• Infection often subclinical. PATHOLOGIC FINDINGS
C • Clinical disease—commonly coinfection • Gross—chronic conjunctivitis with
with other organisms, such as feline herpesvirus mucopurulent ocular discharge; minor
BASICS (FHV) and feline coronavirus (FCV). rhinitis with nasal discharge; sometimes lung
DEFINITION Historical Findings changes indicative of pneumonitis.
A chronic respiratory infection of cats caused • Primarily signs of ocular discharge, • Histopathologic (conjunctiva)—an early
by an intracellular bacterium, characterized blepharospasm. intense infiltration of neutrophils; inflamma-
by mild to severe conjunctivitis, mild upper • Mild upper respiratory infection, with tory response changes to lymphocytes and
respiratory signs, and mild pneumonitis. possible sneezing and oculonasal discharge. plasma cells; inclusions detected with special
• Varying degrees of anorexia, lethargy. stains (inclusions invisible with routine H&E
PATHOPHYSIOLOGY
• Lameness possible (uncommon). stains).
• Chlamydophila felis (previously Chlamydia
psittaci var. felis)—a Gram-negative, obligate Physical Examination Findings
intracellular bacterium spread through close • Conjunctivitis—unilateral or bilateral
contact, aerosolization, or genital contact chemosis, blepharospasm, conjunctival and
during parturition. third eyelid hyperemia; serous to mucopurulent TREATMENT
• Replicates on the mucosa of the upper and discharge without keratitis. APPROPRIATE HEALTH CARE
lower respiratory epithelium; produces a • Mild nasal discharge. Generally outpatient.
persistent commensal flora that causes local • Fever.
irritation, resulting in mild upper and lower NURSING CARE
• Dyspnea and cough extremely unlikely;
respiratory signs and conjunctivitis; can also • Clean eyes and nose as necessary with warm
rales with pneumonitis.
colonize the mucosa of the gastrointestinal water or saline.
and reproductive tracts. CAUSES & RISK FACTORS • Provide access to steam, such as in a bath-
• Incubation period—7–10 days (longer than • Concurrent infections with other respira- room, to clear secretions.
that of other common feline respiratory tory pathogens (FHV, FCV, Bordetella • Provide palatable, soft foods; warming food
pathogens). bronchiseptica, Mycoplasma felis). can improve cat’s olfaction.
• Lack of vaccination. • Generally does not require other supportive
SYSTEMS AFFECTED • Multicat facilities, especially adoption therapy (e.g., fluids), unless complicated by
• Gastrointestinal—cat: infection without shelters and breeding catteries. concurrent infections.
clinical disease; other species: may have • Stress.
clinical gastroenteritis. ACTIVITY
• Presence of asymptomatic shedders.
• Ophthalmic—acute or chronic conjunctivi- • Quarantine affected cats from contact with
tis, unilateral often progresses to bilateral. other cats.
• Reproductive—infection without clinical • Do not allow affected cats to go outside.
disease. DIET
• Respiratory—mild rhinitis, bronchitis, and DIAGNOSIS • No restrictions.
bronchiolitis. DIFFERENTIAL DIAGNOSIS • Special diets—to entice anorectic cats to
GENETICS • Feline herpesvirus infection—short incuba- resume eating.
None tion period (4–5 days), rapid bilateral conjuncti- CLIENT EDUCATION
vitis, severe sneezing, and ulcerative keratitis. Inform clients of the causative organism, the
INCIDENCE/PREVALENCE • Feline calicivirus infection—short
• Incidence of clinical disease—sporadic; anticipated chronic course of disease, and the
incubation period (3–5 days), ulcerative opportunity to vaccinate other cats before
outbreaks of respiratory disease may occur, stomatitis, and potentially pneumonia.
especially in multicat facilities. exposure.
• Mycoplasma felis.
• Prevalence of C. felis in the feline popula-
tion: ~5–10% chronically infected. CBC/BIOCHEMISTRY/URINALYSIS
Leukocytosis possible.
Worldwide IMAGING MEDICATIONS
Thoracic radiographs—consolidation of lung
SIGNALMENT DRUG(S) OF CHOICE
tissue with pneumonia.
• Ophthalmic ointments—usually beneficial;
Species DIAGNOSTIC PROCEDURES oxytetracycline 3-4 times daily for 3 weeks;
• Cat • PCR—preferred; best sensitivity; submit preparations with polymyxin may be
• Human conjunctival swab in a sterile red top tube irritating for cats; alternatively erythromycin
Breed Predilections with a small amount of sterile saline. or fluoroquinolone ointment; resistant to
None • Culture—obtain conjunctival swab with bacitracin, neomycin, gentamicin.
Mean Age and Range vigorous exfoliation and submit on ice within • Systemic antibiotics—tetracyclines are
Usually cats >8 weeks and <1 year of age; any 24 hours in special transport media such as antibiotic of choice; doxycycline (10 mg/kg
age of cat possible. 2-sucrose-phosphate (2-SP). PO q24h or 5 mg/kg PO q12h for 4 weeks to
• Conjunctival cytology—characteristic prevent recrudescence); amoxicillin-clavulanate
Predominant Sex intracytoplasmic basophilic inclusions may be (20–25 mg/kg PO q12h) as alternative for
None seen with Giemsa staining early in disease. young kittens.
SIGNS • Serum antibody titers—limited diagnostic
CONTRAINDICATIONS
value.
General Comments Tetracyclines—risk for esophagitis; may affect
• ELISA kits—variable sensitivity and
• Commonly associated with feline growing teeth of young kittens.
specificity.
conjunctivitis.
(continued) Chlamydiosis—Cats
PRECAUTIONS • If entire course of antibiotics are not SEE ALSO
Colonies/shelters/breeding catteries—all cats completed, persistently infected cats can • Conjunctivitis—Cats. C
may have to be treated; treatment should be become asymptomatic shedders. • Feline Calicivirus Infection.
continued for 4 weeks. • Coinfections increase morbidity. • Feline Herpesvirus Infection.
EXPECTED COURSE AND • Feline (Upper) Respiratory Infections.
None • Mycoplasmosis.
PROGNOSIS • Ophthalmia Neonatorum.
ALTERNATIVE DRUG(S) • Without treatment, tends to be chronic,
None lasting for several weeks or months. ABBREVIATIONS
• Prognosis good with appropriate antibiotic • 2-SP = 2-sucrose-phosphate.
therapy. • FCV = feline calicivirus.
• Improvement in 1–2 days with therapy; 28 • FHV = feline herpesvirus.
days of treatment needed to clear organism. INTERNET RESOURCES
FOLLOW-UP • Look for coinfections if not improving as http://www.abcdcatsvets.org/
PATIENT MONITORING expected. chlamydia-chlamydophila-felis
Monitor for improved health as treatment
Suggested Reading
proceeds.
Hartmann AD, Hawley J, Werckenthin C,
PREVENTION/AVOIDANCE et al. Detection of bacterial and viral
Vaccines MISCELLANEOUS organisms from the conjunctiva of cats with
• Both inactivated and modified live vaccines ASSOCIATED CONDITIONS conjunctivitis and upper respiratory tract
available. Affected cats may be concurrently infected disease. J Feline Med Surg 2010;
• Vaccines do not prevent infection; rather, with FHV or FCV, especially in multicat and 12:775–782.
they reduce severity and duration of clinical breeding facilities. Scherk MA, Ford RB, Gaskell RM, et al.
disease. 2013 AAFP Feline Vaccination Advisory
AGE-RELATED FACTORS Panel Report. J Feline Med Surg 2013;
• American Association of Feline Primarily a disease of young cats.
Practitioners—noncore vaccine; for at-risk 15:785–808.
cats, give a single vaccination at initial visit as ZOONOTIC POTENTIAL Sykes JE. Pediatric feline upper respiratory
early as 9 weeks of age, repeat in 3–4 weeks; C. felis can infect humans, especially immuno- disease. Vet Clin North Am Small Anim
revaccinate annually where C. felis is endemic. compromised individuals; limited number of Pract 2014; 44:331–342.
• Adverse vaccine reactions—mild clinical reports of mild conjunctivitis in humans Sykes JE, Greene CE. Chlamydial infections.
disease with modified live vaccines in small transmitted from infected cats. In: Greene CE, ed., Infectious Diseases of
percentage of vaccinated cats. the Dog and Cat, 4th ed. St. Louis, MO:
Environmental Management • Endemic breeding catteries—treat all cats
Author Sara E. Gonzalez
• Quarantine affected cats by >4 ft perimeter. with doxycycline for at least 4 weeks; then
• Practice appropriate hygiene and beware of vaccinate.
fomites. • Role of C. felis as a pathogen during
• C. felis readily inactivated with common pregnancy—unclear; can colonize the
Fred W. Scott.
disinfectants. reproductive mucosa; severe ophthalmia
neonatorum can occur in neonatal kittens
POSSIBLE COMPLICATIONS infected at or shortly after birth.
• If kittens are affected <2 weeks of age, Client Education Handout
eyelids may need to be surgically opened to SYNONYMS available online
allow for drainage of purulent material Feline pneumonitis.
(ophthalmia neonatorum).
Chocolate Toxicosis
SIGNALMENT OTHER LABORATORY TESTS
C Species • Methylxanthine assay—rarely necessary as
• Dogs most frequently poisoned based on
history and clinical signs usually sufficient for
BASICS diagnosis; can be performed on stomach
proximity to methylxanthine products and
DEFINITION propensity for dietary indiscretion leading to contents, plasma, serum, urine, or liver.
• Chocolate, derived from the seed of the excessive ingestion. • Cats rarely affected. DIAGNOSTIC PROCEDURES
Theobroma cacao plant, contains the naturally • ECG monitoring—sinus tachycardia,
occurring methylxanthine alkaloids theobromine Breed Predilections
• Small dogs may be at higher risk due to
VPCs, and ventricular tachyarrhythmias.
and caffeine. • Excessive intake can lead to • Blood pressure monitoring.
dose-dependent gastroenteric, cardiac, and smaller body weight relative to amount of
neurologic toxicosis. • Theobromine is the largest chocolate consumed. • Breeds prone to PATHOLOGIC FINDINGS
fraction of methylxanthines in chocolate dietary indiscretion, such as Labrador retrievers. • Presence of chocolate in GI tract. • Nonspecific
products; lower concentration of caffeine is SIGNS gastroenteritis. • No distinctive microscopic lesions.
present (Table 1). Other sources of methylxan-
Historical Findings
thines include coffee, tea, diet pills, over-the-
• History of ingestion. • Evidence of chewed
counter (OTC) stimulants, and herbal medications.
packaging. • Vomiting and diarrhea—vomit TREATMENT
PATHOPHYSIOLOGY often contains evidence of chocolate and may
• Variably absorbed orally (caffeine <1 hour; be first sign noted. • Early restlessness and APPROPRIATE HEALTH CARE
theobromine 10 hours), metabolized by liver, hyperactivity. • Polydipsia. • Emesis in stable patients considered low risk for
undergo enterohepatic recirculation; metabo- aspiration; chocolate is slowly absorbed from a
Physical Examination Findings dog’s stomach, so emesis may be rewarding up to
lites primarily excreted via urine and may be
• Physical exam may be normal after recent
reabsorbed from urinary bladder. • Estimated 6–8 hours after ingestion. • Gastric lavage with
ingestion (<1–2 hours). • Vomiting. • Diarrhea. cuffed tube in symptomatic patients with
theobromine and caffeine half-lives in dogs
• Restlessness and hyperactivity. • Panting. large-volume ingestions once stabilized.
17.5 hours and 4.5 hours, respectively.
• Polyuria/polydipsia. • Dehydration. • Activated charcoal may not be necessary with
• Methylxanthines inhibit phosphodiesterase
• Tachycardia. • Cardiac arrhythmias such lower-dose exposures or in cases where most of the
to increase intracellular cyclic adenosine
as VPCs. • Hypertension. • Hyperthermia. chocolate was recovered by induction of vomiting
monophosphate (cAMP), stimulate catechola-
• Tremors. • Hyperreflexia and muscle or gastric lavage; monitor electrolytes for hyperna-
mine release, and increase intracellular calcium,
rigidity. • Seizures. • Advanced signs with tremia if giving multiple doses of activated
which results in vasoconstriction, increased
severe toxicosis—cardiac failure, weakness, charcoal. • IV fluid therapy to correct dehydra-
myocardial and skeletal muscle contractility,
cyanosis, coma, and death. • Death—12–48 tion, promote urinary excretion of methylxan-
and CNS stimulation. • Toxic dosages:
hours after ingestion. thines, and avoid hypernatremia; SC fluids may
◦ Theobromine—LD50 (dog) 250–500 mg/kg;
LD50 (cat) 200 mg/kg. Mild signs (agitation, CAUSES suffice with lower-dose exposures; potassium may
vomiting, diarrhea): 20 mg theobromine/kg. Excessive ingestion of chocolate and other be supplemented in fluids, if needed. • Control
Moderate signs (tachycardia): 40–50 mg methylxanthine products. hyperthermia. • Urine voiding every 4 hours or
theobromine/kg. Severe signs (seizures): 60 mg RISK FACTORS urinary catheterization may reduce urinary
theobromine/kg. ◦ Caffeine—LD50 (dog) 140 • Access to chocolate, which is palatable and bladder resorption. • GI support as needed
mg/kg; LD50 (cat) 80–150 mg/kg. Clinical attractive to dogs, often readily available, and (see Medications). • Control hyperactivity and
signs: >15 mg caffeine/kg. Moderate signs: >25 unprotected in homes and kitchens. • Dogs agitation, tremors, seizures (see Medications).
mg caffeine/kg. Cardiotoxic signs: >50 mg with preexisting heart disease may be more • Treat tachycardia with beta blockers, if sedation
caffeine/kg. • Several aids to assess canine risk sensitive to cardiac effects. not effective; treat arrhythmias with anti-arrhyth-
from chocolate can be found online—see mic drugs as appropriate (see Medications).
Internet Resources. NURSING CARE
SYSTEMS AFFECTED Fluid therapy used to correct electrolyte
• Cardiovascular—tachycardia, hypertension, disturbances and dehydration and to enhance
DIAGNOSIS excretion of methylxanthines.
ventricular premature contractions (VPCs),
other tachyarrhythmias, bradycardia (rare). DIFFERENTIAL DIAGNOSIS
ACTIVITY
• Gastrointestinal (GI)—vomiting, diarrhea, • Convulsant or excitatory alkaloids—
Avoid stress and limit activity until recovered.
regurgitation. • Metabolic—hypokalemia, strychnine, amphetamine, nicotine,
hyperthermia, dehydration. • Nervous— 4-aminopyridine. • Convulsant pesticides DIET
agitation, tremors, seizures, ataxia, muscle such as pyrethroids, organochlorines, • No food until vomiting is controlled.
rigidity, hyperreflexia. • Renal/urologic— bromethalin, zinc phosphide, metaldehyde. • Convalescence—bland, low-fat diet to aid
polyuria, polydipsia. • Respiratory—panting, • Tremorgenic mycotoxins. • Acute psycho- recovery from gastroenteritis and/or pancreatitis.
tachypnea, cyanosis, respiratory failure. genic drugs—LSD, cocaine. • Medications CLIENT EDUCATION
such as phenylpropanolamine, pseudoephed- Warn owners about toxicologic hazards of
INCIDENCE/PREVALENCE rine, tricyclic and selective serotonin reuptake
• Dogs—among 10 most common poisonings chocolate, and advise keeping chocolate out
inhibitor antidepressants. • Cardioactive of reach of dogs.
reported by small animal practices and animal glycosides—Digitalis spp., Nerium oleander.
poison control centers. • More common at • Primary GI, cardiac, or neurologic disease.
holidays when chocolate products readily
available. CBC/BIOCHEMISTRY/URINALYSIS
• Hyperglycemia or hypoglycemia. MEDICATIONS
• Hypokalemia, especially with caffeine
Indoor dogs at risk owing to closer proximity DRUG(S) OF CHOICE
overdose. • Urine may be dilute due to
to chocolate products. • Induce emesis—only if patient is stable
polydipsia.
with low risk of aspiration; apomorphine
(continued) Chocolate Toxicosis

Table 1
C
Comparative concentrations of caffeine and theobromine
Caffeine Source Amount (mg/g) Amount (mg/oz)*

Coffee beans 10–20 284–570
Drip coffee 90–100 mg/6 oz cup 15–20
Cola drinks 30–71 mg/12 oz can 2.5–6
Baking chocolate (unsweetened) 0.8 23
Dark chocolate 0.43–0.8 12–23
Milk chocolate 0.2 6
Cocoa powder (unsweetened) 2.3 70
Guarana 30–50 850–1,400
Caffeine stimulant tablets 50–200 mg/tablet —————
OTC migraine pain control 65 mg/tablet —————
Theobromine Source Amount (mg/g) Amount (mg/oz)
Cacao beans 10–50 300–1500
Baking chocolate (unsweetened) 13–16 370–454
Milk chocolate 1.5–2 42–57
Cacao bean hulls 5–9 142–256
Cacao bean mulch 2–30 57–852
Cocoa powder (unsweetened) 14–29 398–832
* To convert mg/g to mg/oz, multiply by 28.4.
(0.02–0.04 mg/kg IV); hydrogen peroxide 3% ABBREVIATIONS

(1–2 mL/kg PO); do not exceed 50 mL in dogs. • cAMP = cyclic adenosine monophosphate.
• Activated charcoal 1–2 g/kg PO with cathartic • GI = gastrointestinal.
× 1 dose. With large ingestions, repeat activated FOLLOW-UP • OTC = over the counter.
charcoal (no cathartic) q8 up to 24h to prevent PATIENT MONITORING • VPC = ventricular premature contraction.
enterohepatic recirculation. • Hyperactivity— Monitor heart rate, blood pressure, ECG, INTERNET RESOURCES
acepromazine (0.02–0.04 mg/kg IV/IM/SC) or mentation, and temperature closely while • https://www.aspca.org/pet-care/animal-
butorphanol (0.2–0.5 mg/kg IM/IV), with hospitalized. poison-control/apcc-mobile-app
doses repeated/titrated to effect. • Seizures— • https://www.merckvetmanual.com/en-ca/
diazepam (0.5–1 mg/kg IV) or phenobarbital toxicology/food-hazards/chocolate
Warn owners about toxicologic hazards of
(2–6 mg/kg IV) as needed to effect. • Tremors—
chocolate and advise keeping chocolate out of Suggested Reading
diazepam (0.5–1 mg/kg IV) or methocarbamol
reach of dogs. Dolder LK. Methylxanthines. In: Peterson M,
(50–220 mg/kg IV slowly, up to daily dose of
330 mg/kg). • Vomiting—maropitant (1 mg/kg POSSIBLE COMPLICATIONS Talcott P, eds., Small Animal Toxicology,
SC or IV) q24h as needed. • Persistent ventricular • Aspiration can occur rarely secondary to 3rd ed. St. Louis, MO: Elsevier Saunders,
tachycardia—metoprolol (0.04–0.06 mg/kg IV), vomiting. • Pancreatitis can occur in some 2013, pp. 647–652.
esmolol (initial loading dose 0.25–0.5 mg/kg IV patients that consume chocolate. Hoffberg JE. Chocolate and caffeine. In:
slowly over 1–2 min, followed by CRI at Hovda LR, Brutlag AG, Osweiler G,
10–200 μg/kg/min) or propranolol (0.02– Peterson K. The 5 Minute Veterinary
• Expected course—12–36 hours, up to 72
0.06 mg/kg IV); metoprolol or esmolol preferred Clinical Companion Consult: Small Animal
hours in severe cases, depending on dosage and
but may be difficult to obtain. • Ventricular Toxicology, 2nd ed. Ames, IA: Wiley-
effectiveness of decontamination and treatment.
arrhythmias (dogs)—lidocaine (2–4 mg/kg IV Blackwell, 2016, pp. 479–484.
• Successfully treated patients—usually recover
followed by 25–100 μg/kg/min IV CRI); Luiz JA, Heseltine J. Five common toxins
completely. • Prognosis—good if prompt oral
lidocaine not recommended in cats. • In rare ingested by dogs and cats. Compend
decontamination occurs, but guarded with
instance of bradycardia—atropine 0.02–0.04 mg/ Contin Educ Pract Vet 2008, 30:578–587.
advanced signs of seizures and arrhythmias.
kg IV/IM/SC; rule out reflex bradycardia from Author Charlotte Flint
hypertension before use. Consulting Editor Lynn R. Hovda
CONTRAINDICATIONS editors acknowledge the prior contribution of
• Do not use epinephrine concurrent with MISCELLANEOUS Gary D. Osweiler.
lidocaine. • Avoid erythromycin and cortico-
steroids, which may reduce excretion of
Methylxanthines cross the placenta and are
methylxanthines. • Do not use lidocaine in
excreted in milk. Client Education Handout
cats due to risk of seizures. available online
SEE ALSO
PRECAUTIONS
• Antidepressant Toxicosis—SSRIs and SNRIs.
Keep patient under observation until
• Metaldehyde Toxicosis.
recovered and treatment no longer needed.
• Poisoning (Intoxication) Therapy.
Cholangitis/Cholangiohepatitis Syndrome
• NS-CCHS—range: 2–17 years; mostly
C middle-aged cats.
BASICS Predominant Sex DIAGNOSIS
• S-CCHS—male cats may be predisposed.
DEFINITION • NS-CCHS—no sex prevalence. DIFFERENTIAL DIAGNOSES
• Cholangitis—bile duct inflammation. • Feline hepatic lipidosis (FHL)—may
• Cholangiohepatitis—inflammation of bile SIGNS coexist; similar enzyme patterns with jaundice
ducts and adjacent liver parenchyma. General Comments but low γ-glutamyl transferase (GGT) unless
• Cholangitis/cholangiohepatitis syndrome • S-CCHS—most severe clinical illness, acute concurrent biliary or pancreatic inflamm-
(CCHS)—more common in cats; histologically onset (often <5 days); abdominal pain, ation.
classified as suppurative (predominant pyrexia; associated with EHBDO and • EHBDO and obstructive cholelithiasis;
neutrophilic inflammation, S-CCHS); cholelithiasis. variable jaundice, increased alkaline
nonsuppurative (lymphocytic, plasmacytic, • NS-CCHS—ill >3 weeks (months to phosphatase (ALP), GGT, transaminase
NS-CCHS); lymphoproliferative (may transition years). activities; increased cholesterol.
to lymphosarcoma); or granulomatous. • Pancreatitis—may reflect cholelithiasis-
Historical Findings
PATHOPHYSIOLOGY initiated CCHS in cats; lipemia, high
Feline CCHS—cyclic illness with chronic
• Antecedent or coexisting conditions—
cholesterol, hyperbilirubinemia; inconsistent
vague signs: lethargy, vomiting, anorexia,
inflammation or obstruction involving high feline pancreatic lipase activity (fPLI);
weight loss; ductopenic cats demonstrate
extrahepatic bile duct (EHBDO) or high fPLI implicates pancreatic inflammation
polyphagia, acholic stools, variable
pancreatic duct (cat), pancreatitis or but also may reflect IBD, pancreatic duct
steatorrhea, reduced uptake of fat-soluble
inflammatory bowel disease (IBD; dog, cat); inflammation/obstruction from cholelithiasis;
substances.
chronic interstitial nephritis (CIN; cat). ultrasound may differentiate.
Physical Examination Findings • Lymphoproliferative disease and lymphoma—
• Bacterial infection may be primary or
• S-CCHS—fever; painful abdomen; ± may involve any enteric segment, mesenteric/
secondary.
jaundice; dehydration; shock. thoracic lymphadenopathy; shares clinical
• Acute or chronic cholangitis—associates
• NS-CCHS—few physical abnormalities features with CCHS; hepatic infiltrates may
with biliary epithelial hyperplasia and
other than variable hepatomegaly; thickened require immunohistochemical characterization
ductular reaction.
intestines with IBD; variable jaundice; rare and clone evaluation to differentiate
• Chronic inflammation—may cause bile duct
abdominal effusion. lymphoproliferative or lymphoma from
dystrophic mineralization or cholelithiasis.
• Ductopenia (cats)—unkempt coat, cyclic NS-CCHS.
• S-CCHS—usually positive bacterial culture
lateral thoracoabdominal alopecia; jaundiced; • Jaundice of septicemia—hyperbilirubi
or bacteria observed cytologically (tissue or
acholic feces (may be cyclic). nemia dominates clinical biochemical
bile); rarely observed in liver tissue, may
observe in gallbladder (GB). CAUSES features, usually disproportionate to
• NS-CCHS—immune-mediated and
magnitude of liver enzyme activity unless
Suppurative CCHS concurrent CCHS.
self-perpetuating, may evolve from S-CCHS. • Infections acquired as result of ductal plate • DPM occur in dogs, cats, esp. longhaired
• Sclerosing or destructive cholangitis—bile malformations (DPM), all phenotypes but
duct involution/destruction, may be immune cats (Persian and Himalayan)—normal or
most commonly choledochal cyst and caroli modestly increased liver enzymes (see
mediated or infectious; leads to loss of small phenotypes.
and medium-sized bile ducts (ductopenia) Ductal Plate Malformations); variable
• Bacterial infection—more common in mild to moderate suppurative or
with “sclerosing” circumferential fibrosis; cats: E coli and Enterococcus most common,
ductopenia is severe lesion. nonsuppurative portal aggregates,
but numerous bacteria (e.g., Enterobacter, cholangitis, or CCHS.
• Pyogranulomatous CCHS—infectious or β-hemolytic Streptococcus, Klebsiella,
immune mechanisms (dog or cat). Actinomyces, Clostridia, Bacteroides); rare CBC/BIOCHEMISTRY/URINALYSIS
• Lymphoproliferative disease—speculated toxoplasmosis; dogs: usually enteric CBC
transition stage of inflammation to opportunists; rare Campylobacter, • Poikilocytes; nonregenerative anemia;
neoplasia. Salmonella, Leptospirosis, others. anemia of chronic disease; Heinz body
SYSTEMS AFFECTED • Aerobic infections commonest, poly hemolysis.
• Hepatobiliary—liver and biliary system. microbial infections in ~30%. • S-CCHS—variable neutrophilic leukocytosis,
• Gastrointestinal (GI)—pancreas and • May represent sequela to intermittent left shift, toxic neutrophils; NS-CCHS—may
intestines. mechanical bile flow stasis or EHBDO; DPM be normal; lymphoproliferative disorder or
with cholelithiasis most common associated lymphoma may have lymphocytosis ± abnormal
disorder. cell morphology.
NS-CCHS—most common chronic liver
disorder in cats. Nonsuppurative CCHS Serum Biochemistry
Concurrent disorders—cholecystitis, • Consistent findings—high alanine
SIGNALMENT
cholelithiasis, pancreatitis, EHBDO, IBD aminotransferase (ALT), aspartate aminotrans-
Species (dogs, cats); CIN (cats). ferase (AST), ALP, variable GGT.
Cat (common), dog (uncommon). • Variable findings—high total serum bile
RISK FACTORS
Breed Predilections • S-CCHS—EHBDO; cholelithiasis; DPM; acids, bilirubin, cholesterol: depends on
Possibly Himalayan, Persian, Siamese cats. other causes of cholestasis; infections severity and extent of cholestasis, coexistent
Mean Age and Range elsewhere (dental, splenic abscess, pyelo- illness, liver dysfunction, cholelithiasis,
• S-CCHS—range: 0.4–16 years; mostly nephritis). DPM-associated hepatic fibrosis.
young to middle-aged cats. • Feline NS-CCHS—IBD, pancreatitis,
EHBDO, cholelithiasis, CIN; may evolve
from chronic intermittent S-CCHS.
(continued) Cholangitis/Cholangiohepatitis Syndrome

OTHER LABORATORY TESTS allows biopsy of multiple liver lobes, pancreas, • NS-symptomatic cats—fluid therapy as
• Species-specific PLI—may be high with aspiration collection of bile. necessary; if jaundiced: vitamin K1 (0.5– C
pancreatitis, enteritis, or cholelith occlusion • In EHBDO—not recommended, see 1.5 mg/kg SC/IM q12h for 3 doses) before
of bile duct ampulla in cats. Laparotomy. invasive diagnostics; cats with CCHS may
• Vitamin B12—low values indicate small Laparotomy need blood transfusion consequent to surgery
bowel malabsorption, exocrine pancreatic • Esp. if suspected EHBDO or choleliths in
or biopsy.
disease, chronic oral antimicrobials (dysbiosis). CBD or GB. • Polyionic fluids—with B-soluble vitamins
• Coagulation tests—variable results; • Permits inspection and flushing of
(2 mL/L), KCl, and K phosphate if refeeding
prothrombin time most sensitive for vitamin extrahepatic biliary conduits; biliary syndrome possible; avoid dextrose supplements
K1–induced coagulopathy. decompression and biliary enteric anastomosis. unless hypoglycemia (see Hepatic Lipidosis).
• T4—rules out hyperthyroidism as cause of • May be preferable approach in cats with Outpatient Management
increased liver enzyme activity in cats. CCHS as allows biopsy of liver, biliary • S-CCHS—after acute crisis managed.
IMAGING structures, pancreas, intestines, lymph nodes, • NS-CCHS—after resolution of acute crisis,
• Thoracic radiography—sternal lympha bile collection. provide lifelong immunomodulation (if no
denopathy may reflect abdominal Tissue Sampling bacteria observed or cultured), antioxidants,
inflammation or lymphoma, general lympha- If NS-CCHS suspected, also biopsy bowel, hepatoprotectants.
denopathy suggests lymphoma. pancreas, and suspicious lymph nodes. ACTIVITY
• Abdominal radiography—normal to large Restricted while symptomatic.
liver in NS-CCHS; mineralized choleliths or Bile and Tissue Cultures
biliary structures in S-CCHS or NS-CCHS. • Aerobic and anaerobic bacterial cultures— DIET
• Abdominal US—normal to large liver; thick of liver, bile, any choleliths (crushed); bile Nutritional support—avoid FHL in cats by
extrahepatic bile duct or GB wall if choledochitis sample should include particulate debris feeding balanced high-protein, high-calorie
or cholecystitis; echogenic intraluminal debris; (empty GB to collect mucin-laden bile: site of feline diet; supplement water-soluble
choleliths; focal parenchymal lesions (abscess, bacterial biofilm). vitamins; antigen-restricted diet if
infiltrates: inflammation, neoplasia); lympha • If cholecystectomy done—scrape portion of concurrent IBD; fat-restricted diet if
denopathy suggests pancreatic, liver, intestinal GB wall and cut section of GB wall for culture. steatorrhea due to chronic EHBDO or
inflammation or neoplasia; hepatic parenchymal • Put bile, GB wall, crushed cholelith, liver in severe ductopenia or chronic pancreatitis
hyperechogenicity (concurrent FHL, fibrosis); same culture transport medium. causing maldigestion; may require feeding
hypoechogenicity (inflammation); cysts (DPM, Molecular Genetics tube; rarely require parenteral nutrition
cystadenoma). Note: no US lesions apparent in Genetic test for feline polycystic disease may (may provoke FHL).
some animals with CCHS. be appropriate if DPM diagnosis, especially if CLIENT EDUCATION
DIAGNOSTIC PROCEDURES breeding animal. Emphasize chronic nature of NS-CCHS and
PATHOLOGIC FINDINGS requirement for lifelong therapy.
Fine-Needle Aspiration Cytology
• Hepatic aspiration—for culture and • S-CCHS—normal or swollen liver, sharp or SURGICAL CONSIDERATIONS
diagnosis of FHL; cytology may reveal blunt edges, focal discolorations; may note • Cholecystectomy—if cholecystitis.
bacteria not visualized by light microscopy of erythematous, necrotic, or thick-walled GB; • Cholecystoenterostomy—may be necessary
biopsy sections. Note: cytology is diagnostic peripancreatic steatonecrosis or fat saponi for some causes of EHBDO; if choleliths in
for FHL but unreliable for diagnosis of fication (pancreatitis); perihepatic and GB: perform cholecystectomy.
NS-CCHS; hepatocyte vacuolation common peripancreatic lymphadenopathy; EHBDO:
in ill cats, may implicate FHL as primary may observe choleliths or cystic lesions (DPM)
process when consequence of primary hepatic or neoplastic mass lesions.
• NS-CCHS—variable liver size, normal to
disease. MEDICATIONS
• Cholecystocentesis—may disclose firm texture; sharp or blunt margins; variable
suppuration, bacteria, trematode eggs, or surface irregularity; choleliths or cystic lesions DRUG(S) OF CHOICE
neoplasia. (DPM phenotypes). Antibiotics: S-CCHS
• If concurrent FHL—pale yellow friable • Bactericidal—against enteric opportunists;
Percutaneous Biopsy parenchyma, liver floats in formalin.
• US-guided core-needle biopsy—small initial combination of ticarcillin or clavamox
sample size may misdiagnose CCHS; need with enrofloxacin and metronidazole
min 15 portal triads for accuracy; if 18-G (7.5–15 mg/kg PO q12h; low dose if
core needle used, collect min 4 samples. jaundiced).
• Inaccuracy with needle biopsy in feline TREATMENT • Modify initial empiric antimicrobials based
CCHS reflects biopsy of single liver lobe in on culture and sensitivity reports; resistant
APPROPRIATE HEALTH CARE enterococcus may require vancomycin
syndrome with differential lobe involvement
or small sample size. Inpatient Management (10 mg/kg q12h IV slow infusion for
• Postbiopsy complications—esp. cats: • S-CCHS with acute febrile illness, painful 7–10 days).
collapse due to vasovagal response; biliary abdomen, left-shifted leukogram—hydration Immunomodulation: NS-CCHS
trauma; cats and tiny dogs: unintentional support, “best guess” bactericidal antimicro • Glucocorticoids—prednisolone (dogs:
sampling of nonhepatic tissues. bials: initially based on cytology and Gram 2 mg/kg/day prednisone or prednisolone;
stain or start trimodal antibiotics, esp. if cats: 2–4 mg/kg/day prednisolone only) for
Laparoscopy EHBDO or cholecystitis suspected. Antibiotics
• Permits direct visualization of GB, common 14–21 days, taper to lowest effective
essential before surgery; continue antibiotics ≥4 alternate-day dose based on ALT and clinical
bile duct (CBD), porta hepatis, pancreas, weeks with choleretic therapy until enzymes
perihepatic and peripancreatic lymph nodes; signs.
normalize or signs resolve (see Medications).
Cholangitis/Cholangiohepatitis Syndrome (continued)
• Metronidazole—used for cell-mediated concentrations to guide need for chronic

C immunomodulation, antiendotoxin and supplementation.
antibacterial effects, esp. for IBD; as chronic CONTRAINDICATIONS
bacterial involvement possible in feline MISCELLANEOUS
Adjust drug dosages with regard to liver
NS-CCHS, chronic antibiotic treatment may function and cholestasis. Caution with ASSOCIATED CONDITIONS
be beneficial. metronidazole to avoid neurotoxicity—if • Pancreatitis.
• Cats with confirmed ductopenia— jaundiced use 7.5 mg/kg PO BID. • Hepatic lipidosis.
aggressive immunomodulation; do not use • DPM.
azathioprine; clinical experience suggests • Lymphosarcoma.
combination of prednisolone, metronidazole • Lymphoproliferative disease.
with pulsed methotrexate (see below) or • Cholangiocarcinoma—may develop in
chlorambucil 1–2 mg per cat, load q24h for 3 FOLLOW-UP some cats with chronic NS-CCHS or DPM.
days then every 3 days. PATIENT MONITORING SEE ALSO
• Methotrexate protocol feline destructive or • S-CCHS—follow body temperature, CBC, • Bile Duct Obstruction (Extrahepatic).
sclerosing NS-CCHS: 0.4 mg total dose given biochemical profile initially q7–14 days; • Cholecystitis and Choledochitis.
in 3 divided doses on 1 day (0.13 mg total at continue antibiotics until clinical features • Cholelithiasis.
0, 12, and 24h), repeated at 7–10-day normalize; if DPM may require lifelong • Ductal Plate Malformation (Congenital
intervals), PO/IV/IM (parenteral routes antimicrobials. Hepatic Fibrosis).
require 50% dose reduction); concurrently • Animals with intrahepatic cholelithiasis and • Hepatic Lipidosis.
provide folate (folinic acid) 0.25 mg/kg daily. S-CCHS require long-term antibiotics, UDCA, • Inflammatory Bowel Disease.
If lymphoproliferative or neoplastic infiltrates, high-dose SAMe, and monitoring for • Pancreatitis—Cats.
use chemotherapy protocols developed for recurrent sepsis, stone migration (e.g., CBD, • Pancreatitis—Dogs.
enteric lymphoma. EHBDO).
• NS-CCHS—initially monitor enzymes ABBREVIATIONS
Antioxidants
and bilirubin q7–14 days, then monthly • ALP = alkaline phosphatase.
• Vitamin E (α-tocopherol acetate)—
for 3 months to judiciously adjust immuno • ALT = alanine aminotransferase.
10 IU/kg), using oral water-soluble form in
modulatory protocol, then quarterly. • AST = aspartate amino transferase.
chronic EHBDO or ductopenia (fat
• Serum bile acid measurements complicated • CBD = common bile duct.
malabsorption).
by ursodeoxycholic acid administration and • CCHS = cholangitis/cholangiohepatitis
• S-adenosylmethionine (SAMe)—20 mg/kg/
superfluous in circumstance of hepatobiliary syndrome.
day enteric-coated tablet PO 2h before
jaundice • CIN = chronic interstitial nephritis.
feeding; benefits include anti-inflammatory
influence; high dose for glutathione choleresis: PREVENTION/AVOIDANCE • EHBDO = extrahepatic bile duct
40 mg/kg/day. • Control IBD. obstruction.
Other • If S-CCHS in animals with DPM— • FHL = hepatic lipidosis.
• Ursodeoxycholic acid (UDCA)—10– manage long term with appropriate anti • fPLI = feline pancreatic lipase activity.
15 mg/kg/day PO divided, given with food biotics (see Ductal Plate Malformation). • GB = gallbladder.
for best bioavailability; provides immuno • If choleliths in CBD or GB—surgically • GGT = γ-glutamyltransferase.
modulatory, hepatoprotectant, choleretic, intervene: cholecystectomy if GB choleliths; • GI = gastrointestinal.
antifibrotic, antioxidant effects; in immune- flushing CBD free of lithic material essential • IBD = inflammatory bowel disease.
mediated NS-CCHS with developing if EHBDO. • NS-CCHS = nonsuppurative CCHS.
ductopenia, use is controversial based on POSSIBLE COMPLICATIONS • SAMe = S-adenosylmethionine.
work in humans and animal models of • S-CCHS may transform to NS-CCHS or • S-CCHS = suppurative CCHS.
immune-mediated destructive cholangitis: sclerosing CCHS. • UDCA = ursodeoxycholic acid.
findings indicate may hasten small duct • Diabetes mellitus develops in ~30% of cats
injury; liver biopsy recommended before
Suggested Reading
with sclerosing CCHS treated with predni- Center SA. Diseases of the gallbladder and
prescribing UDCA for cats with “suspected” solone. biliary tree. Vet Clin North Am Small Anim
chronic CCHS; taurine supplementation • FHL may develop due to inadequate Pract 2009, 39:543–598.
(250 mg/day) should be considered in cats nutritional intake or as side effect of gluco- Warren AE, Center SA, McDonough SE, et al.
with poor appetite given chronic UDCA corticoids. Histopathologic features, immunophenotyp-
because of obligatory bile acid taurine
EXPECTED COURSE AND PROGNOSIS ing, clonality and eubacterial FISH in cats
conjugation.
• S-CCHS—may be cured. with nonsuppurative cholangitis/cholangio-
• B vitamin supplementation—thiamine (B1)
• NS-CCHS—chronic, long-term, vacillating hepatitis. Vet Pathol 2011, 48:627–634.
and B12: thiamine 50–100 mg PO q24h for 3
illness or remission possible (survival >8 years Author Sharon A. Center
days, then in water-soluble vitamin
documented in some cats). Consulting Editor Kate Holan
supplements while hospitalized; B12 0.25–
1.0 mg SC if suspect gut malabsorption,
using initial and sequential plasma B12 Client Education Handout
available online
Cholecystitis and Choledochitis
ment—DPM lesions including choledochal (“kiwi sign”) in mature GBM; GB rupture
cysts (cats > dogs). • Bacterial infection— implicated by discontinuous GB wall, C
common; retrograde duct bacterial invasion pericholecystic fluid, or generalized effusion,
BASICS from intestines or hematogenous dispersal and hyperechogenicity of pericholicystic
OVERVIEW from splanchnic circulation. • Toxoplasmosis tissue; failure to image GB: may implicate
• Cholecystitis = gallbladder (GB) inflamma- and biliary coccidiosis—rare causes. • rupture or agenesis; mineralized GB wall may
tion. • Choledochitis = large bile duct Necrotizing cholecystitis (dogs)—ruptured indicate dystrophic mineralization (limey or
inflammation. • Associated with cholelithi- GB (common, often secondary to porcelain GB) due to chronic cholecystis often
asis; secondary to GB mucocele (GBM); cholelithiasis or hypermature GBM); E. coli associated with sacculated GB or bile ducts in
extrahepatic bile duct obstruction (EHBDO); and Enterococcus spp.: common isolates. DPM: Caroli’s phenotype; intrahepatic bile
inflammation of intrahepatic biliary • Emphysematous cholecystitis/choledochitis— ducts may be difficult to visualize or be thick
structures (common in ductal plate malfor- rare, associated with diabetes mellitus, traumatic and prominent: ascending cholangitis or
mation [DPM]). • Severe GB inflammation GB ischemia, acute cholecystitis (with or EHBDO (dilated ducts, “too many tubes
can lead to rupture and subsequent bile without cholelithiasis); common gas-forming signs” defined with color-flow Doppler);
peritonitis, necessitating combined surgical organisms: Clostridia spp. and E. coli. pericholecystic fluid: necrotizing cholecystitis
and medical interventions. • Bile duct and surgical emergency. • Choledochitis
obstruction increases risk for biliary infection: involving common bile duct (CBD)—thick
enteric bacteria transmigrate bowel wall, pass wall, intraluminal debris, extends into hepatic
into portal circulation, disseminate within ducts.
DIAGNOSIS
liver, bile, and then GB, dispersing endotox- PATHOLOGIC FINDINGS
ins and bacteria that may cause systemic DIFFERENTIAL DIAGNOSIS
• Gross appearance—erythematous GB; may
sepsis or septic peritonitis. • EHBDO. • GBM. • Cholelithiasis.
appear green-black if necrotizing lesion;
• Cholangitis/cholangiohepatitis. • Pancreatitis.
SIGNALMENT tenacious “inspissated” biliary material
• Focal or diffuse peritonitis. • Bile peritonitis.
• Dog and cat. • No breed or sex predilec- common with GBM; pigmented choleliths if
• Gastroenteritis with biliary involvement.
tion. • Necrotizing cholecystitis (dogs)—usually infection; dark black or frank blood if
• Hepatic necrosis or abscessation. • Septicemia.
middle-aged or older animals. • GBM— hemobilia; CBD with thick wall, variable
predisposition for elderly dogs, dogs with CBC/BIOCHEMISTRY/URINALYSIS intraductal debris (e.g., biliary particulates,
hyperlipidemia or hypercholesterolemia (e.g., • Variable leukocytosis with toxic neutrophils cholelithiasis, suppurative inflammation).
endocrinopathies [hyperadrenocorticism, and inconsistent left shift if necrosis or sepsis. • Microscopic features of GBM without
hypothyroidism, diabetes mellitus]), pancrea • High bilirubin and bilirubinuria common. cholecystitis are benign, with wall thinning,
titis, glucocorticoid administration, nephrotic • High alanine aminotransferase (ALT), mucosal cystic hyperplasia, elongated mucosal
syndrome, idiopathic hyperlipidemia (e.g., aspartate aminotransferase (AST), alkaline fronds extending from flattened mucosa,
Shetland sheepdogs, miniature schnauzers, phosphatase (ALP), and γ-glutamyl trans- without granulation response in GB wall; if
beagles, others); leads to cholestasis and ferase (GGT) activity. • Low albumin with chronic GBM may involve arterial thrombi
possible cholecystitis (see Gallbladder peritonitis. • High cholesterol and bilirubin if and/or transformation to chronic cholecysti-
Mucocele). EHBDO. • Hypercholesterolemia and/or tis. • Microscopic features of cholecystitis
hypertriglyceridemia—breed related, include inflammatory infiltrates in lamina
SIGNS endocrine related, pancreatitis, nephrotic propria (lymphoplasmacytic or suppurative
• Choledochitis—vague signs, variable syndrome, EHBDO, GBM. with macrophages, rarely eosinophilic,
icterus. • Sudden onset—inappetence,
OTHER LABORATORY TESTS occasional lymphoid follicular hyperplasia),
lethargy, vomiting, vague abdominal pain
• Abdominocentesis—inflammatory effusion intraluminal suppurative/necrotic debris; if
(may be postprandial with cholecystitis or
(see Bile Peritonitis). • Bile culture (dogs and chronic cholecystitis—submucosal
GBM, reflecting post-meal GB contraction).
cats)—E. coli, Enterococcus spp., Klebsiella granulation tissue with variable ulcerative/
• Chronic postprandial discomfort/distress—
spp., Pseudomonas spp., Clostridium spp., necrotic mucosa, occasional hemobilia,
position of comfort, stretching, pacing,
many others. • Coagulation tests—abnormal occasional arterial thrombi; if cholelithiasis—
panting. • Mild to moderate jaundice and
if chronic EHBDO (vitamin K deficiency) or hyperplastic mucosa with dense elongated
fever common. • Severe disease—shock due
disseminated intravascular coagulation (DIC) mucosal fronds and glands contrasting with
to endotoxemia, bacteremia, hypovolemia.
in severe conditions with sepsis; cats display flattened appearance of GBM.
• Soft tissue mass in right cranial abdomen
palpable in small dogs and cats, reflecting coagulopathy with EHBDO early.
inflammation or adhesions between GB and IMAGING
pericholecystic tissues. • Abdominal radiography—may reveal loss of
CAUSES & RISK FACTORS cranial abdominal detail with focal or diffuse TREATMENT
peritonitis or effusion; ileus; radiodense • Inpatient—provision of critical care during
• Impaired bile flow at cystic duct or GB
(cholelithiasis, mass lesions), GB dysmotility, choleliths; gas in biliary structures; radiodense diagnostic/presurgical evaluations or if septic. •
or ischemic insult to GB wall (from GB GB (dystrophic mineralization due to chronic Place IV catheter in peripheral vein for
distention)—may precede cholecystitis ± inflammation; porcelain GB is rare). polyionic fluids and blood component therapy
necrotizing lesions. • Irritants in sludged bile • Ultrasonography—diffusely thick GB wall, as needed. • Restore fluid and electrolyte
(e.g., lysolecithin, prostaglandins, choleliths, segmental hyperechogenicity and/or laminated balance; monitor electrolytes frequently. •
flukes) or retrograde flow of pancreatic wall or double-rimmed GB wall observed with Vitamin K—if jaundiced; give parenterally
enzyme into bile duct in cats may initiate/ necrotizing cholecystitis; double-rimmed GB (see Medications) before surgical interventions,
augment GB or duct inflammation. wall also observed with acute cholecystitis, cystocentesis, jugular venipuncture, other
• Previous enteric disorders, trauma, hepatitis, cholangiohepatitis; GB lumen filled iatrogenic trauma. • Plasma—preferred colloid;
abdominal surgery—may be contributing with amorphous echogenic stellate or finely indicated if hypoalbuminemia and
factors. • Anomalous GB or duct develop striated pattern, resembling sliced kiwi fruit coagulopathy or if anticipated surgical
Cholecystitis and Choledochitis (continued)
interventions and complicating coagulopathy feeding; nonbile acid-dependent (GSH) ZOONOTIC POTENTIAL
C uncorrected. • Whole blood or fresh frozen choleresis (40 mg/kg PO q24h); n-acetyl- Campylobacter and Salmonella may cause
plasma—for surgical cases with bleeding cysteine (NAC) IV if oral administration of cholecystitis in dogs; advise owner if
tendencies; if septic, artificial colloids may antioxidants not possible; loading dose diagnosed.
delay recovery; if bleeding, some artificial 140 mg/kg IV over 20 min, follow by 70 mg/ SEE ALSO
colloids impair platelet aggregation. • Monitor kg over 20 min q6–8h. • Vitamin K1—0.5– • Bile Peritonitis.
urine output. • Remain vigilant for vasovagal 1.5 mg/kg SC/IM q12h for 3 doses; caution: • Gallbladder Mucocele.
reflex (abrupt bradycardia, hypotension, never administer IV (anaphylactoid reaction);
cardiac arrest) during biliary tree manipulation treat early to allow response before surgical ABBREVIATIONS
or cholecystocentesis; be prepared with manipulations. • ALP = alkaline phosphatase.
anticholinergics (atropine) and pressor drugs. • ALT = alanine aminotransferase.
CONTRAINDICATIONS/POSSIBLE • AST = aspartate aminotransferase.
• Remain vigilant for cholangiovenous
reflux—systemic dispersal of endotoxin or INTERACTIONS • CBD = common bile duct.
bacteria while handling septic biliary tree: give Ursodeoxycholic acid—contraindicated in • DIC = disseminated intravascular
IV antibiotics promptly (but after culture uncorrected EHBDO or bile peritonitis. coagulation.
collection). • GB resection advised for • DPM = ductal plate malformation.
cholecystis, best based on surgical evaluations, • EHBDO = extrahepatic bile duct
ultrasound images, bedside cytology of obstruction.
bile—bacterial infection mandates cholecystec- FOLLOW-UP • GB = gallbladder.
tomy. • GBM = gallbladder mucocele.
PATIENT MONITORING • GGT = γ-glutamyltransferase.
• After critical crisis resolution and surgery— • GSH = glutathione.
physical examination and pertinent diagnostic • NAC = n-acetylcysteine.
testing: repeat every 1–2 weeks until abnorm- • SAMe = S-adenosylmethionine.
MEDICATIONS alities resolve. • If septic—continue anti
biotics until enzymes, hyperbilirubinemia, Suggested Reading
DRUG(S) OF CHOICE Center SA. Diseases of the gallbladder and
• Antibiotics—before surgery; broad spectrum;
leukocytosis, left shift, and fever resolve.
biliary tree. Vet Clin North Am Small Anim
surgical manipulations may cause bacteremia; POSSIBLE COMPLICATIONS Pract 2009, 39(3):543–598.
select antibiotics for Enterococcus spp., enteric Anticipate protracted clinical course with Lawrence YA, Ruaux CG, Nemanic S, et al.
Gram-negative and anaerobic flora; refine ruptured biliary tract or peritonitis; postop- Characterization, treatment, and outcome
treatment using culture and sensitivity results; erative pancreatitis. of bacterial cholecystitis and bactibilia in
good initial choice is triad combination of dogs. J Am Vet Med Assoc 2015,
metronidazole, ticarcillin (or clavamox), and a 246:982–989.
fluorinated quinolone; reduce standard dose Tamborini A, Jahns H, McAllister H, et al.
for metronidazole by 50% if cholestatic Bacterial cholangitis, cholecystitis, or both
jaundice. • Ursodeoxycholic acid—10–15 mg/
MISCELLANEOUS
in dogs. J Vet Intern Med 2016,
kg PO daily divided BID with food; requires ASSOCIATED CONDITIONS 30:1046–1055.
decompression of EHBDO prior to treatment. • Cholelithiasis. • DPM. • EHBDO. • GBM. Author Sharon A. Center
• Antioxidants—vitamin E (α-tocopherol • Bile peritonitis. Consulting Editor Kate Holan
acetate): 10 IU/kg (see Bile Duct Obstruction AGE-RELATED FACTORS
(Extrahepatic); use water-soluble form if Congenital malformations of biliary
EHBDO); S-adenosylmethionine (SAMe): structures do not predispose patients to
use enteric-coated bioavailable product; on cholecystitis, but do predispose to
empty stomach: used as glutathione (GSH) choledochitis and cholelithiasis that lead to
donor (20 mg/kg PO q24h), 2h before GB disease and infection.
Cholelithiasis
• Fused feline pancreatic and bile duct • Cholelith analysis—infrequently done;
predisposes to concurrent biliary/pancreatic submit to laboratory equipped for cholelith C
cholelithiasis, choledochitis, and bile stasis analyses.
BASICS progressing to EHBDO as well as cholelith- IMAGING
OVERVIEW initiated pancreatitis or signs mistaken for • Abdominal radiography—limited value in
• Radiopaque or radiolucent calculi in pancreatitis. delineating GB structure/content; choleliths
common bile ducts (CBD), gallbladder (GB), • Bile sludge associated with GB distention— often small, may be radiolucent; rarely
or less commonly in intrahepatic bile ducts may enhance mucin production and mistaken for dystrophic biliary mineralization
(hepatolithiasis); gallbladder mucocele coalescence of bile particulates increasing risk in animals with chronic cholangitis or Caroli
(GBM) qualifies as a form of cholelithiasis for choleliths; but EHBDO does not cause DPM phenotype.
(see Gallbladder Mucocele). choleliths. • Ultrasonography—can detect: choleliths
• May be asymptomatic. • Inflammatory mediators and bacterial ≥2 mm diameter, thickened GB wall,
• Symptomatic—signs reflect sludging of enzymes associated with cholecystitis— distended biliary tract, increased hepatic
bile, extrahepatic bile duct obstruction increase risk for stone precipitation. parenchymal echogenicity and extrahepatic
(EHBDO), cholecystitis, cholangiohepatitis, • Hemobilia—bleeding into GB or bile ducts ductal involvement; may facilitate specimen
or bile peritonitis. or chronic hemolysis can lead to heme- collection for culture, cytology, and histopa-
• Primary constituents of choleliths—mucin, initiated cholelith formation. thology; may detect evidence of EHBDO
glycoprotein, calcium carbonate, and • Low-methionine and high-cholesterol within 72h; caution: distended GB with bile
bilirubin pigments; while dog bile is less experimental diet in dogs is proven lithogenic. “sludge” is common in anorectic or fasted
lithogenic than human bile (lower cholesterol patients; do not mistake for GB obstruction.
saturation), dog bile forms calcium bilirubi- Hepatolithiasis usually casts acoustic shadows.
nate sludge upon fasting. Imaging of choleliths within extrahepatic
• 50% feline choleliths are mineralized; may DIAGNOSIS ducts may be difficult owing to enteric gas
be radiographically visible (calcium carbonate). obstructing imaging “window”; confirmation
• Surgical treatment—not recommended DIFFERENTIAL DIAGNOSIS
of distended intrahepatic bile duct done with
without clinical signs or clinicopathologic • EHBDO—inflammatory, infectious, or
color-flow Doppler.
abnormalities (current or historical), with the neoplastic conditions involving liver, CBD, or
exception of preemptive GBM removal. extrahepatic tissues adjacent to porta hepatis; DIAGNOSTIC PROCEDURES
suggested by marked increases in alkaline Histopathologic evaluation of liver necessary
SIGNALMENT phosphatase (ALP), γ-glutamyltransferase in patients undergoing surgical cholelith
• Cat and dog. (GGT), bilirubin, and gradual increase in removal to detect comorbid conditions
• Small-breed dogs may be predisposed; cholesterol. influencing treatment and prognosis,
animals with ductal plate malformations • Cholangiohepatitis. i.e., suppurative cholangitis, nonsuppurative
(DPM) predisposed: particularly Caroli DPM • Cholecystitis/choledochitis. cholangitis, DPM, neoplasia.
phenotypes (i.e., malformative dilated large • Bile peritonitis.
ducts causing bile stasis in sacculated ducts); • GBM.
microhepatolithiasis encountered more often • Consequence of DPM.
in DPM. • Chronic hypercalcemia may increase risk.
• Hyperlipidemic and hypercholesterolemic TREATMENT
dogs—predisposed to GBM; may relate to CBC/BIOCHEMISTRY/URINALYSIS • Controversial whether choleresis with
endocrine disorders, idiopathic condition, or • May have no clinicopathologic ursodeoxycholate (UDCA) is beneficial in
other disorders (see Gallbladder Mucocele). abnormalities—asymptomatic cholelithiasis. animals lacking clinical or clinicopathologic
• CBC—may be normal; may reflect bacterial signs; can resolve cholesterol choleliths in
SIGNS infection, endotoxemia, biliary obstruction, or humans, but these are rare in dogs or cats;
• May be asymptomatic. other underlying causal factors; inflammatory choleresis with UDCA may help move
• When accompanied by infection or causing leukogram in some cases. sludged biliary debris.
intermittent or complete EHBDO (with or • Biochemistry—if symptomatic: variable • Supportive fluids—if hospitalized,
without peritonitis)—vomiting; meal-related hyperbilirubinemia, increase ALP, GGT, according to hydration, electrolyte, and
discomfort, vague abdominal pain; fever; alanine aminotransferase (ALT), and aspartate acid-base status.
± jaundice. aminotransferase (AST) activities; also see • If hyperlipidemia coexistent—prescribe
• Episodic vague peri- or postprandial Bile Duct Obstruction (Extrahepatic). fat-restricted diet, identify and manage
abdominal pain or behavior seeking position endocrinopathies; if failure to control
of relief. OTHER LABORATORY TESTS
• Bacterial culture—bile: aerobic and
hyperlipidemia, may require additional
CAUSES & RISK FACTORS anaerobic bacteria often confirmed in medical management.
• Predisposing factors—stasis of bile flow: symptomatic patients if crushed cholelith, • Control predisposing conditions, especially
GB dysmotility, choledochal cysts (cat sludged bile, ± GB wall (if cholecystectomy) biliary tree infection (with antimicrobials)
especially, form of DPM); lith nidus may submitted for cultures. and GB dysmotility (by GB removal).
evolve from inflammatory debris, infection, • Exploratory surgery, choledochotomy,
• Cholelith nidus—may house associated
epithelial irregularity/exfoliation, neoplasia, bacterial infection. cholecystotomy, and possibly cholecystectomy
residual suture material; bile supersaturation: • Coagulation profile—bleeding associated
or biliary-enteric anastomosis—indicated in
heme-bilirubin pigments, hemobilia, with prolonged clotting times may develop symptomatic cases according to circumstances.
calcium-bilirubinate, enhanced mucin with EHBDO of >7–10 days; see Bile Duct • Warn client that cholelithiasis is chronic
production (inflammation, prostaglandins), Obstruction (Extrahepatic); responsive to problem and that stones may reform even
cholesterol. parenteral vitamin K1 administration. after surgical removal despite chronic medical
treatment; choleliths in GB is strong
Cholelithiasis (continued)
indication for cholecystectomy unless GB choleresis) and thus is potential choleretic

C needed for biliary enteric anastomosis in for patients with high liver enzymes or
certain conditions. confirmed hepatobiliary inflammation;
20–40 mg/kg using enteric-coated tablet PO MISCELLANEOUS
q24h, administer 2h before feeding; higher SEE ALSO
dose recommended for choleresis; also • Bile Duct Obstruction (Extrahepatic).
provides antifibrotic and antiinflammatory • Cholecystitis and Choledochitis.
M EDICATIONS benefits. • Ductal Plate Malformation (Congenital
DRUG(S) OF CHOICE Hepatic Fibrosis).
• Antibiotics—based on culture of bile, • Gallbladder Mucocele.
tissue, and cholelith nidus, cytology and INTERACTIONS
Gram staining of biliary debris or crushed lith Ursodeoxycholic acid—contraindicated with ABBREVIATIONS
if cultures negative; if culture negative then EHBDO before biliary decompression. • ALP = alkaline phosphatase.
directed against enteric microbial opportun- • ALT = alanine aminotransferase.
ists; initial treatment with Timentin or • AST = aspartate aminotransferase.
Clavamox with metronidazole, combined • CBD = common bile duct.
®
with a fluoroquinolone, usually successful. FOLLOW-UP
• Ursodeoxycholic acid—10–15 mg/kg/day • EHBDO = extrahepatic bile duct
PO, divided BID, given with food to increase PATIENT MONITORING obstruction.
bioavailability; provides choleretic, hepato- • Physical examination and pertinent • GB = gallbladder.
protectant, anti-endotoxic, antifibrotic effects, diagnostic testing q2–4 weeks postoperatively • GBM = gallbladder mucocele.
and may facilitate cholesterol stone dissolu- until clinical signs and clinicopathologic • GGT = γ-glutamyltransferase.
tion; therapy often continued lifelong if no abnormalities resolve. • GSH = glutathione.
cause for cholelithiasis identified to augment • Periodic ultrasonography—assess cholelith • SAMe = S-adenosylmethionine.
choleresis thwarting bile stasis. status, integrity/distention of biliary tract, • UDCA = ursodeoxycholate.
• Vitamin K1—parenterally; 0.5–1.5 mg/kg
hepatic parenchymal changes. Suggested Reading
to max 3 doses in 24–36h in jaundiced POSSIBLE COMPLICATIONS Center SA. Diseases of the gallbladder and
patients; do not administer IV (anaphylaxis). Sudden onset of fever, abdominal pain, and biliary tree. Vet Clin North Am Small Anim
Antioxidants malaise—may signify bile peritonitis and/or Pract 2009, 39:543–598.
• Vitamin E (α-tocopherol acetate)—10 IU/kg
sepsis from breakdown in bile containment, van Geffen C, Savary-Bataille K, Chiers K,
per day for patients with high liver enzymes or recurrent cholelith lodged in sphincter of et al. Bilirubin cholelithiasis and haemosi-
or confirmed hepatobiliary inflammation; use Oddi (duodenal papilla) or obstructing derosis in an anaemic pyruvate kinase-
water-soluble form if EHBDO. pancreatic duct (cats only). deficient Somali cat. J Small Anim Pract
• S-adenosylmethionine (SAMe; use form EXPECTED COURSE AND PROGNOSIS 2008, 49:479–482.
with proven bioavailability and efficacy)— • May be asymptomatic. Author Sharon A. Center
glutathione (GSH) donor (important • Symptomatic disease—reflects existing Consulting Editor Kate Holan
hepatic antioxidant, GSH also provides infection, EHBDO, cholecystitis, DPM, or
driving force for non-bile acid–dependent bile peritonitis.
Chondrosarcoma, Bone
Usually normal. C
BASICS IMAGING FOLLOW-UP
• Radiographs of affected area show features
OVERVIEW of aggressive bone lesion (cortical lysis, PATIENT MONITORING
• Chondrosarcoma (CSA) is a malignant nonhomogenous reactive bone formation, Physical examination every 2–3 months and
mesenchymal tumor arising from cartilage and ill-defined zone of transition). • Thoracic thoracic radiographs every 3–4 months to
characterized by production of chondroid and radiographs recommended to screen for monitor for local tumor control and distant
fibrillar matrix. • CSA is the second most pulmonary metastasis. • CT recommended metastases, respectively.
common primary bone tumor in dogs and for axial tumors to more accurately stage local EXPECTED COURSE AND PROGNOSIS
accounts for 5–10% of all primary bone tumors; disease and plan for surgery and/or radiation • Overall, 15–30% of dogs will develop
primary bone tumors are uncommon in cats, and therapy; concurrent CT imaging of thorax metastatic disease, with lungs being most
CSA is third in incidence behind osteosarcoma recommended as more sensitive way to screen commonly affected site; metastatic rates
and fibrosarcoma. • Dogs—majority of CSAs for pulmonary metastasis. • MRI, alone or in approach 50% for high-grade canine tumors;
arise from flat bones (axial skeleton); approxi- combination with CT, may be recommended development of metastasis rare for cats with
mately 30% occur in nasal cavity and 20% of for treatment planning for vertebral CSA. CSA. • With curative-intent surgery, median
CSAs arise from ribs; 20% of CSAs in dogs arise survival >3 years; depending on tumor
from appendicular skeleton; sites are generally DIAGNOSTIC PROCEDURES
• Histopathology needed for definitive diagnosis. location and completeness of excision, up to
similar to where osteosarcoma typically occurs. 40% will develop local recurrence. • With
• Cats: 66% of CSAs arise in appendicular skeleton, • Fine-needle aspirate bone cytology may provide
supportive diagnosis; differentiation of CSA palliative care alone, survival times of >1 year
with 33% occurring in the axial skeleton. • Rarely, still possible.
CSA can arise in soft tissue (extraskeletal) sites. from other sarcomas may be challenging if
sample contains sparse amounts of matrix.
SIGNALMENT
• Dogs—medium- to large-breed dogs, with
mixed-breed dogs, golden retrievers, boxers,
and German shepherd dogs overrepresented;
MISCELLANEOUS
median age is 8 years (range: 1–15 years). TREATMENT SEE ALSO
• Cats—median age is 9 years (range: 2–18 • Amputation recommended for appendicu- • Chondrosarcoma, Nasal and Paranasal Sinus.
years), with males twice as likely to be affected. lar tumors. • For axial tumors, wide surgical • Chondrosarcoma, Oral.
excision recommended whenever possible. • Fibrosarcoma, Bone.
SIGNS • Stereotactic radiation therapy provides • Osteosarcoma.
Historical Findings effective local control for canine osteosarcoma
ABBREVIATIONS
• Patients often present with a visible mass at and might be alternative to surgery for
• CSA = chondrosarcoma.
the affected site. • History of lameness if patients with CSA. • Palliative therapy
involvement of weight-bearing bone. • Rarely, recommended for patients with nonresectable
drug.
CSA of the rib may be associated with local disease or gross metastasis, or when
respiratory signs. • Additional clinical signs definitive therapy is declined; palliative care Suggested Reading
vary with site of involvement. focuses on pain control. Durham AC, Popovitch CA, Goldschmidt
MH. Feline chondrosarcoma: a retrospec-
tive study of 67 cats (1987–2005). J Am
• Findings depend on anatomic location.
Anim Hosp Assoc 2008, 44(3):124–130.
• A firm to hard mass often is palpable, with
Farese JP, Kirpensteijn J, Kik M, et al.
variable degrees of pain elicited on palpation. MEDICATIONS Biologic behavior and clinical outcome of
• CSA of the rib occurs most commonly at
DRUG(S) OF CHOICE 25 dogs with canine appendicular chondro-
the costochondral junction; dyspnea is rare
Pain Management sarcoma treated by amputation: a Veterinary
and associated with space-occupying effect.
• Nonsteroidal anti-inflammatory drugs Society of Surgical Oncology retrospective
CAUSES & RISK FACTORS study. Vet Surg 2009, 38:914–919.
(NSAIDs). • Tramadol. • Gabapentin. • IV
• Etiology largely unknown. Author Jenna H. Burton
aminobisphosphonates (e.g., pamidronate,
• Osteochondromatosis (multiple cartilaginous Consulting Editor Timothy M. Fan
zoledronate) might alleviate bone pain and
exostosis) lesions can transform into CSA. Acknowledgment The author and book
slow pathologic bone resorption.
Chemotherapy Dennis B. Bailey.
Role of chemotherapy has not been defined
in veterinary oncology, but does not
DIAGNOSIS improve outcome in humans.
DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS/POSSIBLE
• Other primary bone tumors (osteosarcoma,
fibrosarcoma, hemangiosarcoma). INTERACTIONS
• Use NSAIDs cautiously in all cats and in
• Metastatic bone tumors (transitional cell,
prostatic, mammary, thyroid, apocrine gland, dogs with renal insufficiency. • Do not
anal sac carcinomas). • Tumors that locally combine NSAIDs with corticosteroids.
invade adjacent bone (especially oral, nasal,
digital, and joint tumors). • Fungal osteomyelitis.
Chondrosarcoma, Nasal and Paranasal Sinus

IMAGING • CT of skull can be considered when clinical
C • Thoracic radiographs to screen for signs recur or progress.
pulmonary metastasis (uncommon). • CT EXPECTED COURSE AND PROGNOSIS
BASICS for detecting soft tissue opacity within nasal • <10% develop metastasis (lungs affected
OVERVIEW cavity and surrounding sinuses, bony most commonly). • Median survival with
• Chondrosarcoma (CSA) is a malignant destruction, and extension through cribriform palliative care alone is 3 months. • With
mesenchymal tumor arising from cartilage plate into brain. • If CT scan is not definitive daily radiation therapy, median
and characterized by production of chondroid accessible, skull radiographs can be performed survival is around 17 months, and 2-year
and fibrillar matrix. • Nasal CSA arises most to assess for soft tissue opacity in nasal cavity survival rate is around 30%; median survival
commonly from the nasal turbinates. • In dogs, and/or frontal sinuses. with palliative radiation protocols is about 9
CSA accounts for 15% of all nasal tumors. DIAGNOSTIC PROCEDURES months. • Recurrence/progression of tumor
SIGNALMENT • Blood pressure, to rule out systemic hyper- and recurrence of clinical signs generally
• Mixed-breed dogs, Labrador retrievers, tension as cause for epistaxis. • Mandibular life-limiting event for nasal CSA. • Brain
golden retrievers, boxers, and German lymph node cytology to screen for possible involvement is poor prognostic sign.
shepherd dogs are overrepresented. • Median metastasis. • Rhinoscopy is helpful for • Unilateral versus bilateral involvement is
age is 7 years (range: 2–13 years). • CSA visualization of mass or fungal plaque and not significant prognostic factor.
tends to develop at a younger age than other guiding subsequent tissue biopsy. • Tissue
nasal tumors. • Rare in cats, with no obvious biopsy and histopathology needed for
breed or sex predilections. definitive diagnosis; biopsy instrument should
not pass caudal to level of medial canthus of
SIGNS
eye to avoid penetrating cribriform plate.
MISCELLANEOUS
Historical Findings • Intranasal approach to obtaining tissue SEE ALSO
• Intermittent unilateral epistaxis and/or biopsy preferable if treatment radiation • Adenocarcinoma, Nasal.
mucopurulent discharge, may progress to therapy planned. • Chondrosarcoma, Bone.
bilateral involvement. • Sneezing, stertorous • Chondrosarcoma, Oral.
breathing, and/or facial deformity. • Decreased • Epistaxis.
appetite and/or halitosis secondary to oral cavity ABBREVIATIONS
invasion. • Seizures, behavior changes, and/or
obtundation secondary to cranial invasion. TREATMENT • CSA = chondrosarcoma.
• Radiation therapy is treatment of choice. • NSAID = nonsteroidal anti-inflammatory
Physical Examination Findings • Conventional linear accelerator used most drug.
• Epistaxis and/or nasal discharge, initially commonly; however, if available, stereotactic Suggested Reading
unilateral but can progress to bilateral. radiation therapy can reduce number of Patnaik AK, Lieberman PH, Erlandson RA,
• Decreased nasal air flow (unilateral or radiation treatments and reduce adverse et al. Canine sinonasal skeletal neoplasms:
bilateral). • Pain on nasal or paranasal sinus effects. • Palliative radiation protocols (fewer chondrosarcomas and osteosarcomas. Vet
palpation or percussion. • Facial deformity, treatments and lower total radiation dose) Pathol 1984, 21(5):475–482.
decreased ocular retropulsion, exophthalmia, might be preferable for dogs with very Sones E, Smith A, Schleis S, et al. Survival times
or epiphora. • Visible mass effect protruding advanced disease. for canine intranasal sarcomas treated with
through the palate into the oral cavity. radiation therapy: 86 cases (1996–2011). Vet
CAUSES & RISK FACTORS Radiol Ultrasound 2013, 54(2):194–201.
Unknown Author Jenna H. Burton
MEDICATIONS Consulting Editor Timothy M. Fan
DRUG(S) OF CHOICE editors acknowledge the prior contribution of
• Nonsteroidal anti-inflammatory drugs Dennis B. Bailey.
DIAGNOSIS (NSAIDs) for pain control. • Prednisone
DIFFERENTIAL DIAGNOSIS (0.5–1 mg/kg PO q24h) to help relieve nasal
• Other nasal tumors—adenocarcinoma, congestion. • Phenylephrine nasal spray can
squamous cell carcinoma, osteosarcoma, be used intermittently to help with epistaxis.
fibrosarcoma, lymphoma, transmissible • Empiric antibiotic therapy can be
venereal tumor (dogs), nasopharyngeal polyp considered for secondary bacterial infections.
(cats). • Fungal rhinitis—aspergillosis and CONTRAINDICATIONS/POSSIBLE
penicilliosis (dogs), cryptococcus (cats), INTERACTIONS
sporotrichosis (both). • Rhinosporidiosis • Use NSAIDs cautiously in all cats and in
(dogs). • Foreign body. • Thrombocytopenia dogs with renal insufficiency. • Do not
or other coagulopathy. • Tooth root abscess. combine NSAIDs with corticosteroids.
• Oronasal fistula.
Usually normal—evaluate for thrombocyto-
penia if signs of epistaxis.
FOLLOW-UP
PATIENT MONITORING
• Nasal flush for cytology and culture—rarely
• Physical examinations every 2–3 months
helpful. • Coagulation profile. • Buccal
and thoracic radiographs every 3–4 months.
mucosal bleeding time.
Chondrosarcoma, Oral
IMAGING
• Thoracic radiographs are recommended to C
screen for pulmonary metastasis.
BASICS • Skull radiographs often will show features FOLLOW-UP
OVERVIEW of an aggressive bone lesion (bone lysis, cortical PATIENT MONITORING
• Chondrosarcoma (CSA) is a malignant destruction, nonhomogenous bone forma- Physical examination with thorough oral
mesenchymal tumor arising from cartilage tion, ill-defined zone of transition); however, examination every 2–3 months and thoracic
and characterized by production of chondroid normal radiographs do not exclude bone radiographs every 3–4 months to monitor for
and fibrillar matrix. involvement. local tumor control and distant metastases,
• CSA accounts for 5–10% of all primary • High-detail dental radiographs may be respectively.
bone tumors; mandibular and maxillary CSAs appropriate for imaging smaller lesions.
have been reported in dogs, but these are not • CT imaging can more accurately determine
• Prognosis depends on tumor size and location,
common locations for this tumor (see extent of local disease and is useful for
and surgical resectability; with complete excision,
Chondrosarcoma, Bone, and surgical planning, particularly caudal lesions;
long-term control may be possible.
Chondrosarcoma, Nasal and Paranasal Sinus). CT is generally required for radiation therapy
• Most patients die or are euthanized due to
planning.
SIGNALMENT local disease progression.
• Dogs—medium- to large-breed dogs, with DIAGNOSTIC PROCEDURES • Overall CSA metastatic rate is 15–30%,
mixed-breed dogs, golden retrievers, boxers, • Fine-needle aspiration (FNA) and cytology with the lungs being affected most com-
and German shepherd dogs overrepresented; of the mass may provide provisional monly; metastatic rates approach 50% for
median age is 8 years (range: 1–15 years). diagnosis. FNA and cytology are recom- high-grade tumors.
• Cats—rarely affected. mended for mandibular lymph nodes,
especially if they are enlarged.
SIGNS
• Histopathology is required to reach a
Historical Findings definitive diagnosis; preoperative incisional
• Visible mass involving the mandible or biopsy is recommended. MISCELLANEOUS
maxilla. • If curative-intent surgery is performed, all SEE ALSO
• Halitosis, dysphagia, and/or hypersalivation. excised tissue should be submitted to the • Chondrosarcoma, Bone.
• Bloody oral discharge and oral pain. pathologist en bloc for evaluation of surgical • Chondrosarcoma, Nasal and Paranasal Sinus.
• Weight loss secondary to a prolonged margin.
ABBREVIATIONS
decrease in food intake.
• CSA = chondrosarcoma.
Physical Examination Findings • FNA = fine-needle aspiration.
• A firm to hard mass centered on the maxilla
Suggested Reading
or mandible is seen most commonly. TREATMENT Verstraete FJ. Mandibulectomy and maxillec-
• The overlying gingival mucosa usually is • Surgical excision—removal of the affected tomy. Vet Clin North Am Small Anim Pract
intact, although trauma and ulceration from segment of bone (maxillectomy or man- 2005, 35(4):1009–1039.
the occlusal teeth are common with larger dibulectomy) with a margin of at least 2 cm is Waltman SS, Seguin B, Cooper BJ, Kent M.
tumors. recommended whenever possible. Clinical outcome of nonnasal chondrosar-
• Loose or missing teeth. • If excision is incomplete, adjuvant radiation coma in dogs: thirty-one cases (1986–
• Difficulty or pain when opening the mouth therapy might help improve local control, 2003). Vet Surg 2007, 36:266–271.
(especially caudal tumors). although there is little information regarding Author Jenna H. Burton
• Facial deformity. efficacy. Consulting Editor Timothy M. Fan
• Mandibular lymphadenopathy. • Radiation therapy can be considered as a sole Acknowledgment The author and book
• Nasal discharge, epistaxis, or decreased air local treatment modality but, because of the editors acknowledge the prior contribution of
flow through the nares (maxillary tumors). chondroid matrix produced by CSAs, radiation Dennis B. Bailey.
CAUSES & RISK FACTORS therapy likely will stabilize tumor size and not
None identified. necessarily cause substantial shrinkage.
• Chemotherapy has not been evaluated, but
is not thought to be effective.
• Palliative care focuses on pain control.
DIAGNOSIS
• Other primary oral tumors, including MEDICATIONS
melanoma, fibrosarcoma, squamous cell
carcinoma, osteosarcoma, and acanthomatous DRUG(S) OF CHOICE
ameloblastoma. • Nonsteroidal anti-inflammatory drugs.
• Maxillary invasion of primary nasal CSA. • Tramadol.
• Craniomandibular osteopathy. • Gabapentin.
• Dentigerous cyst, tooth root abscess, or • Intravenous aminobisphosphonates
osteomyelitis. (pamidronate or zoledronate) might alleviate
bone pain and attenuate bone resorption.
CBC/BIOCHEMISTRY/URINALYSIS • Empiric antibiotic therapy can be consid-
Usually normal. ered for secondary bacterial infections.
Chorioretinitis
• Others—related to underlying systemic chorioretinitis. Thrombocytopenia may result
C disease, retrobulbar disease. in small multifocal or large retinal or vitreal
Lesions hemorrhages with inflammation.
BASICS • Dogs—Vogt-Koyanagi-Harada-like
• Active—indistinct margins, tapetal hypo-
DEFINITION reflectivity, white-gray color, altered course of (uveodermatologic) syndrome: target is
• Inflammation of the choroid and retina. retinal blood vessels. melanin pigment granule (abundant in uveal
• Choroid is also called posterior uvea. • Few or small lesions—no apparent visual
tissue), leading to severe anterior and
• Diffuse inflammation may result in retinal deficits. posterior inflammation (affected dogs may
detachment. • Extensive lesions involving larger areas of
also exhibit depigmentation of the skin,
the retina—blindness or reduced vision. especially at mucocutaneous junctions);
PATHOPHYSIOLOGY
• Inactive (scars)—discrete margins, tapetal
systemic lupus erythematosus (SLE).
• Caused by infectious agents, neoplastic
hyperreflectivity with hyperpigmented central • Cats—periarteritis nodosa, SLE.
cells, or immune complexes (immune-
mediated diseases); hematogenous pathogenic areas, depigmented in the nontapetum and Metabolic
factors inducing choroidal inflammation is some surrounding or central hyperpig- Early hypertensive retinopathy may result in
most common. mentation. multifocal localized lesions.
• Choroid and retina—closely apposed; CAUSES Neoplastic
physiologically interdependent; inflammation Neoplasia (multiple myeloma, lymphoma,
of one usually results in inflammation of the Infectious
malignant histiocytosis) can metastasize to the eye.
other. Dogs
• May also occur as a retinochoroiditis— • Viral—canine distemper, herpesvirus (rare, Toxic
retinal inflammation preceding and inducing usually neonates), rabies. • Ethylene glycol, idiosyncratic drug reactions
choroidal inflammation. • Bacterial—leptospirosis, brucellosis,
(e.g., trimethoprim-sulfa), ivermectin.
pyometra (toxic uveitis), borreliosis, ehrlich- • Photic injury—exposure to bright light can
SYSTEMS AFFECTED burn the retina.
• Nervous. iosis, Rocky Mountain spotted fever,
• Ophthalmic. bartonellosis; discospondylitis, endocarditis Trauma
• Other systems if underlying disease is may be present with bacteremia. Perforating wound or migrating foreign body.
systemic. • Fungal—aspergillosis, blastomycosis,
RISK FACTORS
coccidioidomycosis, histoplasmosis, crypto- • FeLV or FIV infection—may predispose cat
INCIDENCE/PREVALENCE coccosis, acremoniosis, pseudallescheriasis,
• Fairly common. to ocular toxoplasmosis or other infectious
candidiasis, geotrichosis. disease.
• Exact incidence unknown. • Algal—protothecosis. • Immunosuppressive therapy.
GEOGRAPHIC DISTRIBUTION • Protozoal—toxoplasmosis, leishmaniasis
Varies with endemic infectious diseases (rare), neosporosis, and sarcocystosis (dogs).
(e.g., systemic mycoses, rickettsial disease). • Parasitic—ocular larval migrans (Strongyles,
Ascarids, Baylisascaris), Sarcocystis neurona,
SIGNALMENT DIAGNOSIS
and ophthalmomyiasis interna (Diptera larval
Species migrans). DIFFERENTIAL DIAGNOSIS
Dog and cat. • Retrobulbar abscess/cellulitis—uncommon. • Blindness or impaired vision—optic
Breed Predilections Cats neuritis, CNS disease, diffuse retinal
• Systemic mycoses—more common in • Viral—feline leukemia virus (FeLV), feline inflammation.
hunting dogs. immunodeficiency virus (FIV), feline • Retinal dysplasia—bilateral, symmetric
• Uveodermatologic syndrome—Akita, chow infectious peritonitis (FIP). folds or geographic clumps of pigment or
chow, and Siberian husky predisposed. • Bacterial—septicemia or bacteremia, altered fundus reflectivity; no associated signs
• Chorioretinopathy—borzoi, border collie, bartonellosis. of inflammation in the eye.
beagle, German shepherd dog. • Fungal—cryptococcosis, histoplasmosis, CBC/BIOCHEMISTRY/URINALYSIS
• Systemic histiocytosis—Bernese mountain blastomycosis. Normal if problem confined to the eye,
dog, golden retriever. • Parasitic—toxoplasmosis, ophthalmomyia- otherwise may have signs of systemic disease.
Mean Age and Range sis interna (Diptera, Cuterebra), ocular larval
migrans, leishmaniasis (rare). OTHER LABORATORY TESTS
Depends on underlying cause. • Anti-nuclear antibody (ANA)—for
• Protozoal—toxoplasmosis.
Predominant Sex suspected SLE.
Uveodermatologic syndrome—more Idiopathic • Bence-Jones proteinuria—for multiple
common in young male dogs. • Common. myeloma.
• Multifocal chorioretinitis or chorioretin- • Skin biopsy—SLE, uveodermatologic
SIGNS opathy—acquired syndrome; affected dogs
• Not usually painful, except with concurrent
syndrome.
have multifocal retinal edema or chorioretinal • Coagulation profile.
anterior uveitis, secondary glaucoma, or atrophy. • Bacterial culture of ocular or body fluids.
inflammatory retrobulbar disease. • German shepherd dog—choroidal scars in • Serologic or PCR testing—infectious
• Vitreous abnormalities—may note exudate, police dogs: possibly due to physical exertion
hemorrhage, or syneresis (liquefaction). disease (see Causes).
or circulatory disorders; affected dogs had • Cytology of lymph node, mass, or organ
• Interruption or alteration of the course of lower amplitude ERG.
retinal blood vessels—due to retinal aspirates.
Immune • Histopathology of enucleated eyes.
elevation.
• Any immune-mediated disease may cause • Bartonella—PCR, culture on special media
• Ophthalmomyiasis (cats)—curvilinear
tracts from migrating larvae. vasculitis or inflammation, resulting in (BAPGM).
exudative retinal detachment or
(continued) Chorioretinitis
IMAGING glaucoma, which necessitate treatment or eye POSSIBLE COMPLICATIONS
• Thoracic radiography—may show removal; dermatitis may also require management. • Permanent blindness. C
infectious or neoplastic disease. • Cataracts.
• Spinal radiography— may show discospon- • Glaucoma.
dylitis or multiple myeloma. • Chronic ocular pain.
• Ocular ultrasound—retinal detachment, • Death—secondary to systemic disease.
intraocular masses; especially helpful if the
MEDICATIONS
ocular media are not clear; can identify DRUG(S) OF CHOICE
• Prognosis for vision—guarded to good,
retrobulbar disease. • Identify and treat underlying systemic
depending on amount of retina affected;
• Abdominal ultrasound—screen for disease (see specific chapters).
visual deficits or blindness if large areas of the
neoplasia, systemic disease. • Topical medications—not effective in dogs
retina were destroyed; focal and multifocal
• CT/MRI—if signs of retrobulbar or CNS with intact lenses; systemic therapy required.
disease do not markedly impair vision but do
disease. ◦ 1% prednisolone acetate or 0.1%
leave scars.
dexamethasone q6–8h to treat anterior uveitis.
DIAGNOSTIC PROCEDURES • Prognosis for life—guarded to good, depending
◦ Parasympatholytics (e.g., 1% atropine)
• Indirect ophthalmoscopy—screens a large on underlying cause.
can be given at a frequency that dilates the
area of the retina. • Prognosis for globe—secondary glaucoma
pupil and reduces pain.
• Direct ophthalmoscopy—facilitates may necessitate removal of blind painful eye.
◦ 0.5% timolol maleate or 2% dorzolamide
examination of suspicious areas.
may be used to treat secondary glaucoma.
• Cerebrospinal fluid (CSF) tap—indicated
• Corticosteroids at anti-inflammatory
for diagnosis of some CNS disease or optic
doses—prednisone 0.5–1 mg/kg PO q24h
neuritis. MISCELLANEOUS
(dog), prednisolone 1–2 mg/kg q24h (cat),
• Vitreocentesis or subretinal aspirate—if
then taper; avoid use unless large areas of the ASSOCIATED CONDITIONS
other diagnostic tests fail or to identify
retina are affected and vision is severely threatened. Several systemic diseases.
infectious agent or neoplasia; vitreocentesis
• Prednisone for immunosuppression—
may worsen inflammation or induce ZOONOTIC POTENTIAL
2–4 mg/kg PO divided q12 for 3–10 days
hemorrhage or retinal detachment, reducing • Toxoplasmosis—may be transmitted to
(dog, cat), then taper slowly over months (do
chances for restoration of vision. humans if patient is shedding oocysts in feces.
not exceed 80 mg per day).
• Choroidal aspirate—of thickened areas, • Vector-borne diseases—infected animals
ideally ultrasound guided; procedure may CONTRAINDICATIONS may act as reservoirs, i.e., bartonella (cat
aggravate inflammation, induce hemorrhage Systemically administered corticosteroids—do scratch disease), rickettsia, others.
or retinal detachment. not use if systemic infectious disease is present.
Exception: sometimes steroids are used when SYNONYMS
• Measurement of blood pressure.
infectious cause has been identified and is Retinochoroiditis
PATHOLOGIC FINDINGS
being treated. SEE ALSO
• Masses or retinal or choroidal exudates.
• Retinal Degeneration.
• Fungal organisms in exudates and ALTERNATIVE DRUG(S)
• Retinal Detachment.
inflammatory cells. Uveodermatologic syndrome or known
• Uveodermatologic Syndrome (VKH).
• Perivascular inflammation with vasculitis, FIP. autoimmune etiology—may require corticoster-
• Inactive lesions—retinal and choroidal atrophy oids and concurrent use of or transition to other ABBREVIATIONS
(thinning); may note retinal pigment epithelium immunosuppressive medications (e.g., • ANA = antinuclear antibody.
hyperpigmentation and tapetal destruction. azathioprine, cyclosporine, leflunomide, or • CSF = cerebrospinal fluid.
mycophenolate mofetil; see Retinal Detachment). • FeLV = feline leukemia virus.
• FIP = feline infectious peritonitis.
• FIV = feline immunodeficiency virus.
• SLE = systemic lupus erythematosus.
TREATMENT
FOLLOW-UP Suggested Reading
Narfström K, Petersen-Jones S. Diseases of
Depends on physical condition of patient, PATIENT MONITORING
the canine ocular fundus. In: Gelatt KN,
usually outpatient. • As appropriate for underlying cause and
ed., Veterinary Ophthalmology, 5th ed.
type of medical treatment.
NURSING CARE Ames, IA: Blackwell, 2013, pp. 2087–2235.
• For bartonella treatment in cats, consider
Therapy for systemic disease, depending on Stiles J. Infectious diseases and the eye. Vet
follow-up testing to help assess response.
patient status. Clin North Am Small Anim Pract 2000,
• CBC, platelet count, and liver enzymes—
CLIENT EDUCATION 30:971–1167.
monitor for side effects of systemic immuno-
• Chorioretinitis may be a sign of systemic
Author Patricia J. Smith
suppressive drugs.
disease, so diagnostic testing is important. Consulting Editor Kathern E. Myrna
• Intraocular pressure monitoring—for
• Immune-mediated disease requires lifelong anterior uveitis.
therapy.
PREVENTION/AVOIDANCE Client Education Handout
• Dogs with uveodermatologic syndrome
Tick and flea control measures. available online
may have anterior uveitis and secondary
Chronic Kidney Disease

(X-linked dominant); English cocker spaniel • Uremic halitosis.
C (recessive). • Hypertensive retinopathy.
• Renal dysplasia—shih tzu, Lhasa apso, • Renal osteodystrophy may manifest as bone
BASICS golden retriever, Norwegian elkhound, chow pain, particularly in skull.
DEFINITION chow, standard poodle, soft-coated wheaten • Reduced body temperature with uremia.
Chronic kidney disease (CKD) encompasses terrier, Alaskan Malamute, miniature CAUSES
functional or structural lesions (in one or schnauzer, Dutch kooiker, and many other • Unknown in most cases due to late
both kidneys as detected by blood or urine breeds. diagnosis.
tests, imaging studies, or kidney biopsy) INCIDENCE/PREVALENCE • Familial and congenital renal disease,
that have been present for >3 months. This • 9 cases per 1,000 dogs and 16 cases per nephrotoxins, hypercalcemia, hypokalemic
definition includes all cases previously 1,000 cats examined. nephropathy, glomerulopathies, amyloidosis,
described by the terms renal insufficiency • Prevalence increases with age—age >15 pyelonephritis, polycystic kidney disease,
or renal failure, as well as less advanced years, reportedly 57 cases per 1,000 dogs and nephroliths, chronic urinary obstruction,
forms of kidney disease. Patients are 153 cases per 1,000 cats examined. drugs, lymphoma, leptospirosis (following
categorized into stages along a continuum acute kidney injury [AKI]), feline infectious
of progressive CKD (IRIS CKD stages 1–4; GEOGRAPHIC DISTRIBUTION
Worldwide peritonitis.
www.iris-kidney.com) based on >2 serum
creatinine values obtained over several SIGNALMENT RISK FACTORS
weeks when the patient is fasted and well Age, proteinuria, hypercalcemia, hypokalemia,
Species hypertension, urinary tract infection (UTI).
hydrated. The IRIS system uses the term
Dog and cat.
“kidney” rather than “renal” because it is
more universally recognized by pet owners. Breed Predilections
See Genetics.
PATHOPHYSIOLOGY
More than ~67–75% reduction in renal Mean Age and Range D IAGNOSIS
function results in impaired urine- Mean age at diagnosis is 7 years in dogs and 9 DIFFERENTIAL DIAGNOSIS
concentrating ability (leading to polyuria/ years in cats. Animals of any age can be • See Polyuria and Polydipsia for differential
polydipsia [PU/PD]) and retention of affected; prevalence increases with age. diagnosis.
nitrogenous waste products of protein Predominant Sex • Azotemia—includes causes of prerenal and
catabolism (azotemia). CKD is progressive; None postrenal azotemia, AKI, and hypoadreno-
more advanced CKD results in uremia. corticism.
Decreased renal erythropoietin and calcitriol SIGNS
• Prerenal azotemia—azotemia with urine
production results in hypoproliferative General Comments specific gravity (USG) >1.030 in dogs and
anemia and renal secondary hyperpara • Clinical signs related to stage of CKD and >1.035 in cats; rapid reduction in azotemia
thyroidism, respectively. complications such as proteinuria and hyper- after correcting hypoperfusion indicates
SYSTEMS AFFECTED tension. prerenal azotemia; prerenal azotemia
• Cardiovascular—hypertension; uremic • CKD stages 1 and 2 may be asymptomatic; commonly occurs concurrent with primary
pericarditis. overt clinical signs typically become apparent renal azotemia when gastrointestinal signs of
• Endocrine/metabolic—renal secondary in stages 3 and 4. uremia are present.
hyperparathyroidism, activation of renin- • Animals with stable CKD (particularly • Postrenal azotemia—obstruction or rupture
angiotensin-aldosterone system, erythropoietin stages 3 and 4) may decompensate, resulting of excretory system; rapid correction of
deficiency. in uremic crisis. azotemia following elimination of obstruction
• Gastrointestinal—uremic stomatitis and Historical Findings or resolution of leakage from urinary tract
halitosis, nausea, vomiting, anorexia, • PU/PD. supports postrenal azotemia.
gastrointestinal bleeding, diarrhea. • Anorexia. • AKI—differentiated by normal to large
• Hemic/lymphatic/immune—anemia; • Lethargy. renal size, cylindruria, lack of indications of
hemorrhagic diathesis. • Vomiting. chronicity, and history of recent nephrotoxin
• Musculoskeletal—renal osteodystrophy; • Weight loss. exposure or hypotensive episode; AKI can
sarcopenia. • Nocturia. also occur in patients with CKD where rapid
• Neuromuscular—seizures and other • Constipation. developing increase in serum creatinine
neurologic signs, muscle tremors, muscle • Diarrhea. concentration and uremic signs suggests
wasting. • Acute blindness. acute-onset CKD.
• Ophthalmic—retinal detachment, • Seizures or coma. • Hypoadrenocorticism—characterized by
hemorrhage, or edema due to hypertension. • Cats may have ptyalism and muscle hyponatremia and hyperkalemia with hypo-
• Reproductive—impaired reproductive weakness with cervical ventroflexion. cortisolemia.
capacity. CBC/BIOCHEMISTRY/URINALYSIS
• Respiratory—uremic pneumonitis. • Hypoproliferative anemia.
• Kidneys may be small, irregular, enlarged
GENETICS (secondary to polycystic kidney disease or • High blood urea nitrogen (BUN), creatinine,
• Inherited in these breeds (mode of lymphoma), or normal. and symmetric dimethylarginine (SDMA).
inheritance indicated in parentheses)— • Dehydration. • Hyperphosphatemia.
Abyssinian cat (dominant with incomplete • Cachexia. • Metabolic acidosis (normal or high anion
penetrance); Persian cat (dominant); bull • Weakness. gap).
terrier (dominant); Cairn terrier (recessive); • Mucous membrane pallor. • Hypokalemia or hyperkalemia.
German shepherd (dominant); Samoyed • Oral ulceration. • Hypercalcemia or hypocalcemia.
(continued) Chronic Kidney Disease

• USG <1.030 in dogs and <1.035 in cats. DIET CONTRAINDICATIONS
• Proteinuria. • Diets designed for CKD delay onset of Avoid nephrotoxic drugs (aminoglycosides, C
OTHER LABORATORY TESTS uremic crisis and extend survival in dogs and cisplatin, amphotericin B) and corticosteroids.
Urinary protein : creatinine ratio to assess cats with CKD stages 2–4; they are standard PRECAUTIONS
proteinuria. of care for these patients. • Drug dosage or dosing interval may need to
• Important components of renal foods— be modified for some drugs eliminated by the
IMAGING reduced protein, phosphorus, sodium, and
• Abdominal radiographs may demonstrate kidneys.
net acid content, supplementation of n-3 • Use ACE inhibitors and ARB cautiously;
small kidneys, or large kidneys secondary to fatty acids and antioxidants.
polycystic kidney disease or lymphoma. monitor for worsening of azotemia,
• Free access to fresh water.
• Ultrasound demonstrates small kidneys and • Generally avoid nonsteroidal anti-inflam-
hyperechoic renal parenchyma with less CLIENT EDUCATION matory drugs.
• CKD typically progresses to terminal kidney
apparent distinction between cortex and POSSIBLE INTERACTIONS
medulla in some animals. Animals with failure over months to years, but may not be Cimetidine or trimethoprim may cause
lymphoma often have renomegaly with progressive in some cats, which may live for years artifactual increases in serum creatinine
hypoechoic renal parenchyma. • Higher levels of proteinuria associated with concentration by reducing tubular secretion
shorter survival; may be mitigated by anti- in dogs with CKD.
DIAGNOSTIC PROCEDURES proteinuria therapy.
• Blood pressure measurement to detect • Heritability of familial renal diseases. ALTERNATIVE DRUG(S)
hypertension. • Metoclopramide (0.2–0.4 mg PO/SC
• Measurement of glomerular filtration rate SURGICAL CONSIDERATIONS q6–8h) can be used to treat uremic vomiting.
may be useful for detection of loss of kidney • Avoid hypotension during anesthesia. • Hemodialysis and renal transplantation are
function before onset of azotemia. • Renal transplantation has been successfully available at selected referral hospitals.
• Renal biopsy may be indicated in proteinuric performed in cats with CKD.
patients with normal to large kidneys.
PATHOLOGIC FINDINGS
• Gross—small kidneys with irregular FOLLOW-UP
surface; fewer glomeruli found on visualizing MEDICATIONS
PATIENT MONITORING
cut across renal cortex. DRUG(S) OF CHOICE • Monitor at regular intervals; initially weekly
• Histopathologic—variable; complete
Uremic Crisis for patients receiving erythropoietin; every
evaluation of biopsy material requires light,
• Antiemetics (maropitant 1 mg/kg q24h; or 1–3 months for stable patients with CKD
immunofluorescent, and electron microscopy;
ondansetron 0.2–1 mg/kg IV q12h) to minimize stages 3 and 4.
advanced CKD has nonspecific changes
vomiting and hyporexia due to nausea. • Proteinuric patients—monitor at least every
including interstitial fibrosis and foci of
• Potassium chloride in IV fluids or 3–4 months (minimum: serum creatinine and
interstitial mononuclear cells, chronic
potassium gluconate PO (2–6 mEq/cat/day) urine protein : creatine ratio).
generalized nephropathy.
as needed to correct hypokalemia. PREVENTION/AVOIDANCE
• Findings may be specific for diseases
• Sodium bicarbonate to correct metabolic
causing CKD in some patients with less • Do not breed animals with familial renal
acidosis (IV to raise blood pH >7.1). disease.
advanced disease.
Compensated CKD • Include urinalysis and serum creatinine in
• Antiemetic (maropitant) and potassium yearly examination for older pets; if serum
gluconate as above. creatinine increases, increase frequency to
• Mirtazapine (cats, 1.88 mg PO q 24–47h) every 4–6 months.
TREATMENT to promote appetite. POSSIBLE COMPLICATIONS
APPROPRIATE HEALTH CARE • Intestinal phosphate binders as needed to • Systemic hypertension.
Patients with compensated CKD may be correct hyperphosphatemia (see • Uremia.
managed as outpatients; patients in uremic Hyperparathyroidism, Renal Secondary). • Anemia.
crisis should be managed as inpatients. • Darbepoetin (see Anemia of Chronic • UTI.
NURSING CARE Kidney Disease). • Nephrouretrolithiasis.
• Uremic crisis—correct fluid and electrolyte • Amlodipine (dogs, 0.1–0.6 mg/kg PO q24h;
cats, 0.625–1.25 mg/cat PO q24h) or EXPECTED COURSE AND PROGNOSIS
deficits with IV fluids, providing 25% of • Short term—depends on severity.
calculated fluid deficit in first hour; thereafter, angiotensin-converting enzyme (ACE)
inhibitors (0.5 mg/kg PO q24h) or angiotensin • Long term—guarded to poor in dogs (CKD
serially monitor perfusion, blood pressure, and tends to be progressive over months to years);
urine output to assess adequacy of fluid therapy; receptor blockers (ARB; e.g., telmisartan
1–3 mg/kg PO q24h) as needed for hyperten- poor to good in cats (CKD does not progress
if perfusion not improved, additional fluid in some cats).
should cautiously be administered. Provide sion; amlodipine and telmisartan are more
remaining fluid deficit over next 12–24 hours. effective than ACE inhibitors for CKD-induced
Overhydration can result in anuria; once hypertension; if refractory to monotherapy,
patient has been hydrated, only sufficient fluid consider combination of amlodipine and ACE
to sustain hydration should be administered. inhibitor or ARB, with frequent monitoring of MISCELLANEOUS
• Subcutaneous fluid therapy may benefit blood pressure and electrolytes.
• ACE inhibitor (start at 0.5 mg/kg PO ASSOCIATED CONDITIONS
patients with moderate to severe CKD. Continue • Renal secondary hyperparathyroidism.
therapy only if clinical improvement noted. q24h; increase to 1 mg/kg PO q12h) or ARB
(telmisartan 1–3 mg/kg PO q24h) for • Systemic hypertension.
ACTIVITY proteinuria. • Nephroureterolithiasis.
Unrestricted
Chronic Kidney Disease (continued)
AGE-RELATED FACTORS • Hydronephrosis. INTERNET RESOURCES

C Renal function may decrease with aging. • Hyperparathyroidism, Renal Secondary. www.iris-kidney.com
• Hypertension, Systemic Arterial.
ZOONOTIC POTENTIAL Suggested Reading
• Nephrolithiasis.
None Polzin DJ. Chronic kidney disease. In:
• Polycystic Kidney Disease. Ettinger SJ, Feldman EC, eds., Textbook of
PREGNANCY/FERTILITY/BREEDING • Polyuria and Polydipsia.
Patients with mild CKD may maintain Veterinary Internal Medicine, 7th ed.
• Proteinuria. St. Louis, MO: Elsevier, 2010, pp. 1990–2021.
pregnancy; those with moderate to severe • Pyelonephritis.
disease may be infertile or have spontaneous Ross SJ, Polzin DJ, Osborne CA. Clinical
• Urinary Tract Obstruction. progression of early chronic renal failure
abortions; breeding of females not recomm-
ended. ABBREVIATIONS and implications for management. In:
• ACE = angiotensin-converting enzyme. August JR, ed., Consultations in Feline
SYNONYMS • AKI = acute kidney injury. Internal Medicine. St. Louis, MO: Elsevier,
• Chronic kidney failure. • ARB = angiotensin receptor blocker. 2006, pp. 389–398.
• Chronic renal disease or failure. • BUN = blood urea nitrogen. Author David J. Polzin
SEE ALSO • CKD = chronic kidney disease. Consulting Editor J.D. Foster
• Acute Kidney Injury. • PU/PD = polyuria/polydipsia.
• Anemia of Chronic Kidney Disease. • SDMA = symmetric dimethylarginine.
• Azotemia and Uremia. • USG = urine specific gravity. Client Education Handout
• Congenital and Developmental Renal • UTI = urinary tract infection. available online
Diseases.
Chylothorax
when middle-aged. • Shiba Inu—develop and range from yellow to pink. • Protein
when young (<1–2 years of age). content varies, and high lipid content will C
Predominant Sex make refractive index inaccurate. • Total
BASICS nucleated cell count—usually <10,000
None identified.
DEFINITION cells/μL. • Fluid triglycerides—higher
• Accumulation of chyle in the pleural space. SIGNS compared to serum. • Fluid cholesterol—
• Chyle—triglyceride-rich fluid from the General Comments lower compared to serum.
intestinal lymphatics that empties into the • Signs will depend on the rate of fluid Cytology
venous system (usually cranial cava/jugular accumulation and volume of pleural effusion. • Place sample in an EDTA tube to allow cell
vein) in the thorax. • Pseudochylous • Usually not exhibited until there is marked count to be performed. • Initially, cytology
effusion—effusion that contains less triglycer- impairment of ventilation. • Many patients comprises primarily small lymphocytes,
ides and more cholesterol compared to serum, appear to have the condition for prolonged neutrophils, and macrophages containing
but appears fatty grossly. • Thoracic lymphan- periods before diagnosis. lipid. • Chronic effusions contain fewer
giectasia—tortuous, dilated lymphatics found lymphocytes due to continued loss and more
Historical Findings
in many animals with chylothorax. • Fibrosing nondegenerate neutrophils due to inflamma-
• Tachypnea and respiratory difficulty.
pleuritis—condition in which pleural thick- tion from multiple thoracocenteses or
• Coughing—can be present for months
ening leads to constriction of lung lobes; when irritation of pleural lining by chyle. • Atypical
before examination, likely due to lung
severe, results in marked restriction of lymphocytes—suggestive of underlying
compression associated with pleural effusion.
ventilation; can be caused by any chronic neoplasia.
• Lethargy. • Anorexia and weight loss.
pleural exudate, but is most commonly
• Exercise intolerance. IMAGING
associated with chylothorax and pyothorax.
Physical Examination Findings Thoracic Radiography
PATHOPHYSIOLOGY
• Vary with cause of effusion. • Muffled heart • Two to four views if patient is stable—
• Alteration of flow through thoracic duct (TD)
and lung sounds ventrally. • Increased pleural effusion. • Dorsoventral view
leading to leakage of chyle—can be related to
bronchovesicular sounds, particularly in dorsal associated with less stress than ventrodorsal
increased pressure or permeability in TD or
lung fields. • Pale mucous membranes or view in animal with respiratory difficulty.
venous obstruction downstream. • Can be
cyanosis. • Arrhythmia. • Heart murmur. • Repeat radiographs after thoracocentesis to
caused by any disease or process that increases
• Signs of right-sided heart failure (e.g., jugular assess for underlying causes of effusion or
systemic venous pressure at the entrance of the
pulses, ascites, hepatomegaly). • Decreased evidence of fibrosing pleuritis; if collapsed lung
TD to the venous system. • Cardiac causes—
compressibility of anterior chest—common in lobes do not appear to reexpand after pleural
pericardial disease, cardiomyopathy, heartworm
cats with a cranial mediastinal mass. fluid is removed or if respiratory distress
disease, other causes of right-sided heart failure;
thrombosis around pacing lead wire. CAUSES persists with only minimal fluid present,
• Noncardiac causes—neoplasia (especially • Cranial mediastinal masses—lymphoma, suspect underlying pulmonary parenchymal or
mediastinal lymphoma in cats), lung lobe torsion, thymoma. • Cardiac disease—heartworm, pleural disease (e.g., fibrosing pleuritis).
diaphragmatic hernia, venous granuloma, venous cardiomyopathy, pericardial disease, congenital Ultrasonography/Echocardiography
thrombus. • Rare TD rupture/trauma—surgical diseases. • Lung lobe torsion. • Venous • Should be performed before thoracocentesis
(thoracotomy), nonsurgical (e.g., hit by car). obstruction—granuloma, thrombi. • Congenital if patient is stable—fluid acts as an acoustic
• Idiopathic considered most common. abnormality of TD. • Cardiac or thoracic window, enhancing visualization of thoracic
surgery. • Idiopathic—most common cause. structures. • Assess for underlying causes—
SYSTEMS AFFECTED
• Respiratory—due to reduced lung RISK FACTORS detect abnormal cardiac structure and function,
expansion. • Systemic signs can be present Unknown pericardial disease, and mediastinal masses.
secondary to the respiratory distress CT Lymphangiography
(e.g., decreased appetite, weight loss). • Can quantify TD branches more accurately
GENETICS than standard radiographic lymphangiogra-
Unknown DIAGNOSIS phy. • In dogs, percutaneously inject 1–2 mL
DIFFERENTIAL DIAGNOSIS of nonionic contrast material into mesenteric
INCIDENCE/PREVALENCE lymph nodes using ultrasound or CT
Unknown Other causes of pleural effusion—neoplasia,
pyothorax, heart failure, feline infectious guidance. • Acquire helical thoracic CT
GEOGRAPHIC DISTRIBUTION peritonitis (FIP). images before and after injection of contrast
Worldwide media. • Can document location and
CBC/BIOCHEMISTRY/URINALYSIS character of TD and its tributary lymphatics;
SIGNALMENT • Often normal. • Lymphopenia and likely useful for surgical planning.
Species hypoalbuminemia—can be found; hypona-
Dog and cat. tremia and hyperkalemia sometimes noted PATHOLOGIC FINDINGS
due to fluid shifts with repeat thoracocentesis. • Lymphatics (including TD)—difficult to
Breed Predilections identify at necropsy. • Fibrosing pleuritis—
• Dogs—Afghan hound and Shiba Inu. OTHER LABORATORY TESTS lungs appear shrunken; pleural layers (visceral
• Cats—oriental breeds (e.g., Siamese and Heartworm testing. and parietal) are diffusely thickened.
Himalayan). Fluid Analysis • Fibrosing pleuritis—characterized
Mean Age and Range • Classified as an exudate. • Color will depend histologically by diffuse, moderate to marked
• Any age affected. • Cats—more common on fat content from diet and presence of thickening of the pleura by fibrous connective
in older cats; could indicate an association concurrent hemorrhage—usually milky white tissue with moderate infiltrates of lympho-
with neoplasia. • Afghan hound—develop and opaque, but can appear serosanguinous cytes, macrophages, and plasma cells.
Chylothorax (continued)
perform in conjunction with lymphangiog-

C raphy; methylene blue injected in the
mesenteric lymph node greatly facilitates
TREATMENT visualization and complete occlusion of all FOLLOW-UP
APPROPRIATE HEALTH CARE branches. • Thickening of the pericardium PATIENT MONITORING
• Dyspneic animal—immediate thoraco can prevent formation of lymphaticovenous • Monitor for signs of recurrence of pleural
centesis; removal of even small amounts of communications—perform pericardiectomy effusion (tachypnea, labored breathing,
pleural effusion can markedly improve simultaneously with TD ligation; reports of respiratory distress)—perform thoracentesis
ventilation. • Identify and treat the up to 100% success rate when both as needed. • Periodically reevaluate for several
underlying cause, if possible. • Medical techniques are performed; second surgery years to detect recurrence.
management—usually treated on outpatient can be necessary if all branches are not
basis with intermittent thoracocentesis as occluded. • Video-assisted thorascopic
• Fibrosing pleuritis. • Iatrogenic infection
needed based on clinical signs (see Medications). surgery for thoracic duct ligation and
with repeated thoracocentesis—important to
• Chest tubes—place only in patients with pericardiectomy is reported to have similar
use aseptic technique.
suspected chylothorax secondary to trauma success rates to thoracotomy (86%).
(very rare), in cases with rapid fluid EXPECTED COURSE AND PROGNOSIS
Other
accumulation, or after surgery. • Surgery if • Can resolve spontaneously or after surgery.
• Success rates of 83–88% reported for
medical management does not resolve the • Untreated or chronic disease—can result in
cysterna chyli ablation in combination with
problem in 2–3 months (see Surgical severe fibrosing pleuritis and persistent dyspnea.
TD ligation. • Salvage procedures for
Considerations); some clinicians believe • Euthanasia—frequently performed in
recurrence after TD ligation include cisterna
earlier intervention is better to avoid potential patients that do not respond to surgery or
chyli and TD glue embolization, pleuroperi-
for development of restrictive pleuritis. medical management.
toneal or pleurovenous shunts, or placement
NURSING CARE
• Patients undergoing multiple thoraco
®
of a PleuralPort .
centeses can rarely develop electrolyte

abnormalities (hyponatremia, hyperkalemia) MISCELLANEOUS
that may need to be corrected with fluid MEDICATIONS ASSOCIATED CONDITIONS
therapy. • Thoracocentesis—perform under Diffuse lymphatic abnormalities (e.g., intestinal
aseptic conditions to reduce risk of DRUG(S) OF CHOICE
lymphangiectasia, hepatic lymphangiectasia,
iatrogenic infection; antibiotic prophylaxis • Rutin 50–100 mg/kg PO q8h; believed to
pulmonarylymphangiectasia,andchylousascites)—
generally unnecessary if proper technique is increase macrophage removal of proteins,
may be noted; may worsen the prognosis.
used. which promotes absorption of fluid; complete
resolution of effusion appears to occur in AGE-RELATED FACTORS
ACTIVITY some patients; further study is required to Young patients may have a better prognosis
Patients will usually restrict their own exercise determine whether resolution occurs than old animals because of the association of
as pleural fluid volume increases or if they spontaneously or in response to this therapy. neoplasia with advanced age.
develop fibrosing pleuritis. • Somatostatin analog (octreotide)—a ABBREVIATIONS
DIET naturally occurring substance that inhibits • FIP = feline infectious peritonitis.
• Low fat—potentially decreases the amount gastric, pancreatic, and biliary secretions and • TD = thoracic duct.
of fat in the effusion, which would improve prolongs gastrointestinal transit time,
the patient’s ability to resorb fluid from the decreases jejunal secretion, and stimulates Suggested Reading
thoracic cavity; not a cure; may help in gastrointestinal water absorption; in traumatic Allman DA, Radlinsky MG, Ralph AG,
management by facilitating reabsorption. chylothorax, reduction of gastrointestinal Rawlings CA. Thoracoscopic thoracic duct
• Medium-chain triglycerides are transported secretions may aid healing of the TD by ligation and thoracoscopic pericardiectomy
via the TD in dogs and are no longer decreasing TD lymphatic flows; resolution of for treatment of chylothorax in dogs. Vet Surg
recommended. pleural fluid has occurred in dogs and cats 2010, 39(1):21–27.
with idiopathic chylothorax in which Fossum TW, Mertens MM, Miller MW, et al.
CLIENT EDUCATION Thoracic duct ligation and pericardectomy
• Inform client that no specific treatment will
octreotide has been administered, but the
mechanism is unknown; octreotide for treatment of idiopathic chylothorax.
stop the effusion in all patients with the J Vet Intern Med 2004, 18:307–310.
idiopathic form of the disease. • Inform (Sandostatin®; 10 μg/kg SC q8h for 2–3
weeks) is a synthetic analog of somatostatin Johnson EG, Wisner ER, Kyles A, et al.
client that the condition can spontaneously Computed tomographic lymphography of
resolve in some patients after several weeks or that has a prolonged half-life and minimal
side effects. the thoracic duct by mesenteric lymph node
months. injection. Vet Surg 2009, 38(3):361–367.
SURGICAL CONSIDERATIONS CONTRAINDICATIONS Author Elizabeth Rozanski
Cardiac disease or neoplasia—treat the Consulting Editor Elizabeth Rozanski
TD Ligation and Pericardiectomy underlying disease rather than the effusion Acknowledgment The author and book
• Recommended in patients that do not (other than heartworm disease in cats where editors acknowledge the prior contribution of
respond to medical management. • The TD ligation may be beneficial while the Jill S. Pomrantz.
duct usually has multiple branches in the heartworm infection clears).
caudal thorax where ligation is performed;
failure to occlude all branches results in Client Education Handout
continued pleural effusion. • Always available online
Cirrhosis and Fibrosis of the Liver

• Respiratory—tachypnea if tense ascites or • Jaundice—with necroinflammatory
pleural effusion. disease; DPM usually anicteric. C
• Skin—superficial necrolytic dermatitis, • Cats—ascites uncommon with acquired
BASICS unkempt coat. necroinflammatory disease, more common with
DEFINITION GENETICS DPM; ptyalism, aggression, seizures with HE.
• Hepatic fibrosis—replacement/effacement Familial predisposition for chronic hepatitis— Physical Examination Findings
of hepatic parenchyma, intrasinusoidal, Doberman pinscher, cocker spaniel, Labrador • Lethargy.
variable zonal, deposition of extracellular retriever, Maltese, Bedlington terrier (copper • Poor body condition/coat.
matrix (ECM). related), West Highland white terrier, others. • ± Variable jaundice.
• Cirrhosis—regenerative nodules with • ± Ascites.
dissecting fibrotic partitions and regions of INCIDENCE/PREVALENCE
• ± HE.
parenchymal extinction, deranging hepatic High in dogs with chronic necroinflammatory
• Obstructive uropathy—ammonium
architecture; usually reflects chronic necro- liver disease, animals with chronic extrahepatic
bile duct occlusion (EHBDO), dogs with biurates.
inflammatory liver injury. • Anasarca—rare; may develop with over-
severe hepatic copper accumulation.
PATHOPHYSIOLOGY zealous fluid therapy.
• Fibrosis—usually reflects injury-associated SIGNALMENT • Liver size—dogs: microhepatia; cats: variable.
release of cytokines/mediators stimulating Species • Coagulopathy—variable, uncommon in DPM.
production and accumulation of ECM; • Cirrhosis—dogs with chronic hepatitis; cats • Cutaneous lesions—superficial necrolytic
exception: ductal plate malformation (DPM), with chronic cholangitis/cholangiohepatitis; dermatitis.
with congenital hepatic fibrosis (CHF) dogs and cats with chronic EHBDO. CAUSES
phenotype (severe portal-to-portal bridging • Severe fibrosis—dogs and cats with severe • Chronic necroinflammatory, oxidant, or
fibrosis without chronic inflammation). DPM-CHF phenotype. immune-mediated liver injury has many causes;
• Cirrhosis—consequence of chronic hepatic may develop subsequent to chronic inflamma-
Breed Predilection
injury, fibrogenesis, and hepatic regeneration; tory bowel disease (IBD) or pancreatitis.
• Many breeds and mixed-breed dogs.
typified by regenerative nodules, reduced • CuAH.
• Copper associated hepatopathy (CuAH)—
functional hepatic mass, collagen deposition • Drug- or toxin-induced liver injury—anti-
genetics proven only in Bedlington terriers and
in sinusoids (space of Disse) or portal tracts, convulsants; azole antifungals; nonsteroidal
partially in Labrador retrievers; Doberman
compromising parenchymal perfusion. anti-inflammatory drug (NSAID) oxibenda-
pinschers, West Highland white terriers, and
• Cirrhosis/fibrosis—leads to hepatic dysfun- zole; trimethoprimsulfamethoxazole; chronic
Dalmatians appear predisposed; but all breeds at
ction, capillarization of hepatic sinusoids, food-borne toxins (aflatoxins), others.
risk for CuAH due to dietary Cu intake.
collagenization of sinusoids, development of • Infections—leptospirosis, canine adenovirus
• DPM-CHF phenotype—boxers may
sinusoidal hypertension, intrahepatic I, leishmanial, histoplasmosis, protozoal
be predisposed, many breeds of dogs and
shunting through collagenized sinusoids, (toxoplasmosis).
cats; cats with polycystic malformations at
recanalized vascular pathways in fibrotic • Chronic cholangiohepatitis (cats).
risk.
partitions between regenerative nodules; these • Chronic EHBDO (>6 weeks, dogs and cats).
microcirculatory disturbances impair Mean Age and Range • Single episode of massive hepatic necrosis;
exchanges between blood and hepatocytes. • Cirrhosis (dogs)—any age; more common sago palm (cycad toxicity), xylitol, NSAIDs
• Sinusoidal hypertension—leads to in middle-aged to older; CuAH any age. in dogs with substantial Cu accumulation.
hepatofugal portal flow (away from liver); • Biliary cirrhosis (cats)—with chronic
splanchnic hypertension; acquired portosys- cholangiohepatitis often >7 years old. RISK FACTORS
temic shunt (APSS) formation; episodic • Fibrosis—DPM-CHF phenotype (dogs, • Breed predisposition.
hepatic encephalopathy (HE); splanchnic cats)—ECM accumulates with aging • Dietary Cu intake >patient tolerance.
pooling of blood, decreased effective systemic (suspected), genetic cause (see Ductal Plate • Hepatic iron accumulation—
blood volume, stimulation of renal sodium Malformation). supplementation.
and water retention, with ascites formation; • Chronic hepatobiliary inflammation.
Predominant Gender • Chronic EHBDO.
hypertensive splanchnic vasculopathy • Cocker spaniels—may be higher in
predisposing to enteric bleeding. • Chronic phenobarbital administration (dogs).
males. • NSAIDS—dogs, especially carprofen.
SYSTEMS AFFECTED • Doberman pinschers and Labrador
• Gastrointestinal (GI)—splanchnic portal retrievers—no sex predilection.
hypertension leads to ascites and propensity • DPM—no gender predilection.
for enteric bleeding. SIGNS
• Neurologic—HE. DIAGNOSIS
• Hemic—red blood cell (RBC) microcyto- General Comments
sis reflects APSS; bleeding tendencies: failed • Initially—vague and nonspecific.
• Chronic hepatitis—common in dogs.
factor synthesis or activation, thrombocyto- • Later—relate to complications of portal
• Cholangiohepatitis—common in cats.
penia; reduced anticoagulants increases risk hypertension (e.g., HE, ascites, gastroduo-
• Noncirrhotic portal hypertension—dogs.
for thrombosis. denal bleeding) and impaired hepatic
• Chronic EHBDO.
• Renal/urologic—ammonium biurate function.
• Chronic IBD or pancreatitis.
crystalluria; isosthenuria: polyuria/ Historical Findings • Hepatic neoplasia.
polydipsia (PU/PD); hepatorenal syndrome • Chronic intermittent lethargy, anorexia, • Metastatic neoplasia or carcinomatosis.
(rare) may follow therapeutic paracentesis of reduced body condition. • Congenital portosystemic vascular anomaly
large-volume ascites (postcentesis hypoten- • GI signs—vomiting, diarrhea or constipa- (shunt).
sion syndrome [PHS]). tion. Melena—late stage or as APSS develop. • Congenital portal atresia—intrahepatic or
• Endocrine/metabolic—hypoglycemia if • PU/PD. extrahepatic.
end-stage liver failure. • Late onset—ascites, bleeding, HE. • Right-sided heart failure, pericardial disease.
Cirrhosis and Fibrosis of the Liver (continued)
• Cats—hepatic lipidosis, feline infectious • Liver biopsy—for definitive diagnosis; ACTIVITY

C peritonitis, toxoplasmosis. accuracy increased by multiple biopsy samples. Limit
• Hemolytic anemia (jaundice differential). • Ultrasound guided—14–16G.
DIET
• Laparoscopy/laparotomy—best methods,
CBC/BIOCHEMISTRY/URINALYSIS • Withhold oral food in acute severe HE if
permits gross visualization, documents APSS, stupor, coma, or vomiting associated with
CBC biopsy access to multiple liver lobes and focal
• Microcytic RBCs: APSS; mild anemia: enteric bleeding or pancreatitis.
lesions. • Consider partial parenteral nutrition or
small RBCs with normal cell count; anemia
of chronic disease; microangiopathic shearing: PATHOLOGIC FINDINGS total parenteral nutrition.
sinusoidal fibrosis, APSS. Gross • If HE—restrict protein intake, use soy or
• Mild thrombocytopenia variable. • Fibrosis—small, firm irregular to finely dairy protein sources (dogs) with medical
• Leukogram variable. nodular liver; DPM-CHF may not be small; interventions to increase nitrogen tolerance
fibrotic liver may display APSS, ± ascites. (see Hepatic Encephalopathy).
Biochemistry • Supplement water-soluble vitamins.
• Cirrhosis—firm irregular liver; prominent
• Bilirubin variable.
• Liver enzyme activities—high (alanine
micro- or macronodules, APSS, ± ascites. CLIENT EDUCATION
transaminase [ALT] > alkaline phosphatase Histopathology • Treatment palliative and symptomatic.
[ALP]) noted before clinical signs or liver • Immune-mediated hepatitis—periportal, • Fibrosis diminished by control of inflam-
dysfunction; at end-stage enzymes may decline. lobular, or centrilobular lymphoplasmacytic mation and provocative diseases.
• Normal to hypoalbuminemia. infiltrates, hepatic cord disorganization, • Attenuate factors provoking HE—
• Normal to hyperglobulinemia. sinusoidal fibrosis, biliary hyperplasia. azotemia, dehydration; infection; catabolism;
• Hypocholesterolemia—reflects APSS. • CuAH—initially centrilobular, may evolve high-protein meals, hypokalemia; alkalemia;
• Low blood urea nitrogen (BUN)—reduced immune-mediated hepatitis; single necrotic constipation, endoparasitism; enteric
urea cycle activity, APSS, protein-restricted hepatocytes; significant fibrotic tissue may bleeding; certain drugs.
diet, PU/PD. falsely decrease quantitative Cu concentration SURGICAL CONSIDERATIONS
• Hypoglycemia—rare. measurements in biopsy samples. • Cirrhosis—high anesthetic risk; gas
• Hypokalemia—may predispose to HE. • DPM—bridging partitions with proliferative anesthesia preferred: isoflurane or
• Hyponatremia—fluid imbalance with nonfunctional embryonic bile ducts embedded sevoflurane.
ascites. in ECM interconnecting portal regions. • Coagulopathy—predisposes to bleeding;
• Postnecrotic fibrosis—fibrosis marks regen- BMBT may better assess risk for bleeding.
Urinalysis
• Isosthenuria—with PU/PD.
erative repair, disorganized wide hepatic • Postoperative intensive care—avoid HE,
• Ammonium biurate crystalluria.
cords; engorged lymphatics reflect sinusoidal maintain hydration, euglycemia, electrolytes,
• Bilirubinuria, bilirubin crystalluria.
hypertension. acid-base balance (avoid alkalemia).
• Cirrhosis—diffuse lesion; fibrosis, nodular • Predisposed to enteric bacterial transloca-
OTHER LABORATORY TESTS regeneration distorting lobular architecture, tion—judiciously administer antibiotics, esp.
• Ascitic fluid—pure or modified transudate. periportal or sinusoidal fibrosis depending on if surgical procedures involve alimentary canal
• Coagulation tests—inconsistently prolonged zone of chronic injury, engorged lymphatics; or biliary structures.
prothrombin time (PT), activated partial single hepatocyte necrosis if active disease.
thromboplastin time, buccal mucosal
bleeding time (BMBT).
• Low protein C and antithrombin activity—
reflects APSS, synthetic failure, or dissemi- MEDICATIONS
nated intravascular coagulation (DIC). TREATMENT DRUG(S) OF CHOICE
• Serum bile acids—high; reflects APSS or APPROPRIATE HEALTH CARE • Treatments for specific etiologies—chelate
cholestasis in cirrhosis. • Outpatient—minimally symptomatic Cu if CuAH; withdraw potentially hepatotoxic
• Hyperammonemia—inferred from patients. drugs, herbal or natural remedies.
ammonium biurate crystalluria. • Inpatient—diagnostic tests; treatment for • No clinical trials prove efficacy of specific
IMAGING dehydration, severe HE, enteric bleeding, regimens in animals.
tense ascites. Immune Modulation
Radiography
Abdominal—small to normal-sized liver; NURSING CARE • Prednisolone/prednisone—1–2 mg/kg q24h
ascites may obscure details; urate calculi • Fluids—avoid lactate if hepatic failure; PO; taper to 0.5 mg/kg q48h; do not exceed
radiolucent unless calcium complexed. avoid sodium loading if ascites. 40 mg/day/dog.
• B complex vitamins (esp. cats)—2 mL/L • Azathioprine—2 mg/kg (or 50 mg/m2)
Ultrasonography fluid advised. q24h for 14 days, then q48h; contraindicated
• Abdominal—hyperechoic or mixed • Vitamin K1—0.5–1.5 mg/kg SC q12h for 3 in cats (toxic); dogs: with prednisone, anti-
echogenic liver parenchyma; ± nodularity; doses initially; titrate with proteins invoked oxidants, antifibrotics, and polyenylphos-
often small with cirrhosis; abdominal effusion by vitamin K absence or antagonism (PIVKA; phatidylcholine (PPC).
(ascites); APSS (color-flow Doppler); enlarged if available) or PT. • Cyclosporine—5 mg/kg BID tapered to
portal lymph nodes; no parenchymal change • Glucose—if hypoglycemia; 2.5–5% dextrose q24h; has been successful as single agent or
in some cases. in polyionic solution; titrate to response. with corticosteroids.
• Doppler interrogation of portal vasculature— • Potassium chloride—in fluids, as needed. • Mycophenolate—10–15 mg/kg BID; has
may confirm hepatofugal flow or nests of APSS, • Avoid alkalosis—worsens HE. been successful as first- or second-line treat-
esp. near left kidney or splenic vessels. • Therapeutic large-volume abdominocente- ment with corticosteroids.
DIAGNOSTIC PROCEDURES sis if tense ascites nonresponsive to medical Antifibrotics
• Fine-needle aspiration cytology—helps rule treatment; caution: PHS—hypotensive crisis • Immunomodulation, S-adenosylmethionine
out neoplasia; rule in bacterial infection; and acute renal failure. (SAMe), silybin, vitamin E—considered
cannot define fibrosis or nonsuppurative antifibrotics as well as hepatoprotectants.
inflammation.
(continued) Cirrhosis and Fibrosis of the Liver

• Ursodiol—7.5 mg/kg/day PO q12h with PRECAUTIONS SEE ALSO
food; use indefinitely. • Diuretics—dehydration, hypokalemia, • Coagulopathy of Liver Disease. C
• Polyunsaturated phosphatidylcholine with alkalemia worsen HE. • Copper Associated Hepatopathy.
dilinolylphosphatidylcholine (PhosChol®)— • Glucocorticoids—increase susceptibility • Ductal Plate Malformation (Congenital
25 mg/kg/q24h, mix with food. to infection, enteric bleeding, sodium and Hepatic Fibrosis).
• Colchicine—0.025–0.03 mg/kg q24–48h; water retention, ascites, protein catabolism, • Hepatic Encephalopathy.
no evidence of chronic benefit; side effects HE. • Hepatitis, Chronic.
complicate use; no longer recommended. • Avoid drugs or reduce dose if first-pass • Hypertension, Portal.
• Losartan and telmisartan—losartan: 0.5 mg/ hepatic extraction, if require hepatic ABBREVIATIONS
kg/q24h; telmisartan: 0.5–1 mg/kg q24h conjugation or biotransformation (e.g., • ALP = alkaline phosphatase.
initial dose; closely monitor blood pressure, metronidazole—reduce conventional dose to • ALR = alanine transaminase.
renal function, and potassium, reducing dose 7.5 mg/kg PO q12h, as used for HE). • APSS = acquired portosystemic shunt.
if hypotension or hyperkalemia; angiotensin ALTERNATIVE DRUG(S) • BMBT = buccal mucosal bleeding time.
receptor blockers used in humans as antihy- • Dexamethasone—if ascites, replace • BUN = blood urea nitrogen.
pertensives and have been shown to be prednisone/prednisolone to avoid mineralo- • CHF = congenital hepatic fibrosis.
nephroprotective, to protect against some corticoid effect); divide dose by 7–10, • CuAH = copper associated hepatopathy.
forms of drug-induced hepatotoxicity, and to administer q3–4 days; taper dose to efficacy. • DIC = disseminated intravascular coagulation.
inconsistently limit hepatic fibrosis. • DPM = ductal plate malformation.
Antioxidants • ECM = extracellular matrix.
• Necroinflammatory disorders. • EHBDO = extrahepatic bile duct occlusion.
• SAMe—20 mg/kg q24h PO, empty stomach. • GI = gastrointestinal.
• Vitamin E mixed tocopherols—10 U/kg
F OLLOW-UP • HE = hepatic encephalopathy.
q24h PO with food. PATIENT MONITORING • IBD = inflammatory bowel disease.
• Liver enzymes, albumin, BUN, cholesterol, • NSAID = nonsteroidal anti-inflammatory drug.
Hepatoprotectants
bilirubin—monthly to quarterly. • PHS = postcentesis hypotension syndrome.
• Necroinflammatory disorders.
• Serial monitoring of total serum bile • PIVKA = proteins invoked by vitamin K
• Ursodeoxycholate, vitamin E, SAMe.
acids—adds no prognostic or diagnostic absence or antagonism.
• Silibinin—efficacy unclear, use PPC
information. • PPC = polyenylphosphatidylcholine.
complexed form (bioavailable), 2–5 mg/kg
• Body condition score, weight, muscle • PT = prothrombin time.
q24h PO.
mass—reflects nutritional adequacy/nitrogen • PU/PD = polyuria/polydipsia.
• Elemental zinc—1.5–3 mg PO q24h (if
balance. • RBC = red blood cell.
low liver zinc confirmed); adjust dose with
• Abdominal girth—reflects ascites volume. • SAMe = S-adenosylmethionine.
plasma zinc measurements; avoid ≥800 μg/dL;
• Azathioprine, mycophenolate, colchicine—
contraindicated with concurrent d-penicil- Suggested Reading
monitor for bone marrow toxicity (serial
lamine administration. Center SA. Metabolic, antioxidant, nutraceu-
CBCs) and other side effects.
Gastroprotectants tical, probiotic, and herbal therapies relating
POSSIBLE COMPLICATIONS to the management of hepatobiliary disorders.
• Gastric acid inhibitors—if enteric bleeding
HE, septicemia, bleeding—may be life- Vet Clin North Am Small Anim Pract 2004,
(see Hepatitis, Chronic).
threatening; DIC—may be terminal event. 34:67–172.
• Eliminate endoparasitism.
EXPECTED COURSE AND PROGNOSIS Eulenberg VM, Lidbury JA. Hepatic fibrosis
Ascites in dogs. J Vet Intern Med. 2018, 32:26–41.
• Flare-ups of HE and ascites may require
• Restrict activity and sodium intake Strickland JM, Buchweitz JP, Smedley RC,
hospitalization to adjust nutritional and
combined with diuretic therapy. et al. Hepatic copper concentrations in 546
medical interventions.
• Dietary sodium restriction (0.2% dry dogs (1982–2015). J Vet Intern Med 2018,
• Sodium restriction and diuretics may
matter basis or <0.05 g/100 kcal). 32:1943–1950.
require titration to achieve optimal control of
• Diuretics (see Hypertension, Portal; Hepatitis, Webster CRL, Center SA, Cullen JM, et al.
ascites.
Chronic); slowly mobilize effusion: furosemide ACVIM consensus statement on the
• Presence of ascites indicates severe disease.
(0.5–1 mg/kg IV/SC/PO q12h) with spironol- diagnosis and treatment of chronic hepatitis
• DPM—survival up to 12 years after diagnosis.
actone (0.5–2 mg/kg PO q12h); adjust dose to in dogs. J Vet Intern Med 2019,
• Cirrhosis—variable: poor long-term prognosis
response (7–10 day recheck; if no response 33(3):1173–1200.
in limited studies, <6 months; however, some
titrate up q3–5d to max dose 4 mg/kg/day). Authors Alysha Vincent and Kate Holan
can survive years (>5) with careful interventional
• Therapeutic large-volume abdominocentesis Consulting Editor Kate Holan
management depending on whether histologic
if nonresponsive ascites mobilization after Acknowledgment The author and book
changes truly “end-stage” or not.
7–14 days of diuretics and sodium restriction. editors acknowledge the prior contribution of
• Consider vasopressin V2 antagonists with Sharon A. Center.
low-dose diuretics for treatment-resistant
ascites (no published data for dogs or cats).
CONTRAINDICATIONS MISCELLANEOUS Client Education Handout
NSAIDs—avoid; potentiate enteric bleeding; available online
ZOONOTIC POTENTIAL
may worsen ascites; potentiate centrilobular Dogs with leptospirosis-associated chronic
hepatic necrosis-hepatotoxic metabolites and liver disease (rare) may shed organisms.
CuAH.
Claw and Clawfold Disorders

SIGNS OTHER LABORATORY TESTS
C • Licking at the feet and/or ungual folds. • Feline leukemia virus (FeLV).
• Lameness. • Serum thyroxine.
BASICS • Pain. • Antinuclear antibody (ANA) titer.
DEFINITION • Swelling, erythema, and exudate of ungual fold.
IMAGING
• Ungual fold—crescent-shaped tissue • Deformity or band formation of claw.
Radiographs—osteomyelitis of third phalanx,
surrounding the proximal claw. • Sloughing of claw.
neoplastic change.
• Coronary band and dorsal ridge (dorsal • Discoloration of claw.
ridge of the ungual crest)—produces most of • Hemorrhage from claw or at loss of a claw. DIAGNOSTIC PROCEDURES
the claw; contributes to the curvature of the • Biopsy—often involves a third phalanx
CAUSES amputation; inclusion of the coronary band
claw.
• Paronychia—inflammation of soft tissue Paronychia required for diagnosis of most diseases; punch
around the claw. • Infection—bacteria, dermatophyte, yeast biopsy of the claw (onychobiopsy).
• Onychomycosis—fungal infection of the (Candida, Malassezia). • Cytology of exudate from the claw and/or
claw. • Demodicosis. fold.
• Onychorrhexis—brittle claws that tend to • Immune-mediated—pemphigus, bullous • Skin scraping.
split or break. pemphigoid, systemic lupus erythematosus • Bacterial and fungal culture.
• Onychomadesis—sloughing of the claw. (SLE), drug eruption, SLO.
• Onychodystrophy—deformity caused by • Neoplasia—subungual squamous cell
abnormal growth; often a sequela of a carcinoma, melanoma, eccrine carcinoma,
osteosarcoma, subungual keratoacanthoma,
disorder.
inverted squamous papilloma.
TREATMENT
• Onychomalacia—softening of the claw.
• Arteriovenous fistula. PARONYCHIA
PATHOPHYSIOLOGY • Surgical removal of claw plate (shell).
• Claws and ungual folds—subject to trauma, Onychomycosis
• Antimicrobial soaks.
infection, vascular insufficiency, immune- • Dogs—Trichophyton mentagrophytes—
• Systemic antibiotics as per culture results.
mediated disease, parasites, neoplasia, defects usually generalized.
• Identify underlying condition and treat
in keratinization, and congenital abnormal- • Cats—Microsporum canis.
specifically.
ities. Onychorrhexis
• A particular claw deformity may be
Onychomycosis
• Idiopathic—especially in dachshunds;
• Antifungal soaks—chlorhexidine, povidone
caused by a variety of diseases—claw disease multiple claws.
is most often associated with other dermatoses: iodine, lime sulfur.
• Trauma.
• Surgical removal of claw plate—may
rarely the only epithelial structure affected. • Infection—dermatophytosis, leishmaniasis.
• A single disease can present with various
improve response to systemic medication.
Onychomadesis • Amputation of third phalanx.
claw lesions.
• Trauma.
• One foot affected—top differentials include Onychorrhexis
• Infection.
foreign body, neoplasia, trauma, fungal • Repair with fingernail glue (type used to
• Immune-mediated—pemphigus, bullous
infection, bacterial infection. attach false nails in humans).
pemphigoid, SLE, drug eruption, SLO.
• Multiple feet affected—allergy, endocrine, • Remove splintered pieces and maintain
• Vascular insufficiency—vasculitis, cold
secondary infections, demodicosis, with rotary sander (Dremel).
agglutinin disease.
immune-mediated disorders, epidermolysis • Treat underlying cause.
• Neoplasia—see above.
bullosa, symmetric lupoid onychodystrophy • Amputate third phalanx, last resort.
• Idiopathic.
(SLO), plasma cell pododermatitis, super- Onychomadesis
ficial necrolytic dermatitis, nutritional deficien- Claw Dystrophy
• Antimicrobial soaks.
cies, psychogenic dermatoses, idiopathic. • Acromegaly.
• Treat underlying cause.
• Feline hyperthyroidism.
SIGNALMENT Neoplasia
• Zinc-responsive dermatosis.
• Dog and cat. • Determined by biologic behavior of specific
• Congenital malformations.
• Claw and clawfold diseases—1.3% of dogs tumor.
• Leishmaniasis.
and 2.2% of cats. • Surgical excision.
• Mean age range—SLO 3–8 years. • Amputation of digit or leg.
• No predominant sex reported. • Chemotherapy and/or radiation therapy.
• Dachshunds—onychorrhexis.
• German shepherd dogs, Rottweilers, DIAGNOSIS Claw Dystrophy
possibly giant schnauzers and Doberman Treat underlying cause.
pinschers—SLO. • Trauma or neoplasia often affects a single
• Siberian huskies, dachshunds, Rhodesian claw.
ridgebacks, Rottweilers, cocker spaniels— • Involvement of multiple claws suggests a
idiopathic onychodystrophy. systemic disease. MEDICATIONS
• German shepherd dogs, whippets, English • Immune-mediated diseases (except SLO)
springer spaniels—idiopathic onychomadesis DRUG(S) OF CHOICE
usually have other skin lesions in addition to • Bacterial paronychia—systemic antibiotics
• Shorthair dog breeds—paronychia in claw or ungual fold lesions.
multiple digits. based on culture and sensitivity.
• Devon Rex cats—Malassezia paronychia. CBC/BIOCHEMISTRY/URINALYSIS • Yeast paronychia—Candida or Malassezia
May show evidence of SLE, diabetes mellitus, paronychia: ketoconazole (5–10 mg/kg PO
hyperthyroidism, or other systemic illness. q12–24h); topical nystatin or miconazole.
(continued) Claw and Clawfold Disorders

• Onychomycosis—griseofulvin (50–150 mg/ • NSAID = nonsteroidal anti-inflammatory
kg PO/day) or ketoconazole (5–l0 mg/kg PO drug. C
q12h) for 6–12 months until negative • SLE = systemic lupus erythematosus.
cultures; itraconazole (10 mg/kg PO q24h) FOLLOW-UP • SLO = symmetric lupoid onychodystrophy.
for 3 weeks and then pulse therapy until EXPECTED COURSE AND PROGNOSIS Suggested Reading
resolved. • Slow claw growth cycle may require 6–8 Helton Rhodes KA, Werner A. Blackwell’s
• Onychomadesis—determined by cause; months of therapy to fully correct an Five-Minute Veterinary Consult: Clinical
immunomodulation therapy for immune- abnormality; improvement may be noted Companion: Small Animal Dermatology,
mediated diseases (e.g., SLO); options include after 6–8 weeks of appropriate treatment. 3rd ed. Hoboken, NJ: Wiley-Blackwell,
essential fatty acid supplementation; cycline • Bacterial or yeast paronychia and 2018.
antibiotics: tetracycline 250 mg PO TID for onychomycosis—treatment may be Miller WH, Griffin CE, Campbell KL.
dogs <10 kg; 500 mg PO TID dogs >10 kg); prolonged and response may be influenced Muller & Kirk’s Small Animal Dermatology,
doxycycline 10 mg/kg PO q24h; minocycline by underlying factors; weight reduction in 7th ed. St. Louis, MO: Elsevier Mosby,
5 mg/kg PO BID, often administered with obese patients. 2013.
niacinamide 250 mg PO for dogs <10 kg and • Onychorrhexis—may require amputation Author Guillermina Manigot
500 mg PO for dogs >10 kg; pentoxifylline of the third phalanx for resolution. Consulting Editor Alexander H. Werner
10–15 mg/kg PO BID to TID; corticoster- • Onychomadesis—prognosis determined by Resnick
oids and cyclosporine 5 mg/kg PO q24h; underlying cause; immune-mediated diseases Acknowledgment The author and book
vitamin E; appropriate chemotherapeutic and vascular problems carry a more guarded editors acknowledge the prior contribution of
agents (e.g., azathioprine, chlorambucil). prognosis than do trauma or infectious causes. Karen Helton Rhodes.
• Nonsteroidal anti-inflammatory drugs • Neoplasia—excised by amputation of the
(NSAIDs) or tramadol if pain is present. digit; malignant tumors metastasize by the
PRECAUTIONS time of diagnosis. Client Education Handout
• Griseofulvin—teratogenic; may cause bone available online
marrow suppression, anorexia, vomiting, and
diarrhea; absorption enhanced if given with a
high-fat meal. MISCELLANEOUS
• Ketoconazole—avoid use in cats; may cause
anorexia, gastric irritation, hepatic toxicity, ABBREVIATIONS
and lightening of the hair coat. • ANA = antinuclear antibody.
Clostridial Enterotoxicosis
been voluminous diarrhea or vomiting. Enterotoxin Assay
C • Fever is uncommon. • Evidence of systemic • Fecal ELISA for identification of CPE in
illness or debilitation is rare. patients with diarrhea suspected to be due to
BASICS CP is the current recommendation; since
CAUSES
DEFINITION • In humans, CP-associated diarrhea is
CPE is present in the feces of 5–14% of
A complex disorder characterized by diarrhea usually due to ingestion of enterotoxigenic clinically normal dogs, this may or may not
in dogs and cats associated with Clostridium isolates. In dogs, it is thought to be secondary be clinically useful. • Fecal ELISA should be
perfringens enterotoxins (CPEs). to disruption of the intestinal microenviron- run in conjunction with PCR to detect
ment. • Anything that disrupts normal enteric enterotoxigenic strains. • Real-time polymer-
PATHOPHYSIOLOGY ase chain reaction (RT-PCR) for detection of
• Clostridium perfringens (CP) is a Gram- microbiota can lead to CP overgrowth and
diarrhea. • CP toxins have been implicated in the CPE gene and the alpha toxin gene is
positive, spore-forming, strictly anaerobic available; the CPE gene has been found in up
bacterium. • CP is a normal commensal dogs with AHDS.
to 33.7% of healthy dogs, therefore its
organism found in the intestinal tract of RISK FACTORS presence in a dog with GI disease does not
humans and animals. • A strong link between • Dietary changes. • Antibiotic use. • Stress. confirm that CP is the cause.
canine acute hemorrhagic diarrhea syndrome • Primary small intestinal bacterial
(AHDS; formerly hemorrhagic gastroenteritis Fecal Cytology
overgrowth.
[HGE]) and the presence of CP has been • CP endospores, characterized by “safety-
identified. • Certain strains of CP (primarily pin” appearance with oval form and dense
Type A) produce a potent enterotoxin (CPE) body at one end of spore wall, can be seen on
as well as pore-forming toxins (NetE and microscopic evaluation of heat-fixed thin fecal
NetF). • CPE is a cytotoxic enterotoxin that DIAGNOSIS smear stained with Romanowsky-type stain
causes tissue destruction; it has been identified • Diagnostic testing should occur during the (e.g., Diff-Quik®), Wright’s stain, or new
in the feces of up to 14% of dogs without acute phase. • In the absence of sepsis, methylene blue. • High numbers of CP
diarrhea, thus its role in causing diarrhea is antibiotic therapy has not been shown to endospores on fecal cytology correlates poorly
unclear. • NetF-producing CP isolates have alter resolution of clinical signs, therefore with clinical disease or fecal CPE activity.
not been found in healthy dogs. • Not all response to antibiotics cannot be used as • High numbers of fecal endospores can be
strains of CP produce CPE or NetF and not all diagnostic criterion. found in feces of healthy dogs.
dogs that have CPE in feces are clinical, DIFFERENTIAL DIAGNOSIS DIAGNOSTIC PROCEDURES
therefore it is undetermined why some develop Any cause of diarrhea can be considered, • Abdominal ultrasound can help rule out
diarrhea. • CPE production is coregulated including, but not limited to, viral, bacterial, other causes of GI disease. • Colonoscopy
with sporulation of the organism; conditions or parasitic infection, dietary indiscretion, and endoscopy with biopsy can be used to
that precipitate sporulation in animals include chronic enteropathy, metabolic disease, confirm presence of acute mucosal necrosis
a sudden change in diet, dietary indiscretion, neoplasia. and neutrophilic infiltration, as well as
injudicious use of antibiotics causing a severe adherence of rod-shaped bacteria to these
dysbiosis, and underlying intestinal disease. CBC/BIOCHEMISTRY/URINALYSIS
• If dehydration is present—increased necrotic areas, and can rule out other causes
SYSTEMS AFFECTED packed cell volume (PCV) from hemocon- of GI disease.
Gastrointestinal (GI). centration, increased total plasma protein, PATHOLOGIC FINDINGS
INCIDENCE/PREVALENCE increased amylase, and increased blood urea • Grossly hyperemic or ulcerated mucosa. • Acute
Incidence is unknown; up to 34% of canine nitrogen (BUN) from prerenal azotemia. intestinal mucosal destruction and neutrophilic
diarrhea cases are suspected to be CP related. • Dogs with AHDS will often have infiltration. • Immunohistochemical staining of
The infection is far less common in cats. increased PCV with discordantly low total bacterial plaques on necrotic areas may be
plasma protein. • Leukocytosis with clostridial antigen positive.
SIGNALMENT neutrophilia and monocytosis. • Decreased
Species albumin secondary to loss and decreased
Dog and cat. production. • Increased alanine aminotrans-
ferase (ALT) and aspartate aminotransferase
Mean Age and Range
(AST) activities from organ hypoxia TREATMENT
Any age.
secondary to hypovolemia. APPROPRIATE HEALTH CARE
SIGNS • There are no research-based recommenda-
General Comments There is no gold standard diagnostic test for tions for optimal treatment of patients with
Can include both large and small bowel confirming CP-associated diarrhea. CP-associated illness. • If vomiting or
diarrhea. diarrhea is not severe, animals may be treated
Microbiology as outpatients with antiemetics and subcuta-
Historical Findings • Fecal culture alone should not be used to neous fluids. • If more severe diarrhea,
• Large bowel diarrhea—tenesmus, mucous, diagnose CP-associated illness because the vomiting, dehydration, or evidence of
frank blood, and increased frequency of organism is a normal commensal; CP can hypovolemia, hospitalization with IV
defecation. • Small bowel diarrhea—large be isolated from feces of >80% of healthy replacement crystalloids and antiemetics is
volumes of soft to liquid diarrhea. • Vomiting dogs and 43–63% of normal cats. • Fecal recommended.
and abdominal discomfort. • Severity varies endospore cultures are not useful, as
from mild, self-limiting diarrhea to fatal, sporulation of enterotoxigenic strains of DIET
acute, hemorrhagic diarrhea. • Diet change plays a role in treatment and
CP occurs in dogs with and without
diarrhea. management of cases with chronic recurring
Physical Examination Findings disease; diets high in either soluble (ferment-
• Abdominal discomfort. • Hematochezia. able) or insoluble fiber often result in clinical
• Mucoid feces. • Dehydration if there has improvement by reducing enteric CP
(continued) Clostridial Enterotoxicosis

number, possibly through acidification of the probiotics than with no treatment. • Diet • ALT = alanine aminotransferase.
distal intestine, which limits CP sporulation change can be instituted following resolution • AST = aspartate aminotransferase. C
and enterotoxin production. of clinical signs. • BUN = blood urea nitrogen.
• Commercial diets can be supplemented • CP = Clostridium perfringens.
with psyllium (1/2–2 tsp/day) as a source of • CPE = Clostridium perfringens enterotoxin.
soluble fiber. • GI = gastrointestinal.
• Diets low in fiber should be supplemented • HGE = hemorrhagic gastroenteritis.
with fiber (coarse bran 1–3 tbs/day) as a
FOLLOW-UP • PCV = packed cell volume.
source of insoluble fiber or psyllium added as PATIENT MONITORING • RT-PCR = real-time polymerase chain
a source of soluble fiber. • Probiotics might • Ensure adequate hydration and intravascu- reaction.
help restore the normal intestinal microbiota, lar volume, with replacement fluid adminis-
Suggested Reading
thereby reducing risk of recurrent CP- tration as needed. • Monitor PCV, total
Albini S, Brodard I, Jaussi A. Real-time
associated diarrhea. plasma protein, acid-base balance, and
multiplex PCR assays for reliable detection
electrolyte concentrations.
CLIENT EDUCATION of Clostridium perfringens toxin genes in
• Acute disease is often self-limiting. • There PREVENTION/AVOIDANCE animal isolates. Vet Microbiol 2008,
have been no documented reports of trans- • Regular use of high-fiber diets or probiot- 127:179–185.
mission of CP from animals to humans; ics. • Avoiding or anticipating stressful events Marks SL, Rankin SC, Byrne BA, et al.
however, if there are immunosuppressed (e.g., kenneling) and using anxiolytics. ACVIM Consensus Statement: enteropath-
members in the household, strict hygiene EXPECTED COURSE AND PROGNOSIS ogenic bacteria in dogs and cats: diagnosis,
protocols should be followed. • Overall excellent prognosis; many animals epidemiology, treatment, and control. J Vet
will have resolution of clinical signs without Intern Med 2011, 25:1195–1208.
in-hospital treatment. • Acute hemorrhagic Minamoto Y, Dhanani N, Markel ME, et al.
diarrheal events should be addressed with Prevalence of Clostridium perfringens,
Clostridium perfringens enterotoxin and
MEDICATIONS aggressive resuscitation and hospitalization; if
dysbiosis in fecal samples of dogs with
the animal responds to therapy, the prognosis
DRUG(S) OF CHOICE is good. diarrhea. Vet Microbiol 2014, 174:463–473.
Antiemetics Weese SJ, Staempfli HR, Prescott JF, et al.
• Maropitant—1 mg/kg IV/SC q 24h. The roles of Clostridium difficile and
• Ondansetron—0.5–1 mg/kg IV/PO q24h. enterotoxigenic Clostridium perfringens in
diarrhea in dogs. JVIM 2001, 15:374–378.
Antibiotics MISCELLANEOUS Ziese AL, Suchodolski JS, Hartmann K, et al.
• Antibiotics are unnecessary in animals with Effect of probiotic treatment on the clinical
mild disease as the infection is typically course, intestinal microbiome, and toxigenic
• CP enterotoxicosis can be associated with
self-limiting. • If signs of systemic disease or Clostridium perfringens in dogs with acute
AHDS. • The connection to chronic
sepsis are present, antibiotics should be hemorrhagic diarrhea. Plos One 2018,
enteropathies is less well understood.
administered. • Antibiotics that are recom- 13(9):e0204691.
mended are ampicillin: 22 mg/kg IV q8h; ZOONOTIC POTENTIAL Author Jennifer Good
amoxicillin: 22 mg/kg PO q8h; metronida- Unknown Consulting Editor Amie Koenig
zole: 10–25 mg/kg IV/PO q12h for 5–7 days; PREGNANCY/FERTILITY/BREEDING Acknowledgment The author and book
tylosin: 5–10 mg/kg PO q24h. Antibiotic therapy may be contraindicated. editors acknowledge the prior contribution of
• Tetracyclines are no longer recommended Stanley L. Marks.
due to resistance of CP isolates. SEE ALSO
• Colitis and Proctitis.
ALTERNATIVE DRUGS(S) • Small Intestinal Dysbiosis.
• Probiotics (e.g., lactobacillus) may alter the Client Education Handout
intestinal microbiota, reducing likelihood of ABBREVIATIONS available online
recurrences. • One study reported faster • AHDS = acute hemorrhagic diarrhea
resolution of clinical signs with use of syndrome.
Coagulation Factor Deficiency

CAUSES OTHER LABORATORY TESTS
C • Acquired—synthetic failure (liver disease); • Coagulation screening tests (activated
vitamin K deficiency (cholestasis, anticoagulant clotting time [ACT], APTT, PT, TCT) are
BASICS rodenticide toxicity, malabsorption, long-term functional tests that measure the time for in
DEFINITION antibiotics, coumadin); factor inhibition vitro clot formation; coagulation factor and
Hemostatic defects characterized by a lack (anticoagulant overdose, envenomation, fibrinogen deficiencies prolong clotting time
of one or more procoagulant proteins auto- or alloantibodies); factor consumption (see Figure 1).
(coagulation factors). and depletion (disseminated intravascular • ACT is a point-of-care screening test that
coagulopathy [DIC]); factor dilution detects severe deficiencies of all factors (except
PATHOPHYSIOLOGY
(high-volume transfusion, crystalloid, or factor VII); ACT may be influenced by
• Coagulation involves a complex series of
colloid fluid therapy); hyperfibrinolysis anemia, thrombocytopenia, and changes in
enzymatic reactions that generate a burst of
(secondary fibrinogen depletion). blood viscosity.
thrombin (factor IIa) at sites of blood vessel
• Hereditary—distinct mutations in • APTT is a screening test of the contact
injury; thrombin then cleaves plasma
coagulation factor genes. pathway (prekallikrein, high molecular weight
fibrinogen into fibrin monomers that
kininogen, factor XII), intrinsic system (factors
subsequently polymerize and cross-link to
XI, IX, VIII), common system (factors X, V,
form an insoluble fibrin clot.
II), and severe fibrinogen deficiency.
• Functional and/or quantitative coagulation
factor deficiencies cause a failure of fibrin clot DIAGNOSIS • PT is a screening test of factor VII, common
system, and severe fibrinogen deficiency.
formation. DIFFERENTIAL DIAGNOSIS • The TCT is a screening test of functional
• The liver is the sole or primary site of synthesis • Thrombocytopenia should be the first rule-out fibrinogen and is sensitive to the presence of
of most coagulation factors; after synthesis, for any patient with abnormal hemorrhage; fibrinogen inhibitors.
factors II, VII, IX, and X require a vitamin K– thrombocytopathies may also cause bleeding • Acquired coagulation factor deficiencies
dependent modification to become fully active. (see Thrombocytopenia, Thrombocytopathies). generally cause prolongation of more than one
SYSTEMS AFFECTED • Hereditary coagulation factor deficiencies cause screening test; the most common hereditary
• Coagulation factor deficiency can cause prolongation of coagulation screening tests, factor deficiencies (hemophilia and factor XII
spontaneous hemorrhage, prolonged post- whereas vonWillebrand disease (vWD) does not. deficiency) specifically prolong APTT.
traumatic hemorrhage, and ultimately blood • Hyperfibrinolysis may cause hemorrhage in • Individual factor assays can be performed
loss anemia. patients with hypovolemic shock, acute blood for definitive diagnosis of hereditary or
• Spontaneous hemorrhage—often develops loss, or trauma, but generally does not cause complex coagulopathies.
in body cavities or potential spaces (i.e., prolongation of activated partial thromboplastin
time (APTT) or prothrombin time (PT) tests; Drugs That May Alter Laboratory Results
hemothorax, hemoperitoneum, hemarthrosis,
a breed predisposition for hyperfibrinolysis Therapeutic dosages of unfractionated
subcutaneous, or intramuscular hematoma).
may exist in sighthounds. heparin, coumadin, and plasma expanders
GENETICS • Acquired coagulopathies often develop (dextran, hetastarch) prolong coagulation
• Hemophilia A and B (factor VIII and IX because of liver disease, anticoagulant screening tests.
deficiencies)—X-linked recessive traits. rodenticide ingestion, or DIC. Disorders That May Alter Laboratory
• All other factor deficiencies are autosomal • Liver disease is accompanied by changes in
traits. Results
the chemistry profile (see Coagulopathy of
• Specific defects are more likely to be • Improper sample collection (poor venipuncture
Liver Disease).
propagated within a single breed, but all breeds technique, partially or overfilled citrate collection
• Anticoagulant rodenticide toxicity prolongs
are at risk for developing new mutations. tubes, use of heparin or clot activator tubes) will
the PT and/or APTT, but does not affect
invalidate coagulation test results.
SIGNALMENT thrombin clotting time (TCT) or fibrinogen
• Extreme lipemia, hemoglobinemia, or
• Dog and cat. concentration.
icterus may interfere with clot detection by
• Hereditary factor deficiencies—severe defects • DIC always develops secondary to systemic
photo-optical coagulation analyzers.
manifest by 3–6 months of age, milder hemostatic disease (especially sepsis, neoplasia, other
• Because of factor lability, samples should be
defects manifest after surgery or trauma. inflammatory conditions) and is often
assayed on site or plasma separated and sent
• For X-linked recessive traits, males express the accompanied by low or falling platelet count.
on ice to the laboratory.
bleeding tendency, female carriers are clinically • Massive transfusion (>1 blood volume)
normal. with stored blood products may dilute Valid if Run in Human Laboratory?
• For autosomal traits, males and females functional factors, fibrinogen, and platelets • Interpretation of coagulation assay
express signs with equal frequency. below hemostatic levels; hypocalcemia may results requires same-species reference
• Hemophilia A is a common hereditary also result. intervals and controls; for example, human
factor deficiency and may be seen in all • Contamination of blood samples (e.g., with APTT values are generally twice those of
breeds and mixed-breed dogs and cats. heparin flush) or delayed processing can dogs and cats.
• Factor XII deficiency is common in cats, but generate spurious PT and APTT abnormalities. • The laboratory should confirm cross-
does not cause a clinical bleeding tendency. reactivity of antigenic assays and optimization
• Acquired factor deficiencies—depends on of functional tests for animal species.
• Regenerative anemia develops over the
underlying disease process. course of days after blood loss. DIAGNOSTIC PROCEDURES
SIGNS • Platelet count is normal unless the patient Buccal mucosal bleeding time (BMBT) is
• Hematoma formation. has DIC or massive bleeding. prolonged in patients with severe thrombocyto
• Intracavitary hemorrhage. • Resorption of blood from a large hematoma penia, platelet dysfunction, vWD, and
• Prolonged hemorrhage after surgery or trauma. may cause hyperbilirubinemia. fibrinogen deficiency, but BMBT is insensitive
• Blood loss anemia. to coagulation factor deficiencies.
(continued) Coagulation Factor Deficiency
COAGULATION SCREENING TESTS: APTT, PT, TCT C

APTT: LONG PT: LONG APTT& PT: LONG ALL TESTS
PT, TCT: NORMAL APTT, TCT: NORMAL TCT NORMAL LONG
INTRINSIC FACTOR EXTRINSIC FACTOR COMMON PATHWAY FIBRINOGEN AND

DEFECTS DEFECTS OR COMBINED COMBINED DEFECTS
DEFECTS
Factor VIII (Hemophilia A) Factor VII deficiency Fibrinogen
Factor IX (Hemophilia B) Common Pathway Severe deficiency
Factor II (Thrombin) High concentration inhibitors
Contact Deficiencies Factor V
Factor XI Factor X Combined Deficiency
Factor XII (Hageman trait) Deficiency of fibrinogen and
Prekallikrein Combined Deficiency intrinsic, extrinsic, and
HMW Kininogen Vitamin K dependent factors: common pathway factors
Factor II, VII, IX, X
Figure 1.
Diagnostic algorithm for coagulation factor deficiencies
• Intravenous administration of vitamin K is

not recommended because of the risk of
anaphylaxis.
TREATMENT MISCELLANEOUS
• Transfusion of fresh whole blood, fresh ALTERNATIVE DRUG(S)
Antifibrinolytic drugs (aminocaproic acid and PREGNANCY/FERTILITY/BREEDING
plasma, and fresh frozen plasma will supply Patients with hereditary factor deficiencies
all coagulation factors. tranexamic acid) help correct coagulopathy
due to acute trauma and reduce transfusion should not be bred.
• Cryoprecipitate is a specific source of factor
VIII, fibrinogen, and von Willebrand factor; requirements for orthopedic procedures in SYNONYMS
cryo-supernatant plasma supplies all other factors. humans, and have shown benefit to prevent • Coagulation defects.
• Component therapy is preferred for surgical postoperative bleeding in greyhounds. These • Coagulopathies.
prophylaxis and nonanemic patients to prevent drugs may also be used topically (e.g.,
SEE ALSO
red cell sensitization and volume overload. bleeding from tooth extraction).
• Coagulopathy of Liver Disease.
• Patients with severe acquired or hereditary • Disseminated Intravascular Coagulation.
factor deficiencies may require repeated • Thrombocytopathies.
transfusion (q8–12h) to control or prevent • Thrombocytopenia.
hemorrhage. • Von Willebrand Disease.
FOLLOW-UP
ABBREVIATIONS
PATIENT MONITORING
• ACT = activated clotting time.
• PT or factor VII assays can be used to
• APTT = activated partial thromboplastin time.
MEDICATIONS monitor effectiveness of vitamin K admin
• BMBT = buccal mucosal bleeding time.
istration in animals with anticoagulant toxicity;
DRUG(S) OF CHOICE • DIC = disseminated intravascular coagulation.
test results should normalize after 24–48 hours
Vitamin K1 (1.0 to 2.0 mg/kg SQ using a • NSAID = nonsteroidal anti-inflammatory drug.
of initiating therapy.
small needle, or preferably PO q24h) is an • PT = prothrombin time.
• ACT is a less specific but reasonable
effective treatment for patients with anti- • TCT = thrombin clotting time.
substitute for monitoring response to
coagulant rodenticide poisoning and other • vWD = von Willebrand disease.
vitamin K.
causes of vitamin K deficiency. • Hereditary defects can be monitored by INTERNET RESOURCES
CONTRAINDICATIONS cessation of bleeding, stabilization of http://eclinpath.com/hemostasis
Nonsteroidal anti-inflammatory drugs hematocrit, resolution of hematoma, and, if Suggested Reading
(NSAIDs), anticoagulants, and plasma needed, specific factor analyses. Brooks MB and DeLaforcade A. Acquired
expanders should be avoided to prevent coagulopathies. In: Weiss DJ, Wardrop KJ, eds.,
further compromise of hemostasis. Schalm’s Veterinary Hematology, 6th ed. Ames,
Transfusion poses a risk of immune and
PRECAUTIONS nonimmune reactions (see Blood Transfusion IA: Wiley-Blackwell, 2010, pp. 654–660.
• IM injections and jugular venipuncture Reactions). Author Marjory B. Brooks
should be avoided, when possible, because of Consulting Editor Melinda S. Camus
the risk of inducing additional bleeding.
Coagulopathy of Liver Disease

• Abdominal trauma, gastrointestinal
C infiltrative disorders.
BASICS CBC/BIOCHEMISTRY/URINALYSIS MEDICATIONS
• CBC—normal or regenerative anemia;
OVERVIEW microcytosis; thrombocytopenia. DRUG(S) OF CHOICE
• The liver is the sole/primary site of • Biochemistry—high liver enzymes; • Based on cause of hepatic abnormality.
synthesis of procoagulant, anticoagulant, and bilirubinemia; low albumin; hypoglobulin • Vitamin K deficiency—parenteral vitamin K1
fibrinolytic proteins, except factors V, VIII, emia; low cholesterol. (0.5–1.5 mg/kg q12h SC up to 3 doses in
von Willebrand factor (vWF), tissue plasmin- • Urinalysis—hematuria; bilirubinuria. 24h interval initially); vitamin K1 PO
ogen activator (TPA). (Mephyton , 1 mg/kg q24h) if normal
• Some patients develop prolonged in vitro OTHER LABORATORY TESTS enteric bile ®acid uptake.
clotting times, but few exhibit spontaneous Hemostatic tests—thrombocytopenia; • DIC—correct primary disease; consider
bleeding. prolonged APTT (activated clotting time heparin for overt thrombosis (unfractionated
• Causes of hemostatic imbalance: [ACT]), prothrombin time (PT), thrombin heparin [UFH]: 200 U/kg q6–12h; or low
◦ reduced synthesis or activation of clotting time (TCT), and proteins induced by molecular weight heparin [enoxaparin]: 1 mg/
procoagulant proteins; vitamin K absence (PIVKA); low fibrinogen kg q12–24h), dose titration based on clinical
◦ vitamin K deficiency; and coagulation factors; low anticoagulant status and laboratory monitoring (ACT,
◦ dysfibrinogenemia due to abnormal factors (antithrombin [AT], protein C); high APTT [UFH], heparin anti-Xa activity [all
fibrin polymerization; FDP and D-dimer. heparins]).
◦ reduced clearance of fibrin/fibrinogen IMAGING • Blood products—fresh whole blood:
degradation products (FDP); 12–20 mL/kg q24h; fresh frozen plasma:
Abdominal Ultrasonography
◦ thrombocytopenia or thrombocytopathy; 10–20 mL/kg q12h; plasma cryosupernatant
• Effusion (ascites, hemorrhage).
◦ enhanced fibrinolysis. (albumin, vitamin K–dependent factors):
• Liver changes—variable.
• Vitamin K deficiency—linked to severe 10–20 mL/kg q12h; cryoprecipitate
• Abnormal enteric motility, thickening in
intra- or extrahepatic cholestasis, steatorrhea, (fibrinogen, vWF, factor VIII): 1 U/10 kg or
area of bleeding.
or prolonged oral antibiotic administration. dose to effect.
• Desmopressin acetate (DDAVP)—
SIGNALMENT
Dog and cat of any age, breed, or sex. 0.5–1 μg/kg IV in saline; may increase
coagulation factors, shortens bleeding times,
SIGNS TREATMENT reduces bleeding tendencies; empirically used
• Often minor or absent. • Not necessary unless invasive procedures for biopsy-induced bleeding.
• Melena, hematemesis, hematochezia, hematuria. planned or spontaneous hemorrhage noted. • Antifibrinolytics—epsilon aminocaproic
• Prolonged bleeding if provoked—venipunc- • Fresh whole blood—provides replacement acid (EACA): 100 mg/kg loading, 30 mg/
ture, cystocentesis, biopsy, surgical wounds. of red cells, coagulation factors, functional kg/h up to 8h; tranexamic acid: 25 mg/kg
• Spontaneous bruising/hematomas—rare platelets. q8h; if evidence of hyperfibrinolysis.
unless severe vitamin K deficiency or • Fresh frozen plasma—provides coagulation
fulminant disseminated intravascular CONTRAINDICATIONS/POSSIBLE
factors, other hemostatic proteins, and
coagulation (DIC). reduces risk of red cell sensitization or volume INTERACTIONS
overload. • Stored whole blood—may provoke hepatic
CAUSES & RISK FACTORS encephalopathy (HE).
• Severe hepatic failure of any etiology. • Cryoprecipitate—for severe hypofibrino-
genemia or bleeding with coexistent von • Vitamin K1 (cats)—high dose causes Heinz
• Acute viral liver disease.
Willebrand’s disease (vWD). body hemolysis and oxidant liver injury.
• Extrahepatic bile duct obstruction
• Platelet-rich plasma—rarely indicated. • Aspirin or other nonsteroidal anti-
(EHBDO). inflammatory drugs (NSAIDs)—may
• Chronic liver disease—especially cirrhosis. • Avoid synthetic colloids if bleeding
tendencies observed. predispose to renal failure, worsen ascites,
• Concurrent small bowel disease (e.g., cats provoke emesis and spontaneous bleeding,
with cholangiohepatitis or hepatic lipidosis) Biopsy • High-volume transfusion in citrate-based
predisposing to vitamin K deficiency. • High risk for bleeding—PIVKA, PT, anticoagulants (especially in animals <5 kg)
• High central venous pressure (CVP) and APTT, or ACT prolonged by >50%; may induce symptomatic hypocalcemia.
portal hypertension. thrombocytopenia <50,000/μL; prolonged • Avoid provocative procedures—e.g., jugular
• Portosystemic vascular anomaly (PSVA)— mucosal bleeding time. venipuncture or catheter placement,
asymptomatic factor deficiency common; • Iatrogenic hemorrhage—grave prognosis if cystocentesis, if recognized bleeding
overt bleeding uncommon. spontaneous bleeding with undetermined tendencies.
cause.
• Hemostasis support—postprocedure
bleeding.
DIAGNOSIS • Ultrasound-guided needle core—highest
risk; observe biopsy site for 15 minutes, then FOLLOW-UP
DIFFERENTIAL DIAGNOSIS sequentially over several hours postprocedure. PATIENT MONITORING
• Toxicities—see Hepatotoxins. • Laparoscopy—affords visibility and allows • PT, PIVKA (limited availability), factor
• Hereditary hemostatic defects. hemostasis (cautery, Gelfoam pack biopsy VII—most sensitive coagulation tests to detect
• Thrombocytopenia. site). vitamin K deficiency; if no improvement after
• DIC—any cause. • Laparotomy—wedge biopsy; ill-advised in 48h of vitamin K1 injection, unlikely correction
• Hepatic amyloidosis. patients with overt bleeding. by further dosing.
(continued) Coagulopathy of Liver Disease

• Heart rate, blood pressure, mucous POSSIBLE COMPLICATIONS • EHBDO = extrahepatic bile duct
membrane color and refill, packed cell Hemorrhage, anemia, hypovolemia, HE. obstruction. C
volume (PCV), and total solids to monitor EXPECTED COURSE AND PROGNOSIS • FDP = fibrin/fibrinogen degradation
response if active bleeding. Spontaneous hemorrhage, refractory product.
• Biopsy site—observe immediately and • HE = hepatic encephalopathy.
coagulopathy, and DIC—poor prognosis.
sequentially (ultrasonography) for hemorrhage. • NSAID = nonsteroidal anti-inflammatory
• Sample abdominal effusion to differentiate drug.
hemorrhage from ascites. • PCV = packed cell volume.
• PIVKA = proteins induced by vitamin K
• Well-balanced diet replete with vitamins.
MISCELLANEOUS absence.
SEE ALSO • PSVA = portosystemic vascular anomaly.
• Consider impaired vitamin K availability or
synthesis from chronic oral antimicrobials. • Hepatotoxins. • PT = prothrombin time.
• TCT = thrombin clotting time.
• Invasive procedures—anticipate bleeding; ABBREVIATIONS
pretreat with vitamin K1; give DDAVP within • TPA = tissue plasminogen activator.
• ACT = activated clotting time. • UFH = unfractionated heparin.
20 min of anticipated biopsy or if bleeding • APTT = activated partial thromboplastin
tendencies persist despite vitamin K1 therapy • vWD = von Willebrand’s disease.
time. • vWF = von Willebrand factor.
(repeated DDAVP of no use); fresh frozen • AT = antithrombin.
plasma for factor/fibrinogen replacement and Author Marjory B. Brooks
• CVP = central venous pressure. Consulting Editor Kate Holan
active bleeding; avoid volume overload and • DDAVP = desmopressin acetate.
increased CVP. • DIC = disseminated intravascular
• Eliminate enteric parasitism. coagulation.
• EACA = epsilon aminocaproic acid.
Cobalamin Deficiency
• Hereditary (Chinese Shar-Pei, giant
C schnauzer, beagle, border collie, Australian
shepherd dog).
BASICS • Dietary—being fed exclusively vegan or M EDICATIONS
OVERVIEW vegetarian diet without concurrent supple- DRUG(S) OF CHOICE
• Cobalamin deficiency occurs in patients mentation. • Cobalamin supplements:
with cobalamin malabsorption when all body ◦ Cyanocobalamin—usually at 1,000 μg/mL
stores of cobalamin have been utilized and for parenteral use; or 1,000 μg tablets or 250 μg
cobalamin is deficient on a cellular level. and 1000 μg chewable tablets for oral use.
• Cobalamin is required by virtually all cells DIAGNOSIS ◦ Hydroxocobalamin—usually at 1,000 μg/
in the body and plays a major role in beta- mL; for parenteral use.
oxidation, conversion of certain amino acids, DIFFERENTIAL DIAGNOSIS ◦ Methylcobalamin—usually 1 mg capsule;
and the formation of tetrahydrofolate, and is Other diseases causing chronic GI disease, for oral use.
thus crucial for energy production, amino immunosuppression, central neuropathies, or • Traditionally, cobalamin supplementation
acid metabolism, and DNA and RNA peripheral neuropathies. in cobalamin-deficient patients has been
synthesis. CBC/BIOCHEMISTRY/URINALYSIS administered parenterally (usually SC)
• Cobalamin deficiency is associated with • May be within normal limits. using cyanocobalamin or rarely hydroxo-
gastrointestinal (GI) signs and systemic • May show changes associated with under- cobalamin.
complications, such as immunodeficiencies, lying disease process (e.g., hypoalbuminemia ◦ Cats receive 250 μg/injection; dogs
central neuropathies, and peripheral neuro- in patients with severe inflammatory bowel receive between 250 μg (small dog) and
pathies. disease). 1,500 μg (giant dog) per injection; doses
• Cobalamin is absorbed exclusively in the • May show anemia, neutrophilia with left should approximate 50 μg/kg per injection
ileum of dogs and cats via a receptor- shift, or neutropenia. Rubricytes have been within this dose range.
mediated mechanism. documented in cobalamin-deficient dogs and ◦ In either species there are 6 weekly
• The main causes of cobalamin deficiency in have been interpreted as evidence of injections, one more injection a month
dogs and cats include chronic GI disease ineffective erythropoiesis. Hypersegmented later, and reevaluation of serum cobalamin
involving the ileum (e.g., inflammatory bowel neutrophils can also be observed. concentration a month later.
disease, small intestinal dysbiosis, intestinal • Recent studies have shown that oral
lymphoma), exocrine pancreatic insufficiency OTHER LABORATORY TESTS cobalamin supplementation with cyanoco-
• Serum and urine methylmalonic acid
(EPI), short bowel syndrome, and, in rare balamin is equally efficacious regardless of
cases, inherited cobalamin malabsorption or concentrations are increased in patients with the underlying cause of cobalamin
dietary deficiencies. cobalamin deficiency. deficiency.
• Decreased or low normal serum cobala-
◦ Cats receive 250 μg/day; dogs receive
SIGNALMENT min concentrations. Studies measuring
• In the United States, Chinese Shar-Pei have between 250 μg (small dog) and 1,000 μg
methylmalonic acid in serum from dogs and (giant dog) per day.
a high prevalence of cobalamin deficiency. cats have shown that patients with low ◦ Reevaluation of serum cobalamin
Isolated families of other breeds, such as the normal serum cobalamin concentrations
giant schnauzer, beagle, border collie, and concentration 2–4 weeks after the last
may be cobalamin deficient on a cellular dose.
Australian shepherd dog, have also been level. Note that all assays used for the
described as having cobalamin deficiency. • Continue therapy at the original dosing
measurement of serum cobalamin concen- scheme if serum cobalamin is still low; continue
• No other breed, sex, or age predilections are tration in dogs and cats have been devel-
known for canine or feline patients with at a decreased interval if cobalamin is in the
oped for use in humans and thus must be mid-normal range; discontinue if serum
cobalamin deficiency. analytically validated for dogs and cats cobalamin is in the high end of the reference
SIGNS before routine clinical use. In addition, each interval.
• Clinical signs attributable to the underlying laboratory should develop specific reference
disease process: intervals. CONTRAINDICATIONS/POSSIBLE
◦ Chronic enteropathy—diarrhea, weight IMAGING INTERACTIONS
loss, vomiting, poor appetite, or others. Not useful, other than for evaluation of None known.
◦ EPI—weight loss, failure to thrive, loose underlying intestinal disease.
stools, steatorrhea, polyphagia or pica,
borborygmus, flatulence. DIAGNOSTIC PROCEDURES
• Clinical signs attributable to cobalamin
None for the diagnosis of cobalamin deficiency.
However, intestinal biopsies may be useful to FOLLOW-UP
deficiency—weight loss, failure to thrive, Depending on the severity of the underlying
poor hair coat, lethargy, anorexia; less confirm and characterize chronic
enteropathies. disease process, the complications from
commonly signs of peripheral and central cobalamin deficiency, and treatment
neuropathy such as a plantigrade stance or response.
encephalopathy.
PATIENT MONITORING
CAUSES & RISK FACTORS • See above; reevaluation of serum cobalamin
• Intestinal disease involving the distal small TREATMENT
Treatment of the underlying disease process, concentration either 1 month after the last
intestine (i.e., the ileum)—inflammatory cobalamin injection or 2–4 weeks after the
bowel disease, food-responsive enteropathy, if identified (e.g., inflammatory bowel
disease, EPI, lymphoma, small intestinal last oral dose of cobalamin.
lymphoma, others. • Additional monitoring as required for the
• EPI. dysbiosis).
underlying disease process.
• Short bowel syndrome.
(continued) Cobalamin Deficiency

INTERNET RESOURCES deficiency in Chinese Shar-Peis. Vet J 2011,
http://vetmed.tamu.edu/gilab 191:41–45. C
Suggested Reading Maunder CL, Day MJ, Hibbert A, et al.
MISCELLANEOUS Serum cobalamin concentrations in cats
Batchelor DJ, Noble P-JM, Taylor RH, et al.
SEE ALSO Prognostic factors in canine exocrine with gastrointestinal signs: correlation with
• Diarrhea, Chronic—Cats. pancreatic insufficiency: prolonged survival histopathological findings and duration of
• Diarrhea, Chronic—Dogs. is likely if clinical remission is achieved. clinical sigs. J Feline Med Surg 2012,
• Exocrine Pancreatic Insufficiency. J Vet Intern Med 2007, 21:54–60. 14:686–693.
• Inflammatory Bowel Disease. Berghoff N, Parnell NK, Hill SL, et al. Serum Toresson L, Steiner JM, Suchodolski JS, et al.
• Protein-Losing Enteropathy. cobalamin and methylmalonic acid Oral cobalamin supplementation in dogs
concentrations in dogs with chronic with chronic enteropathies and hypocobala-
ABBREVIATIONS
gastrointestinal disease. American J Vet Res minemia. J Vet Intern Med 2016,
• EPI = exocrine pancreatic insufficiency.
2013, 74:84–89. 30:101–107.
Bishop MA, Xenoulis PG, Berghoff N, et al. Author Jörg M. Steiner
Partial characterization of cobalamin Consulting Editor Mark P. Rondeau
Coccidioidomycosis
SIGNS OTHER LABORATORY TESTS
C Historical Findings • Serologic tests (generally by agar gel
• Coughing (ranges from dry/harsh to wet/
immunodiffusion [AGID] or ELISA) for
BASICS antibody to C. immitis may provide a
productive). • Fever unresponsive to anti-
DEFINITION biotics. • Anorexia, weight loss. • Weakness, presumptive diagnosis; may aid in monitoring
A systemic mycosis caused by the inhalation lameness (bone or joint involvement). response to therapy. • Antigen testing has not
of infective arthroconidia of the soil-borne • Seizures, paraparesis, back and neck pain proven to be sensitive.
fungus Coccidioides immitis. (CNS involvement). • Visual changes IMAGING
PATHOPHYSIOLOGY (ophthalmic involvement). • Radiography of lung (interstitial infiltrates,
• Grows in soil in the mycelial state. Physical Examination Findings granulomas, tracheobronchial lymphadenopa-
• Inhalation of infective arthroconidia is the thy) and bone lesions (osteolysis) may aid in
primary route of infection; at body tempera- Dogs diagnosis. • MRI may help in diagnosing
ture, all but one nucleus is shed and an • Signs with pulmonary involvement— granulomas in the CNS.
immature spherule is produced within 2–3 coughing and dyspnea. • Fever. • Bone
swelling, joint enlargement, and lameness. DIAGNOSTIC PROCEDURES
days. • Spherule matures and ruptures, • Serologic testing; repeat serology titers in
releasing 200–300 endospores that can • Lymphadenomegaly, skin lesions, and
draining tracts. • Neurologic dysfunction 4–6 weeks when low titers are accompanied by
produce new spherules. • Neutrophils cannot clinical signs. • Microscopic identification of
penetrate the spherule wall but can phago including ataxia, spinal or cranial nerve
deficits, and behavioral changes. • Blindness, the large spherule form of C. immitis in lesion
cytize the endospores. • Fewer than 10 inhaled or biopsy material is the definitive method of
arthrospores are sufficient to cause disease in uveitis, keratitis, and iritis.
diagnosis (large 10–80 μm round, double-
susceptible animals. • Respiratory signs are Cats walled structure containing endospores).
often noted 1–3 weeks after exposure; signs of Like dogs, although skin lesions are most • Lymph node aspirates and impression smears
dissemination may not be evident for several common type of infection in cats. of skin lesions or draining exudate may yield
months. • Most infections are mild or organisms. • Cultures should be performed by
CAUSES
subclinical, although dogs appear more trained laboratory personnel using protective
C. immitis grows several inches deep in the soil,
susceptible than cats to development of hoods. • Biopsy of infected tissue often is
where it survives high ambient temperatures
disseminated disease. • Fever, lethargy, preferred to avoid false-negative results; tissues
and low moisture. After a period of rainfall, the
inappetence, coughing, and joint pain or involved, however, may not be readily accessible
organism returns to the soil surface where it
stiffness may be noticed. • Dissemination and finding the organism can be challenging;
sporulates, releasing many arthroconidia that
may occur within 10 days, resulting in signs therefore, serologic testing is often a more
disseminate by wind and dust storms.
related to the organ system involved; skin logical approach.
lesions are usually associated with RISK FACTORS
dissemination. • Aggressive nosing in contaminated soil and PATHOLOGIC FINDINGS
underbrush may expose susceptible animals to • Granulomatous, suppurative, or pyogranu-
SYSTEMS AFFECTED lomatous inflammation present in many
large numbers of arthroconidia. • Dust storms
• Respiratory—site of initial infection. tissues. • Presence of the characteristic
after the rainy season; increased incidence noted
• Extrapulmonary—musculoskeletal, spherule forms in affected tissues.
after earthquakes. • Land development with
ophthalmic, cardiovascular, skin, neuromus-
earth disruption may lead to increased exposure.
cular, reproductive, and visceral organs.
Not an uncommon disease in endemic areas, TREATMENT
rare in nonendemic areas. It occurs more
commonly in dogs and rarely in cats.
DIAGNOSIS APPROPRIATE HEALTH CARE
DIFFERENTIAL DIAGNOSIS • Generally treated as outpatient.
GEOGRAPHIC DISTRIBUTION • Concurrent clinical symptoms (e.g., seizures,
• Pulmonary lesions may resemble those of
• C. immitis is found in the southwestern pain, coughing) should be treated appropriately.
other systemic mycoses (e.g., histoplasmosis,
United States in the geographic Lower
blastomycosis) or neoplasia (single mass or ACTIVITY
Sonoran life zone. • More common in
multiple nodules). • Lymphadenomegaly may Restrict activity until clinical signs begin to
southern California, Arizona, and southwest
be seen in lymphoma, other systemic mycoses, subside.
Texas. • Less prevalent in New Mexico,
and localized bacterial infections. • Bone
Nevada, and Utah. DIET
lesions may resemble those caused by primary
SIGNALMENT or metastatic bone tumors or bacterial osteo- Feed a high-quality palatable diet to maintain
myelitis. • Skin lesions must be differentiated body weight.
Species
Dog and cat. from routine abscesses or other infective CLIENT EDUCATION
processes. • For seizures and ataxia, consider • Treatment is potentially long (>6–9
Breed Predilections inflammatory and neoplastic etiologies. months) and expensive. • Relapse (especially
None with disseminated disease) is common.
Mean Age and Range • Hemogram—mild nonregenerative anemia, • Reassure client that infection is not
Though most commonly diagnosed in young neutrophilic leukocytosis, monocytosis. zoonotic.
animals (<4 years of age), it is seen in animals • Serum chemistry profile—hyperglobuline- SURGICAL CONSIDERATIONS
of all ages. mia, hypoalbuminemia, other changes may In cases of focal granulomatous organ
Predominant Sex be consistent with organ of involvement. involvement (e.g., consolidated pulmonary
None • Urinalysis—proteinuria with inflammatory lung lobe, eye, kidney), surgical removal of
glomerulonephritis. the affected organ may be indicated.
(continued) Coccidioidomycosis
the recommended dose if the animal is able to
tolerate the drug; newer azoles (ITZ and C
FCZ) have fewer side effects. • Side effects of
MEDICATIONS AMB therapy can be severe, especially renal MISCELLANEOUS
DRUG(S) OF CHOICE dysfunction, fever; use with caution if patient ZOONOTIC POTENTIAL
Coccidioidomycosis is considered one of the is azotemic, but not an absolute contraindica- • The spherule form of the fungus, as found
most severe and life-threatening of the tion if the infection is life-threatening. in animal tissues, is not directly transmissible
systemic mycoses. Treatment of disseminated to humans or to other animals. • Under
disease often requires at least 1 year of certain rare circumstances, however, there
aggressive antifungal therapy. could be reversion to growth of the infective
Dogs FOLLOW-UP mold form of the fungus on or within
• Ketoconazole (KTZ)—5–10 mg/kg PO
bandages placed over a draining lesion or in
PATIENT MONITORING contaminated bedding; draining lesions can
q12h; ideally given with food; treatment • Serologic titers should be monitored every
typically requires at least 1 year of therapy; if lead to contamination of the environment
3–4 months; animals should be treated until with arthrospores; care should be exercised
titers rise or clinical signs deteriorate over first clinical and radiographic signs resolve/stabilize
4–6 weeks of treatment, alternative therapy whenever handling an infected draining
and their titers ideally fall to less than 1 : 4; lesion. • Special precautions should be
should be considered. • Fluconazole (FCZ)— titers frequently do not become negative
10 mg/kg PO q12h; noted to greatly increase recommended to households in which the
throughout treatment. • Consider ITZ levels owners may be immunosuppressed.
success of treatment; cost of the drug has (2–4h post pill) in patients showing poor
significantly decreased with availability of response to ITZ therapy, especially if using PREGNANCY/FERTILITY/BREEDING
medical-grade generic compound; treatment generic or compounded formulation. Azole drugs can be teratogenic and should be
failures have been noted with use of chemical- • Creatinine and urinalysis should be used in pregnant animals only if the potential
grade compounded formulations. monitored in all animals treated with AMB; benefit justifies the potential risk to offspring.
• Itraconazole (ITZ)—5 mg/kg PO q12h; treatment should be temporarily discontinued SYNONYMS
administered similarly to KTZ, it has been if creatinine rises above reference range or • Desert rheumatism (in humans).
reported to have higher penetration rate than greater than 20% above baseline, or if • San Joaquin Valley fever. • Valley fever.
KTZ; some suggest greater efficacy of ITZ over granular casts are noted in urine.
FCZ. • Amphotericin B (AMB) is rarely ABBREVIATIONS
recommended because most patients do not PREVENTION/AVOIDANCE • AGID = agar gel immunodiffusion.
require this aggressive therapy and effective • No vaccine is available for dogs or cats. • ALP = alkaline phosphatase.
oral medications are readily available; AMB • Contaminated soil in endemic areas should • ALT = alanine transaminase.
can be administered at a dosage of 0.5 mg/kg be avoided, particularly during dust storms • AMB = amphotericin B.
IV 3 times per week, for a total cumulative after the rainy season. • FCZ = fluconazole.
dosage of 8–10 mg/kg; given IV either as a POSSIBLE COMPLICATIONS • ITZ = itraconazole.
slow infusion (in dogs that are gravely ill) or as Pulmonary disease resulting in severe • KTZ = ketoconazole.
a rapid bolus (in fairly healthy dogs); for slow coughing may temporarily worsen after Suggested Reading
infusion, add AMB to 250–500 mL of 5% therapy is begun owing to inflammation in Arbona N, Butkiewicz CD, Keyes M, et al.
dextrose solution and administer as a drip over the lungs. Anti-inflammatory short-term Clinical features of cats diagnosed with
4–6 hours; to lessen adverse renal effects of (2 weeks to 2 months) oral prednisone and coccidioidomycosis in Arizona, 2004–2018.
AMB, consider 0.9% NaCl (2 mL/kg/h) for cough suppressants may be required to J Feline Med Surg 2020, 22(2):129–137.
several hours before initiating AMB therapy. alleviate the respiratory signs. Graupmann-Kuzma A, Valentine BA, Shubitz
Cats EXPECTED COURSE AND PROGNOSIS LF, et al. Coccidioidomycosis in dogs and
Any of the following azoles may be used in • Prognosis for localized respiratory disease is cats: a review. J Am Anim Hosp Assoc
cats: KTZ 50 mg total dose PO q12h; FCZ good. • Prognosis for disseminated disease is 2008, 44:226–235.
25–50 mg total dose PO q12h; ITZ guarded; many dogs will improve following Johnson LR, Herrgesell EJ, Davidson AP,
25–50 mg total dose PO q12h. oral therapy with resolution of signs reported et al. Clinical, clinicopathologic, and
in up to 90% cases; however, relapses may be radiographic findings in dogs with
CONTRAINDICATIONS coccidioidomycosis: 24 cases (1995–2000).
• Drugs metabolized primarily by the liver should common, especially if therapy is shortened;
overall recovery rate has been estimated at J Am Vet Med Assoc 2003, 222:461–466.
be used with caution alongside azole drugs. Shubitz LE, Butkiewicz CD, Dial SM, et al.
• Drugs metabolized primarily by the kidneys 60%. • Prognosis with CNS involvement may
be guarded to poor. • Prognosis for cats is not Incidence of coccidioides infection among
should be used with caution alongside AMB. dogs residing in a region in which the
well documented, but long-term therapy
PRECAUTIONS should be anticipated and relapses are organism is endemic. J Am Vet Med Assoc
• Side effects of azoles include inappetence, common. • Serologic testing every 3–4 2005, 226:1846–1850.
vomiting, and hepatotoxicity (typically months after completion of therapy is Author Daniel S. Foy
alanine transaminase [ALT] > alkaline recommended to monitor possibility of rising Consulting Editor Amie Koenig
phosphatase [ALP]); liver values should be titer and potential relapse. • Spontaneous
monitored monthly initially; drugs may be recovery from disseminated coccidioidomyco-
stopped until signs abate and restarted at a sis without treatment is extremely rare. Client Education Handout
lower dose, which may be slowly increased to available online
Coccidiosis
• Cystoisospora oocysts should be 40 μm long; CONTRAINDICATIONS/POSSIBLE
C cysts of Cryptosporidium are approximately INTERACTIONS
5 μm diameter. Sulfa medications—caution in patients with
BASICS preexisting renal or hepatic disease.
OVERVIEW
• An enteric infection, traditionally associated
with Cystoisospora canis (dogs) and Cystoisospora TREATMENT
felis (cats) as potential pathogens; other
species of Cystoisospora may be present.
• Usually treated as an outpatient. FOLLOW-UP
• Inpatient if debilitated. Fecal flotation (for Cystoisospora spp. oocysts)
• Strictly host specific (i.e., no cross-transmission). • Fluid therapy if dehydrated.
• Eimeria spp. are not parasitic for dogs or
or DFA (for Cryptosporidium spp. oocysts)
cats. 1–2 weeks following treatment.
• Cryptosporidium can cause an acute, life-
threatening coccidiosis (cryptosporidiosis) in
neonatal pups and kittens; can also cause MEDICATIONS
non-life-threatening small bowel diarrhea in DRUG(S) OF CHOICE MISCELLANEOUS
dogs and cats (see Cryptosporidiosis) • Sulfadimethoxine—55 mg/kg PO on the AGE-RELATED FACTORS
• Voluminous watery diarrhea is characteris- first day, then 25–50 mg/kg PO q24h for up More severe disease in young or immuno-
tic; auto-infection and recycling within the to 10–14 days, or until dog is asymptomatic compromised patients.
intestinal tract result in a rapid loss of for Cystoisospora and fecal examination is
mucosal lining with cryptosporidiosis. negative for oocysts. SEE ALSO
• Sulfadiazine/trimethoprim—15–30 mg/kg • Cryptosporidiosis.
SIGNALMENT
sulfadiazine PO q24h up to 10 days. • Toxoplasmosis.
Dog and cat (especially puppies and kittens).
• Amprolium (extra-label)—dogs: 100– ABBREVIATIONS
SIGNS
400 mg (total dose) PO q24h for 7 days; cats • DFA = direct fluorescent antibody.
• Watery to mucoid, sometimes blood-
with Cystoisospora: 60–100 mg (total dose) Suggested Reading
tinged, diarrhea; vomiting; abdominal
PO q24h for 7 days. Bowman DD, Lynn RC, Eberhard ML.
discomfort; inappetence.
• No effective or approved treatment for
• Weak puppies and kittens. Georgis’ Parasitology for Veterinarians,
Cryptosporidium—paromomycin 165 mg/kg 8th ed. St. Louis, MO: Saunders (Elsevier
• Immunocompromised animals.
PO q12h for 5 days has been suggested Science), 2003, pp. 92–100.
CAUSES & RISK FACTORS (extra-label); however, the drug is potentially Dubey JP, Greene CE. Enteric coccidiosis.
• Infected dogs or cats contaminating nephrotoxic and ototoxic in cats and should In: Greene CE, ed., Infectious Diseases of
environment with oocysts of Cystoisospora not be used; azithromycin has been used at a the Dog and Cat, 4th ed. St. Louis, MO:
spp. or Cryptosporidium spp. dosage of 7–10 mg/kg PO q12h for 7 days Elsevier Saunders, 2012, pp. 828–839.
• Stress. for eradication of Cryptosporidium spp. in Lappin, MR. Update on the diagnosis and
• Immunocompromise. dogs and cats; however, efficacy is unknown. management of Isospora spp. infections in
• Ponazuril at 30–50 mg/kg PO q24h for
dogs and cats. Top Companion Anim Med
1–7 consecutive days in dogs, or 15 mg/kg 2010, 25(3):133–135.
PO q24h for 7 consecutive days in cats; Author Gavin L. Olsen
DIAGNOSIS treatment can be repeated after 3- to 5-day Consulting Editor Amie Koenig
break to increase efficacy; single doses of the
DIFFERENTIAL DIAGNOSIS drug are generally ineffective.
Enteric viral infections and other intestinal • Toltrazuril—10–30 mg/kg PO q24h for
parasites. 1–6 consecutive days in dogs.
CBC/BIOCHEMISTRY/URINALYSIS Precautions
Usually unremarkable; may be hemoconcen- • Mild gastrointestinal upset with antibiotics.
trated if dehydrated. • Amprolium—not recommended to be used
OTHER LABORATORY TESTS for more than 12 consecutive days in puppies,
N/A exogenous thiamine in high doses may
decrease efficacy; neurologic abnormalities
IMAGING have been reported in some dogs: if observed,
N/A discontinue medication and begin thiamine
DIAGNOSTIC PROCEDURES supplementation.
• Fecal flotation (preferably centrifugation • Sulfadimethoxine—caution with dimin-
flotation technique) for oocysts (distinguish from ished hepatic or renal function.
pseudoparasitic Eimeria sp.); use sucrose solution • Sulfadiazine/trimethoprim—potentially
or zinc sulfate; acid-fast stains should be teratogenic; dog: associated with irreversible
considered for detection of Cryptosporidium spp. keratoconjunctivitis sicca, type 1 or type 3
• Direct fluorescent antibody (DFA) assay is hypersensitivity (especially in larger-breed
a sensitive dual assay (can detect Giardia cysts dogs), thrombocytopenia; cat: anorexia,
and Cryptosporidium oocysts very well) and leukopenia, anemia, hematuria.
can be performed at reference laboratories or
university parasitology laboratories.
Cognitive Dysfunction Syndrome

SIGNS CBC/BIOCHEMICAL/URINALYSIS
Historical Findings Normal with CDS, but concurrent disease C
• Clinical signs have been categorized using processes common in aged dogs.
BASICS
the acronym DISHAA. • Disorientation, OTHER LABORATORY TESTS
DEFINITION including getting lost in familiar environ Normal with CDS.
Syndrome associated with brain aging. ments, confusion, inability to navigate
Leads to alterations in awareness, decreased IMAGING
through familiar routes (e.g., goes to hinge • Used to rule out primary organic/structural
responsiveness to stimuli, deficits in side of door), dropping food and not retrieving.
learning and memory, agitation, and cause. • Most important when there are
• Interactions with humans or other animals abnormalities on the neurologic examination
anxiety. Subtle signs seen in early stages of may be altered (irritability, decreased interest
cognitive decline may include alterations in or when the onset is sudden; less likely to be
in play/affection, or increased attention of diagnostic value if signs are slowly
activity, social interactions and increasing seeking). • Sleep–wake cycle alterations
anxiety. progressive in the absence of other neurologic
including night waking, vocalization, and/or findings.
PATHOPHYSIOLOGY increased sleep during the day.
• Neuronal loss, decreased frontal lobe • Housetraining and other previously learned DIAGNOSTIC PROCEDURES
volume, increased ventricular volume, and behaviors might deteriorate. • Activity may • Diagnosis is based on identifying clinical
neurotoxic deposits including lipofuscin and be altered—including a decline in activity signs on screening questionnaire, e.g., DISHAA
beta-amyloid. • Toxic free radicals (reactive level, exploration, and self-care; however, as (Pan et al.), CADEs (Madari et al.), and
oxygen species) increase with age because of the condition progresses, activity may increase CCDR (Salvin et al.), ruling out possible
illness and stressors, age-related decline in with signs of restlessness, pacing, aimless medical causes. • Early and mild signs not
mitochondrial efficiency, and decreased wandering, vocalization, or excessive licking. likely to be reported; therefore veterinarians
clearance mechanisms. • Unclear which • Anxiety and agitation. must ask (e.g., with screening questionnaire).
changes are associated with the clinical signs; • Endoscopy, radiography, ultrasound, and
Physical Examination other specialized diagnostic procedures may
possible correlation between cognitive • No specific abnormalities associated with
decline, amount of beta-amyloid in the be necessary to rule out other causes of the
cognitive dysfunction. • Other age-related clinical signs. • Further ophthalmic and
cerebral cortex, and increases in toxic free medical disorders might be noted.
radicals. • Compromised cerebral vascular neurologic assessment if indicated to rule out
blood flow and infarcts may be contributory. CAUSES visual or auditory deficits and neurologic
• Neurotransmission is compromised; may be • Exact cause is unknown and animals are disease. • Therapeutic trial might be
a decline in catecholamine and cholinergic variably affected. • Environmental factors considered to rule out and treat other
transmission. may contribute to age-related degeneration. potential causes of the signs, e.g., pain.
• May be predisposing genetic factors.
SYSTEMS AFFECTED PATHOLOGIC FINDINGS
• Diet, enrichment, and stress management
• Behavioral. • Nervous. Loss of frontal and temporal lobe volume,
may be in part preventive. • See neuronal loss, meningeal calcification,
GENETICS Pathophysiology. microhemorrhage and infarcts, beta-amyloid
Unknown; may be genetic factors contrib RISK FACTORS deposition and hyperphosphorylated tau.
uting to beta-amyloid deposition and the • Chronic oxidative stress and chronic
age at which it begins to accumulate. low-grade inflammation. • Conditions that
INCIDENCE/PREVALENCE affect cerebral vascular blood supply (e.g.,
• Clinical signs of cognitive dysfunction systemic hypertension, anemia). • Deficiency
in docosahexaenoic acid (DHA), B6, B12,
TREATMENT
syndrome (CDS) have been reported to arise
in 41–68% (or higher) of dogs over 14. and folic acid, high homocysteine, low- NURSING CARE
• Overall prevalence in dogs over 10 quality diets. Support and home care by pet owners.
estimated as at least 14.2%. • Clinical signs ACTIVITY
reported to arise in 50% of cats over 15. • Maintain exercise, play, reward-based
• Prevalence in cats over 10 estimated at training, work, feeding enrichment (e.g.,
35%. • Progressive—over 6 months, 24% of DIAGNOSIS food-filled toys), and daily routines that are
dogs with mild signs progressed to moderate appropriate for the pet’s age and health.
and 42% with no impairment progressed to DIFFERENTIAL DIAGNOSIS • Maintaining mental stimulation and
mild. • Any medical condition that affects the pet’s physical activity have been shown to reduce
mental attitude or behavior must be ruled or slow progression of cognitive decline.
SIGNALMENT out. • Pain (e.g., arthritis, dental disease) can
Species lead to increased irritability, anxiety, and DIET
Dogs and cats. altered response to stimuli. • If mobility is • Diet should be fed that meets and
affected, the pet may be less able to avoid prioritizes medical and cognitive health care
Mean Age and Range needs. • For dogs, diet supplemented with
• Increased prevalence with increasing age.
fearful stimuli and less able to access its
elimination area. • Impaired sight or hearing antioxidants including vitamins E and C,
• Neuropsychological testing in dogs and cats selenium, beta carotene, and flavonoids and
has identified a decline in memory and might lead to decreased responsiveness or
increased reactivity to stimuli. • Diseases of carotenoids, omega-3 fatty acids, and
learning as early as 6–8 years of age. • Initial carnitine and alpha lipoic acid (for mitochon
signs may not be noticed by pet owners, the urinary or gastrointestinal tract can cause
house-soiling. • Organ failure, tumors, drial health) has been shown to improve
except perhaps in dogs trained to perform memory, learning ability, and clinical signs of
more specialized tasks (e.g., guide and hearing immune diseases, and endocrinopathies can
also affect behavior. • Diseases that affect the cognitive dysfunction (Hills Prescription Diet
dogs, drug detection, agility). b/d). • As cerebral glucose metabolism
CNS or its circulation can affect behavior.
declines with increasing age in dogs, a diet
Cognitive Dysfunction Syndrome (continued)
supplemented with 5.5% medium-chain • Nicergoline—alpha-adrenergic antagonist 30–60 days and the dose adjusted or
C triglyceride (MCT) oil to provide ketone that may improve cognitive function treatment changed if there is insufficient
bodies as an alternative source of energy for through vasodilatory effects on cerebral improvement. • If the pet is stable, twice-
aging neurons has been demonstrated to circulation; 0.25–0.5 mg/kg PO q24h. yearly checkups are recommended unless new
improve cognitive function in middle-aged Cats problems arise before reassessment is due.
and senior dogs (e.g., Purina ProPlan Bright • No therapeutic agents licensed for PREVENTION/AVOIDANCE
Mind 7+®). • A brain support blend treatment of CDS. • Selegiline (0.5–1 mg/kg • Providing an enriched environment,
containing arginine (to enhance nitrous oxide PO q24h), propentofylline (1/4 of 50 mg ongoing training, and physical activity that is
synthesis), antioxidants including vitamins C, tablet PO q24h), and nicergoline (0.25– appropriate and practical for the pet’s age and
E, and selenium; B vitamins; and omega-3 0.5 mg/kg PO q24h) have been used off-label health may help to prevent or delay the onset
fatty acids has been demonstrated to improve in cats, with anecdotal evidence of effect. of cognitive decline. • Early CDS dietary
cognitive function in laboratory studies in intervention may address risk factors and slow
senior dogs and middle-aged cats. • A CONTRAINDICATIONS
• Selegiline should not be used concurrently
the progression of disease.
combination of the brain support blend and
6.5% MCT supplementation has been with MAO inhibitors such as amitraz, EXPECTED COURSE AND PROGNOSIS
demonstrated to improve clinical signs of narcotics, alpha-adrenergic agents such as Diet and medication may improve signs and
cognitive dysfunction in dogs (Purina Pro phenylpropanolamine or ephedrine, or slow progression in most cases; however, with
Plan Veterinary Diets NC NeuroCare®). • For selective serotonin reuptake inhibitors increasing age, CDS may progress and other
dogs—supplements containing phosphati- (e.g., fluoxetine) or tricyclic antidepressants concurrent health problems will ultimately
dylserine (Senilife, CEVA Animal Health and (e.g., clomipramine). • A 2-week washout is arise.
Activait, VetPlus), S-adenosyl-L-methionine- suggested following most tricyclic antidepress-
tosylate disulfate (SAMe; Novifit, Virbac ants and up to 5 weeks following fluoxetine
Animal Health), and apoaequorin have before starting selegiline.
demonstrated some evidence of efficacy. • For PRECAUTIONS MISCELLANEOUS
cats—SAMe and diets containing fish oil, • Choose medications that are least sedating
arginine, B vitamins, and antioxidants have SYNONYMS
and least anticholinergic. • Potential drug
demonstrated beneficial effects. • Age-related cognitive and affective
interactions must be considered with
disorders, involutional depression, dysthymia.
CLIENT EDUCATION concurrent use of drugs and over-the-counter
• Dementia. • Senility.
• Lifelong therapy is required, and medications.
concurrent medications may be necessary if ABBREVIATIONS
the pet has multiple problems. • Any changes • CDS = cognitive dysfunction syndrome.
See Contraindications.
in the pet’s health or behavior should be • DHA = docosahexaenoic acid. • GABA =
reported immediately, as this may be due to ALTERNATIVE DRUG(S) γ-aminobutyric acid. • MAO = monoamine
cognitive dysfunction or new health problems. • Consider potential benefits vs. risks oxidase. • MCT = medium-chain triglyceride.
• Considering the pet’s health and cognitive
including contraindications, side effects, • SAMe = S-adenosyl-L-methionine-tosylate
status, the owner must be advised on any off-label use, and evidence of effect. • Anti- disulfate.
limitations on what might be achieved. inflammatory medications and natural
supplements such as gingko biloba and
Suggested Reading
• Signs are generally progressive; treatment is Landsberg GM, Madari A, Zilka N., eds.
aimed at slowing the progression of the curcumin might be considered based on
Canine and Feline Dementia: Molecular
disease, not cure. preliminary work in other species.
Basis, Diagnostics, and Therapy. Cham:
• Medication used in humans for Alzheimer’s
Springer, 2017.
disease to enhance cholinergic transmission
Madari A, Farbakova J, Katina S, et al.
might be useful, but doses and pharmaco
Assessment of severity and progression of
kinetics in dogs have not been determined;
MEDICATIONS canine cognitive dysfunction syndrome
side effects might include nausea, vomiting,
using the Canine Dementia Scale
DRUG(S) OF CHOICE diarrhea, and sleep-wake disturbances. • For
(CADES). Appl Anim Behav Sci 2015,
anxiety, agitation, apathy, and night waking
Dogs 17:138–145.
consider adjunctive therapeutics including
• Selegiline—monoamine oxidase (MAO) Pan Y, Landsberg G, Mougeot I, et al.
buspirone or fluoxetine for ongoing use, or
B inhibitor, may contribute to improved Efficacy of a therapeutic diet on dogs with
trazodone, benzodiazepines, and alpha-2
catecholamine transmission, decrease in free signs of cognitive dysfunction syndrome
agonists for as needed use. • Natural
radicals, and neuroprotective effect; (CDS): a prospective double blinded
supplements including pheromones,
0.5–1 mg/kg PO q24h in the morning and placebo controlled clinical trial. Front Nutr,
melatonin, valerian, l-theanine, alpha-
maintained if effective; reevaluate clinical 2018, doi: 10.3389/fnut.2018.00127.
casozepine, γ-aminobutyric acid (GABA),
signs for improvement after 1–2 months; Salvin HE, McGreevy PD, Sachdev PS, et al.
magnolia and phellodendron (Solliquin®), or
side effects might include occasional The canine cognitive dysfunction rating
Souroubea (Zentrol®) might help to reduce
gastrointestinal upset and restlessness, and scale (CCDR): a data-driven and ecologi-
signs related to anxiety and night-time
repetitive behavior at higher doses. cally relevant assessment tool. Vet J 2011,
waking.
• Propentofylline—not licensed in North 188:331–336.
America but is licensed in other countries; Authors Gary M. Landsberg and Sagi
xanthine derivative; purported to inhibit Denenberg
platelet aggregation and thrombus Consulting Editor Gary M. Landsberg
formation, make the red cells more pliable, FOLLOW-UP
and increase blood flow; may increase PATIENT MONITORING
oxygen supply to CNS without increasing Client Education Handout
• If a drug or diet for CDS is dispensed,
glucose demand; 3–5 mg/kg PO q12h. available online
therapeutic response should be evaluated after
Cold Agglutinin Disease

(SLE), lymphoma, frostbite, lead poisoning, • IgG cold agglutinins—immunosuppressive
and pemphigus. therapy. C
• Other causes of anemia (including hemo-
BASICS CONTRAINDICATIONS/POSSIBLE
lytic anemias).
INTERACTIONS
OVERVIEW CBC/BIOCHEMISTRY/URINALYSIS Use warmed IV fluids if indicated.
• Rare type II autoimmune disorder in which • Laboratory abnormalities secondary to
anti-erythrocyte antibodies have enhanced hemolysis, if present.
activity at temperatures <99 °F (37.2 °C). • Autoagglutination of RBCs may be
• Cold agglutinins are typically immuno- observed at room temperature.
globulin (Ig) M, although IgG alone and in F OLLOW-UP
combination with IgM may result in disease. OTHER LABORATORY TESTS • Keep patient in warm environments.
• Cold agglutinins cause direct erythrocyte • Cold agglutinins should be suspected when • Cold agglutinin disease usually character-
agglutination at low body temperatures blood in heparin or EDTA on a glass slide ized by acute onset and rapid progression.
(primarily peripheral microvasculature), agglutinates spontaneously at room tempera- • Prognosis is guarded to fair; recovery may
leading to vaso-occlusive disease, initiated or ture with enhancement at 39 °F (3.9 °C), and take weeks.
intensified by cold exposure. the erythrocytes disperse again upon warming
• Fixation of complement and hemolysis is a to 99 °F (37.2 °C).
warm reactive process occurring at higher • If no agglutination can be induced in vitro,
body temperatures; at those temperatures cold it will not occur in vivo in extremities.
agglutinins have eluted off the red blood cells • Coombs’ test at 99 °F—cold agglutinins MISCELLANEOUS
(RBCs), lowering the rate of complement usually not detected because they may be SEE ALSO
binding; therefore, acute hemolytic anemias eluted off the erythrocytes during washing; Anemia, Immune-Mediated.
are uncommon with this condition. thus test requires the use of anti-complement
factor serum. ABBREVIATIONS
• Most cold agglutinins cause little or no • Ig = immunoglobulin.
shortening of erythrocyte lifespan. • Coombs’ test at 39 °F—incidence of a
positive result in healthy dogs has been • RBC = red blood cell.
• High thermal amplitude cold agglutinins • SLE = systemic lupus erythematosus.
(rare)—may cause mild chronic hemolysis, reported to be >50%, which may be caused
but exposure to cold may greatly augment by unspecific binding of the reagent itself or Suggested Reading
binding of cold agglutinins and cause by binding of naturally occurring nonpatho- Dickson NJ. Cold agglutinin disease in a
intravascular hemolysis. genic low-titer cold agglutinins. puppy associated with lead intoxication.
• The globulin class can be established by J Small Anim Pract 1990, 31:105–108.
SIGNALMENT immunoelectrophoresis of the patient’s Author Jörg Bucheler
• Rare; genetics, age, breed, and sex predilec- erythrocytes, which may be important for Consulting Editor Melinda S. Camus
tions unknown. prognosis and treatment.
• Low titer of cold agglutinins (1 : 32 or less)
may be found in healthy pets without clinical PATHOLOGIC FINDINGS
significance. • Dermal necrosis and ulceration with
• More likely to occur following exposure to possible opportunistic infections.
cold temperatures. • Vascular thrombosis, ischemic necrosis.
SIGNS
• Cyanosis of the extremities associated with
sludging of erythrocyte agglutinates in
microvasculature. TREATMENT
• Erythema, skin ulceration with secondary • Hospitalization in a warm environment
crusting. until the disease is nonprogressive.
• Dry, gangrenous necrosis of ear tips, tail tip, • Supportive care and wound management.
nose, and feet. • Splenectomy is of little benefit in patients
• Anemia may cause signs of pallor, tachycar- with IgM-mediated hemolysis, but may be
dia, tachypnea, icterus, and pigmenturia. helpful in those with IgG-mediated hemolysis.
• Inform the client to keep the patient in a warm
CAUSES & RISK FACTORS environment at all times to prevent relapse.
• Idiopathic; cold exposure is a risk factor. • Exercise restriction.
• Secondary disease—associated with upper • In humans, plasmapheresis, IV gamma
respiratory infection (cats), neonatal globulins, and rituximab with or without
isoerythrolysis, lead intoxication (dogs), fludarabine have been tried.
Mycoplasma pneumonia, and neoplasia.
MEDICATIONS
DIAGNOSIS
DRUG(S) OF CHOICE
DIFFERENTIAL DIAGNOSIS • IgM cold agglutinins—immunosuppressive
• Skin lesions—vasculitis, hepatocutaneous therapy not very effective against IgM-
syndrome, toxic epidermal necrolysis, mediated disorders, but can be tried (i.e.,
dermatomyositis, systemic lupus erythematosus corticosteroids, leflunomide, cyclosporine).
Colibacillosis
• Purulent skin disease, otitis, meningoencephalo- RISK FACTORS
C myelitis. Neonates
BASICS Dogs • Bitch/queen in poor health and nutritional
• ETEC—2.7–29.5% of diarrheic dogs; status—unable to provide good care and
DEFINITION strains: STa/STb+/−, and CNF+ isolated from colostrum.
• Escherichia coli (EC)—Gram-negative diarrheic dogs along with hemolysin. • Lack of colostrum or insufficient colostrum.
member of the Enterobacteriaceae; normal • β-hemolytic EC—major cause of septice- • Dirty birthing environment.
inhabitant of intestine of most mammals. mia in newborn puppies exposed in utero, • Difficult or prolonged labor and birth.
• Acute infection of puppies and kittens in during birth, or from mastitic milk. • Crowded facilities—feces in environment,
first week of life characterized by septicemia chance for fecal–oral spread.
and multiple organ involvement. Cats
• Isolation from stool of young animals— • AEEC/enteropathic EC (EPEC)—diarrheic Puppies/Kittens and Adults
inconclusive evidence of pathogenic potential cats; strains: eae+, hemolysin. • Concurrent disease—parvovirus, heavy
because it is normal flora; molecular methods • Extraintestinal pathogenic EC (ExPEC)— parasitism.
can assess virulence potential. acute necrotizing and hemorrhagic pneumo- • Antimicrobial drugs—upset gastrointestinal
• Isolation from blood cultures or internal nia and pleuritis; strains: CNF-1 plus other microbial flora.
organs—better evidence of causality. adhesions. • Immunosuppression.
• Infection of older dogs and cats— • UPEC—cystitis; strains: CNF-1+, • Postparturient mastitis.
documented; virulence of individual strains P-fimbria, hemolysin.
poorly characterized. GEOGRAPHIC DISTRIBUTION
PATHOPHYSIOLOGY Worldwide
• Virulence factors—not well defined; likely SIGNALMENT DIAGNOSIS
EC as a cause of septicemia in neonatal dogs DIFFERENTIAL DIAGNOSIS
Species
and cats reflects balance between immuno- • Infectious enteritis—viral: feline panleuko-
Dog and cat.
logic immaturity and intestinal barrier penia, feline leukemia virus, feline immuno-
function of host and resident enteric EC Breed Predilections deficiency virus, enteric coronavirus, canine
rather than a single virulent strain. Boxer dogs may be predisposed to colitis. parvovirus, rotavirus, canine distemper;
• Enterotoxigenic EC (ETEC), attaching and Mean Age and Range bacterial: Salmonella, E. coli, Campylobacter
effacing EC (AEEC), uropathogenic EC • Neonatal infections common (diarrhea, jejuni, Yersinia enterocolitica, bacterial
(UPEC), cytotoxic necrotizing factor (CNF) septicemia) up to 2 weeks of age. overgrowth syndrome, Clostridium difficile,
+ EC strains—recovered from dogs, similar in • Puppies/kittens and adult animals— Clostridium perfringens; parasitic: hookworms,
cats. sporadic disease often associated with other ascarids, whipworms, Strongyloides, Giardia,
• Intestinal strains colonize and multiply in infectious agents. coccidia, cryptosporidia, rickettsiae (salmon
small intestine; ETEC then elaborates poisoning).
uncharacterized adhesins and enterotoxins Predominant Sex
• Dietary-induced enteritis—overeating,
(STa); attaching and effacing factor of AEEC None
abrupt changes, starvation, thirst, food
(intimin [eae]+). SIGNS intolerance or allergy, indiscretions
• Many strains of EC from dogs and cats are (e.g., foreign material, garbage).
General Comments
hemolytic. • Drug- or toxin-induced enteritis—antimi-
One of the most common causes of septice-
• An EC reported in boxer dogs with granu- crobial agents, antineoplastic agents, anthel-
mia and death in puppies and kittens.
lomatous colitis characterized by ability to mintics, heavy metals, organophosphates.
adhere, invade, and replicate in macrophages, Historical Findings • Extraintestinal disorders or metabolic
resulting in massive inflammatory response • Neonates—sudden-onset vomiting, diseases—acute pancreatitis; hypoadrenocor-
within intestinal wall. weakness/lethargy, diarrhea, cold skin; one or ticism; liver or kidney disease; pyometra;
more animals affected in a litter. peritonitis.
SYSTEMS AFFECTED
• Puppies/kittens and adults—vomiting and • Functional or mechanical ileus— gastroin-
• Neonates—small intestine (enteritis);
diarrhea. testinal obstruction, intussusception,
multiple body systems (septicemia).
• Puppies/kittens and adults—small intestine Physical Examination Findings electrolyte disorder, gastrointestinal foreign
(enteritis); urogenital (cystitis, endometritis, • Neonates—acute depression, anorexia, body.
pyelonephritis, prostatitis); mammary gland vomiting, tachycardia, weakness, hypothermia, • Neurologic disorders—vestibular disease,
(mastitis); large intestine (colitis). cyanosis, watery diarrhea. psychogenic (e.g., fear, excitement, pain).
• Puppies/kittens and adults—ETEC • Fading neonates.
GENETICS
associated with acute vomiting, diarrhea, CBC/BIOCHEMISTRY/URINALYSIS
Boxer dogs may be predisposed.
anorexia, rapid dehydration, fever. • Few abnormalities noted, owing to rapidity
INCIDENCE/PREVALENCE of death in puppies.
CAUSES
• Few statistics available. • Adults with enteritis may show nonspecific
• EC—endogenous microbial flora of
• More common in neonatal puppies and abnormalities, depending on condition.
adult gastrointestinal tract, prepuce, and
kittens <1 week old that have not received
vagina. DIAGNOSTIC PROCEDURES
any or adequate amounts of colostrum.
• Many strains; poorly characterized • Routine bacterial culture and identification
• Problem in overpopulated kennels and
regarding virulence factors; need molecular of EC from blood (antemortem) or necropsy
catteries.
methods to assess virulence. tissue (bone marrow, heart blood, liver, spleen,
• Sporadic accounts in older dogs and cats
• Often found in older dogs and cats brain, mesenteric lymph node) required.
(mainly diarrhea and urogenital problems).
concurrently with other infectious agents.
(continued) Colibacillosis
• False-negative results can occur if antimi- • Enrofloxacin—dog: 10–15 mg/kg IM/IV ZOONOTIC POTENTIAL
crobials are used before obtaining bacterial q24h; cat: 5 mg/kg IV q24h. • Little information of virulence potential of C
cultures. • Ticarcillin–clavulanate—dogs and cats: EC strains from dogs or cats for humans,
• Appropriate testing of strains—identify 50 mg/kg IV q6h. although recently similarities have been found
adhesins and toxins (by DNA colony CONTRAINDICATIONS between canine fecal and UPEC and human
hybridization, PCR) in ETEC and verotoxi- Fluoroquinolones—avoid use in pregnant, EC associated with urinary tract infections,
genic EC (VTEC) strains. neonatal, or growing animals (medium-sized sepsis, and meningitis.
PATHOLOGIC FINDINGS dogs <8 months of age; large or giant breeds • Growing concern for presence of multidrug
• Acute enteritis. <12–18 months of age) because of potential resistance determinants in EC strains from
• Inflammation of small intestinal mucosa. cartilage lesions. companion animals.
• Petechiae and hemorrhagic lesions on • Children and immunosuppressed persons
PRECAUTIONS should be kept away from pets with diarrhea.
serosal surface of gastrointestinal mucosae and Ensure adequate hydration and perfusion
all body cavities. • Whole genome sequencing has linked
when using aminoglycosides. commercially available raw meat diets to
• Fibrin on abdominal wall.
• Necrosis of liver/spleen. pathogens found in dogs and cats, including
EC, Salmonella, and Listeria.
SYNONYMS
FOLLOW-UP • E. coli septicemia.
PATIENT MONITORING • Neonatal enteritis.
TREATMENT
• Physical exam—mentation, rectal ABBREVIATIONS
APPROPRIATE HEALTH CARE temperature, pulse quality. • AEEC = attaching and effacing E. coli.
Acutely ill puppies/kittens—inpatient care. • Behavior—puppies should be eating, • CNF = cytotoxic necrotizing factor.
NURSING CARE drinking, and/or nursing; adequate weight • EC = Escherichia coli.
• Balanced parenteral polyionic isotonic gain. • EPEC = enteropathogenic E. coli.
solution (e.g., lactated Ringer’s)—restore fluid PREVENTION/AVOIDANCE • ESBL = extended spectrum beta-lactamase.
balance. • Bitch/queen—good health; vaccinated; • ETEC = enterotoxigenic E. coli.
• Oral hypertonic glucose solution—for good nutritional status. • ExPEC = extraintestinal pathogenic E. coli.
secretory diarrhea, as indicated. • Clean and disinfect parturition environ- • UPEC = uropathogenic E. coli.
ACTIVITY ment (1 : 32 dilution of bleach); clean • VTEC = verotoxigenic E. coli.
Acutely ill immature puppies/kittens bedding frequently after birth. Suggested Reading
(bacteremic/septicemic)—restricted activity, • Ensure adequate colostrum intake of all Craven M, Mansfield CS, Simpson KW.
cage rest, monitoring, and warmth. littermates. Granulomatous colitis of boxer dogs. Vet
• Separate mother with nursing litter from Clin North Am Small Anim Pract, 2011
DIET
Puppies—likely to still be nursing when other cats or dogs. 41:433–445.
• Keep density low in kennel or cattery Marks SL, Rankin SC, Byrne BA, et al.
affected; good nursing care needed with
bottle-feeding and/or IV nutrients. rooms. Enteropathogenic bacteria in dogs and cats:
• Wash hands and change clothes and shoes diagnosis, epidemiology, treatment, and
CLIENT EDUCATION after handling other cats/dogs and before control. J Vet Intern Med 2011, 25:1195–208.
Neonates—life-threatening with poor prognosis. dealing with neonates. Sabshin SJ, Levy JK, Tupler T, et al.
EXPECTED COURSE AND PROGNOSIS Enteropathogens identified in cats entering
• Neonates—life-threatening; prognosis often a Florida animal shelter with normal feces
poor; neonate may rapidly succumb; quick or diarrhea. J Am Vet Med Assoc 2012,
M EDICATIONS treatment with supportive care essential for 241:331–337.
survival. Tupler T, Levy JK, Sabshin SJ, et al.
DRUG(S) OF CHOICE Enteropathogens identified in dogs entering
• Antimicrobial therapy—septicemia. • Adults—self-limiting with supportive care,
depending on degree of dehydration and a Florida animal shelter with normal feces
• Guided by culture and susceptibility (and or diarrhea. J Am Vet Med Assoc 2012,
minimal inhibitory concentration) testing of existence of other diseases.
241:338–343.
EC; empiric therapy until results available. Weese JS. Bacterial enteritis in dogs and cats:
Extended-spectrum β-lactamase (ESBL) diagnosis, therapy, and zoonotic potential.
and/or plasmid mediated AmpC (pAmpC) Vet Clin North Am Small Anim Pract 2011,
strains becoming more common. MISCELLANEOUS 41:287–309.
• Amikacin—dog and cat: 15–20 mg/kg IV Author Patrick L. McDonough
q24h. AGE-RELATED FACTORS
Neonates—greatest risk of infection and Consulting Editor Amie Koenig
• Cefazolin—dog and cat: 15–35 mg/kg IV
q6–8h. subsequent septicemia.
• Cefoxitin—dog and cat: 30 mg/kg IV once,
then 15 mg/kg IV q6–8h. available online
Colitis and Proctitis
distribution in North America, Australasia, CBC/BIOCHEMISTRY/URINALYSIS
C Europe, and Asia. • Results usually unremarkable; neutrophilia
SIGNALMENT with left shift can be seen with severe
BASICS inflammatory causes; eosinophilia secondary
DEFINITION Species to eosinophilic colitis, parasitism, histoplas-
• Colitis—inflammation of the colon (large Dog and cat. mosis, pythiosis/phycomycosis. • Mild
intestine); colitis may be acute and self- Breed Predilections microcytic, hypochromic anemia may occur
limiting or chronic. • Colitis does not infer • Boxers, French bulldogs, border collies secondary to chronic intestinal bleeding
causality, and an underlying cause of the colitis (GC). • German shepherd dogs—perianal and iron deficiency. • Hyperglobulinemia in
should be investigated, particularly in chronic fistulas and concurrent colitis. some patients (especially cats) with chronic
cases. • Proctitis—inflammation of the rectum. disease.
Mean Age and Range
PATHOPHYSIOLOGY • Any age; boxers and French bulldogs are OTHER LABORATORY TESTS
• Inflammation of the colon causes accumu- typically younger (<2 years). • Cats infected with • Examination of fecal centrifugation
lation of inflammatory cytokines, disrupts Tritrichomonas blagburni are typically younger flotation, direct fecal smear (only on fresh
tight junctions between epithelial cells, (<2 years), but can also be infected when older. diarrheic feces), detection of netE and netF
stimulates colonic secretion, stimulates goblet toxin genes of C. perfringens and C. difficile
SIGNS toxins A and B genes via PCR, serum ELISA
cell secretion of mucus, and disrupts motility.
• These mechanisms reduce the ability of the Historical Findings test for Pythium when indicated. • Rectal
colon to absorb water and electrolytes, and • Fecal consistency can be variable from scraping for cytology for Histoplasma
store feces, which causes frequent diarrhea, semi-formed to liquid. • Marked increase in organisms and Prototheca spp. • Biopsy of
often with mucus and/or frank blood. frequency of defecation (6–15 times per day) colon or regional lymph nodes for detection
with small fecal volume. • Tenesmus. of Prototheca spp., or biopsy of gastrointesti-
SYSTEMS AFFECTED
• Increased fecal mucus. • Hematochezia; cats nal tract and regional lymph nodes for
Gastrointestinal
may have formed feces with hematochezia. detection of Histoplasma organisms.
GENETICS • Occasional dyschezia (painful defecation). • Microscopic examination of urine sediment
• Breeds predisposed to histiocytic ulcerative • Increased urgency to defecate. • Vomiting in or cerebrospinal fluid (CSF) in dogs with
colitis (granulomatous colitis [GC]) include approximately 30% of dogs and cats with colitis. disseminated protothecosis and associated
boxers, French bulldogs, and, less commonly, clinical signs can be excellent means of
border collies. • German shepherd dogs are detecting organisms. • Culture and sensitivity
• Usually unremarkable. • Rectal examination
predisposed to perianal fistulae (anal furuncu- testing for diagnosis of Prototheca spp.
may reveal thickened and irregular colorectal
losis) that can be associated with colitis.
mucosa. • Dogs with GC may show systemic ®
• MVista Histoplasma quantitative antigen
test performed on serum, plasma, urine, or
INCIDENCE/PREVALENCE signs of weight loss and anorexia.
• Approximately 30% of dogs with chronic CSF can aid diagnosis and management of
CAUSES histoplasmosis. • Fecal PCR or In Pouch TF
diarrhea examined at one university hospital.
• Dietary—food-responsive enteropathy is medium for culture of Tritrichomonas foetus.
• 71% of dogs with a food-responsive
common and important cause of colitis;
enteropathy had clinical signs of colitis (either IMAGING
dietary indiscretion; food intolerance. • Drug
alone or in association with enteritis (entero- • Abdominal radiographs—usually unre-
administration (antibiotics, nonsteroidal
colitis). • Prevalence of colitis probably higher markable. • Abdominal ultrasonography—
anti-inflammatory drugs [NSAIDs]).
than perceived, because many diarrheic dogs may reveal masses, diffuse thickening or
• Infectious—Trichuris vulpis, Entamoeba
and cats manifesting small bowel diarrhea altered architecture of the colon, or enlarged
histolytica, Balantidium coli, Tritrichomonas
have evidence of colitis histopathologically associated lymph nodes. • Contrast studies—
blagburni, Clostridium perfringens and
when biopsied. barium may be administered transcolonically
Clostridium difficile, Campylobacter jejuni and
GEOGRAPHIC DISTRIBUTION Campylobacter coli, Yersinia enterocolitica, to evaluate colorectal mucosa for irregularities
• N/A except for certain infectious diseases. Prototheca, Histoplasma capsulatum, pythiosis/ or filling defects and colorectal strictures;
• Pythiosis—predominantly Gulf Coast and phycomycosis. • Traumatic—foreign body, however, procedure rarely indicated in dogs
southeast United States, although becoming abrasive material. • Inflammatory—secondary to and cats with colitis and of low sensitivity in
more widespread, including California. pancreatitis (transverse colitis). • Inflammatory/ general.
• Histoplasmosis—Midwest, eastern United immune—inflammatory bowel disease DIAGNOSTIC PROCEDURES
States. • Prototheca spp.—ubiquitous in (lymphoplasmacytic, eosinophilic, granuloma- • Colonoscopy with biopsy—procedure of
nature, especially prevalent in warm, humid tous) colitis. choice for diagnosis of chronic or refractory
climates (e.g., southern and southeastern cases; animals must be adequately prepared
United States, northeastern Australia, for colonoscopy by being fasted and
southern continental Europe, Japan) in administered osmotic cathartics such as
aqueous environments where decaying OsmoPrep® or GoLYTELY®; mucosal changes
organic matter present. • Entamoeba DIAGNOSIS visible grossly in animals with colitis include
histolytica—prevalent in tropical and DIFFERENTIAL DIAGNOSIS disappearance of submucosal blood vessels,
subtropical regions worldwide; in United • Neoplasia—colonic lymphoma, adenocarci- granular appearance of mucosa, hyperemia,
States, much higher rate of amebiasis-related noma, sarcomas. • Irritable bowel syndrome. excessive mucus, ulceration, pinpoint
mortality in California and Texas, which • Colorectal polyps do not typically cause hemorrhage (small ulcerations), or mass(es).
might be caused by their proximity to signs of colitis, but instead cause hematoche- • Always obtain multiple biopsy specimens
E. histolytica-endemic areas, such as Mexico, zia in association with formed stool defecated from multiple locations (ascending colon,
other parts of Latin America, and Asia. at normal frequency. • Cecal inversion. transverse colon, descending colon, rectum)
• Tritrichomonas blagburni—widespread • Ileocecocolic intussusception.
(continued) Colitis and Proctitis

because extent of mucosal change assessed syndrome, can be self-limiting and avoidance dose over course of therapy. • Cyclosporine
histologically does not necessarily reflect of antimicrobials recommended whenever (5 mg/kg PO q12–24h for 6 weeks for C
severity of colitis or proctitis. feasible. • Clostridium difficile—metronida- immune disease). • GC (histiocytic ulcerative
PATHOLOGIC FINDINGS zole (10 mg/kg PO q12h for 5 days). colitis) usually managed with fluoroquinolo-
Histopathologic findings depend on histologic • Campylobacter jejuni—erythromycin nes such as enrofloxacin at 10 mg/kg q24h
type of colitis—lymphoplasmacytic, eosino- (10–15 mg/kg PO q8h) or azithromycin for 6–8 weeks; however, evidence of marked
philic, or histiocytic represent most common (5–10 mg/kg PO q24h) can be given for increase in antimicrobial resistance to this
subtypes; hyperplastic mucosa may be seen with 7–10 days; azithromycin better tolerated than class of drugs underscores importance of
irritable bowel syndrome; various infectious erythromycin. • Yersinia spp.—select drug on culture and sensitivity testing to optimize
agents may be seen with special stains. basis of bacterial culture and sensitivity antimicrobial therapy. • Reconsider diagnosis
testing. • Prototheca—combination therapy of food-responsive colitis or nonspecific
with amphotericin B and itraconazole, colitis carefully in dogs that do not respond
although disseminated cases typically fatal. to dietary therapy, fenbendazole administra-
• Histoplasma—itraconazole (dogs: 10 mg/kg tion, and tylosin therapy.
TREATMENT PO q24h; cats: 5 mg/kg PO q12h; several Motility Modifiers
DIET months of therapy necessary); amphotericin B • Indicated for symptomatic relief only in
• No inherent benefit to fasting patients with (0.25–0.5mg/kg slow IV q48h up to animals with intractable diarrhea; must be
diarrhea, unless cause of diarrhea has osmotic cumulative dose of 4–8 mg/kg) in advanced avoided in all animals with suspected infectious
component. • Animals that do not have severe cases. • Pythiosis—itraconazole (10 mg/kg enteropathy. • Loperamide—0.1 mg/kg PO
clinical signs can be managed with elimination PO q24h) and terbinafine (10 mg/kg PO q8–12h. • Diphenoxylate—0.1–0.2 mg/kg PO
diet or hypoallergenic diet for 2 weeks; q24h) are drugs of choice following surgical q8h. • Propantheline bromide—0.25–0.5 mg/
response to dietary therapy typically seen debridement of affected portions of bowel; kg PO q8h, if colonic spasm contributing to
within first 5–7 days following dietary however, combination of itraconazole, clinical signs.
implementation; obtain comprehensive dietary terbinafine, and prednisone (without surgical
resection) was shown to be highly effective in Anthelminthics
history to optimize selection of novel, single
small cohort of dogs with focal involvement • Broad-spectrum anthelminthics such as
protein source diet; strict dietary compliance
of colon; antifungal therapy often adminis- fenbendazole (50 mg/kg q24h for 5
pivotal during this trial period to optimize
tered for 3–4 months or longer in affected consecutive days) or Drontal® Plus in
interpretation of response. • Fiber supplemen-
animals. conjunction with dietary therapy (elimina-
tation with poorly fermented fiber (e.g., bran
tion diet) for first 2 weeks is mainstay of
and alphacellulose) recommended to increase Anti-inflammatory therapy for most patients with chronic
fecal bulk, improve colonic muscle contractil- and Immunosuppressive Drugs colitis, unless a boxer breed that should have
ity, and bind fecal water to produce formed
for Inflammatory/Immune Colitis endoscopy and biopsy to confirm presence of
feces. • Some fermentable fiber sources (e.g.,
• Sulfasalazine (dogs: 25–40 mg/kg PO q8h GC, which has different therapy and
psyllium or diet containing beet pulp or
for 3–6 weeks with progressive tapering of prognosis. • Tylosin is highly effective
fructooligosaccharides) may be beneficial—
dose throughout course of drug therapy; cats: antimicrobial that can be administered
short-chain fatty acids produced by fermenta-
20 mg/kg PO q12h for 3 weeks); use with following assessment of response to dietary
tion may be beneficial for colonocyte function.
caution, particularly in cats, in which adverse and anthelminthic therapy.
SURGICAL CONSIDERATIONS effects on gastrointestinal tract and kidneys PRECAUTIONS
Segments of colon severely affected by fibrosis can be observed; sulfasalazine has been • Monitor patients on sulfasalazine for signs
from chronic inflammation and subsequent associated with irreversible keratoconjuncti- of KCS; measure tear production (Schirmer
stricture formation may need surgical excision, vitis sicca (KCS). • Corticosteroids— tear test) at baseline and every 2 weeks
especially in patients with granulomatous prednisone for dogs and prednisolone for throughout course of therapy; discontinue
form of disease; cecal inversion and ileoceco- cats: 1–2 mg/kg PO q12h for 5–7 weeks drug if tear production decreases; use of
colic intussusception require surgical with gradual, progressive tapering of dose; sulfasalazine therapy has decreased markedly
intervention; pythiosis/phycomycosis often most cats can be started on 5 mg (per cat) over past decade in light of excellent
requires surgical excision or debulking. q12h with gradual taper; never use more response to dietary and tylosin therapy in
than 50 mg total of prednisone (per day) for most dogs. • Monitor patients on azathio-
any animal, regardless of size. • Azathioprine prine for bone marrow suppression—CBC
(dogs) 1–2 mg/kg PO q24h for 10–14 days, every 2–3 weeks; stop treatment or go to
followed by taper to 1–2 mg/kg q48h for 4–6
MEDICATIONS weeks; drug is markedly myelosuppressive in
alternate day if white blood cell count falls
below 3,000 cells/μL. • Azathioprine can
DRUG(S) OF CHOICE cats and should be avoided even though also increase risk of pancreatitis and should
Antimicrobial Drugs lower dose (0.3 mg/kg PO q48h) for this be used extremely cautiously in any dog at
• Trichuris—fenbendazole (50 mg/kg PO species has been published. • Chlorambucil— increased risk for pancreatitis; azathioprine
q24h for 5 consecutive days, repeat in effective immunomodulator in both dogs can also cause hepatopathy. • Chlorambucil
3 months). • Entamoeba, Balantidium— and cats and usually administered in can cause progressive neutropenia and CBC
metronidazole (25 mg/kg PO q12h for 5–7 conjunction with prednisone or predniso- should be repeated q2–3 weeks in all animals
days). • Tritrichomonas blagburni—ronidazole lone; several dosing regimens have been receiving this drug. • Cyclosporine can cause
(30 mg/kg q24h for 14 days). • Clostridium published—cats: 2 mg per cat q3–4 days for hepatotoxicity and chemistry panel should
perfringens—metronidazole (10 mg/kg PO 2–3 months (or longer if managing lym- be performed as baseline before starting the
q12h for 5 days), tylosin (5–10 mg/kg PO phoma) or 15 mg/m2 given for 4 consecutive drug and repeated q2–3 months.
q24h for 5 days), ampicillin or amoxicillin days every 3 weeks for 2–3 months; dogs: • Amphotericin B is nephrotoxic and
(20 mg/kg PO q8h for 5 days); diarrhea, 0.1–0.2 mg/kg PO q24h for 8–12 weeks for requires close assessment of renal function
including acute hemorrhagic diarrheal immune disease, with gradual tapering of
Colitis and Proctitis (continued)
via urinalyses and serum biochemistry sis—poor long-term prognosis in most SYNONYMS
C panels. • Enrofloxacin-resistant cases of GC animals, despite surgical intervention, given • Inflammatory bowel disease. • Large bowel
are increasing in prevalence due to antimi- advanced stage of disease at diagnosis; diarrhea.
crobial resistance, necessitating alternative addition of anti-inflammatory dose of ABBREVIATIONS
antimicrobial therapy in select cases. prednisone with antifungal therapy appears • CSF = cerebrospinal fluid.
to enhance effectiveness and benefit of • GC = granulomatous colitis.
therapy. • Cecal inversion, ileocecocolic • KCS = keratoconjunctivitis sicca.
intussusception—good with surgical • NSAID = nonsteroidal anti-inflammatory
resection if diagnosed in timely fashion. •
FOLLOW-UP Inflammatory—fair to good with treatment
drug.
PATIENT MONITORING in patients with lymphoplasmacytic or Suggested Reading
• Infrequent recheck examinations or client eosinophilic colitis or GC. • Most dogs with Marks SL, Kather EJ, Kass PH, et al.
communication by phone. • Recheck of CBC mild to moderate nonspecific colitis respond Genotypic and phenotypic characterization
is important for animals on immunomodula- favorable to combination of fenbendazole, of Clostridium perfringens and Clostridium
tory therapy. feeding of elimination or hypoallergenic difficile in diarrheic and healthy dogs. J Vet
diet, and tylosin therapy. Intern Med 2002, 16:533–540.
Reagan KL, Marks SL, Pesavento PA, et al.
• Most bacterial and parasitic infectious
Successful management of 3 dogs with
causes have excellent prognosis, with high
colonic pythiosis using itraconzaole,
likelihood of cure following therapy.
terbinafine, and prednisone. J Vet Intern
• Prototheca—grave; no known treatment M ISCELLANEOUS Med 2019, 33(3):1434–1439.
except excision and itraconazole and
ZOONOTIC POTENTIAL Author Stanley L. Marks
amphotericin B following early diagnosis
Entamoeba, Balantidium, Campylobacter Consulting Editor Mark P. Rondeau
and before dissemination. • Histoplasma
spp.—poor in advanced or disseminated jejuni, Yersinia in immunosuppressed
disease; mild to moderate cases generally individuals.
respond to therapy. • Pythiosis/phycomyco-
available online
Colitis, Histiocytic Ulcerative

DIAGNOSTIC PROCEDURES Anti-inflammatory/Immunosuppressive
• Proctoscopy or colonoscopy to obtain Drugs C
colonic biopsies. • Most Boxer dogs with • Rarely indicated in dogs with GC, and used
BASICS GC have involvement of descending colon, at anti-inflammatory dose in conjunction
OVERVIEW underscoring diagnostic utility of procto with appropriate antimicrobial therapy.
• Relatively common cause of colitis in scopy. • Common changes in appearance to • Diagnosis must be reconsidered if no
Boxer breeds and infrequently seen in colonic wall include erythema, irregularity, dramatic improvement in clinical signs
French bulldogs and border collies. • Boxer and ulceration of colonic and rectal wall. following administration of fluoroquinolone
colitis is also referred to as granulomatous Microbiologic Testing therapy, because not all boxers with signs of
colitis (GC) in light of the granulomatous E. coli commonly isolated on routine colitis have GC.
inflammation (macrophages) in the colon. bacteriologic media from feces of both healthy CONTRAINDICATIONS/POSSIBLE
• Etiology of GC is an adherent-invasive dogs and dogs with diarrhea; however,
E. coli (AIEC) strain. INTERACTIONS
attempts to isolate E. coli from colonic Avoid anticholinergics or other motility
SIGNALMENT biopsies is recommended for sensitivity testing modifiers such as Imodium® in dogs with
• Dogs—primarily affects young Boxers, and optimization of antimicrobial therapy. infectious cause of diarrhea.
usually <3 years of age. • Reported in French PATHOLOGIC FINDINGS
bulldogs and border collies less frequently. • Histopathologic lesions include neutrophilic
SIGNS inflammation, epithelial ulceration, crypt
• Bloody, mucoid diarrhea with marked hyperplasia and distortion, decreased numbers FOLLOW-UP
increase in frequency of defecation. • Tenesmus. of goblet cells, and large numbers of macro
phages that stain positive with periodic acid– PATIENT MONITORING
• Weight loss and anorexia can occur and
Schiff (PAS) stain. • Presence of E. coli within • Monitor clinical signs, stool consistency
debilitation may develop.
macrophages can be confirmed using and frequency, and body weight. • Dogs
CAUSES & RISK FACTORS showing favorable response should improve
fluorescent in-situ hybridization (FISH).
GC appears to be a genetic disorder in boxer within 5 days of starting effective antimicrobial
breeds associated with reduced macrophage therapy.
phagocytic function and inability to kill AIEC.
• Generally good prognosis following
TREATMENT appropriate antimicrobial therapy. • Increasing
• Outpatient medical management following
injudicious administration of fluoroquinolones
DIAGNOSIS confirmation of diagnosis. • Antimicrobial
to dogs is increasing resistance of E. coli to this
therapy utilizing fluoroquinolones (unless
DIFFERENTIAL DIAGNOSIS class of antimicrobials, necessitating use of
resistance is observed) is mainstay of therapy.
• Other causes of colitis—nonhistiocytic alternative antimicrobials in a subset of dogs.
• Diet change to include moderately
inflammatory bowel disease (IBD), lymphocytic, fermentable fiber source can be used in cases
plasmacytic, eosinophilic colitis, other that do not show complete resolution of
infectious causes of colitis (pythiosis, diarrhea.
protothecosis, entamoeba), parasitic colitis MISCELLANEOUS
(whipworms), food-responsive diarrhea.
• Cecal inversion. • Ileocolic intussusception. PREGNANCY/FERTILITY/BREEDING
• Neoplasia—lymphoma, adenocarcinoma. Boxers, French bulldogs, and border collies
• Foreign body. • Colorectal polyps—dogs MEDICATIONS with GC should not be bred.
with colorectal polyps do not have diarrhea or DRUG(S) OF CHOICE SEE ALSO
increased mucus in stools, and instead have Colitis and Proctitis.
normal defecation frequency with formed Antimicrobials—First-Line Therapy
• Enrofloxacin (10 mg/kg q24h) for minimum ABBREVIATIONS
stools (can have altered shape) coated with • AIEC = adherent-invasive E. coli.
frank blood. • Irritable bowel syndrome. duration of 6–8 weeks is typically associated
with rapid resolution of clinical signs and • FISH = fluorescent in-situ hybridization.
• Differentiate by clarifying history (colitis vs.
resolution of histopathologic abnormalities. • GC = granulomatous colitis. • IBD =
colorectal neoplaia), fecal flotations, inflammatory bowel disease. • PAS =
abdominal imaging, and colonoscopy or • Because enrofloxacin resistance has been
documented in up to 70% of isolates from periodic acid–Schiff.
proctoscopy and biopsy.
dogs with GC, attempts to isolate E. coli from Suggested Reading
CBC/BIOCHEMISTRY/URINALYSIS colonic biopsies before treatment recommended Craven M, Dogan B, Schukken A, et al.
• Usually unremarkable; microcytic anemia such that antimicrobial susceptibility testing Antimicrobial resistance impacts clinical
may be present in Boxer dogs with GC can be performed. • Antimicrobials that outcome of granulomatous colitis in boxer
secondary to intestinal bleeding. • Chemistry penetrate intracellularly, such as fluoroquinolones, dogs. J Vet Intern Med 2010, 24(4):819–824.
panel may reveal hypoalbuminemia, chloramphenicol, rifampin, or trimethoprim- Manchester AC, Hill S, Sabation B, et al.
electrolyte abnormalities, and prerenal sulfonamides, should be preferentially chosen Association between granulomatous colitis in
azotemia in dogs with severe diarrhea and for treatment based on results of antimicrobial French Bulldogs and invasive Escherichia coli
anorexia. susceptibility testing. • Chloramphenicol, and response to fluoroquinolone antimicro-
IMAGING trimethoprim-sulfa, clarithromycin, imipenem, bials. J Vet Int Med 2013, 27(1):56–61.
Abdominal ultrasound in Boxer dogs with and meropenem should be considered for cases Author Stanley L. Marks
GC often reveals mild or moderate mesen- resistant to fluoroquinolones. Consulting Editor Mark P. Rondeau
teric or sublumbar lymphadenomegaly, and
colonic wall can appear thickened.
Compulsive Disorders—Cats
SIGNS and associated neuritis. • Feline hyperesthesia
C General Comments syndrome. • Pain/neuropathy.
BASICS • Behaviors may quickly increase in frequency if Fabric Chewing/Sucking
reinforced with attention by owner. • Scolding • Lead intoxication. • Hyperthyroidism.
DEFINITION or punishment may increase cat anxiety and • Thiamin deficiency. • Gastrointestinal upset.
• Compulsive disorders are relatively invariant stress and worsen expression of behavior.
exaggerated behavior patterns, often derived Hyperesthesia Syndrome
from normal behaviors but out of context and Historical Findings • Seizure disorder. • Skin disorders including
repetitive, without apparent function; may be • Onset may be coincident with environmen- external parasites, hypersensitivity to food,
performed to the exclusion of other normal tal change (e.g., move or new household flea bites, and parasites; atopy. • Spinal
behaviors or to the detriment of the animal. member) suggesting stress effect; cat may hide disorder/neuropathy. • Myositis, myopathy.
• May be a heterogeneous group of conditions to avoid punishment. • Psychogenic dermatitis/ CBC/BIOCHEMISTRY/URINALYSIS
with differing pathologies including compul- alopecia—may be associated with excessive Minimum database to rule out metabolic
sive, stereotypic, and neurologic; therefore grooming to exclusion of other activities; may abnormalities. No consistent clinicopatholo-
abnormal repetitive behaviors might be used be history of flea exposure or diet change. • gies associated with compulsive disorders.
to describe the clinical presentation. • Considered Compulsive fabric chewing/sucking—some
patients show preference for specific fabric OTHER LABORATORY TESTS
here are psychogenic dermatitis/alopecia,
compulsive fabric chewing/sucking, and type such as wool or may have general texture Psychogenic Alopecia
hyperesthesia syndrome. preference; grind fabric with molars; may Microscopic examination of hairs (tricho-
ingest fabric leading to foreign body gram), skin scraping, skin biopsy, fungal
PATHOPHYSIOLOGY obstruction. • Hyperesthesia syndrome— culture, bacterial culture, examination for
• Diagnosis of exclusion; must rule out may be triggered by tactile contact (petting external parasites, exclusion diet to rule out
pathophysiologic causes, including psycho- along dorsum and rump); may be episodic; dermatologic condition.
motor seizures, before a presumptive flea exposure.
diagnosis is made. • Can be a behavioral Fabric Chewing
response to confinement, specific anxiety- Physical Examination Findings • Serum lead level—if indicated for pica.
producing event, or undefined environmental • Psychogenic dermatitis/alopecia—focal, • Serum T4.
conditions (e.g., conflict, stress, anxiety, partial, and bilateral dermatitis or alopecia;
most common locations: groin, ventrum, and Hyperesthesia Syndrome
frustration); over time, can become fixed and Rule out dermatologic conditions as above.
independent of the environment; affected cats medial or caudal thigh regions; appearance of
may lack control of onset or termination. skin variable (normal or abnormal; erythematous IMAGING
• Behaviors may be self-reinforcing—allowing to abraded). • Fabric chewing/sucking— • CT or MRI—if indicated by abnormalities
some animals to cope with conditions that do often normal; secondary gastrointestinal on examination, i.e., to diagnose neurologic,
not meet their species-specific needs. inflammation or obstruction may occur if cat pain. • Fabric chewing/sucking—imaging
ingests material. • Hyperesthesia syndrome— gastrointestinal tract if obstruction or foreign
SYSTEMS AFFECTED episode may be prompted by petting or body suspected.
• Behavioral. • Gastrointestinal—fabric scratching dorsum; signs may include dilated
chewing/sucking. • Musculoskeletal—feline DIAGNOSTIC PROCEDURES
pupils, salivation, alarming vocalization,
hyperesthesia (involves cutaneous trunci “rippling skin” (hyperresponsive cutaneous Psychogenic Alopecia
muscle), tail attack/mutilation. • Skin/ trunci muscle), inappropriate urination or Complete dermatologic evaluation.
exocrine—psychogenic dermatitis/alopecia. defecation, tail twitching, frantic grooming, Hyperesthesia Syndrome
• Nervous—feline hyperesthesia syndrome. self-directed (especially to tail) or owner- Skin and/or muscle biopsy (as necessary).
GENETICS directed aggression, escape behavior.
PATHOLOGIC FINDINGS
None identified, although the association of CAUSES
compulsive fabric chewing/sucking with Unidentified Psychogenic Alopecia
Asian breeds suggests a heritable component. • Microscopic examination of hairs—typically
RISK FACTORS shafts are cleanly broken off at variable length
INCIDENCE/PREVALENCE • Changes in environment might predispose as a result of trauma from the tongue. • If
Unknown, uncommon. cat to compulsive disorder. • More commonly primarily behavioral, results of other
SIGNALMENT reported in indoor cats. • Cats fed ad libitum dermatologic testing will be generally normal.
may have lower prevalence of fabric chewing/
Species
sucking; must be balanced with nutritional
Cat
needs.
Breed Predispositions
Siamese, Burmese, Birman, and crosses may T REATMENT
be overrepresented for fabric chewing and APPROPRIATE HEALTH CARE
sucking. Supportive care.
DIAGNOSIS
Mean Age and Range NURSING CARE
• Compulsive disorders can develop at any
Rule out medical, including psychomotor Fabric chewing/sucking—create a “safe place”
time, generally not seen in kittens. for when the cat is left alone, devoid of fabric
• Psychogenic dermatitis/alopecia—6 months seizures, before behavioral diagnosis is made.
of the sort favored for chewing.
to 12 years. • Fabric chewing/sucking—12–49 Psychogenic Dermatitis/Alopecia
months; generally around 24 months. • Hyper- • Skin conditions—especially if associated
ACTIVITY
esthesia syndrome—1–5 years. with pruritus including external parasites; Increase opportunities for play and social
hypersensitivity to parasites, fleas, or food; interactions by providing outlets favored by
Predominant Sex the affected cat. Insure environmental needs
None atopy; neoplasia; fungal or bacterial dermatitis.
• Nervous system disorders. • Disk rupture are fully addressed.
(continued) Compulsive Disorders—Cats

Table 1
C
Drugs and dosages used to manage feline compulsive disorder.
Drug Drug Class Oral Dosage in Cats Frequency Side Effects—Usually Transient
Fluoxetine SSRI 0.5–1.0 mg/kg q24h Decreased appetite, sleepiness
Paroxetine SSRI 0.25–0.50 mg/kg q24h Constipation
Clomipramine TCA 0.25–1.0 mg/kg q24h Sleepiness, urine retention
Amitriptyline TCA 0.25–1.0 mg/kg q24h Sleepiness, urine retention
Gabapentin Anticonvulsant 3–5 mg/kg q12h Sleepiness, sedation
DIET PRECAUTIONS
• Fabric chewing—increasing fiber in the diet • Start behavioral drugs at low dose to avoid
has been suggested. • Presumptive psycho- side effects; may give at bedtime to reduce
genic alopecia—exclusion diet. complaints of sedation; may be given with M ISCELLANEOUS
CLIENT EDUCATION food. • No drugs approved by FDA for ASSOCIATED CONDITIONS
• Identify and remove triggers for the behavior,
treatment of these disorders in cats; inform Avoidance behavior or aggression toward the
if applicable. • Do not reward the behavior. client of extra-label use and risks involved; owner—if the owner punishes the patient
• Ignore the behavior as much as possible; document the discussion in the medical when it exhibits a compulsive behavior.
distract the cat and initiate an acceptable record or with a release form.
AGE-RELATED FACTORS
behavior. • Note details of the time, place, and POSSIBLE INTERACTIONS None
social milieu so that an alternative behavior Do not use TCAs or SSRIs with monoamine
ZOONOTIC POTENTIAL
(play or feeding or food-dispensing toy) may oxidase inhibitors, including selegiline.
None
be scheduled prior to initiation of the ALTERNATIVE DRUG(S)
compulsive behavior. • Punishment is PREGNANCY/FERTILITY/BREEDING
• Phenobarbital if seizure disorder suspected.
contraindicated and can increase the unpre- • Do not breed animals that display
• Selegiline if cognitive dysfunction.
dictability of the patient’s environment, compulsive behavior. • TCAs—contraindi-
• Presumptive psychogenic alopecia—
increase patient fear or aggressive behavior, and cated in pregnant animals.
exclusion diet, parasite treatment/preventative,
disrupt the human–animal bond. • Reduce trial course of steroids. SYNONYMS
environmental stress—increase the predictabil- • Psychogenic alopecia—barbering, overg-
ity of household events (feeding, play, exercise, rooming. • Hyperesthesia syndrome—
and social time with the client); eliminate rippling skin disease, neurodermatitis.
unpredictable events as much as possible.
FOLLOW-UP SEE ALSO
Compulsive Disorders—Dogs.
N/A unless obstructed. PATIENT MONITORING
• Before initiating treatment, record frequency of ABBREVIATIONS
compulsive behavior so that progress can be • SSRI = selective serotonin reuptake
monitored. • Successful treatment requires a inhibitor. • TCA = tricyclic antidepressant.
schedule of follow-up examinations; a INTERNET RESOURCES
M EDICATIONS recommended schedule is a phone check 1 week https://www.vet.cornell.edu/departments-
DRUG(S) OF CHOICE after the initial consultation and an office recheck centers-and-institutes/cornell-feline-health-
• If a specific etiology cannot be identified, 4–6 weeks later; if improvement is evident, the center/health-information/feline-health-topics
anti-compulsive or anti-anxiety drugs may be treatment regime should be continued; if there is
helpful; relatively high doses may be required no improvement, differential diagnoses should be Suggested Reading
(Table 1). • Goal—use the drugs until control considered or an alternative drug should be Horwitz D, ed. Blackwell’s 5 Minute Consult
is achieved for 2 months; attempt gradual considered. • If a medication is not effective after Clinical Companion: Canine and Feline
withdrawal by decreasing dosage at 2-week dosage adjustment, select an agent from another Behavior, 2nd ed. Ames, IA: Wiley-Blackwell,
intervals; treatment should be resumed at the drug class. 2018, pp. 391–403, 425–455, 481–492.
last effective dose at the first sign of relapse; Landsberg G. Stereotypic and compulsive
PREVENTION/AVOIDANCE disorders. In: Landsberg G, Hunthausen W,
may be life-long. • Drugs are listed with Create an enriched environment with
dosage used to manage behavior and common Ackerman L. Behavior Problems of the Dog
distributed resources, safe and accessible and Cat, 3rd ed. New York: Saunders/
side effects. • Hyperesthesia syndrome— elevated resting sites, exercise and play
gabapentin has been reported anecdotally Elsevier, 2013, pp. 163–179.
opportunities, and predictable social Tynes VV, Sinn L. Abnormal repetitive
to reduce the frequency and intensity of bouts. interactions with people. behaviors in dogs and cats: a guide for
CONTRAINDICATIONS POSSIBLE COMPLICATIONS practitioners. Vet Clin Small Anim Pract
• Selective serotonin reuptake inhibitors 2014, 44:543–564.
• Treatment failure. • Realistic expectations
(SSRIs)—depending on agent: poor appetite, must be created; immediate control of a Authors Margaret E. Gruen and Barbara L.
constipation, sedation. • Tricyclic antidepres- longstanding problem is unlikely. Sherman
sants (TCAs)—cats with history of cardiac Consulting Editor Gary M. Landsberg
conduction disturbances, urinary or fecal EXPECTED COURSE AND PROGNOSIS
retention, megacolon, lower urinary tract With treatment, prognosis for improvement
blockages, seizures, and glaucoma. is good; treatment can be lifelong. Client Education Handout
• Transdermal route does not appear to available
consistently produce satisfactory drug levels.
Compulsive Disorders—Dogs
transmission via the 5-HT3 receptor, as well RISK FACTORS
C as other aspects of synaptic transmission. • Environmental stress (e.g., kenneling—
INCIDENCE/PREVALENCE spinning), management. • Owner/environmental
BASICS reinforcement of the behavior. • Punishment of
Generally uncommon, although recent
DEFINITION studies report in up to 16%; more common the behavior further contributing to stress and
• Heterogeneous group of abnormal repetitive in certain breeds/families. conflict. • Medical disease, pain, neuropathy—
behaviors with differing pathologies (compulsive, may increase anxiety or may be primary cause.
stereotypic, neurologic). • Categorized as SIGNALMENT • Sensory abnormalities (e.g., visual deficits) may
locomotor (spinning, tail chasing, circling, Species contribute.
fence running, pacing, light/shadow chasing); Dog
oral (licking, sucking/mouthing an object/
Breed Predispositions
body part, e.g., flank, tail, limb; pica, excessive
Bull terrier—spinning, freezing/”trancing”;
drinking, “fly biting”); or hallucinatory (“fly DIAGNOSIS
German shepherd—spinning, tail chasing;
biting,” hind end checking, freezing, staring),
Great Dane, German shorthaired pointer— DIFFERENTIAL DIAGNOSIS
with/without vocal and affective responses.
self-directed oral behaviors, fence running, • Dermatologic (e.g., atopy). • Gastrointestinal
• Compulsive disorders (CDs) are abnormal,
hallucinations; Doberman—flank/blanket (e.g., inflammatory bowel disease [IBD],
repetitive, exaggerated, and/or sustained,
sucking; miniature schnauzer—hind end neoplasia, gastroesophageal reflux).
variable in form and fixated on a goal; they are
checking; border collie—light/shadow chasing; • Metabolic/endocrine (e.g., Cushing’s).
derived from normal maintenance behaviors
cavalier King Charles spaniel—fly catching. • Neurologic (e.g., seizure focus, forebrain
(e.g., grooming, predation, ingestion);
motivational conflict or frustration appears to Mean Age and Range neoplasia, neurodegenerative disorder).
trigger the behaviors in specific contexts often May be presented at any age; usually develops • Orthopedic (e.g., degenerative joint disease
associated with high arousal; with repeated/ from onset of sexual (6 months) to social [DJD]). • Any disorder causing abnormalities
sustained conflict, the behavior becomes (12–24 months) maturity; earlier onset (3–6 of sensation such as dysesthesia, paresthesia
emancipated from the original trigger(s) and months) reported for some CDs. (e.g., sensory neuropathy). • Other problem
displayed in diverse contexts; the animal may behaviors—displacement/conflict behaviors,
Predominant Sex
lack control of onset or termination. play and attention seeking, behaviors
Some CDs may be more common in males.
• Stereotypies are repetitive behaviors that are occurring secondary to lack of stimulation or
unvaried in sequence and have no obvious SIGNS due to resource restriction (e.g., water
function or purpose; they may arise in General Comments restriction—excessive drinking). • Rule out
situations of conflict/frustration related to • Wide variety of manifestations—behaviors physical/medical causes.
confinement or husbandry practices, when the may be repetitive or static (e.g., freezing). CBC/BIOCHEMISTRY/URINALYSIS
environment lacks sufficient outlets for the • Signs may not be observed during exam- • Usually within reference range—use for
normal behavior repertoire, and with maternal ination; descriptions may be unclear; video general health screening; prior to drug use.
deprivation. aids diagnosis and treatment planning. • Hematocrit, cholesterol, triglyceride
PATHOPHYSIOLOGY Historical Findings increases have been reported.
• Alterations in brain neurotransmitter • May be other signs of anxiety/concurrent OTHER LABORATORY TESTS
functions likely—primarily serotonin; also behavioral diagnoses (e.g., separation anxiety, Specific to differential diagnoses (e.g.,
dopamine, glutamate, endorphins; different fears, aggression) and/or a history of stress endoscopy, biopsy, echocardiography).
CDs may preferentially involve different (e.g., inadequate stimulation, punishment,
brain regions. • Abnormal serotonin IMAGING
change in routine/household). • Behavior may
• For neurologic differentials, CT or MRI to
transmission has been identified as a primary first be displayed as play or in situations of
mechanism by which compulsive disorders rule out structural brain/spinal disease; altered
high arousal/stress; eventually may occur in
are induced; stereotypies might be induced by brain/gray matter volume/density reported in
multiple contexts independent of identifiable
dopaminergic stimulation. CD. • Radiography, ultrasound if needed to
triggers. • Certain repetitive behaviors are
rule out underlying physical causes.
SYSTEMS AFFECTED expressed in situations with little to no external
• Behavioral—fear, anxiety, aggression. stimulation or evidence of arousal (e.g., DIAGNOSTIC PROCEDURES
• Cardiovascular—tachycardia. • Endocrine/ blanket sucking). • May occur whether or not History, video clips.
metabolic— hypothalamic–pituitary–adrenal the owner is present; if punished, pet may
(HPA) axis upregulation. • Gastrointestinal— avoid detection. • Hallmarks—behavior is
inappetence, gastroenteritis, foreign body ritualized, often exaggerated in form, and with
obstruction. • Hemic/lymphatic/immune— time increases in frequency, intensity, and TREATMENT
stress leukogram. • Musculoskeletal—weight duration. • Behavior may be difficult/ Repetitive behaviors may represent a normal
loss, self-injury. • Respiratory—tachypnea. impossible to interrupt. • Behavior may coping mechanism. If not harmful nor
• Skin/exocrine—abrasions/wounds/ interfere with normal functioning (e.g., eating, interfering with normal functioning, health,
infections secondary to self-trauma. sleeping, social interactions). or human–animal bond, intervention may be
GENETICS Physical Examination Findings unnecessary or contraindicated.
• Higher than expected occurrence among • May be unremarkable. • May see skin
first-generation relatives (manifestations may lesions/injuries related to self-trauma • Generally outpatient. • Sedation—stop-gap
differ). • Certain breeds overrepresented for (especially tail, forelimbs, distal extremities); measure; if needed to stop serious self-
specific CDs. • Genetic studies implicate excessive tooth wear/damage; lameness or mutilation. • Treat associated physical
N-methyl-D-aspartate (NMDA) glutamatergic poor body condition. conditions (primary or secondary).
neurotransmission, particularly via neural CAUSES • Combination of environmental
cadherin (CDH2); also serotonergic No direct cause. modification, behavior modification, and
(continued) Compulsive Disorders—Dogs

pharmacologic treatment. • Pharmacologic low end of dose range for 4–6 weeks; intensity of behavior modification, addition
intervention—implement early; reduction of gradually increase dosage if ineffective and no of short-term, shorter-acting anxiolytics C
anxiety facilitates behavioral therapy. adverse events. • SSRIs—fluoxetine 1–2 mg/ (e.g., benzodiazepines).
• Environmental modification—reduce stress kg q24h; sertraline 1–3 mg/kg q24h; PREVENTION/AVOIDANCE
and anxiety; identify and remove sources paroxetine 1–2 mg/kg q24h. • TCAs— Monitor for affected relatives; early recogni-
(e.g., triggers) and/or begin desensitization clomipramine is most serotonergic (most tion and intervention.
and counter-conditioning exercises. effective, fewest side effects): 2–3 mg/kg
• Punishment—contraindicated; increases q12h. • If symptoms resolve, continue POSSIBLE COMPLICATIONS
anxiety, may worsen behavior and increase medication for >1 month; taper dose no Dermatologic/musculoskeletal injury;
patient secrecy. • Provide structured, faster than 25% every two weeks; recurrence gastrointestinal disorders.
consistent interactions, routine, and sufficient common. EXPECTED COURSE AND PROGNOSIS
exercise, enrichment/mental stimulation CONTRAINDICATIONS • Untreated CDs almost always progress.
appropriate to species and individual; • Hepatic or renal compromise—medications • >50% reduction in CD in approximately
includes interactive play, food puzzles, and metabolized by these organs. • Cardiac two-thirds of cases with appropriate medication
reward-based training. • Behavior conduction anomalies—TCAs. • Use extreme and behavioral and environmental modification.
modification—teach the patient to relax in a care combining serotonergic drugs (e.g., SSRI
variety of settings; also teach a calm, desirable with tramadol); risk of serotonin syndrome.
behavior incompatible with the stereotypic • Do not use SSRIs or TCAs within 2 weeks
one, coupled to a verbal cue (e.g., for circling, of monoamine oxidase (MAO) inhibitors
teach to lie down with head and neck MISCELLANEOUS
(e.g., selegiline, amitraz).
outstretched in response to “Head down”). In ASSOCIATED CONDITIONS
some cases, a head collar (e.g., Gentle Leader, PRECAUTIONS Various; specific to type of CD.
Halti) left on the dog (when the owner is • Use of listed medications for CD is extra-
or off-label. • TCA overdose—cardiac PREGNANCY/FERTILITY/BREEDING
home) in the problem contexts may allow the
conduction disturbances. • TCA/SSRI • Listed medications not evaluated/
owner to use gentle physical guidance along
overdose—serotonin syndrome. • Side effects contraindicated in pregnant animals; avoid
with verbal encouragement/cues to interrupt
of SSRIs and TCAs—most common: use. • Do not breed affected animals.
the behavior and redirect it more effectively;
monitor for situation in which behavior lethargy, appetite change; less common: SYNONYMS
occurs and preempt it by engaging the pet in increased anxiety/reactivity, vomiting/ Obsessive-compulsive disorder.
an incompatible activity; if behavior occurs, diarrhea; severe side effects may necessitate
SEE ALSO
disrupt immediately, redirect the animal to discontinuation.
Acral Lick Dermatitis.
alternative incompatible activity and reward POSSIBLE INTERACTIONS
(with food/play/other reinforcer); dogs with ABBREVIATIONS
SSRIs competitively inhibit cytochrome P450
CD may be more perseverant and thus not • CD = compulsive disorder. • DJD =
enzymes: may increase warfarin, many TCAs,
respond well to extinction procedures. • Have degenerative joint disease. • HPA =
some benzodiazepines and anticonvulsants,
clients monitor behaviors via videos and hypothalamic–pituitary–adrenal. • IBD =
other medications; check compatibility and
written logs (e.g., rate severity) for objective inflammatory bowel disease. • MAO =
adjust dosage if necessary.
assessment of response to therapy; improve monoamine oxidase. • NMDA = N-methyl-
ment may be seen in frequency and/or ALTERNATIVE DRUG(S) D-aspartate. • SSRI = selective serotonin
intensity. • Bandages, collars, braces, and • Synthetic pheromones (Adaptil), l-theanine, reuptake inhibitor. • TCA = tricyclic
crates increase distress, do not address the or alpha-casozepine—may reduce anxiety. antidepressant.
behavioral condition, and may worsen it; if • Adjunctive use of memantine (NMDA
receptor antagonist) 0.3–1 mg/kg q12h;
Suggested Reading
needed to ensure healing, use as briefly as Crowell-Davis SL, Murray T, Dantas L.
possible. second-line TCAs, e.g., amitriptyline 1–6 mg/
Veterinary Psychopharmacology, 2nd ed.
kg q12h. • Selegiline (MAO inhibitor)
ACTIVITY Hoboken, NJ: Wiley, 2019.
0.5–1 mg/kg q24h—may be effective in some
Environmental enrichment. Overall KL, Dunham AE. Clinical features
cases. • Narcotic antagonists (e.g., naltrexone,
and outcome in dogs and cats with
CLIENT EDUCATION naloxone)—may be effective but not a practical
obsessive-compulsive disorder; 126 cases
• Cure unlikely; usually requires lifelong therapeutic option. • Antipsychotics (e.g.,
(1989–2000). J Am Vet Med Assoc 2002,
management. • Teach client to recognize all thioridazine, haloperidol)—not recommended:
221:1445–1452.
body language/behaviors reflecting anxiety. risk of adverse effects, efficacy undocumented.
Tynes VV, Sinn L. Abnormal repetitive
SURGICAL CONSIDERATIONS behaviors in dogs and cats: a guide for
Tail/limb mutilation—avoid amputation practitioners. Vet Clin Small Anim Pract
unless medically indicated; will not resolve 2014, 44:543–564.
the CD. FOLLOW-UP Author Mary P. Klinck
PATIENT MONITORING Consulting Editor Gary M. Landsberg
• CBC, biochemistry, T4 (TCAs may
artificially lower), and urinalysis—semi- editors acknowledge the prior contribution of
Karen L. Overall
MEDICATIONS annually to yearly if chronic treatment; adjust
dosages accordingly. • Medications may take
DRUG(S) OF CHOICE 8–12 weeks or longer to affect CDs; first sign
• Selective serotonin reuptake inhibitors Client Education Handout
of efficacy may be reduced duration/ available online
(SSRIs) and tricyclic antidepressants (TCAs)— frequency. • Relapses common during
CNS serotonin effects. • Generally treat at stressful situations; manage with increased
Congenital and Developmental Renal Diseases

keeshond, Lhasa apso, miniature schnauzer, some patients with renal telangiectasia or
C Norwegian elkhound, Rhodesian ridgeback, renal neoplasms. • Patients with unilateral
shih tzu, soft-coated wheaten terrier, standard renal agenesis, ectopic kidneys, and isolated
BASICS poodle. ◦ Glomerulopathy—Airedale terrier, renal tubular transport defects are frequently
DEFINITION beagle, Belgian shepherd, Bernese mountain asymptomatic.
• Functional or morphologic abnormalities dog, Brittany spaniel, bull terrier, bullmastiff, Physical Examination Findings
resulting from heritable (genetic) or acquired Dalmatian, Doberman pinscher, English • Signs associated with advanced chronic
disease processes affecting differentiation and cocker spaniel, Newfoundland, Pembroke kidney disease. • Ascites or pitting edema in
growth of the developing kidney. • Renal Welsh corgi, Rottweiler, Samoyed, soft-coated some patients with protein-losing glomeru-
agenesis—complete absence of one or both wheaten terrier. ◦ Polycystic renal disease— lopathies or amyloidosis. • Renomegaly or
kidneys. • Renal dysplasia—disorganized renal beagle, bull terrier, Cairn terrier, West abdominal mass lesions in some patients with
parenchymal development. • Renal ectopia— Highland white terrier; Persian, exotic polycystic kidneys, renal neoplasms, or fused
congenital malposition of one or both shorthair, Himalayan, British blue cats. ectopic kidneys.
kidneys. • Glomerulopathy—glomerular ◦ Renal telangiectasia—Pembroke Welsh
disease of any type. • Polycystic renal corgi. ◦ Renal amyloidosis—Abyssinian, CAUSES
disease—formation of multiple, variable-sized oriental shorthair, Siamese cats; beagle, Nonhereditary
cysts throughout the renal medulla and cortex. English foxhound, shar-pei. ◦ Renal cystad- • Infectious agents—feline panleukopenia
• Renal telangiectasia—multifocal vascular enocarcinoma—German shepherd. ◦ Fanconi virus and canine herpesvirus infection
malformations involving the kidneys and syndrome—basenji and border terrier. associated with renal dysplasia. • Drugs—
other organs. • Renal amyloidosis—extracel- ◦ Primary renal glucosuria—Norwegian corticosteroids, diphenylamine, and biphenyls
lular deposition of amyloid in glomerular elkhound, Scottish terrier, basenji. associated with polycystic kidneys; chloram-
capillaries, glomeruli, and interstitium. ◦ Cystinuria—American pit bull terrier, basset bucil and sodium arsenate associated with
• Nephroblastoma—congenital renal hound, English bulldog, dachshund, mastiff, renal agenesis. • Dietary factors—hypo- or
neoplasm arising from the pluripotent Newfoundland, Rottweiler, among others. hypervitaminosis A associated with renal
metanephric blastema. • Multifocal renal ◦ Xanthinuria—cavalier King Charles spaniel, ectopia.
cystadenocarcinoma—hereditary renal wirehaired dachshund; domestic shorthair
neoplasm in dogs. • Fanconi syndrome— cats. ◦ Hyperuricuria—Dalmatian, black
generalized renal tubular functional anomaly Russian terrier, English bulldog. ◦ Primary
characterized by impaired reabsorption of hyperoxaluria—domestic shorthair cats;
glucose, phosphate, electrolytes, amino acids, Tibetan spaniel. D IAGNOSIS
and uric acid. • Primary renal glucosuria— INCIDENCE/PREVALENCE DIFFERENTIAL DIAGNOSIS
defect in renal tubular reabsorption of glucose. Uncommonly recognized, but occur more • Rule out acquired and nondevelopmental
• Cystinuria—excessive urinary excretion of frequently in related animals from more than causes of primary renal disease. • Rule out
cystine due to defect in renal tubular one generation than in the general popu- nonrenal causes of hematuria, proteinuria,
reabsorption of cystine and other amino acids. lation. glucosuria, abdominal distention, or ascites.
• Xanthinuria—excessive urinary excretion of
xanthine caused by a deficiency in xanthine SIGNALMENT CBC/BIOCHEMISTRY/URINALYSIS
• Nonregenerative anemia. • Azotemia and
oxidase. • Hyperuricuria—excessive urinary Species
excretion of uric acid, sodium urate, or urine specific gravity <1.030 in dogs and
Dog and cat.
ammonium urate. • Primary hyperoxaluria— <1.035 in cats. • Proteinuria, hypoalbumine-
Breed Predilections mia, and hypercholesterolemia with nephrotic
intermittent hyperoxaluria, l-glyceric aciduria,
Sporadic cases can occur without apparent syndrome. • Normoglycemic glucosuria in
and oxalate nephropathy. • Congenital
familial predisposition in any breed of dog or cat. Fanconi syndrome or primary renal glucosuria.
nephrogenic diabetes insipidus—polyuria
caused by diminished renal responsiveness to Mean Age and Range • Hematuria with congenital renal neoplasia
antidiuretic hormone. Most are <5 years old at time of diagnosis. or renal telangiectasia. • Cystine crystalluria
with cystinuria. • Xanthine crystalluria with
PATHOPHYSIOLOGY Predominant Sex xanthinuria. • Urate crystalluria with hyper-
Many congenital and developmental renal • Familial cystinuria occurs primarily in male uricuria.
disorders are caused by genetic abnormalities dogs. • Samoyed hereditary glomerulopathy
that disrupt the normal development and more common in males. • Familial glomeru- OTHER LABORATORY TESTS
interaction of multiple embryonic tissues lonephropathy of Bernese mountain dogs is Genetic tests are available for some specific
involved in formation of the mature kidney. more common in females. genetic mutations associated with hereditary
Nongenetic factors are also possible. renal disorders.
SIGNS
IMAGING
SYSTEMS AFFECTED General Comments Survey abdominal radiography, renal ultra-
Renal/urologic. Most congenital and developmental disorders sonography, and excretory urography may
GENETICS cannot be distinguished from acquired renal identify and characterize congenital and
• Familial renal disorders have been reported disease without kidney biopsy. developmental renal disorders and their
in the following breeds: ◦ Renal agenesis— Historical Findings associated sequelae.
beagle, Doberman pinscher, Shetland • Indicate chronic kidney disease. • Some DIAGNOSTIC PROCEDURES
sheepdog. ◦ Renal dysplasia—Alaskan glomerulopathies associated with abdominal Consider light microscopic evaluation of
Malamute, border terrier, boxer, bullmastiff, distension, edema, or other signs of nephrotic kidney biopsy specimens from patients with
bulldog, Cairn terrier, cavalier King Charles syndrome. • Abdominal distension in some morphologic or functional abnormalities of
spaniel, chow chow, cocker spaniel, Dutch patients with polycystic kidneys or renal the kidney for which a definitive diagnosis
kookier, golden retriever, Finnish harrier, neoplasms. • Hematuria or abdominal pain in has not been established.
(continued) Congenital and Developmental Renal Diseases

PATHOLOGIC FINDINGS • Refer to chapters describing specific renal
• Renal dysplasia—primary lesions include diseases or clinical syndromes. C
immature glomeruli, persistent mesenchyme,
persistent metanephric ducts, atypical MISCELLANEOUS
tubular epithelium, and dysontogenic ASSOCIATED CONDITIONS
metaplasia; primary lesions usually associ- • Polycystic renal disease associated with
ated with, and may be obscured by, MEDICATIONS hepatic biliary cysts. • Cystinuria, xanthinu-
secondary degenerative, inflammatory, and DRUG(S) OF CHOICE ria, and hyperuricuria associated with
compensatory lesions. • Glomerulopathies— Refer to chapters describing specific renal formation of uroliths. • Amyloidosis in
usually normal-to-small kidneys; most are diseases or clinical syndromes. Chinese Shar-Pei dogs associated with
characterized by a primary membranoprolif- CONTRAINDICATIONS intermittent pyrexia or swelling of the hocks.
erative glomerulonephritis with variable Avoid potentially nephrotoxic drugs or • Renal neoplasms associated with hyper-
degrees of tubulointerstitial disease, others anesthetic agents that decrease renal function. trophic osteoarthropathy, polycythemia, or
have cystic atrophic membranous glomeru- other paraneoplastic syndromes.
lopathy. • Polycystic renal disease—see PRECAUTIONS
Avoid drugs requiring renal excretion in SYNONYMS
Polycystic Kidney Disease. • Renal amyloidosis—
patients with renal failure; if necessary, • Familial renal disease. • Juvenile renal
see Amyloidosis. • Renal telangiectasia—
modify dosage regimens to compensate for disease.
multiple, variable-sized, red-black, blood-filled
nodules and clots in the renal cortex and decreased renal clearance of drugs and other SEE ALSO
medulla, interstitial fibrosis, interstitial metabolites. • Acute Kidney Injury.
mononuclear cell infiltrate, and hydronephrosis. • Amyloidosis.
• Nephroblastoma—unilateral renal mass; • Anemia of Chronic Kidney Disease.
contains both embryonic mesenchymal and • Chronic Kidney Disease.
epithelial tissue components. • Multifocal FOLLOW-UP • Fanconi Syndrome.
renal cystadenocarcinoma—bilaterally • Hematuria.
enlarged kidneys with irregular protruding PATIENT MONITORING • Hyperparathyroidism, Renal Secondary.
cystic structures or multifocal neoplastic Refer to chapters describing specific renal • Nephrotic Syndrome.
renal tubular epithelial cell proliferations. • diseases or clinical syndromes. • Oliguria and Anuria.
Renal ectopia—kidneys abnormally located PREVENTION/AVOIDANCE • Polycystic Kidney Disease.
in the retroperitoneal space or abdomen; Congenital and developmental renal disorders • Polyuria and Polydipsia.
horseshoe kidneys are symmetrically fused are irreversible, so control lies in preventing • Renal Tubular Acidosis.
along the medial border of either pole. • breeding of affected animals. • Renomegaly.
Fanconi syndrome— • Urolithiasis, Cystine.
inconsistent findings of tubular atrophy, Suggested Reading
• Acute or chronic renal failure. • Nephrotic
interstitial fibrosis, and acute papillary necrosis. Segev G. Familial and congenital renal
syndrome. • Urolithiasis. • Hydronephrosis.
• Primary hyperoxaluria—large, irregularly diseases of cats and dogs. In: Ettinger SJ,
• Urinary tract infection.
shaped kidneys; renal tubular deposition of Feldman EC, Cote E, eds., Textbook of
calcium oxalate crystals and variable interstitial EXPECTED COURSE AND PROGNOSIS Veterinary Internal Medicine, 8th ed.
and periglomerular fibrosis. • Highly variable; depends on the specific
St. Louis, MO: Elsevier, 2017, pp. 1981–1984.
disorder, the extent of primary lesions, and Author John M. Kruger
the severity of renal dysfunction. • Congenital Consulting Editor J.D. Foster
and developmental disorders are irreversible Acknowledgment The author and book
and may result in advanced chronic kidney
TREATMENT disease; some patients with mild to moderate
editors acknowledge the prior contributions
• Congenital and developmental renal of Carl A. Osborne, and Scott D. Fitzgerald.
renal dysfunction may remain stable for long
disorders often have no specific treatment. periods. • Patients with some disorders may
• Supportive strategies are similar to those for remain asymptomatic unless the disorder is
acquired chronic kidney disease and may Client Education Handout
complicated by urolithiasis, infection, or
improve quality of life and minimize available online
other disease processes that promote
progression in patients with renal dysfunction. progressive renal dysfunction.
Congenital Ocular Anomalies

• Optic nerve hypoplasia—miniature and toy • Pupillary abnormalities—polycoria, acorea,
C poodle, sporadically in other breeds: unknown aniridia, or dyscoria.
mode of inheritance. • Congenital cataracts—primary, inherited,
BASICS • Photoreceptor dysplasia*—Abyssinian, or developmental defect; associated with
DEFINITION Somali, and Ocicat cat breeds: dominant anomalies of lens, including microphakia,
Solitary or multiple abnormalities that affect trait. lenticonus or lentiglobus, and coloboma (see
the globe or its adnexa; observed in dogs and INCIDENCE/PREVALENCE Web Figures 5 and 6).
cats at birth or within the first 6–8 weeks of • PHTVL and PHPV—persistence of parts
• Incidence—low; dogs > cats.
life. • CEA—>50% in collies, lower in other
of hyaloid vasculature; developmental
breeds. aberrations of vitreous, lens, and lens capsule;
PATHOPHYSIOLOGY
may show leukocoria as result of retrolental
• Breed-related inherited defects. SIGNALMENT fibrovascular plaques and/or cataracts, or
• Spontaneous malformations.
Species reddish sheen from pupillary area with
• In utero systemic infections and inflamm
Dog and cat. intralenticular bleeding.
ations, exposure to toxic compounds, and
• Retinal dysplasia—effect on retinal
lack of specific nutrients in pregnant dams or Breed Predilections structure depends on severity; ranges from
bitches. See Genetics. focal neuroretinal folds (multifocal defects
SYSTEMS AFFECTED SIGNS often along major blood vessels in central
Ophthalmic—entire eye or any part; unilateral tapetal fundus) to geographic dysplasia
General Comments
or bilateral. (abnormal central tapetal fundus area with
• Depends on defect.
GENETICS • May cause no signs of disease; often
elevated retina and surrounding hyperpig
• * Indicates availability of genetic testing for incidental finding. mentation and scarring) to complete retinal
all or most affected breeds. • May be congenitally blinding disease.
detachment.
• Congenital keratoconjunctivitis sicca • CEA—bilateral area of choroidal
Historical Findings hypoplasia temporal to optic nerve head:
(KCS) and KCS ichthyosiform dermatosis
Ranges from none to severe visual impair- focal increased visibility of white sclera and
(KCSID)*—cavalier King Charles spaniel
ment to blindness. scarce, irregularly shaped choroidal blood
(dry eye and curly coat syndrome):
recessive trait. Physical Examination Findings vessels; visual impairment or blindness can
• Persistent pupillary membranes (PPM)— • Anophthalmos—congenital lack of globe; rare. be caused by optic nerve coloboma and
Basenji and other breeds: unknown mode of • Microphthalmos—congenitally small eye; retinal detachment.
inheritance. often associated with other hereditary defects, • MOD—microphthalmia, microcornea,
• Persistent hyperplastic tunica vasculosa including MOD. heterochromia irides, pupillary abnormalities,
lentis (PHTVL) and persistent hyperplastic • Eyelid agenesis or colobomas of eyelids in cataract, fundus coloboma, retinal
primary vitreous (PHPV)—Doberman cats—result in congenitally open eyelids; detachment, intraocular hemorrhage.
pinscher and Staffordshire bull terrier: affects temporal portion of upper eyelid; may • Coloboma of posterior segment—primary
dominant allele with variable expression. cause blepharospasm, epiphora, and corneal or in conjunction with CEA or MOD;
• Retinal dysplasia—English springer spaniel: changes as result of trichiasis. focal, well-defined tissue depression,
recessive trait. • Dermoids—islands of aberrant skin tissue typically at 6 o’clock position in optic nerve
• Collie eye abnormality (CEA)*—collie and involving either eyelids, conjunctiva, or head in CEA, or in fundus periphery in
other dog breeds: recessive trait. cornea; may cause blepharospasm and MOD; may be in other locations of fundus
• Merle ocular dysgenesis (MOD)— epiphora (see Web Figure 1). near optic nerve head.
Australian shepherd: autosomal recessive trait • Atresia and imperforate puncta of lacrimal • OSD—heterozygous carriers typically
with incomplete penetrance. system, common in dogs—results in tear display signs of focal/multifocal retinal
• Oculo-skeletal dysplasia (OSD)*— streak at nasal canthus. dysplasia, whereas homozygous animals
Labrador retriever and Samoyed: autosomal • Congenital KCS—usually unilateral; display complete phenotype, including
dominant trait with incomplete penetrance. affected eye appears smaller; thick mucous skeletal (short-limbed dwarfism) and ocular
• Retinal dystrophy*—Briard: recessive trait. discharge from red and irritated eye. defects (ranging from retinal dysplasia to
• Rod cone dysplasia*—collies, Irish setter, • KCSID—therapy-resistant KCS, curly coat retinal detachments; corneal and lens
Cardigan Welsh corgi, sloughi: recessive traits; and progressive dermatologic signs, including opacities also possible).
nonallelic disease. footpad hyperkeratosis that can cause • Retinal dystrophy—congenital night
• Early retinal degeneration*—Norwegian lameness. blindness, variable severity and progression of
elkhound: recessive trait. • PPMs—remnants of pupillary membrane day blindness.
• Photoreceptor dysplasia—Belgian shepherd. spanning from iris collarette to another • Rod cone dysplasia, early retinal degeneration,
• Cone rod dystrophy*—American pit bull portion of iris, lens, or cornea; may coexist photoreceptor dysplasia, and cone rod
terrier, American Staffordshire terrier, springer with other defects (see Web Figures 2 and 3). dystrophy—pupillary abnormalities and
spaniel, long-, short- and wirehaired • Iris cysts—pigmented or nonpigmented visual impairment in first few months of life;
dachshunds: recessive traits; nonallelic disease. spherical structures may float freely in disease progression depends on specific
• Cone degeneration, achromatopsia, or day anterior chamber or be attached to posterior disease and breed affected.
blindness*—Alaskan Malamute, Australian iris, ciliary body, or corneal endothelium (see • Cone degeneration—apparent day blindness
shepherd, German shepherd dog, miniature Web Figure 4). from 8–10 weeks of age; vision in dim light
American shepherd, German shorthaired • Congenital glaucoma—rare; buphthalmic never affected.
pointer, Australian cobberdog, Labrador eye, often associated with multiple anterior • Retinal detachment—often in conjunction
retriever and Labrador crosses (incl. segment changes. with other hereditary ocular diseases; signs
Labradoodles): recessive traits. depend on extent of detachment and include
widely dilated pupils, weak to absent
(continued) Congenital Ocular Anomalies

pupillary light reflexes; presence of fundus • Tonometry—when glaucoma or uveitis
areas that appear out of focus, vascularized suspected. C
membranous structure (retina) visible within • Direct and/or indirect ophthalmoscopy—
pupillary aperture behind lens, blindness with evaluation of posterior segment anomalies; MEDICATIONS
complete bilateral detachment. pharmacologic pupil dilation necessary; DRUG(S) OF CHOICE
• Optic nerve hypoplasia—avascular, dark, difficult to perform in patients with opacities • Congenital KCS—frequent application of
abnormally small, circular optic nerve head, in cornea, anterior chamber, lens, or anterior tear substitutes; antibiotics may be added;
may result in blindness. vitreous. cyclosporine ophthalmic ointment q12h.
• Gonioscopy—evaluation of width of and • Congenital cataracts—if only in nuclear
CAUSES
• Genetic.
presence of signs of dysgenesis in iridocorneal region of lens, mydriatics used to increase
• Spontaneous malformations.
angle when glaucoma suspected; critical to visual capability.
• Infections or inflammation during pregnancy.
include examination of unaffected eye.
• Electroretinography (ERG).
• Toxicity during pregnancy.
• Optical coherence tomography (OCT).
• Nutritional deficiencies.
• Referral to ophthalmologist necessary for
RISK FACTORS gonioscopic, ERG, and OCT examinations. FOLLOW-UP
Breeding dogs or cats that are homozygous or PATIENT MONITORING
heterozygous for hereditary disease with • Congenital KCS—repeated monitoring of
recessive inheritance, or affected animals tear production and status of external eye.
where disease has dominant inheritance. • Congenital cataracts and severe PHTVL
TREATMENT and PHPV—regular checkups, usually on
APPROPRIATE HEALTH CARE 6-month basis; monitor progression.
• Patients usually referred to ophthalmologist. • Large colobomatous defects of the fundus
• No treatment for most congenital and geographic retinal dysplasia—regular
DIAGNOSIS
abnormalities, except symptomatic treatment checkups to monitor possible retinal
DIFFERENTIAL DIAGNOSIS or surgery. detachment.
• Infectious and inflammatory processes in
adnexa—may mimic and mask congenital NURSING CARE PREVENTION/AVOIDANCE
abnormalities. • In KCS—removing discharge and flushing Restrict breeding of affected animals and of
• Cataracts induced at early age may be
with saline. known carriers of hereditary defects; DNA-
interpreted as congenital. • Accommodate handicap of blind animals— based tests available for various diseases (see
• Postinflammatory ophthalmic lesions with
leash walking, supervision. Internet Resources).
anterior or posterior synechia—easily confused ACTIVITY POSSIBLE COMPLICATIONS
with iris to cornea or iris to lens PPMs. Visually impaired or blind animals need • In congenital KCS with parotid duct
• Tumors of anterior segment may be adequate exercise. transposition, keratitis and dermatitis may
confused with iris cysts. DIET occur due to excessive deposition of minerals
• Focal, multifocal, or generalized retino- from saliva.
Provide diet adequate in vitamins, antioxi-
pathy of inflammatory origin—resulting dants, and omega-3 fatty acids, especially in • Cataract surgery can result in glaucoma,
retinal atrophy may appear to be retinal photoreceptor degenerations. retinal detachment, and corneal scarring in
dysplasia or photoreceptor dysplasia. puppies and kittens; surgery seldom
• Retinal detachment as result of trauma or CLIENT EDUCATION recommended before age 8–12 weeks.
uveitis in young dogs. Discuss visual capacity, possible progression,
and sequelae. EXPECTED COURSE AND PROGNOSIS
• Optic nerve atrophy due to inflammatory
• Most abnormalities affecting adnexa can be
process may be difficult to differentiate from SURGICAL CONSIDERATIONS corrected in young dogs and cats.
congenital optic nerve hypoplasia. • Adnexal abnormalities—surgery as soon as • Prognosis for most anterior segment
IMAGING possible. abnormalities good to fair.
• Routine ophthalmic ultrasound—use of • Congenital KCS—parotid duct trans- • Prognosis for glaucoma poor.
10–20 MHz probes for evaluation of position. • For photoreceptor abnormalities prognosis
intraocular changes in case of opacities that • Cataract extraction—congenital cataract for vision poor, but eyes should remain
prevent proper ophthalmic examination. may be associated with other anomalies, comfortable.
• High-resolution ultrasound—use of decreasing chances for visual rehabilitation or • For most other abnormalities prognosis
20–50 MHz probes for evaluation and causing surgical complications; presurgical depends on severity of condition.
measurement of corneal and anterior chamber evaluation should include imaging and ERG.
structures, e.g., anterior chamber cysts or • Congenital glaucoma—surgical options
iridocorneal angle. depend on presence of vision, size of patient/
eye, and level of motivation of owners;
DIAGNOSTIC PROCEDURES enucleation or intrascleral prosthesis typical MISCELLANEOUS
• Examination with diffuse and focal treatments of choice; consider euthanasia if
illumination, including slit-lamp biomicro PREGNANCY/FERTILITY/BREEDING
bilateral. • Dogs and cats affected with congenital
scopy—evaluation of adnexal and anterior • Barrier retinopexy to prevent occurrence of
segment anomalies, including lens and ocular anomalies resulting in blindness and/or
retinal detachments with large colobomatous pain should not be used for breeding.
anterior vitreous (following pharmacologic or dysplastic lesions of fundus—carries risk of
pupil dilation). • Many congenital ocular anomalies are
inducing retinal detachment. hereditary and use of affected animals in
• Schirmer tear test—evaluate tear
production. breeding should be prohibited or severely
Congenital Ocular Anomalies (continued)
restricted. Breeding advice should be sought ◦ www.CatDNAtest.org Suggested Reading

C from kennel club and breed associations. ◦ www.aht.org.uk Gelatt KN, Gilger BC, Kern TJ, ed.
◦ www.laboklin.co.uk Veterinary Ophthalmology, 5th ed. Ames,
ABBREVIATIONS
◦ https://breeder.wisdompanel.com/ IA: Wiley-Blackwell, 2013.
• CEA = collie eye anomaly.
◦ https://vgl.ucdavis.edu/services Maggs DJ, Miller PE, Ofri R, ed. Slatter’s
• ERG = electroretinography.
◦ www.vetgen.com Fundamentals of Veterinary
• KCS = keratoconjunctivitis sicca.
◦ www.caninegeneticdiseases.net Ophthalmology, 6th ed. St. Louis, MO:
• KCSID = KCS ichthyosiform dermatosis.
◦ www.optimal-selection.com Saunders, 2017.
• MOD = merle ocular dysgenesis.
◦ www.mydogdna.com Author Simon A. Pot
• OSD = oculo-skeletal dysplasia.
◦ www.pawprintgenetics.com Consulting Editor Kathern E. Myrna
• PHPV = persistent hyperplastic primary
vitreous. ◦ https://www.vet.upenn.edu/research/
• PHTVL = persistent hyperplastic tunica
academic-departments/clinical-sciences-
vasculosa lentis. advanced-medicine/research-labs-centers/ Client Education Handout
• PPM = persistent pupillary membrane.
penngen/penngen-tests available online
• Good summaries of genetic basis and
INTERNET RESOURCES clinical signs of diseases, relevance of test
• These laboratories offer DNA-based tests: results, and relevant references are listed on
◦ www.antagene.com most of these websites.
Congenital Spinal and Vertebral Malformations

• Sacrococcygeal dysgenesis—Manx cat. • CT myelography and 3D reconstructed
• Spina bifida—bulldog, Manx cat, and other imaging—to characterize bony abnormali- C
screw-tailed breeds. ties and associated spinal cord
BASICS • Spinal dysraphism—Weimaraner. compression.
DEFINITION • Congenital spinal stenosis—Doberman • MRI—sensitive modality to visualize
Anomalous development of spinal structures, pinscher; chondrodystrophic breeds. abnormalities of spinal cord parenchyma,
which are apparent at birth or within the first Mean Age and Range cauda equina, nerve roots, and surrounding
weeks of life. • Often silent, vertebral malformation
soft tissues.
PATHOPHYSIOLOGY may cause clinical disease during the DIAGNOSTIC PROCEDURES
• Malformation of the occipital bones, atlas, rapid growth of the animal (e.g., 5–9 Cerebrospinal fluid analysis to rule out
and axis; malformation of the odontoid months of age). infectious/inflammatory conditions.
process; occipitoatlantoaxial malformation; • Spinal cord anomalies cause clinical disease
PATHOLOGIC FINDINGS
and occipital dysplasia—may cause atlanto- from birth on. • Multiple congenital malformations—often
axial subluxation with secondary compression SIGNS present concomitantly; pathologic changes
and trauma to the first segments of the • Distortion of the spinal column—lordosis; reflect several disease processes.
cervical spinal cord. kyphosis; and scoliosis in cases of vertebral • Acute compression of the spinal cord
• Other embryonic or developmental malformations. secondary to congenital malformation(s)—
anomalies of the vertebrae such as hemiverte- • Ataxia and paresis associated with spinal may result in spinal cord ischemia, hemor-
bra, transitional vertebra, block vertebra, and cord compression and trauma. rhage, ballooning of the myelin sheath at the
butterfly vertebra—these defects cause • Signs vary with spinal cord segment(s) point of compression or trauma, and axonal
deformity and instability of the vertebral involved. swelling or loss; in chronic spinal cord
canal and, on rare occasions, compression of compression, myelin degeneration, astrocyto-
the associated spinal cord or nerve roots. CAUSES
Breed-related inherited defects are suspected sis, and fibrosis are more prominent; at spinal
• Sacrococcygeal dysgenesis—characterized sites, cranial and caudal to the primary injury,
by absence or partial development of the for most congenital spinal abnormalities,
although interactions between several genes Wallerian degeneration can be observed in
sacrocaudal spinal cord segments; often ascending or descending pathways, respect-
associated with additional malformations and environmental factors (e.g., teratogenic
compounds, nutritional deficiencies) are ively.
(e.g., spina bifida). • Chronic changes—may result from
• Spina bifida—caused by failure of fusion of likely involved and would explain some of
these complex pathologic changes. vertebral malformations secondary to bony
the vertebral arches; may be associated with proliferation, thickening of the joint capsule,
protrusion of the spinal cord and meninges; RISK FACTORS hypertrophy of articular processes, and
other malformations often linked to this • Teratogenic compounds. thickening of the ligaments surrounding the
syndrome include spinal dysplasia, dysraphism, • Toxins. spinal cord.
syringomyelia/hydromyelia, and myelodysplasia. • Nutritional deficiencies. • Atlantoaxial subluxation—congenital
• Congenital spinal stenosis—can occur when • Stress. aplasia or hypoplasia of the odontoid process
vertebral malformations cause segmental or and surrounding ligaments.
diffuse narrowing of the spinal cord; inborn • Occipitoatlantoaxial malformations—
errors in skeletal growth, hypertrophy of fusion of the atlas to the occipital bone
ligamentum flavum, and bony proliferation (cats) and dorsal angulation of the dens
may also contribute to the stenosis. DIAGNOSIS
(dogs).
SYSTEMS AFFECTED DIFFERENTIAL DIAGNOSIS • Occipital dysplasia—anomaly of the
• Metabolic disease (e.g., storage diseases). foramen magnum in which the occipital
Nervous—spinal cord; spinal nerve roots; and
• Nutritional disease (e.g., hypovitaminosis bone is incompletely formed and fibrous
vertebral column.
and hypervitaminosis A, thiamine tissue membrane covers the caudal
GENETICS deficiency). cerebellum.
• A genetic background, with unknown • Early-onset inflammatory or infectious • Sacrococcygeal dysgenesis—caudal vertebral
mode of inheritance, is suspected in most processes (e.g., viral, protozoal, and rarely aplasia or hypoplasia.
congenital spinal diseases. bacterial). • Spina bifida—incomplete fusion of the
• Sacrococcygeal dysgenesis—autosomal • Toxin exposure (e.g., lead, organophos- dorsal vertebral arches where the meninges
dominant. phates, hexachlorophene, organochlorine). or spinal cord can protrude; most com-
• Thoracic hemivertebra of German • Trauma. monly seen in the caudal lumbar or sacral
shorthaired pointers—autosomal recessive.
CBC/BIOCHEMISTRY/URINALYSIS area; a dimple can be observed in a few
GEOGRAPHIC DISTRIBUTION Usually within normal limits. cases secondary to the lack of separation
N/A between the neuroectoderm and other
SIGNALMENT ectodermal structures, leaving a small
N/A
attachment between the spinal cord or
Species and Breed Predilections IMAGING meninges and the skin; often seen with
• Malformation of the occipital bones, atlas, • Survey radiography—to reveal vertebral myelodysplasia, central canal defects,
and axis—most common in small-breed dogs. malformation(s) and deviation of the spinal syringomyelia or hydromyelia, and
• Hemivertebra, transitional vertebra, block column. abnormal gray-matter differentiation.
vertebra, and butterfly vertebra—most • Myelography—to determine the level(s) of • Spinal stenosis—pathologic changes
common in brachycephalic, “screw-tailed” spinal cord compression; flexed and extended observed within the spinal cord are most
breeds (e.g., French and English bulldog, pug, views may cause neurologic deterioration if commonly chronic and are caused by focal or
Boston terrier). instability present. diffuse narrowing of the spinal canal.
Congenital Spinal and Vertebral Malformations (continued)
• Spina bifida associated with spinal cord

C malformation, chronic neurologic disease
despite surgical treatment, and lower motor
T REATMENT M EDICATIONS neuron incontinence—prognosis is poor.
APPROPRIATE HEALTH CARE DRUG(S) OF CHOICE • Medical treatment usually is insufficient to
• Depends on severity of neurologic deficits. Corticosteroids may be used in some cases, alleviate moderate to severe neurologic signs
• Outpatient—if animal is ambulatory. with variable results. caused by spinal cord compression secondary
• Inpatient—if animal is nonambulatory CONTRAINDICATIONS to congenital vertebral malformation(s).
or requires emergency surgical treatment Avoid steroids with concomitant infections.
(e.g., for atlantoaxial subluxation).
PRECAUTIONS
NURSING CARE Steroids may cause ulcerations of the gastro-
• Restricted activity combined with physical intestinal tract and inhibit bone growth. M ISCELLANEOUS
therapy—may help neurologically disabled ASSOCIATED CONDITIONS
patients in the postoperative period; a cart POSSIBLE INTERACTIONS
Steroids reduce immune response following N/A
may be necessary for severely affected
patients. vaccination. AGE-RELATED FACTORS
• Management of urination—essential for ALTERNATIVE DRUG(S) N/A
cases in which disorders of micturition N/A ZOONOTIC POTENTIAL
accompany the spinal injury. N/A
ACTIVITY PREGNANCY/FERTILITY/BREEDING
Restricted, especially if vertebral subluxation N/A
is present. F OLLOW-UP SEE ALSO
DIET PATIENT MONITORING • Ataxia.
Maintaining a lean bodyweight limits stress • Frequent neurologic examinations—to • Atlantoaxial Instability.
on the spinal column. monitor the progression of clinical signs in • Cervical Spondylomyelopathy (Wobbler
CLIENT EDUCATION developing animals (e.g., every 4–6 weeks). Syndrome).
• Many congenital vertebral malformations • Neuroimaging—repeat as needed. • Paralysis.
are clinically silent. • Spinal Dysraphism.
• Perform a thorough workup when a Avoid breeding affected animals. Suggested Reading
congenial malformation results in neurologic de Lahunta A, Glass E, Kent M. Veterinary
abnormalities. POSSIBLE COMPLICATIONS Neuroanatomy and Clinical Neurology,
• Heritability is suspected; avoid breeding. • Depend on the type and severity of 4th ed. St Louis, MO: W.B. Saunders,
• Many neurologically affected dogs and cats neurologic signs. In cases of subluxation of 2015, pp. 45–77.
left untreated are euthanized. the atlantoaxial joint, acute death may occur. Dewey CW, Da Costa RC. Myelopathies:
• Early surgical intervention often necessary • Acute paralysis can also be seen with disorders of the spinal cord. In: Dewey
to alleviate compression of the spinal cord vertebral subluxation, with further trauma CW & Da Costa RC, ed., Practical Guide
and prevent further damage. and spinal cord compression. to Canine and Feline Neurology, 3rd ed.
• Implant failure may be observed after Ames, IA: John Wiley & Sons, Inc. 2016,
SURGICAL CONSIDERATIONS surgical decompression/stabilization.
• In general, surgical decompression is pp. 361–371, 412–415.
required when congenital malformation(s) EXPECTED COURSE AND PROGNOSIS Summer BA, Cummings JF, de Lahunta A.
cause narrowing of the spinal canal and • Prognosis varies depending on the type of Veterinary Pathology. Philadelphia, PA:
compression of the spinal cord. In cases of malformation, degree of spinal cord Mosby-Year Book, 1995, pp. 86–90.
chronic or diffuse spinal cord compression, compression or injury, and surgical decom- Wyatt S, Gonçalves R, Gutierrez-Quintana &
improvement following surgery is minimal. pression or stabilization techniques. al. Outcomes of nonsurgical treatment for
• Atlantoaxial subluxation—surgical ventral • Vertebral malformation without compres- congenital thoracic vertebral body malfor-
decompression combined with stabilization of sion of the spinal cord—prognosis is good. mations in dogs: 13 cases (2009–2016).
the atlantoaxial joint with pins or screws is • Atlantoaxial subluxation following surgical J Am Vet Med Assoc 2016;253:768–773.
the treatment of choice. decompression or stabilization—prognosis is Author Joane M. Parent.
• Spina bifida—meningoceles can be closed fair to good.
surgically to prevent leakage of cerebrospinal fluid • Spinal cord compression treated surgically—
and infections; surgery usually not attempted prognosis is fair. Client Education Handout
when the spinal cord parenchyma is involved. available online
Congestive Heart Failure, Left-Sided

CAUSES involving right caudal lung lobe in acute
Pump (Muscle) Failure of Left Ventricle edema of dog, but may be patchy, especially C
• Dilated cardiomyopathy (DCM)/diet-induced
in cats; acute pulmonary edema may begin in
BASICS right caudal lung lobe.
DCM. • Trypanosomiasis (rare). • Doxorubicin
DEFINITION cardiotoxicity (dogs). • Hypothyroidism (rare). Echocardiography
Failure of the left side of the heart to advance • Hyperthyroidism (rarely causes pump failure; • Findings vary markedly with cause, but left
blood at a sufficient rate to meet the metabolic more commonly causes high output failure). atrial enlargement relatively consistent finding
needs of the patient or to prevent blood from • Tachycardia-induced cardiomyopathy (caused in cardiogenic pulmonary edema. • Diagnostic
pooling within the pulmonary venous circulation. by persistent pathologic supraventricular or test of choice for documenting congenital
PATHOPHYSIOLOGY ventricular tachyarrhythmia). defects, cardiac masses, and pericardial effusion.
• Low cardiac output causes lethargy, exercise Pressure Overload of Left Heart DIAGNOSTIC PROCEDURES
intolerance, syncope, and prerenal azotemia. • Systemic hypertension (uncommon cause
• High hydrostatic pulmonary venous pressure ECG
of heart failure in animals). • Subaortic • Atrial or ventricular arrhythmias.
causes leakage of fluid from pulmonary venous stenosis. • Aortic coarctation (rare; Airedale
circulation into pulmonary interstitium and • Evidence of left cardiomegaly (e.g., wide P
predisposed). • Left ventricular tumors (rare). waves, tall and wide QRS complexes, and left
alveoli; when fluid leakage exceeds ability of
lymphatics to drain affected areas, pulmonary Volume Overload of Left Heart axis orientation). • May be normal.
edema develops. • Degenerative mitral valve disease (dogs). PATHOLOGIC FINDINGS
• Mitral valve dysplasia (cats and dogs). Cardiac findings vary with disease.
SYSTEMS AFFECTED • Patent ductus arteriosus (dogs). • Ventricular
• All systems can be affected by poor septal defect, especially if complicated by aortic
perfusion. • Respiratory—increased rate and valve insufficiency. • Aortic valve insufficiency
effort because of elevated pulmonary venous secondary to endocarditis (dogs). • Chronic,
pressures/edema. • Cardiovascular. severe anemia. • Inadvertent high-volume fluid TREATMENT
GENETICS administration. • Steroid administration (cats, APPROPRIATE HEALTH CARE
Some congenital heart defects, cardiomyo often with previously asymptomatic underlying • Usually treat as outpatient unless dyspneic
pathies, and valvular heart disease have hypertrophic cardiomyopathy [HCM]). or severely hypotensive. • Identify and correct
genetic basis in some breeds. Impediment to Filling of Left Ventricle underlying cause whenever possible.
INCIDENCE/PREVALENCE • Restrictive cardiomyopathy (rare in dogs, • Minimize handling of critically dyspneic
Common more common in cats). • Pulmonary vein animals—stress can kill!
GEOGRAPHIC DISTRIBUTION stenosis (rare). • HCM. • Left atrial masses NURSING CARE
Seen everywhere; prevalence of causes varies (e.g., tumor or thrombus). • Mitral stenosis Oxygen supplementation and postural
with location. (rare). • Cor triatriatum sinister (cats, rare). support in dyspneic patients.
SIGNALMENT Rhythm Disturbances ACTIVITY
• Bradyarrhythmia (high-grade atrioventricular Restrict activity when dyspneic or tachypneic.
Species block). • Tachyarrhythmia (e.g., atrial
Dog and cat. fibrillation, sustained supraventricular tachy- DIET
Breed Predilections cardia, ventricular tachycardia). Initiate moderately sodium-restricted diet with
Varies with cause. adequate protein and calories. Severe sodium
RISK FACTORS restriction indicated with advanced disease.
Mean Age and Range Conditions causing chronic high cardiac
Varies with cause. output (e.g., hyperthyroidism and anemia). CLIENT EDUCATION
With few exceptions (e.g., animals with thyroid
Predominant Sex
disorders, anemia, arrhythmias, nutritionally
Varies with cause.
responsive heart disease, congenital heart
SIGNS disease), L-CHF is not curable.
General Comments DIAGNOSIS
Signs vary with underlying cause and species. DIFFERENTIAL DIAGNOSIS • Surgical intervention, coil embolization,
Historical Findings Must differentiate from other causes of Amplatz occluder placement, or balloon
• Weakness, lethargy, exercise intolerance. coughing, dyspnea, and weakness. valvuloplasty may benefit selected patients
• Coughing (dogs with large left atria, CBC/BIOCHEMISTRY/URINALYSIS with some forms of congenital and acquired
concurrent tracheobronchial disease, or such • CBC usually normal; maybe stress leuko- valvular heart disease; response to these
severe edema that large airways affected) and gram. • Mild to moderate liver enzyme interventions varies. • Pericardiocentesis in
dyspnea (increased respiratory rate and effort); elevation; bilirubin generally normal. animals with pericardial effusion.
respiratory signs often worsen at night and may • Prerenal azotemia in some animals.
require assuming standing, sternal, or “elbows OTHER LABORATORY TESTS
abducted” position (orthopnea). • Cats rarely • Thyroid disorders may be detected.
cough from heart failure; coughing should • Serum NT-proBNP and cardiac troponin I MEDICATIONS
prompt search for primary airway disease. concentrations higher in animals with DRUG(S) OF CHOICE
Physical Examination Findings left-sided congestive heart failure (L-CHF)
• Tachypnea and dyspnea. • Coughing, often than in normal animals. Diuretics
soft in conjunction with tachypnea (dogs). • Furosemide (1–2 mg/kg q8–24h) or other
IMAGING loop diuretic is initial diuretic of choice; diuretics
• Pulmonary crackles and wheezes. • Pale/
gray/cyanotic mucous membranes. Radiography indicated to reduce preload and remove
• Prolonged capillary refill time. • Possible • Left heart and pulmonary veins enlarged. pulmonary edema; critically dyspneic animals
murmur or gallop. • Weak femoral pulses. • Pulmonary edema, often hilar, especially often require high doses (2–4 mg/kg) IV to
Congestive Heart Failure, Left-Sided (continued)
stabilize; dose can be repeated in 1h if animal still especially in animals with severe sodium
C severely dyspneic; IV bolus of 0.66 mg/kg restriction. • Combination diuretic therapy
followed by CRI of 0.66–1 mg/kg/h for 1–4h adds to risk of dehydration and electrolyte
causes greater diuresis than equal dose divided disturbances. • Combination vasodilator FOLLOW-UP
into two IV boluses given 4h apart; once edema therapy predisposes animal to hypotension. PATIENT MONITORING
resolves, taper to lowest effective dose. ALTERNATIVE DRUG(S) • Monitor resting respiratory rate and effort,
• Spironolactone (0.5–2 mg/kg PO q12–24h) appetite, renal status, electrolytes, hydration, heart
increases survival in humans with CHF and is in Arterial Dilators rate, bodyweight. • If azotemia develops, reduce
clinical trials in dogs; use in combination with • Hydralazine (0.5–2 mg/kg PO q12h; diuretic dose; if azotemia persists and animal is
furosemide. • Thiazide diuretics can be added to 0.5 mg/kg PO to start when added to ACE also on ACE inhibitor, reduce or discontinue
furosemide and spironolactone in refractory inhibitor) or amlodipine (0.05–0.2 mg/kg ACE inhibitor; use digoxin with caution if
heart failure cases. • Torsemide (0.2–0.8 mg/kg PO q24h) can be substituted for ACE azotemic. • Monitor ECG if arrhythmias
q24h) may be useful as substitute for furosemide inhibitor in patients that do not tolerate the suspected. • Check digoxin concentration
in animals requiring daily furosemide dosing in drug or have advanced renal failure; monitor (0.5–1.5 ng/mL, 8–10 hours post dose).
excess of 12 mg/kg, and it may be more effective for hypotension and tachycardia; can be
cautiously added to ACE inhibitor in animals PREVENTION/AVOIDANCE
than furosemide at delaying death due to cardiac
with refractory L-CHF. • Nitroprusside • Minimize stress, exercise, and sodium
disease in dogs with CHF secondary to degen-
(1–10 μg/kg/min) is potent arterial dilator intake in patients with heart disease.
erative valve disease.
usually reserved for short-term support of • Pimobendan delays onset of CHF in
Angiotensin-Converting Enzyme ACE) Doberman pinschers, and in dogs with
patients with life-threatening edema.
Inhibitors hemodynamically significant myxomatous
• ACE inhibitors such as enalapril (0.5 mg/kg Digoxin mitral valve regurgitation; prescribing an
q12–24h) or benazepril (0.25–0.5 mg/kg • Digoxin (dogs: 0.22 mg/m2 q12h; cats: ACE inhibitor with pimobendan early in
q12–24h) indicated in most animals with 0.01 mg/kg q48h) is used in animals with course of heart disease in patients with DCM
L-CHF. • ACE inhibitors improve survival and atrial fibrillation and myocardial failure (e.g., may slow progression of heart disease and
quality of life in dogs with L-CHF secondary to DCM); commonly used in combination with delay onset of CHF; role of ACE inhibitors in
degenerative valve disease and DCM. diltiazem to control rate of atrial fibrillation. asymptomatic animals with mitral valve
• Digoxin is also indicated to treat dogs with disease remains controversial.
Positive Inotropes refractory heart failure from either myocardial
• Pimobendan (0.25–0.3 mg/kg PO q12h) is a failure or volume loads; however, its use as a POSSIBLE COMPLICATIONS
calcium channel sensitizer that dilates arteries and primary agent in myocardial failure has been • Syncope. • Aortic thromboembolism (cats).
increases myocardial contractility; first-line agent replaced by pimobendan. • Arrhythmias. • Electrolyte imbalances.
in treating DCM or CHF due to degenerative • Digoxin toxicity. • Azotemia and renal
valve disease efficacy in cats with CHF is not Calcium Channel Blockers failure.
known, but possibly beneficial. • Dobutamine Diltiazem (0.5–1.5 mg/kg PO q8h) is frequently
used in L-CHF patients for rate control in EXPECTED COURSE AND PROGNOSIS
(dogs: 2.5–10 μg/kg/min; cats: 0.5–5 μg/kg/ Prognosis varies with underlying cause; cats
min) is a potent positive inotropic agent that animals with supraventricular arrhythmias.
and dogs that survive initial episode of
may provide valuable short-term support of a Beta Blockers pulmonary edema and can be reliably
heart failure patient with poor cardiac • Atenolol and metoprolol are sometimes used medicated often survive months to more than
contractility. • Positive inotropes in general are for rate control in animals with supraventricular a year with good quality of life. Animals with
potentially arrhythmogenic—monitor carefully. tachycardia, hypertrophic cardiomyopathy, and reversible causes of L-CHF may recover to
Venodilators hyperthyroidism. • Used alone or with a class 1 normal lives.
• Nitroglycerin ointment (one-fourth antiarrhythmic drug for control of ventricular
inch/5 kg q6–8h) causes venodilation, lowering arrhythmias; these drugs depress contractility
left atrial filling pressures. • Used for acute (negative inotropes), so use cautiously in patients
stabilization of patients with severe pulmonary with myocardial failure or active signs of CHF.
edema and dyspnea, but uncertain benefit. • On basis of human studies, may enhance MISCELLANEOUS
survival in animals with idiopathic DCM; AGE-RELATED FACTORS
Antiarrhythmic Agents treatment is best initiated under guidance of a
Treat arrhythmias if clinically indicated. • Congenital causes seen in young animals.
cardiologist, starting with very low dosage and • Degenerative heart conditions and
CONTRAINDICATIONS gradually increasing; carvedilol is sometimes used neoplasia generally seen in old animals.
Avoid vasodilators in patients with pericardial for this purpose, starting at 0.1 mg/kg q24h and
effusion or fixed outflow obstruction. titrating to 0.5 mg/kg q12h. SEE ALSO
Pulmonary Edema, Noncardiogenic.
PRECAUTIONS Nutritional Supplements
• ACE inhibitors and arterial dilators must be • Potassium and magnesium supplementation ABBREVIATIONS
used with caution in patients with possible if deficiency is documented; use potassium • ACE = angiotensin-converting enzyme.
outflow obstruction. • Pulmonary hypertension, supplements cautiously in animals receiving • DCM = dilated cardiomyopathy.
hypothyroidism, and hypoxia increase risk for ACE inhibitor or spironolactone. • Taurine • HCM = hypertrophic cardiomyopathy.
digoxin toxicity; hyperthyroidism diminishes supplementation in cats with DCM and dogs • L-CHF = left-sided congestive heart failure.
effects of digoxin. • ACE inhibitors and with DCM and taurine deficiency (e.g., Authors Francis W.K. Smith, Jr. and Bruce
digoxin—use cautiously in patients with renal American cocker spaniels) • L-carnitine W. Keene
disease. • Dobutamine—use cautiously in cats. supplementation may help some dogs with Consulting Editor Michael Aherne
• Spironolactone—may cause facial pruritis DCM. • Coenzyme Q10 is of potential value
in cats. based on results in humans with DCM.
POSSIBLE INTERACTIONS • Ensure animal receiving a nutritionally
available online
• Combination of high-dose diuretics and balanced diet (see Cardiomyopathy,
ACE inhibitors may cause azotemia, Nutritional).
Congestive Heart Failure, Right-Sided

Physical Examination Findings effusion due to heart failure should have
• Jugular venous distention. • Hepatojugular jugular venous distension. C
reflux. • Jugular pulse in some animals.
B ASICS CBC/BIOCHEMISTRY/URINALYSIS
• Hepatomegaly. • Ascites common in dogs
• CBC usually normal; animals with
DEFINITION and rare in cats with R-CHF. • Possible
heartworm disease may have eosinophilia.
Failure of the right side of the heart to regurgitant murmur in tricuspid valve
• Mild to moderately high alanine aminotrans
advance blood at a sufficient rate to meet the region or ejection murmur at left heart base
ferase, aspartate aminotransferase, and
metabolic needs of the patient or to prevent (pulmonic stenosis). • Muffled heart sounds
alkaline phosphatase due to passive liver
blood from pooling within the systemic if animal has pleural or pericardial effusion.
congestion; bilirubin generally normal.
venous circulation. • Weak femoral pulses. • Rapid, shallow
• Prerenal azotemia in some animals.
respiration if animal has pleural effusion or
PATHOPHYSIOLOGY severe ascites.• Peripheral edema (infrequent). OTHER LABORATORY TESTS
• High hydrostatic pressure leads to leakage of • Heartworm test may be positive. • NT-proBNP
fluid from venous circulation into the pleural CAUSES
concentrations higher in animals with cardiac
and peritoneal space and potentially into the Pump (Myocardial) Failure of Right causes of fluid accumulation.
pericardium and interstitium of peripheral Ventricle
tissue. • When fluid leakage exceeds ability of IMAGING
• Idiopathic dilated cardiomyopathy (DCM).
lymphatics to drain the affected areas, pleural • ARVC. • Hypertrophic cardiomyopathy Thoracic Radiography
effusion, ascites, pericardial effusion, and (cats). • Restrictive cardiomyopathy (cats). • Right cardiomegaly in some animals.
peripheral edema develop. • Trypanosomiasis. • Doxorubicin • Dilated caudal vena cava (diameter greater
SYSTEMS AFFECTED cardiotoxicity. • Chronic hyperthyroidism. than the length of the vertebra directly above
All systems can be affected by either poor the heart). • Pleural effusion (especially cats).
Volume Overload of Right Ventricle
delivery of blood or the effects of passive • Hepatosplenomegaly and possible ascites
• Chronic atrioventricular (AV) valve (mitral
congestion from backup of venous blood. (especially dogs).
± tricuspid) insufficiency due to myxomatous
valvular degeneration. • Tricuspid valve Echocardiography
GENETICS
dysplasia. • Large atrial septal defect. • Findings vary with underlying cause;
• Some congenital cardiac defects have a genetic
basis in certain breeds. • Arrhythmogenic right especially useful for documenting congenital
Pressure Overload of Right Ventricle
ventricular cardiomyopathy (ARVC) appears to defect, cardiac mass, and pericardial effusion.
• Heartworm disease. • Chronic obstructive
have a genetic basis in boxers and possibly some • Abdominal ultrasound reveals hepatomeg-
pulmonary disease with pulmonary hypertension. aly with hepatic vein dilation, flow reversal in
cats. • Pulmonary thromboembolism. • Pulmonic the hepatic veins (Doppler), and possibly
INCIDENCE/PREVALENCE stenosis. • Tetralogy of Fallot. • Right ventricular ascites.
Common tumors. • Heart base tumors (occasionally,
compression of the pulmonary artery). • Primary DIAGNOSTIC PROCEDURES
GEOGRAPHIC DISTRIBUTION pulmonary hypertension. ECG Findings
Syndrome seen everywhere; prevalence of
Impediment to Right Ventricular Filling • Small (<1 mV) QRS complexes in all frontal
various causes varies with location.
• Pericardial effusion (tamponade). • Constrictive/ axis leads if pericardial or pleural effusion.
SIGNALMENT restrictive pericarditis. • Right atrial or caval masses. • Electrical alternans or elevated ST segment
Species • Tricuspid stenosis. • Cor triatriatum dexter. with pericardial effusion. • Evidence of right
Dog and cat. cardiomegaly (e.g., tall [>0.4 mV] P waves in
Rhythm Disturbances
lead II, deep S waves in leads I, II, aVF, and
Breed Predilections • Bradycardia, generally complete AV block.
right axis deviation). • Atrial or ventricular
Vary with cause. • Tachyarrhythmias, generally sustained arrhythmias. • ECG may be normal.
supraventricular tachycardia.
Mean Age and Range Abdominocentesis
Vary with cause. RISK FACTORS Analysis of ascitic fluid in patients with
• No heartworm prophylaxis. • Offspring of
Predominant Sex R-CHF generally reveals modified transudate
animal with right-sided congenital cardiac with total protein >2.5 mg/dL.
Varies with cause.
defect. • Conditions that augment demand
SIGNS for cardiac output (e.g., hyperthyroidism, Thoracentesis
anemia, pregnancy). • Cats with pleural effusion associated with
General Comments
• Signs vary with underlying cause and
R-CHF may have transudate, modified
between species. • Pleural effusion without transudate, or chylous effusion. • Dogs with
ascites and hepatomegaly is rare in dogs pleural effusion and R-CHF may have
transudate or modified transudate.
with right-sided congestive heart failure DIAGNOSIS
(R-CHF). • Ascites without pleural Central Venous Pressure
effusion is rare in cats with R-CHF. DIFFERENTIAL DIAGNOSIS Central venous pressure is high (>9 cmH2O)
• Small-volume pericardial effusion • Must differentiate from other causes of or rises dramatically to that level and remains
without tamponade is relatively common pleural effusion and ascites; generally elevated for more than 1h following a fluid
in cats with R-CHF. • Interstitial periph- requires complete diagnostic workup bolus (e.g., 5–10 mL/kg IV).
eral edema is a rare manifestation of including CBC, biochemistry profile,
heartworm test, thoraco- or abdominocen- PATHOLOGIC FINDINGS
R-CHF in both species. • Cardiac findings vary with disease.
tesis with fluid analysis and cytology, and
Historical Findings sometimes thoracic and abdominal • Hepatomegaly in animals with centrolobu-
• Weakness. • Lethargy. • Exercise intolerance. ultrasound. • Animals with ascites or pleural lar necrosis (chronic condition).
• Abdominal distension. • Dyspnea, tachypnea.
Congestive Heart Failure, Right-Sided (continued)
Vasodilators arrhythmias if clinically indicated. • Taurine

C • Angiotensin-converting enzyme (ACE) supplementation in cats with DCM and dogs
inhibitors such as enalapril (0.5 mg/kg with DCM and taurine deficiency. • Carnitine
TREATMENT q12–24h) or benazepril (0.25–0.5 mg/kg supplementation may help some dogs with
APPROPRIATE HEALTH CARE q24h) are helpful when CHF is secondary to DCM (e.g., cocker spaniels and boxers).
Most animals treated as outpatients unless DCM or chronic AV valve insufficiency.
dyspneic or collapsed (e.g., significant pleural • Sildenafil (0.5–1 mg/kg PO q12h up to
or pericardial effusion). 2–3 mg/kg q8h) may be beneficial for
pulmonary hypertension.
NURSING CARE FOLLOW-UP
Thoracentesis and abdominocentesis may be Pimobendan
• Calcium sensitizer that acts as an inodilator,
PATIENT MONITORING
required periodically for patients no longer • Monitor renal status, electrolytes, hydration,
responsive to medical management or those causing arterial vasodilation and increasing
myocardial contractility. • Especially useful in respiratory rate and effort, bodyweight, and
with severe dyspnea due to pleural effusion or abdominal girth (dogs). • If azotemia develops,
ascites. myocardial failure. • Dose—0.25–0.3 mg/kg
PO q12h. reduce diuretic dosage; if azotemia persists and
ACTIVITY the animal is also on an ACE inhibitor, reduce or
Restrict activity. Digoxin discontinue this drug; if azotemia develops,
• Digoxin (dogs: 0.22 mg/m2 q12h; cats: reduce digoxin dosage to avoid toxicity.
DIET 0.01 mg/kg q48 h) is used in animals with
Restrict sodium moderately; severe sodium • Monitor ECG periodically to detect arrhyth-
myocardial failure (e.g., DCM) and atrial mias. • Monitor digoxin concentrations—
restriction indicated for animals with fibrillation. • Digoxin indicated in animals
advanced disease. normal value 0.5–1.5 ng/mL for serum sample
with refractory CHF that have supraventricu- obtained 8–10h after dose is administered.
CLIENT EDUCATION lar arrhythmias.
• With few exceptions (e.g., in heartworm
CONTRAINDICATIONS • Pulmonary thromboembolism. • Arrhythmias.
disease, arrhythmias, hyperthyroidism, and • Avoid diuretics in patients with pericardial
idiopathic pericardial effusion), R-CHF is not • Electrolyte imbalances. • Digoxin toxicity.
effusion/tamponade. • Avoid vasodilators in • Azotemia and renal failure.
curable. • Most patients improve with initial patients with pericardial effusion or fixed
treatment but often have recurrent failure. outflow obstructions. EXPECTED COURSE AND PROGNOSIS
SURGICAL CONSIDERATIONS Prognosis varies with underlying cause.
PRECAUTIONS
• Surgical intervention or balloon valvuloplasty
• ACE inhibitors and arterial dilators must be
is indicated to treat certain congenital defects used with caution in patients with possible
such as pulmonic stenosis or cor triatriatum outflow obstructions. • Pulmonary hyperten-
dexter, and Amplatz occluder placement for sion, hypothyroidism, and hypoxia increase MISCELLANEOUS
morphologically appropriate atrial septal risk for digoxin toxicity; hyperthyroidism AGE-RELATED FACTORS
defects. • Pericardiocentesis or pericardectomy diminishes effects of digoxin. • ACE • Congenital causes seen in young animals.
for pericardial effusion. • Removal of heart- inhibitors and digoxin—use cautiously with • Degenerative heart conditions and
worms from the heart via the jugular vein in renal disease. • Dobutamine—use cautiously neoplasia generally seen in old animals.
dogs with caval syndrome. in cats. • Spironolactone—may cause facial
SEE ALSO
pruritis in cats.
• Ascites.
POSSIBLE INTERACTIONS • Chylothorax.
• Combination of high-dose diuretics and • Pleural Effusion.
MEDICATIONS ACE inhibitors may alter renal perfusion and
ABBREVIATIONS
DRUG(S) OF CHOICE cause azotemia. • Combination diuretic
• ACE = angiotensin-converting enzyme.
Drugs should be administered only after a therapy promotes risk of dehydration and
• ARVC = arrhythmogenic right ventricular
definitive diagnosis is made. electrolyte disturbances.
cardiomyopathy.
Diuretics ALTERNATIVE DRUG(S) • AV = atrioventricular.
• Furosemide (1–2 mg/kg q8–24h) or another • Patients unresponsive to furosemide, • DCM = dilated cardiomyopathy.
loop diuretic is the initial diuretic of choice; spironolactone, vasodilator, pimobendan, and • R-CHF = right-sided congestive heart failure.
diuretics are indicated to remove excess fluid digoxin (if indicated) may benefit from triple Authors Francis W.K. Smith, Jr. and Bruce
accumulation. • Torsemide (0.2–0.8 mg/kg diuretic therapy by adding a thiazide diuretic, W. Keene
q24h) may be a useful substitute for furosem- or substitution of torsemide for furosemide, Consulting Editor Michael Aherne
ide in animals requiring a daily furosemide generally at 0.1–0.2 mg of torsemide for each
dose in excess of 12 mg/kg. • Spironolactone 1 mg of furosemide previously administered.
(2 mg/kg PO q12–24h) increases survival in • Potassium and magnesium supplementation Client Education Handout
humans with heart failure; use in combination if deficiency documented; use potassium available online
with furosemide. supplements cautiously in animals receiving
ACE inhibitors or spironolactone. • Treat
Conjunctivitis—Cats
Secondary to Adnexal Disease useful with mass lesions and immune-medi-
• May develop keratoconjunctivitis sicca ated disease or chronic disease. • PCR testing C
(KCS) as a result of scarring. • Eyelid diseases for chlamydia or FHV. • Virus isolation or
B ASICS (e.g., entropion, trichiasis, distichia, or eyelid immunofluorescence antibody (IFA) testing
DEFINITION agenesis)—cause frictional irritation or for FHV; false-positive result if fluorescein
Inflammation of the conjunctiva, the exposure. • Dacryocystitis or nasolacrimal staining is done before IFA testing.
vascularized mucous membrane that covers system outflow obstruction. • Serologic test for FHV antibodies—not
the anterior sclera (bulbar conjunctiva), lines Referred Inflammation from Other useful (widespread exposure, vaccination).
the eyelids (palpebral conjunctiva), and lines Ocular or Periocular Diseases PATHOLOGIC FINDINGS
the third eyelid. • Ulcerative keratitis. • Corneal sequestrum. • Biopsy—signs of inflammation, possible
PATHOPHYSIOLOGY • Anterior uveitis. • Glaucoma. • Orbital infectious agents. • Histopathology of mass
May be primary or secondary to adnexal or disease. • Pyoderma. lesions may reveal neoplasia (e.g., squamous
ocular disease. cell carcinoma and lymphoma).
RISK FACTORS
SYSTEMS AFFECTED Stress or immune system compromise (FHV).
Ophthalmic
GENETICS
N/A TREATMENT
INCIDENCE/PREVALENCE DIAGNOSIS APPROPRIATE HEALTH CARE
• Primary—often outpatient. • Secondary to
Common DIFFERENTIAL DIAGNOSIS other diseases (ulcerative keratitis, uveitis,
GEOGRAPHIC DISTRIBUTION • Must distinguish primary conjunctivitis from
glaucoma)—may need hospitalization to
N/A secondary conjunctival hyperemia. • Thorough address severe underlying ophthalmic issue.
ophthalmic exam rules out other diseases (e.g.,
SIGNALMENT ulcers, uveitis, glaucoma, orbital disease); assess NURSING CARE
Species pupil size and symmetry, look for aqueous flare, • Irritant-induced conjunctivitis—flush ocular
Cat perform intraocular pressure testing and surfaces and remove foreign body if observed.
fluorescein staining. • Deeper, darker, more • Topical hyaluronate-based artificial tear, q8h
Breed Predilections to benefit tear film. • Frequent cleaning of
linear and immobile blood vessel injection
Infectious—purebred cats may be eyelid margins and periocular skin to remove
indicates episcleral vasculature congested due to
predisposed. ocular discharge.
intraocular disease. • Conjunctival mass biopsy
Mean Age and Range will identify neoplasia (lymphoma and ACTIVITY
Infectious—commonly affects young animals. squamous cell carcinoma most common). • Generally, no restrictions. • Suspected contact
Predominant Sex CBC/BIOCHEMISTRY/URINALYSIS irritant or acute allergic disease—prevent contact
N/A Normal, except with systemic disease. with the offending agent. • Suspected FHV—
SIGNS minimize stress. • Do not expose patients with
OTHER LABORATORY TESTS infectious disease to susceptible animals.
• Blepharospasm. • Conjunctival hyperemia. Infectious—serologic testing for feline
• Ocular discharge—serous, mucoid, or leukemia virus (FeLV) and feline immuno- DIET
mucopurulent. • Chemosis. • Conjunctival deficiency virus (FIV). • No change for most patients. • Suspected
follicles. • Upper respiratory infection—pos- underlying skin disease and/or food allergy—
IMAGING food elimination diet.
sible with infectious etiologies.
N/A
CAUSES CLIENT EDUCATION
DIAGNOSTIC PROCEDURES • When solutions and ointments are prescribed,
Viral • Thorough adnexal examination—rule out
• Feline herpesvirus (FHV)—most common
instruct the client to use solution(s) before
eyelid abnormalities and foreign bodies under ointment(s) and wait at least 5 minutes between
infectious cause; only one that leads to eyelids or third eyelid. • Complete ophthal-
corneal changes (e.g., dendritic or geographic treatments. • If copious discharge is noted,
mic examination—rule out other ocular instruct client to clean eyes before giving
ulcers). • Calicivirus—may cause conjuncti- disease (e.g., uveitis, glaucoma). • Fluorescein
val ulcerations. medication. • Instruct client to call for instruc-
stain—assess for corneal ulceration or dendritic tions if condition fails to improve or worsens.
Bacterial lesions (FHV) and observe nares for stain
• Chlamydophila felis—chemosis is common passage to indicate nasolacrimal system SURGICAL CONSIDERATIONS
patency. • Nasolacrimal flush—considered to • Lipogranulomatous conjunctivitis—surgical
clinical sign. • Mycoplasma spp.—may be
overgrowth of normal flora. • Conjunctivitis rule out dacryocystitis or nasolacrimal system incision and curettage of glandular material
neonatorum—accumulation of exudates obstruction. • Schirmer tear test—measures and inflammatory infiltrates. • Entropion,
under closed eyelids prior to natural opening; aqueous tears to diagnose or rule out KCS; distichia, or other eyelid disease—perform
bacterial or viral component. performed before anything is placed in the temporary or permanent surgery depending on
eye. • Conjunctival cytology—rarely reveals the findings, signalment, and history.
Immune-Mediated cause; eosinophils with eosinophilic conjunc- • Nasolacrimal duct obstruction—difficult;
• Eosinophilic. • Lipogranulomatous. tivitis; degenerate neutrophils and intracyto- treatment often not recommended (see
• Allergic. • Related to systemic immune- plasmic bacteria indicate bacterial infection; Epiphora). • Conjunctival neoplasia—depend-
mediated disease. intracytoplasmic inclusion bodies indicate ing on tumor type and extent of involvement,
Trauma or Environmental Causes chlamydial or mycoplasmal infection; rarely may involve local excision and adjunctive
• Conjunctival foreign body. • Irritation from dust, see intranuclear FHV inclusions. therapy (β-irradiation, cryotherapy), enuclea-
smoke, chemicals, or ophthalmic medications. • Conjunctival biopsy—“snip biopsy” may be tion, or exenteration. • Symblepharon
Conjunctivitis—Cats (continued)
(adhesions between the conjunctiva and 0.2% ointment 1–2% compounded solution, EXPECTED COURSE AND PROGNOSIS
C cornea)—adhesions may require surgical or tacrolimus 0.03% compounded solution— • FHV—most patients become chronic
resection (poor prognosis). • Corneal topical therapy q8–24h. • Topical 0.5% carriers; may see repeated exacerbations, but
sequestration—keratectomy often recom- megestrol acetate solution (available from episodes less common as patient matures; more
mended (see Corneal Sequestrum—Cats). compounding pharmacies)—q8–12h; safe with severe clinical signs at times of stress or
concurrent corneal ulceration and/or concur- immunocompromise. • Bacterial conjunctivi-
rent FHV ocular disease. • Oral megestrol tis—usually resolves with appropriate admin-
acetate—may help resistant condition, but istration of antibiotic. • Immune-mediated
rarely used given possible systemic side effects. diseases (e.g., eosinophilic)—control not cure;
MEDICATIONS may require chronic treatment at lowest level
CONTRAINDICATIONS
DRUG(S) OF CHOICE possible. • If underlying disease is found (e.g.,
• Topical corticosteroids—avoid with known
Herpetic or suspected infectious conjunctivitis; may KCS, entropion), resolution may depend on
• Condition usually mild and self-limiting. result in FHV recrudescence and predispose appropriate treatment of the disease.
• Antiviral treatment—indicated for severe to corneal sequestrum formation; never use if
intractable conjunctivitis, herpetic keratitis, corneal ulceration is noted. • Valacyclovir
and before keratectomy for corneal sequestra should never be used in cats.
suspected to be related to FHV; for all
PRECAUTIONS MISCELLANEOUS
antivirals treat 2 weeks past resolution of
• Topical medications may be irritating. ASSOCIATED CONDITIONS
clinical signs. • 0.5% cidofovir solution
• Monitor all patients treated with topical FeLV and FIV—may predispose patient to
(available from compounding pharmacies)—
corticosteroids for signs of corneal ulceration; chronic carrier state of FHV conjunctivitis.
topical, q12h. • 0.1% idoxuridine solution or
discontinue agent immediately if corneal
0.5% ointment (compounding pharma- AGE-RELATED FACTORS
ulceration occurs.
cies)—topical, q4h. • Vidarabine 3% FHV—tends to be more severe in kittens and
ointment—topical, q4h. • Trifluridine 1% POSSIBLE INTERACTIONS in old cats with waning immunity.
solution—topical, q4h; potentially irritating. N/A
ZOONOTIC POTENTIAL
• Oral famciclovir is effective and safe; ALTERNATIVE DRUG(S) Chlamydophila felis—low.
recommended dosage 90 mg/kg PO q12h. Other corticosteroids—1% prednisolone
• Lysine 500 mg PO q12h for adult cat PREGNANCY/FERTILITY/BREEDING
acetate.
(250 mg PO q12h for kitten). • FortiFlora® Use topical and systemic medications with
probiotic PO q24h may decrease incidence of caution, if at all, in pregnant animals.
conjunctivitis associated with FHV. SEE ALSO
Chlamydial or Mycoplasmal • Corneal Sequestrum—Cats.
FOLLOW-UP • Keratoconjunctivitis Sicca.
• Tetracycline, erythromycin, or chloram-
phenicol ophthalmic ointment—topically PATIENT MONITORING • Ophthalmia Neonatorum.
q6–8h; continue for several days past Recheck shortly after beginning treatment (at • Red Eye.
resolution of all clinical signs; recurrence or 5 days), then in 2 weeks or as needed. ABBREVIATIONS
reinfection common. • Topical ciprofloxacin PREVENTION/AVOIDANCE • FeLV = feline leukemia virus.
ophthalmic solution q6–8h as alternative to • Treat any underlying disease that may be • FHV = feline herpesvirus.
ophthalmic ointment. • Doxycycline 10 mg/ exacerbating the conjunctivitis. • Minimize • FIV = feline immunodeficiency virus.
kg PO q24h for 3–4 weeks may be superior to stress for patients with herpetic disease. • Isolate • IFA = immunofluorescent antibody.
or used along with topical treatment. • Based patients with infectious conjunctivitis to prevent • KCS = keratoconjunctivitis sicca.
on bacterial culture and sensitivity results. spread. • Prevent reexposure to infectious Suggested Reading
Neonatal sources. • Vaccination recommended; infection Maggs DJ, Miller PE, Ofri R. Slatter’s
Carefully open the eyelid margins (medial to is still possible if the cat was exposed to an Fundamentals of Veterinary
temporal), establish drainage, and treat with infectious agent before being vaccinated (e.g., Ophthalmology, 6th ed. St. Louis, MO:
topical antibiotic ointment q6–8h and an FHV infection from an infected queen). Elsevier, 2018, pp. 158–177.
antiviral for suspected FHV. POSSIBLE COMPLICATIONS Author Rachel A. Allbaugh
Eosinophilic • Corneal sequestration (see Corneal Consulting Editor Kathern E. Myrna
• Topical corticosteroid—0.1% dexamethasone Sequestrum—Cats)—usually requires surgical
sodium phosphate q6–8h generally effective; keratectomy. • Symblepharon—may require
taper gradually to lowest effective dose or surgery. • KCS—most likely from chronic Client Education Handout
transition to cyclosporine. • Cyclosporine FHV. available online
Conjunctivitis—Dogs
chronic superficial keratitis (pannus). else is placed in eye. • Fluorescein stain—no
• Systemic immune-mediated disease (e.g., corneal retention rules out ulcerative keratitis; C
pemphigus). stain flow to nares rules out nasolacrimal disease.
B ASICS • Tear film breakup time—assesses tear film
Trauma or Environmental Causes
DEFINITION • Conjunctival foreign body. • Irritation (dust,
stability to rule out qualitative tear deficiency.
Inflammation of the conjunctiva, the smoke, ophthalmic medications). • Toxin or • Intraocular pressures—rule out glaucoma.
vascularized mucous membrane that covers chemical contact. • Globe retropulsion—rule out orbital disease.
the anterior sclera (bulbar conjunctiva), lines • Examine for signs of anterior uveitis (e.g.,
the eyelids (palpebral conjunctiva), and lines Other hypotony, aqueous flare, miosis) or other
the third eyelid. Ligneous conjunctivitis—rare, young female intraocular disease (e.g., cataracts, lens luxation).
Dobermans may be predisposed. • Consider nasolacrimal duct flush if fluorescein
PATHOPHYSIOLOGY
• Primary—allergic, infectious, environmental. Secondary to Adnexal Disease stain did not pass to nares. • Conjunctival
• Secondary to other ocular disease—kerato- • Aqueous tear film deficiency (KCS) or cytology—lymphocytes and plasma cells
conjunctivitis sicca (KCS), entropion, qualitative tear deficiency. • Eyelid diseases— diagnostic for lymphocytic/plasmacytic
distichiasis. entropion, ectropion, medial canthal pocket conjunctivitis; eosinophils in allergic
syndrome, eyelid mass. • Hair or eyelash conjunctivitis; degenerate neutrophils and
SYSTEMS AFFECTED disorders—trichiasis, distichiasis, ectopic cilia. intracellular bacteria with bacterial infection;
Ophthalmic • Exposure—facial nerve paralysis, lagoph- rarely distemper virus intracytoplasmic
GENETICS thalmos. • Dacryocystitis or nasolacrimal inclusions. • Conjunctival biopsy—may be
N/A system outflow obstruction (e.g., obstructed useful with mass lesions and nodular episcleritis
duct or imperforate punctum). or chronic undiagnosed disease. • PCR or viral
INCIDENCE/PREVALENCE isolation testing for canine herpesvirus-1.
Common Referred Inflammation from Other • Intradermal skin testing—if suspect allergic
GEOGRAPHIC DISTRIBUTION Ocular or Periocular Diseases conjunctivitis.
N/A • Ulcerative keratitis. • Nodular episcleritis.
• Anterior uveitis. • Glaucoma. • Orbital PATHOLOGIC FINDINGS
SIGNALMENT disease. • Pyoderma. • Biopsy—inflammation, may note infectious
Species
agents, neoplasia, or nodular episcleritis.
RISK FACTORS • Ligneous conjunctivitis—thick, amorphous
Dog Atopy, KCS. eosinophilic hyaline-like material.
Breed Predilection
Breeds predisposed to allergic or immune-
mediated skin diseases (e.g., atopy) tend to have
more problems with allergic conjunctivitis or
KCS.
DIAGNOSIS TREATMENT
DIFFERENTIAL DIAGNOSIS APPROPRIATE HEALTH CARE
Mean Age and Range
• Distinguish primary conjunctivitis from • Primary—outpatient. • Secondary to other
N/A
secondary conjunctival hyperemia. • Thorough disease (e.g., ulcerative keratitis, uveitis,
Predominant Sex systematic ophthalmic exam identifies other glaucoma, lens luxation)—may require
None potential diseases (e.g., KCS, ulcers, uveitis, hospitalization to address underlying
SIGNS glaucoma, orbital disease); assess pupil size and ophthalmic issue.
• Blepharospasm. • Conjunctival hyper- symmetry, look for aqueous flare, attempt globe
retropulsion, perform Schirmer tear test, NURSING CARE
emia. • Ocular discharge—serous, mucoid, • Irritant-induced conjunctivitis—flush ocular
or mucopurulent. • Chemosis. • Follicle intraocular pressure measurement, and
fluorescein staining. • Deeper, darker, more surfaces and remove foreign body if observed.
formation on posterior third eyelid surface. • Allergic or follicular conjunctivitis—apply
• Enophthalmos and third eyelid elevation. linear and immobile blood vessel injection
indicates congested episcleral vasculature due to viscous artificial tear gel to both eyes before
CAUSES episcleritis or intraocular disease. • Mass biopsy patient is active outdoors (q8–12h), then flush
will differentiate conjunctival neoplasia (rare: ocular surface with eye wash when returning
Infectious
squamous cell carcinoma, melanoma, indoors to remove “trapped” allergens.
• Bacterial—rare as primary condition,
hemangioma/sarcoma, lymphoma, papilloma, • Secondary to ectropion or medial canthal
usually secondary to KCS; conjunctivitis
mast cell tumor) or episcleritis. pocket syndrome—flush ocular surface with
neonatorum involves accumulation of
eye wash daily to remove dust, dirt, or other
exudates under closed eyelids prior to natural CBC/BIOCHEMISTRY/URINALYSIS matter that collects ventrally. • Warm pack
opening. • Viral—canine herpes virus-1, Normal unless systemic disease. eyelids and periocular skin to soften crusted
canine distemper virus, or canine adenovi-
OTHER LABORATORY TESTS secretions and improve comfort.
rus-2. • Parasitic—Leishmania, Onchocerca,
or Thelazia. • Conjunctival manifestation of N/A ACTIVITY
systemic infectious disease IMAGING • No restriction for most. • Suspected contact
N/A irritant or allergic disease—prevent contact with
Immune-Mediated
offending agent. • Do not expose patients with
• Allergic—especially in atopic patients. DIAGNOSTIC PROCEDURES infectious viral disease to susceptible animals.
• Follicular conjunctivitis—common in • Adnexal examination—rule out facial nerve
dogs <18 months, secondary to chronic paralysis, lagophthalmos, eyelid abnormalities, DIET
antigenic stimulation. • Lymphocytic/ hair or eyelash disorders, and foreign bodies in • No change for most. • Suspected underlying
plasmacytic conjunctivitis—especially in cul-de-sacs or under third eyelid. • Schirmer tear skin disease and/or food allergy—food
German shepherd dogs with or without test—rule out KCS; perform before anything elimination diet trial.
Conjunctivitis—Dogs (continued)
CLIENT EDUCATION Immune-Mediated EXPECTED COURSE AND PROGNOSIS

C • When solutions and ointments are prescribed, • Depends on severity. • Allergic and • Good prognosis when underlying cause
the client should use solution(s) before follicular conjunctivitis—attempt nursing identified and treated (e.g., KCS, adnexal disease,
ointment(s) and wait 5 minutes between care first with viscous artificial tear gel eyelash disorder). • Bacterial—usually resolves
treatments. • If copious discharge is noted, lubricants and ocular flushing q8–12h; if with appropriate antibiotics; may depend on
clean eyes before giving medication. • Call for nonresponsive consider antihistamine eye control of underlying disease (e.g., KCS).
instructions if condition fails to improve or drops (e.g., ketotifen) q8–12h, or topical • Allergic or follicular—nursing care or medical
worsens. • An Elizabethan collar should be corticosteroid (e.g., dexamethasone) q8–12h. treatment may be needed during peak allergy
placed on the patient to prevent self-trauma. • Lymphocytic/plasmacytic conjunctivi- times. • Lymphocytic/plasmacytic—tend to be
SURGICAL CONSIDERATIONS tis—0.1% dexamethasone q8h, then taper controlled and not cured; may require chronic
• Follicular conjunctivitis—if follicles are
gradually to lowest effective dose; could treatment at lowest level possible.
unresponsive to medication, consider debride- attempt transition to cyclosporine 0.2%
ment. • Entropion, distichia, ectopic cilia, or ointment, cyclosporine 1–2% compounded
other eyelid disease—perform temporary or solution q12–24h, or tacrolimus 0.03%
compounded solution q12–24h. • Treatment
permanent surgery depending on findings,
of any underlying disease (e.g., atopy) often MISCELLANEOUS
signalment, and history. • Nasolacrimal duct
improves clinical signs of allergic conjunc- ASSOCIATED CONDITIONS
obstruction—if repeated flushing attempts at
tivitis. • Atopy. • Pyoderma.
weekly intervals along with medical therapy are
unsuccessful, consider contrast study and Tear Deficiencies AGE-RELATED FACTORS
surgery (see Epiphora). • Conjunctival • Aqueous tear film deficiency (see N/A
neoplasia—depending on tumor type and Keratoconjunctivitis Sicca). • Qualitative tear ZOONOTIC POTENTIAL
extent of involvement, may involve local deficiency—cyclosporine 0.2% ointment, N/A
excision and adjunctive therapy (β-irradiation, cyclosporine 1–2% compounded solution
cryotherapy), enucleation, or exenteration. q12h, or tacrolimus 0.03% compounded PREGNANCY/FERTILITY/BREEDING
solution q12–24h, and viscous artificial tear Use topical and systemic medications with
lubricants q6–12h. caution, if at all, in pregnant animals.
CONTRAINDICATIONS SEE ALSO
MEDICATIONS Topical corticosteroids—avoid if corneal • Epiphora.
ulceration is present, patient is at high risk for • Keratoconjunctivitis Sicca.
DRUG(S) OF CHOICE ulceration (e.g., entropion, lagophthalmos, • Red Eye.
Bacterial severe KCS), or with known or suspected ABBREVIATIONS
• Initial treatment—broad-spectrum topical infectious conjunctivitis. • KCS = keratoconjunctivitis sicca.
triple antibiotic q6–8h continuing several PRECAUTIONS
days past resolution of clinical signs; revise Suggested Reading
• Topical medications may be irritating. • Topical Hendrix DVH. Diseases and surgery of the
based on bacterial culture and sensitivity corticosteroids—monitor all patients carefully for
results. • Systemic antibiotic (e.g., cephalo- canine conjunctiva and nictitating
signs of corneal ulceration; discontinue agent membrane. In: Gelatt KN, Gilger BC,
sporin)—occasionally indicated, especially for immediately if corneal ulceration occurs.
more generalized disease (e.g., pyoderma). Kern T, eds., Veterinary Ophthalmology,
POSSIBLE INTERACTIONS 5th ed. Ames, IA: Wiley-Blackwell, 2013,
Neonatal pp. 945–975.
N/A
Carefully open eyelid margins (medial to Maggs DJ, Miller PE, Ofri R. Slatter’s
lateral), establish drainage, and treat with ALTERNATIVE DRUG(S) Fundamentals of Veterinary
topical antibiotic ointment q6–8h. Other corticosteroids—1% prednisolone Ophthalmology, 6th ed. St. Louis, MO:
acetate, betamethasone, hydrocortisone. Elsevier, 2018, pp. 158–177.
Herpetic
• Condition usually mild and self-limiting. Author Rachel A. Allbaugh
• Antiviral treatment—indicated for severe Consulting Editor Kathern E. Myrna
intractable canine herpesvirus-1 conjunc
tivitis or herpetic keratitis. • 0.15% FOLLOW-UP
ganciclovir gel—topical q4h for 7 days, Client Education Handout
PATIENT MONITORING available online
then q8h. • 1% trifluridine solution— Recheck shortly after beginning treatment (at
topical q4h for 2 days, then q6h. • 0.1% 5 days), then recheck in 2 weeks or as needed.
idoxuridine solution (compounding
pharmacies)—topical q4h for 2 days, then PREVENTION/AVOIDANCE
q6h. • 0.5% cidofovir solution Treat any underlying disease that may be
(compounding pharmacies)—topical q12h; exacerbating the conjunctivitis (e.g., KCS,
generally avoided: reduces duration of allergic or immune-mediated skin disease).
shedding but may worsen clinical disease POSSIBLE COMPLICATIONS
due to local ocular toxic effects. N/A
Constipation and Obstipation
• Other findings depend on underlying
cause. • Rectal examination may reveal mass, C
stricture, perineal hernia, anal sac disease,
B ASICS foreign body or material, prostatic enlarge- DIAGNOSIS
DEFINITION ment, or narrowed pelvic canal. DIFFERENTIAL DIAGNOSIS
• Constipation is defined as infrequent, CAUSES • Dyschezia and tenesmus (e.g., caused by
incomplete, or difficult defecation with colitis or proctitis)—unlike constipation,
passage of hard or dry feces. This does not Dietary associated with increased frequency of
imply abnormal motility or loss of function. • Bones. • Hair. • Foreign material. • Excessive attempts to defecate and frequent production
• Obstipation denotes intractable constipation fiber. • Inadequate water intake. of small amounts of liquid feces containing
that has failed several consecutive treatments; Environmental blood and/or mucus; rectal examination
defecation is impossible in the obstipated • Lack of exercise. • Change of environment— reveals diarrhea and lack of hard stool.
patient. hospitalization, dirty litter box. • Inability to • Stranguria (e.g., caused by cystitis/
PATHOPHYSIOLOGY ambulate. urethritis)—unlike constipation, can be
• Constipation can develop with any disease
associated with hematuria and abnormal
Drugs
that impairs the passage of feces through the findings on urinalysis (pyuria, crystalluria,
• Anticholinergics. • Antihistamines.
colon. Potential causes include congenital bacteruria).
• Opioids. • Barium sulfate. • Sucralfate.
vertebral malformation, spinal cord disease, • Antacids. • Kaopectolin. • Iron supple- CBC/BIOCHEMISTRY/URINALYSIS
pelvic canal narrowing (trauma), rectal mass ments. • Diuretics. • Usually unremarkable. • May detect
lesions causing obstruction, and perianal disease hypokalemia, hypercalcemia. • High packed
Painful Defecation (Dyschezia)
causing painful defecation. Often in cats no cell volume (PCV) and total protein in
• Anorectal disease—anal sacculitis, anal sac
underlying etiology can be identified. • Delayed dehydrated patients. • High white blood cell
abscess, perianal fistula, anal stricture, anal
fecal transit allows removal of additional salt and (WBC) count in patients with severe
spasm, rectal foreign body, rectal prolapse,
water, producing drier feces. Clinical signs are obstipation secondary to bacterial or
proctitis. • Trauma—fractured pelvis,
attributable to dehydration and potential endotoxin translocation, abscess, perianal
fractured limb, dislocated hip, perianal bite
toxemia resulting from fecal retention. fistula, prostatic disease. • Pyuria and
wound or laceration, perineal abscess.
• Peristaltic contractions may increase during hematuria with prostatitis.
constipation, but eventually motility diminishes Mechanical Obstruction
because of smooth muscle degeneration • Extraluminal—healed pelvic fracture with
• If patient is hypercholesterolemic, consider
secondary to chronic overdistension. narrowed pelvic canal, prostatic hypertrophy,
thyroid panel to rule out hypothyroidism. • If
prostatitis, prostatic neoplasia, intrapelvic
SYSTEMS AFFECTED patient is hypercalcemic, consider parathyroid
neoplasia, sublumbar lymphadenopathy.
Gastrointestinal. hormone assay.
• Intraluminal and intramural—colonic or
GENETICS rectal neoplasia or polyp, rectal stricture, IMAGING
N/A rectal foreign body, rectal diverticulum, • Abdominal radiography documents
INCIDENCE/PREVALENCE perineal hernia, rectal prolapse, congenital severity of colonic impaction. Other findings
Common clinical problem in older cats; less defect (atresia ani). may include colonic or rectal foreign body,
common in dogs. colonic or rectal mass, prostatic enlarge-
Neuromuscular Disease
ment, fractured pelvis, dislocated hip, or
GEOGRAPHIC DISTRIBUTION • Central nervous system—paraplegia, spinal
perineal hernias. • Pneumocolon (after
N/A cord disease, intervertebral disc disease,
enemas to clean colon) may better define
cerebral disease (lead toxicity, rabies).
SIGNALMENT intraluminal mass or stricture.
• Peripheral nervous system—dysautonomia,
• Ultrasonography may help define
Species sacral nerve disease, sacral nerve trauma (e.g.,
extraluminal mass and prostatic disease.
• Dog and cat. • More common in cat. tail fracture/pull injury). • Colonic smooth
muscle dysfunction—idiopathic megacolon DIAGNOSTIC PROCEDURES
Breed Predilections Colonoscopy may be needed to identify a
in cats.
N/A mass, stricture, or other colonic or rectal
Metabolic and Endocrine Disease
Mean Age and Range lesion; rectal/colonic mucosal biopsy
• Impaired colonic smooth muscle
Any age; most common in older cats. specimens should always be obtained.
function—hyperparathyroidism, hypothy-
Predominant Sex roidism, hypokalemia (chronic renal PATHOLOGIC FINDINGS
N/A failure), hypercalcemia. • Debility— Dependent on underlying disease process.
SIGNS general muscle weakness, dehydration,
neoplasia.
Historical Findings
• Reduced, absent, or painful defecation. RISK FACTORS
• Hard, dry feces. • Small amount of • Manx cats may be predisposed due to TREATMENT
liquid, mucoid stool, sometimes with vertebral (sacral) abnormalities. • Drug
blood present produced after prolonged therapy—anticholinergics, narcotics, barium
• Remove or ameliorate any underlying cause
tenesmus. • Occasional vomiting, sulfate. • Metabolic disease causing dehydra-
if possible. • Discontinue any medications
inappetence, and/or lethargy. tion. • Feline dysautonomia. • Intact
that may cause constipation. • May need to
male—perineal hernia, benign or infectious
Physical Examination Findings treat as inpatient if obstipation and/or
prostatic disease. • Castrated male—prostatic
• Colon filled with hard feces. Severe dehydration present.
neoplasia. • Perianal fistula.
impaction may cause abdominal distention.
Constipation and Obstipation (continued)
NURSING CARE modifiers can be administered—cisapride and ulceration can lead to fecal
C Dehydrated patients should receive IV (dogs: 0.3–0.5 mg/kg PO q8–12h; cats: incontinence.
(preferably) or SC balanced electrolyte 2.5–10 mg/cat PO q8–12h) may stimulate EXPECTED COURSE AND PROGNOSIS
solutions (with potassium supplementation if colonic motility; indicated with early • Fair to good prognosis with early diagnosis
indicated). megacolon. and intervention. • Recurring bouts of
ACTIVITY CONTRAINDICATIONS constipation/obstipation may occur
Encourage activity. • Lubricants such as mineral oil and white dependent on underlying cause.
petrolatum are not recommended because of
DIET the danger of fatal lipid aspiration pneumonia
Dietary supplementation with a bulk-forming due to their lack of taste. • Fleet (sodium
agent (bran, methylcellulose, canned phosphate) enemas. • Anticholinergics.
pumpkin, psyllium) is often helpful, though • Diuretics.
MISCELLANEOUS
they can sometimes worsen colonic fecal ASSOCIATED CONDITIONS
distension; in this instance, feed a low-residue PRECAUTIONS
Vomiting—with severe/prolonged
diet. Cisapride and cholinergics—can be used with
obstipation.
caution; contraindicated in obstructive
CLIENT EDUCATION processes. Avoid the use of metoclopramide AGE-RELATED FACTORS
• Feed appropriate diet and encourage because it does not affect the colon. N/A
activity. • Survey cat boxes daily to ensure POSSIBLE INTERACTIONS ZOONOTIC POTENTIAL
level of defecation activity. N/A N/A
SURGICAL CONSIDERATIONS ALTERNATIVE DRUG(S) PREGNANCY/FERTILITY/BREEDING
• Manual removal of feces through the anus • Ranitidine causes contraction of colonic N/A
with the animal under general anesthesia smooth muscle in vitro. • Misoprostol causes
(after rehydration) may be required if enemas SYNONYMS
contraction of colonic smooth muscle in • Colonic impaction. • Fecal impaction.
and medications are unsuccessful. • Subtotal vitro. • Newer-generation cisapride-like drugs
colectomy may be required with recurring may be available soon. • One recent pilot SEE ALSO
obstipation that responds poorly to assertive study using multistrain probiotic SLAB51® Megacolon
medical therapy. showed clinical improvement in a feline ABBREVIATIONS
cohort having chronic constipation and • PCV = packed cell volume.
idiopathic megacolon. • WBC = white blood cell.
Suggested Reading
MEDICATIONS Chandler M. Focus on nutrition: dietary
DRUG(S) OF CHOICE management of gastrointestinal disease.
• Emollient laxatives—docusate sodium or FOLLOW-UP Compend Contin Educ Vet 2013,
docusate calcium (dogs: 50–100 mg PO PATIENT MONITORING 35(6):E1–E3.
q12–24h; cats: 50 mg PO q12–24h). Monitor frequency of defecation and stool Rossi G, Jergens A, Cerquetella M, et al.
• Stimulant laxatives—bisacodyl (5 mg/ consistency at least twice a week initially, then Effects of a probiotic (SLAB51™) on clinical
animal PO q8–24h). Ensure that animal is weekly or biweekly in response to dietary and histologic variables and microbiota of
not obstructed prior to use of stimulant and/or drug therapy. cats with chronic constipation/megacolon:
laxatives. • Saline laxatives—isosmotic a pilot study. Benef Microbes 2018,
mixture of polyethylene glycol and poorly PREVENTION/AVOIDANCE 9:101–110.
absorbed salts; usually administered as a Keep pet active and feed appropriate diet. Tam FM, Carr AP, Myers SL. Safety and
trickle amount via nasoesophageal tube over Subcutaneous fluids to ensure hydration can palatability of polyethylene glycol 3350 as
6–12h. • Disaccharide laxative—lactulose help reduce frequency of constipation, an oral laxative in cats. J Feline Med Surg
(1 mL/4.5 kg PO q8–12h to effect). • Warm particularly in cats. 2011, 13(10):694–697.
water enemas may be needed; a small POSSIBLE COMPLICATIONS Author Albert E. Jergens
amount of mild soap or docusate sodium • Chronic constipation or recurrent Consulting Editor Mark P. Rondeau
can be added but is usually not needed; obstipation can lead to acquired megacolon.
sodium phosphate retention enemas (e.g., • Overuse of laxatives and enemas can
Fleet®) are contraindicated because of their cause diarrhea. • Colonic mucosa can be lient Education Handout
C
association with severe hypocalcemia. damaged by improper enema technique, available online
• Suppositories can be used as a replacement repeated rough mechanical breakdown of
for enemas; use glycerol, bisocodyl, or feces, or ischemic necrosis secondary to
docusate sodium products. • Motility pressure of hard feces. • Perineal irritation
Contact Dermatitis
C
BASICS DIAGNOSIS FOLLOW-UP
OVERVIEW DIFFERENTIAL DIAGNOSIS PREVENTION/AVOIDANCE
• Irritant and allergic contact dermatitis—rare • Hypersensitivity dermatitis. • Drug reaction. Remove offending substances from the
syndromes with similar clinical signs but • Pelodera dermatitis. • Hookworm dermatitis. environment.
different pathophysiology; differentiation may be • Pyoderma. • Malassezia dermatitis.
more conceptual. • Irritant contact dermatitis • Demodicosis. • Solar dermatitis. • Thermal
(ICD)—direct damage to keratinocytes by injuries. • Trauma from rough surfaces. ICD
exposure to particular irritant or sensitizer • Acute condition—may occur after only one
DIAGNOSTIC PROCEDURES exposure; can be manifested within 24 hours of
induces inflammatory response directed at skin • ACD—closed-patch test (corticosteroids
without prior sensitization. • Allergic contact exposure. • Corticosteroids rarely helpful.
and nonsteroidal anti-inflammatory drugs • Lesions resolve 1–2 days after irritant removal.
dermatitis (ACD)—type IV (delayed) hypersen- [NSAIDs] must be discontinued for 3–6
sitivity: immunologic event requiring sensitiza- weeks); materials taken from environment or ACD
tion and elicitation; Langerhans cells and home applied to upper thorax skin under • Requires chronic exposure for hypersensitivity
keratinocytes interact with environmental bandage; examine for erythema, edema, to develop. • Reexposure results in development
haptens to create antigens, leading to sensitiza- pruritus at 48, 72 hours, and 7 days. of clinical signs within 1–5 days; signs may
tion of T-lymphocytes and activation following • ICD—eliminate exposure to contact irritant persist for several weeks. • Responds well to
reexposure with release of cytokines (mainly or antigen, followed by provocation. • Open corticosteroids; pruritus returns after discon-
tumor necrosis factor alpha • [TNF-α], patch test—apply substance to inside pinnae; tinuation if antigenic stimulus persists.
IL1βGM-CSF). • Recent reports blur monitor for mild erythema, edema, pruritus; • Hyposensitization not effective. • Prognosis—
distinction between ICD, ACD, and atopic examine daily for 5–15 days. • Human patch good if allergen is identified and removed,
dermatitis. test kits (TRUE Test®). • Skin biopsy. otherwise poor: may require lifelong treatment.
SIGNALMENT PATHOLOGIC FINDINGS
• ICD—Any age as direct result of irritation • Intraepidermal vesiculation and spongiosis;
from offending chemical. • ACD—older dogs; superficial dermal edema with perivascular
chronic exposure to antigen (months to years); mononuclear cell infiltrate in ICD and ACD; MISCELLANEOUS
extremely rare in cats, (except exposure to polymorphonuclear cell infiltrate in ICD; ABBREVIATIONS
d-limonene-containing insecticides). • ACD— leukocyte exocytosis common. • Lymphocytic • ACD = allergic contact dermatitis.
German shepherd dog, poodle, wirehaired fox spongiotic or eosinophilic and lymphocytic • ICD = irritant contact dermatitis.
terrier, Scottish terrier, West Highland white spongiotic infiltrate with intraepidermal • NSAID = nonsteroidal anti-inflammatory
terrier, Labrador and golden retriever. eosinophilic pustules in canine ACD. drug.
SIGNS • TNF-α = tumor necrosis factor alpha.
Lesions Suggested Reading

• Location determined by antigen contact; Ho KK, Campbell KL, Lavergne SN. Contact
commonly limited to glabrous skin and
TREATMENT dermatitis: a comparative and translational
• Eliminate offending substance(s). • Bathe review of the literature. Vet Dermatol 2015;
regions frequently in direct contact with the
with hypoallergenic shampoos to remove 26:314–327.
environment. • Extreme erythroderma stops
antigen from skin. • Create mechanical Author Liora Waldman
abruptly at hairline. • Initial erythema,
barriers, if possible—socks, shirts, restriction Consulting Editor Alexander H. Werner
edema, and papules leading to crusts and
from environment. Resnick
excoriations; lichenification and hyperpigmen-
tation with chronicity; vesicles uncommon.
Others
• Localized reactions to topical medications.
• Generalized reactions to shampoos or MEDICATIONS
insecticide sprays. • Pruritus—moderate to DRUG(S) OF CHOICE
severe (most common). • Seasonal incidence • Prednisolone (1 mg/kg PO q24h for 5–7
may indicate plant or outdoor antigen. days, then q48h for 2 weeks). • Topical
corticosteroids for focal lesions. • Topical
CAUSES & RISK FACTORS tacrolimus. • Pentoxifylline (10–25 mg/kg
• Reported offending substances—plants,
PO q8–12h initially). • Cyclosporine
mulch, cedar chips, fabrics, rugs, carpets, (modified, 5 mg/kg q24h).
plastics, rubber, leather, nickel, cobalt,
concrete, soaps, detergents, floor waxes, epoxy CONTRAINDICATIONS/POSSIBLE
resin, carpet and litter deodorizers, herbicides, INTERACTIONS
fertilizers, insecticides (including topical flea Pentoxifylline—do not administer with
treatments), flea collars, topical preparations alkylating agents, cisplatin, or amphotericin B;
(neomycin). • Increased incidence with cimetidine may increase serum levels of
atopic disease. pentoxifylline.
Coonhound Paralysis (Acute Polyradiculoneuritis)

Breed Predilections
C • CHP—Coonhounds; any breed in contact
with raccoons susceptible. • ACIP, postvac-
BASICS cinal polyradiculoneuritis—none. DIAGNOSIS
DEFINITION Mean Age and Range DIFFERENTIAL DIAGNOSIS
• Acute inflammatory disorder involving the N/A • Other acute polyneuropathy (i.e., paraneo-
axons and myelin of nerve roots, spinal plastic neuropathy). • Distal denervating
nerves, and peripheral nerves in dogs, with or Predominant Sex disease. • Botulism. • Tick bite paralysis.
without a previous history of contact with N/A • Fulminant myasthenia gravis. • Black
raccoon saliva, vaccination, or a gastrointesti- SIGNS widow spider bite envenomation, coral snake
nal or respiratory infection. • Proposed Historical Findings envenomation. • Intoxications (lasalocid,
animal model for Guillain-Barré syndrome in • Appear 7–14 days after contact with
blue-green algae). • Generalized (diffuse) or
humans. raccoon saliva (bite or scratch), receipt of multifocal myelopathy (involving both
PATHOPHYSIOLOGY vaccination, or development of respiratory or cervical and lumbosacral intumescences).
• Etiology uncertain, appears to be immune gastrointestinal infection. • Initial signs— CBC/BIOCHEMISTRY/URINALYSIS
mediated. • Immune-mediated inflammation stiff, stilted gait in all limbs, typically starting Usually normal.
develops 7–14 days after antecedent event in the pelvic limbs and eventually progressing OTHER LABORATORY TESTS
(delayed hypersensitivity reaction?). to the thoracic limbs. • Rapid progression • Serum immunoglobulins (Ig)—high serum
• Thought to be the dog’s immune system (2–4 days) to a flaccid, lower motor neuron IgG but not IgM in some patients.
reaction to a cross-reacting antigen (suspect tetraparesis to tetraplegia. • Owners may • Immunologic—serum reaction to raccoon
molecular mimicry phenomenon between notice loss or change of voice. • Appetite and saliva on ELISA; dogs with CHP have a strong
external antigen and gangliosides from dog’s water consumption—usually normal. positive reaction that decreases in intensity
neural tissue, with the development of • Urination and defecation—normal. over time; dogs without disease but with
antiganglioside autoantibodies). • Coonhound • Progressive phase of the disease—clinical raccoon contact have a strong positive reaction;
paralysis (CHP)—antecedent event is recent signs can continue to worsen up to 5–10 days dogs with ACIP but with no raccoon contact
contact with raccoon saliva. • Acute canine after onset. have a negative reaction. • Immunologic—for
idiopathic polyradiculoneuritis (ACIP)— Neurologic Examination Findings dogs with ACIP, identification of anti-GM2
affected dogs with identical clinical signs to • Usually symmetric. • Stiff, stilted gait that ganglioside antibodies reached a diagnostic
those with CHP but without a history of usually progresses rapidly to lower motor sensitivity of 60% and a specificity of 97%.
raccoon exposure; may have history of recent neuron tetraparesis or tetraplegia; some dogs
respiratory or gastrointestinal infection. IMAGING
may remain ambulatory tetraparetic. Thoracic radiographs and abdominal
• Postvaccinal polyradiculoneuritis—ante-
• Generalized hyporeflexia to areflexia, with ultrasound—normal.
cedent event is recent vaccination (rare). the exception of a normal perineal reflex.
• Toxoplasma gondii infection—dogs with DIAGNOSTIC PROCEDURES
• Generalized hypotonia to atonia, severe
ACIP more likely to have positive titers than neurogenic muscle atrophy. • Affected dogs
control dogs (possible triggering factor?). Cerebrospinal Fluid Analysis
often show inability to hold the head up. • Lumbar—high protein without an increase
SYSTEMS AFFECTED • Aphonia or dysphonia common; no in leukocytes at all stages of disease. • Albumin
• Peripheral nervous system—most severe megaesophagus. • Facial paresis—bilateral leakage across the disrupted blood–nerve
involvement in the ventral (motor) nerve incomplete palpebral closure in some barrier of the affected ventral nerve roots is the
roots and ventral root components of the patients. • Respiration—labored in severely primary cause of the protein increase.
spinal nerves; lumbosacral nerve roots affected dogs; occasional progression to
Electrodiagnostics
affected more severely than cervical and respiratory paralysis. • Pain sensation intact;
• Electromyography (EMG)—generalized
thoracic nerve roots. • Cranial nerves—nerve hyperesthesia common—may reflect variable
spontaneous activity (fibrillation potentials
VII often affected; nerves IX, X occasionally dorsal nerve root inflammation. • Motor
and positive sharp waves) consistent with
affected. • Respiratory failure—secondary to dysfunction—always predominates; even
denervation; EMG normal in first 4–5
intercostal and/or phrenic nerve involvement tetraplegic patient can usually wag its tail.
days. • Markedly low compound muscle
in some patients. • Mental status, urination, and defecation—
action potential amplitudes after motor
GENETICS unaffected.
nerve stimulation. • F waves (late waves
No proven basis. CAUSES that indicate proximal motor nerve and
INCIDENCE/PREVALENCE • CHP—contact with a raccoon; perhaps more ventral nerve root function)—prolonged
• Most commonly recognized acute poly- important, contact with raccoon saliva. minimum latencies, increased F ratio,
neuropathy in dogs. • Low incidence. • ACIP—none proven; possibly previous decreased amplitudes. • Motor nerve
respiratory or gastrointestinal viral or bacterial conduction velocities—usually normal;
GEOGRAPHIC DISTRIBUTION infection. • Postvaccinal polyradiculoneuritis— severely affected patients may have mildly
• CHP—relative to distribution of raccoons recent vaccination (rare). decreased values. • Sensory nerve func-
(e.g., North and Central America; parts of tion—usually normal. • Abnormalities
South America). • ACIP—worldwide. RISK FACTORS
• CHP—coonhounds tend to be predisposed provide evidence of severe peripheral motor
SIGNALMENT primarily because of the nature of their activities; axonopathy (more severe in proximal
previous disease does not confer immunity and portions of nerves and ventral nerve roots),
Species
may increase risk of redevelopment; multiple along with demyelination in the proximal
Dog, very occasionally cat.
bouts not uncommon. • ACIP—unknown. motor nerves and ventral nerve roots.
(continued) Coonhound Paralysis (Acute Polyradiculoneuritis)

PATHOLOGIC FINDINGS SURGICAL CONSIDERATIONS
• Ventral nerve roots and the ventral root N/A C
components of the spinal nerves—most
severe lesions, various degrees of axonal MISCELLANEOUS
degeneration, paranodal and segmental ASSOCIATED CONDITIONS
demyelination, and leukocyte infiltration N/A
(predominantly monocytes and macrophages).
M EDICATIONS
DRUG(S) OF CHOICE AGE-RELATED FACTORS
• Peripheral nerves—affected to a lesser
• None proven effective. • Immunoglobulin— N/A
degree; might be normal. • Dorsal nerve
roots—much less severely affected. 1 g/kg IV daily for 2 consecutive days, 0.5 g/ ZOONOTIC POTENTIAL
kg IV daily for 3 consecutive days, or 0.4 g/kg N/A
IV daily for 5 consecutive days; given early PREGNANCY/FERTILITY/BREEDING
may shorten recovery time in ACIP. Unknown effect on the fetuses of an affected
T REATMENT CONTRAINDICATIONS bitch.
Corticosteroids—do not improve clinical signs SYNONYMS
APPROPRIATE HEALTH CARE or shorten course of disease; may reduce survival
• Inpatient—closely monitor patients in the Coondog paralysis.
in humans with Guillain-Barré syndrome.
progressive phase of the disease (especially during SEE ALSO
first 5 days) for respiratory problems. • Severe PRECAUTIONS • Botulism.
respiratory compromise—mechanical ventilation Monitor for possible adverse reactions • Myasthenia Gravis.
as required. • IV fluid therapy—administer if (anaphylaxis, hematuria) after IV immuno- • Polyneuropathies (Peripheral Neuropathies).
patient is dehydrated. • Outpatient—once globulin administration. • Tick Bite Paralysis.
patient is stable and the progressive phase of the
disease is over. ABBREVIATIONS
• ACIP = acute canine idiopathic
NURSING CARE polyradiculoneuritis.
• Patients are usually able to eat and drink; F OLLOW-UP
• CHP = coonhound paralysis.
hand feed in sternal position until able to PATIENT MONITORING • EMG = electromyography.
reach food and water. • Intensive physical • Outpatient—keep in close contact with • Ig = immunoglobulin.
therapy—important to decrease muscle client regarding complications or changes in
atrophy; severe neurogenic muscle atrophy is the patient’s condition. • Urinalysis—perform Suggested Reading
inevitable. • Frequent turning and excellent periodically to check for cystitis in tetraplegic Añor S. Acute lower motor neuron tetraparesis.
padding—essential to prevent pressure sores. or severely tetraparetic patients. • Ideally, Vet Clin North Am Small Anim 2014,
reevaluate at least every 2 weeks. 44:1201–1222.
ACTIVITY Cuddon PA. Electrophysiologic assessment of
Encourage as much movement as possible. PREVENTION/AVOIDANCE acute polyradiculoneuropathy in dogs:
• CHP—if possible, avoid contact with comparison with Guillain-Barré syndrome in
DIET
• No restrictions. • Make sure patient is able to
raccoons. • Postvaccinal polyradiculoneuritis—if people. J Vet Intern Med 1998, 12:294–303.
reach food and water. • Cervical weakness—may strong association with a specific vaccination, Cummings JF, de Lahunta A, Holmes DF,
need to hand feed patient in sternal position. avoid that particular vaccine in the future. Schultz RD. Coonhound paralysis: further
POSSIBLE COMPLICATIONS clinical studies and electron microscopic
CLIENT EDUCATION observations. Acta Neuropathol 1982,
• Respiratory paralysis—in progressive phase
• Inform client that good nursing care is
of disease. • Pressure sores, urine scalding, 56:167–178.
essential. • Discuss importance of prevent- Hirschvogel K, Jurina K, Steinberg TA, et al.
ing pressure sores and urine scalding and of cystitis—common in chronically recumbent
dogs. Clinical course of acute canine polyradicu-
limiting the degree of muscle atrophy by loneuritis following treatment with human
frequent daily physical therapy (passive limb EXPECTED COURSE AND PROGNOSIS IV immunoglobulin. J Am Anim Hosp
movement, swimming as the patient’s • Signs stabilize once progressive phase of
Assoc 2012, 48:299–309.
strength begins to improve). • Patient needs disease is over. • Most affected dogs recover Northington JW, Brown MJ. Acute canine
soft bedding that must be kept free of urine fully over 3–6 weeks; severely affected cases idiopathic polyneuropathy: a Guillain-
and feces, frequent turning (every 3–4 may take up to 3–4 months to recover; Barré-like syndrome in dogs. J Neurol Sci
hours), frequent bathing, and adequate incomplete recoveries can happen. 1982, 56:259–273.
nutrition. Author Paula Martín Vaquera
Copper Associated Hepatopathy

• Focal hepatitis initiated by Cu may progress • West Highland white terrier—maximum
C to chronic hepatitis, eventually cirrhosis. Cu accumulation observed by 12 months of
• Rarely, acute severe hepatic necrosis releases age and may vacillate or decline with clinical
BASICS Cu into systemic circulation causing disease at any time; however, some dogs with
DEFINITION hemolysis and/or acute-onset acquired high hepatic Cu survive to old age (15 years)
• Severe hepatic accumulation of copper (Cu) Fanconi syndrome (proximal renal tubular without evidence of liver injury.
causes acute or chronic hepatitis leading to injury causing euglycemic glucosuria). • Labrador retriever, Doberman pinscher,
cirrhosis or death from liver failure. SYSTEMS AFFECTED Dalmatian, other breeds—young adult to
• Mild to moderate hepatic Cu accumulation • Hepatobiliary—centrilobular hepatitis,
middle-aged at diagnosis for chronic hepatitis.
augments oxidative injury and increases risk for chronic hepatitis, eventual cirrhosis. • Doberman pinscher—often develop
liver disease caused by other hepatobiliary insults, • Hemic/lymphatic—hemolytic anemia rare
hepatitis with ALT increases and Cu
notably hepatotoxicity from nonsteroidal sequel to acute hepatic necrosis in dogs. accumulation at 1–3 years of age; clinical
anti-inflammatory drugs (NSAIDs). • Renal—rare reversible Fanconi syndrome
signs of liver disease often recognized by 5–7
• Primary copper associated hepatopathy causes euglycemic glycosuria, granular casts, years of age.
(CuAH) depicts copper accumulation in the ± clinicopathologic evidence of compromised Predominant Sex
absence of other liver disorders or as the major renal function. None
cause of liver injury.
• Secondary CuAH depicts Cu accumulation GENETICS SIGNS
caused by severe chronic cholestasis in cats • Autosomal recessive COMMD1 mutation in Historical Findings
(not dogs) or fulminant hepatic failure (rare). Bedlington terriers reduces biliary Cu excretion. • Primary CuAH—4 categories:
• Genetic primary CuAH—only proven in • Gene mutations remain unproven in other ◦ no clinical signs;
Bedlington terriers. breeds and in cats; gene associations may ◦ subclinical disease: increased ALT activity
• Acquired primary CuAH—most common modify susceptibility in Labrador retrievers, with no clinical illness;
canine cause of CuAH, reflects dietary Cu but no genetic test and liver biopsy remains ◦ acute disease associated with severe acute
availability in commercial dog food that gold standard for diagnosis of CuAH. hepatic necrosis;
exceeds individual’s tolerance limit. • Predisposition to CuAH recognized in ◦ chronic progressive hepatitis eventually
• Congenital primary CuAH (no gene mutation Labrador retriever, West Highland white terrier, evolving cirrhosis.
characterized)—comparatively rare in cats. Doberman pinscher, Dalmatian, keeshond, • Secondary CuAH accompanies feline
• Some animals with primary CuAH corgi, Staffordshire terrier, and other breeds. cholestatic necroinflammatory liver disease
accumulate Cu without histologic evidence of INCIDENCE/PREVALENCE (cholangiohepatitis) or rarely in dogs with
liver damage despite vacillating liver enzyme • Bedlington terrier—at one time up to 2/3 of fulminant liver necrosis.
activity (alanine aminotransferase [ALT] most dogs carried COMMD1 mutation; incidence • Acute signs—with extreme hepatic Cu
common); in absence of inflammation or significantly declined with genetic testing. accumulation, sudden-onset lethargy, anorexia,
hepatocyte necrosis, the term hepatopathy is • Prevalence of excess hepatic Cu remains high vomiting; may have rapid course, dogs
most correct. in West Highland white terrier, Labrador succumb despite intensive supportive care.
PATHOPHYSIOLOGY retriever, Doberman pinscher, and other breeds. • Chronic signs—variable, intermittent
• Hepatic Cu homeostasis involves complex • CuAH currently most common cause of lethargy, hyporexia, weight loss, vomiting,
regulatory system including protein transporters, chronically increased ALT activity in dogs diarrhea, with later polydipsia and polyuria;
chaperones, membrane receptors, intracellular (since mid-1990s) likely caused by increased eventual liver injury leads to ascites,
binding proteins, canalicular egress pumps; Cu Cu availability in manufactured dog foods. jaundice, bleeding tendencies, hepatic
absorbed from small intestine, stored in liver, • CuAH comprises ≥20% of liver biopsy encephalopathy (HE).
with excess excreted in bile. submissions for abnormal enzyme activity Physical Examination Findings
• A single gene mutation (COMMD1) causes in dogs. • Acute signs—lethargy, weakness, jaundice,
genetic primary CuAH in Bedlington terriers. • Primary congenital CuAH occurs in cats pallor (anemia), vomiting, diarrhea, dark
• More commonly, canine hepatic Cu but comparatively rare. urine (bilirubinuria); rare hemoglobinemia
accumulation reflects Cu intake exceeding GEOGRAPHIC DISTRIBUTION and hemoglobinuria if intravascular
capacity to maintain neutral Cu balance; Reported worldwide. Cu-mediated hemolysis.
suspected pharmacogenetic basis. • Chronic signs—weight loss, ascites,
SIGNALMENT
• Secondary CuAH reflects reduced jaundice, nodular microhepatia; melena and
canalicular Cu egress associated with severe Species petechial hemorrhage in animals with
cholestasis (cats only) or severe panlobular Dog and cat; more common in dog. significant panlobular injury.
liver injury (fulminant hepatic failure, rare). Breed Predilections CAUSES
• Primary CuAH—hepatocyte cytosolic Cu first Bedlington terrier, West Highland white • Genetic primary CuAH—single gene
accumulates in zone 3 (centrilobular region). terrier, Labrador retriever, Doberman mutation in Bedlington terriers.
• Secondary CuAH (cats)—hepatocyte pinscher, Dalmatian, Welsh corgi, keeshond, • Acquired primary CuAH—either
cytosolic Cu accumulates in zone 1 Staffordshire terrier with observed increased Bedlington mutation or suspected
(periportal) or adjacent to injured regions. incidence of high hepatic Cu concentrations; pharmacogenetic differences involving
• Hepatic Cu concentrations widely variable— no canine breed exempt. regulatory pathways influencing Cu
primary CuAH: range 500 to >10,000 μg/g
Mean Age and Range homeostasis, making them intolerant to
dry weight liver (DWL); secondary CuAH in
• Bedlington terrier—Cu slowly accumulates current levels of dietary Cu supplementation.
cats rarely exceeds 1,000 μg/g DWL.
to max at ∼6 years of age; dogs can be • Secondary acquired CuAH—necroinflamm-
• Cu accumulation causes oxidative membrane
clinically affected at any age; most present as atory chronic cholestatic liver disease in cats
injury—cell and organelles; high hepatic Cu
middle-aged to older dogs with chronic or diffuse severe panlobular injury in dogs or
concentration not always associated with
hepatitis. cats (rare).
histologic evidence of liver injury.
(continued) Copper Associated Hepatopathy

RISK FACTORS liver injury, remodeling, or portal hyper • Digital scanning of rhodanine-stained biopsy
• Primary—feeding diets or providing water tension associated with APSS. sections—validated against atomic absorption C
with Cu concentrations exceeding individual’s • Prolonged prothrombin time (PT), spectroscopy, accurately quantifies liver Cu
tolerance to maintain neutral Cu balance. activated partial thromboplastin time (Cornell University) on biopsy sections;
• Stress or concurrent illnesses may precip (APTT), activated clotting time (ACT), allows rhodanine staining of all sections to
itate acute illness in dogs with hepatocyte Cu mucosal bleeding time in severe liver injury. determine accurate hepatic Cu distribution
accumulation. • Rare increased serum Cu concentration— and quantification.
• Asymptomatic dogs with primary CuAH dogs with acute severe CuAH liver necrosis; Hepatic Cu Concentrations (DWL)
may become symptomatic when additional otherwise serum Cu does not reflect liver Cu • Normal hepatic Cu ≤400 μg/g.
disease processes or toxicities (e.g., NSAID concentrations; low-yield screening test. • Hepatic Cu concentration in dogs with
administration; CCNU chemotherapy) • Hepatic Cu measurements must be primary diet-induced or genetic CuAH (μg/g
impose oxidative challenge, expose hepato reconciled with histopathologic findings. DWL)—Bedlington terrier (COMMD1
cytes to inflammatory cytokines, or another • Genetic marker testing in Bedlington mutation): 850–12,000; West Highland white
primary liver disease develops. terrier—microsatellite markers or specific terrier: up to 3,500; Labrador retriever:
COMMD1 mutation; however, kindreds of 400–9,000; Doberman pinscher: 1,000–10,000;
Bedlington terriers with CuAH have had Dalmatian: 750–22,000; cat: 700–8,000.
negative PCR-based gene tests. • Avoid analytic methods “estimating” sample
DIAGNOSIS IMAGING hydration or reporting Cu on wet weight basis.
• Radiography—unremarkable in most dogs;
DIFFERENTIAL DIAGNOSIS PATHOLOGIC FINDINGS
small liver in chronic hepatic injury, poor • Cu accumulates in lysosomes and
• Acute diseases—infectious (e.g., infectious
abdominal detail if ascites. mitochondria in zone 3 (centrilobular)
canine hepatitis, leptospirosis, septicemia,
• Ultrasonography—early: normal hepatic hepatocytes in dogs.
suppurative bacterial cholangiohepatitis),
imaging; later: hyperechoic to heterogeneous • Oxidative injury—mechanism of hepato
acute hepatic necrosis, hepatic abscess,
nodular echogenicity; ascites in some cases. cellular injury.
drug- or toxin-induced hepatic injury, acute
pancreatitis, hepatic lymphoma, immune- DIAGNOSTIC PROCEDURES • In some cases, apparent immune-mediated
mediated hemolytic anemia, zinc toxicity. • Liver biopsy—gold standard diagnostic test; hepatitis accompanies CuAH injury.
• Chronic diseases—chronic hepatitis or confirms and characterizes liver injury; needle • Rhodanine Cu staining confirms affiliation
cholangiohepatitis of any other cause, drug- samples may not provide adequate liver lobe of Cu with histologic injury.
or toxin-induced liver injury, severe diffuse assessment as Cu is differentially distributed • Histologic features commonly include
glycogen-type vacuolar hepatopathy (dogs), across lobes and liver sections; biopsy at least formation of “copper granulomas” in areas of
infectious hepatitis, chronic obstructive 3 lobes. hepatocyte necrosis—reflects response to
biliary disease, chronic fibrosing pancreatitis, • Routine H&E staining—can overlook oxidatively mediated hepatocyte necrosis;
congenital portosystemic shunt, primary or pathologic Cu accumulation. adjacent copper-laden hepatocytes.
metastatic hepatic neoplasia. • Cu-specific staining—rhodanine (preferred); • Chronic untreated necroinflammatory
confirms Cu-protein aggregates, details zonal injury progresses to chronic hepatitis,
distribution. parenchymal extinction, liver fibrosis,
• CBC—may be normal; regenerative
• Semi-quantitative scoring system— eventually to cirrhosis and formation of
anemia, leukocytosis, neutrophilia if acute
estimates severity of Cu accumulation; APSS.
Cu-associated hemolysis; microcytic or
variation among interpreters confounds • CuAH causing necroinflammatory liver
normocytic, normochromic nonregenerative
comparisons between biopsy reports. injury leads to development of microhepatia,
anemia in chronic progressive liver injury;
• Cu measurements—can be completed on regenerative nodules, fibrotic “firm” liver
microcytosis usually reflects acquired
fresh, frozen, formalin fixed liver, liver tissue texture.
portosystemic shunting.
extracted from paraffin blocks, or liver sections.
• Biochemistry—increased liver enzymes
• Distribution of hepatocytes with cytosolic
(ALT, aspartate transaminase [AST],
Cu granules and quantification of Cu should
γ-glutamyl transferase [GGT], and alkaline
be reconciled—areas of dense fibrosis,
phosphatase [ALP] with increase in ALT >
parenchymal extinction, regenerative nodules
TREATMENT
ALP); hyperbilirubinemia in dogs with severe APPROPRIATE HEALTH CARE
contain lower Cu concentrations than
liver injury; increased ALT without clinical • Outpatient for most dogs.
unremodeled liver tissue; this phenomenon
signs increases suspicion for early or cyclic • Inpatient evaluation and treatment for dogs
causes discordance between measured and
CuAH necrosis. with hepatic failure or severe acute hepatitis.
assessed Cu accumulations.
• As hepatic function deteriorates—onset of • See Hepatitis, Chronic; Cirrhosis and
• In dogs with severe illness with high risk for
hypoalbuminemia, ± hyperglobulinemia, low Fibrosis of the Liver for detailed management
general anesthesia and liver biopsy, hepatic
blood urea nitrogen (BUN), hypoglycemia, of liver disease.
aspiration cytology with samples stained with
hypocholesterolemia.
rhodanine may identify Cu accumulation; NURSING CARE
• Urinalysis—usually normal, bilirubinuria
qualitative with variable accuracy; not • Animals in liver failure require fluid and
escalates with hyperbilirubinemia; hepatic
recommended method for definitive diagnosis. electrolyte correction; may require treatment for
insufficiency: dilute urine, ammonium
biurate crystalluria reflects acquired porto Cu Measurement HE and coagulopathies and should be treated
systemic shunts (APSS); glucosuria, granular • Atomic absorption spectroscopy—gold with IV N-acetylcysteine (NAC) for oxidative
casts if acquired Fanconi syndrome. standard method of Cu determination; injury, d-penicillamine chelation protocol
requires at least full needle biopsy (≥16 g) started as soon as oral treatment possible.
OTHER LABORATORY TESTS • Dogs with hemolytic anemia may require
sample; larger samples improve accuracy.
• High fasting or postprandial total serum whole or packed red blood cell (RBC)
• Cu must be expressed per DWL.
bile acid (TSBA) values—dogs with severe transfusion, IV NAC.
Copper Associated Hepatopathy (continued)
• Dogs with acquired Fanconi syndrome Zinc—Blocking Enteric Cu Uptake

C require IV fluid therapy and IV NAC to • Zinc oral administration may assist in
protect against acute renal failure. chronic control of CuAH; zinc use predicated
MEDICATIONS on study of only 6 dogs.
ACTIVITY
Normal; rest if severe acute hepatic necrosis. DRUG(S) OF CHOICE • Reduces intestinal Cu absorption—study
See other liver topics for specific treatments of demonstrated reduced hepatic Cu concen
DIET chronic hepatitis and cirrhosis. trations after 2 years.
• Feed Cu-restricted diets to all affected dogs • 100 mg elemental zinc PO q12h 1h before
for their lifetime. Chelation
feeding as loading dose for 2 months, then
• Merely feeding Cu-restricted diet is unreliable d-Penicillamine 25–50 mg PO q12h for Bedlington terrier-sized
intervention for dogs with pathologic hepatic • 10–15 mg/kg PO q12h on empty stomach dog; zinc acetate best tolerated as zinc source.
Cu accumulation (see Suggested Reading). (1h before feeding); bioavailability reduced • In humans, zinc therapy less effective than
• Avoid Cu in water if copper pipes—run 50% if given with food. chelation for chronic management.
water for 5 min to remove eluted Cu; restrict • Mechanism—chelates Cu, promotes urinary • May be useful in early CuAH with lower
access to water with Cu >0.2 ppm. excretion of Cu, other Cu-protective effects. hepatic Cu concentrations: <1,000 μg/g DWL.
• Prescription-type liver diets contain lowest • Supplement vitamin B6 (pyridoxine)— • Effects too slow to achieve therapeutic
Cu content, only provide 2.2–2.5 g protein/ 25 mg PO q24h for duration of d-penicillamine utility in dogs with high Cu concentrations
kg body weight when fed for maintenance treatment. and hepatitis where chelation therapy required
energy requirements; however, dietary protein • Initiate treatment in dogs with increased for acute Cu mobilization and elimination.
content should only be reduced for dogs ALT activity associated with biopsy- • Coadministration of zinc and Cu strongly
exhibiting signs of HE or developing confirmed centrilobular Cu accumulation in contraindicated as will negate efficacy of each
ammonium biurate crystalluria. >25% centrilobular hepatocytes or that treatment.
• Supplemental protein added to base reconciles with lobular injury/remodeling and • Vomiting and inappetence commonly
prescription “liver” diets to increase protein Cu affiliation. associated with zinc-induced gastritis.
intake by 0.5 g up to 1.5 g protein/kg body • Hepatic Cu as low as 600 μg/g DWL may • Evidence suggests low zinc utility in CuAH
weight using low Cu-containing foods; select require chelation and chronic management. in dogs—low concentrations of oral zinc
supplemental low Cu-containing protein • Dogs with hepatic Cu <1,500 μg/g DWL concurrent with Cu-restricted diet in previously
sources using USDA food tables (freely usually cleared with 6 months of d-penicillamine chelated Labrador retrievers provided no
available on internet). chelation based on cases with biopsy-proven additional benefit (see Suggested Reading).
• Alternative dietary management—balanced response.
homemade Cu-restricted diets (avoid organ • Dogs with hepatic Cu >3,000 μg/g may Antioxidants
meats, nuts, certain grains) formulated by require ≥9–12 months chelation or longer. • d-α-tocopherol (vitamin E)—10 U/kg
veterinary clinical nutritionist. • Drug-associated vomiting or hyporexia— q24h PO; may be mixed in food.
• Supplement water-soluble vitamins but abated with starting ½ dose d-penicillamine • S-adenosylmethionine (SAMe)—20 mg/kg
avoid ascorbate (vitamin C supplements) and titrating upward or concurrent low-dose q24h, given on empty stomach.
during Cu hepatotoxicity as may augment prednisone; giving with morsel of meat Hepatoprotectants
oxidative injury. anecdotally reported to solve nausea but may • Silibinin (milk thistle extract, form bound
• Avoid mineral supplements containing Cu compromise drug bioavailability. to phosphatidylcholine [PPC] improves
if homemade diet; use specifically formulated • Monitoring—most clinicians use ALT as bioavailability)—5 mg/kg PO q24h; no
supplements (e.g., Balance-It®). surrogate marker because of cost and risks proven benefit aside from high-dose IV
• Chelation protocol must be adjunctively used associated with follow-up liver biopsy; silibinin for Amanita toxicity.
with commercial diets for initial Cu removal. post-treatment biopsy optimal. • Ursodeoxycholic acid—10–15 mg/kg PO
• Expect substantial decline in ALT by 8 divided BID given with food for best
CLIENT EDUCATION
weeks of chelation; do not discontinue daily bioavailability (see Hepatitis, Chronic).
• Educate all Bedlington terrier owners about
chelation until ALT within normal range for • Polyunsaturated PPC
genetic basis of CuAH in this breed and
several months, coordinating with anticipated (dilinolylphosphatidylcholine [DLPC])—
appropriate genetic testing, but inform that
chelation duration based on hepatic biopsy 20–50 mg/kg PO q24h (soy bean extract;
some dogs require liver biopsy for diagnosis.
Cu quantification. PhosChol® form providing 52% DLPC)
• Other breeds—monitor for increased ALT
• Successful chelation achieves remarkable mixed with food, advised for membrane-
activity with liver biopsy.
histologic improvement and resolution of protectant and antifibrotic effects; apparent
• Dogs receiving NSAIDs with circumstantial
ALT activity. benefit with described chelation protocol
increase in ALT activity should be investigated
for potential asymptomatic or “silent” hepatic Trientine hydrochloride based on post-treatment biopsy evaluations.
Cu accumulation. • Alternative Cu chelator—as effective as CONTRAINDICATIONS
• Dietary management and chronic inter- d-penicillamine with similar guidelines; dose: • Ascorbic acid (vitamin C) may augment Cu
mittent chelation or zinc administration 5–7 mg/kg PO q12h given 1h before meals; hepatotoxicity.
needed for life in most dogs rescued from higher dosing associated with acute renal injury. • Avoid treatment with NSAIDs in affected
CuAH. • Trientine currently restrictively expensive dogs.
and difficult to acquire.
SURGICAL CONSIDERATIONS PRECAUTIONS
• Ammonium tetrathiomolybdate—
• Animals with hepatic failure are surgical • Remain aware of altered drug metabolism
alternative method for chelating Cu in
and anesthetic risks. related to reduced first-pass extraction if
circulation, from liver, and blocking enteric
• Hypoxia encountered during anesthesia or APSS develop or altered hepatic metabolism/
uptake in humans with Wilson’s disease;
surgery can provoke Cu-driven oxidative injury. biotransformation in dogs with severe centri-
limited use in dogs.
lobular necrosis and remodeling.
• Avoid NSAID administration.
(continued) Copper Associated Hepatopathy

POSSIBLE INTERACTIONS EXPECTED COURSE AND PROGNOSIS • BUN = blood urea nitrogen.
Penicillamine or trientine may not be • Prognosis poor in acutely affected young • CuAH = copper associated hepatopathy. C
effective if giving concurrent zinc therapy. dogs with fulminant hepatic failure or older • DLPC = dilinolylphosphatidylcholin.
dogs with cirrhosis; however, some respond to • DWL = dry weight liver.
acute care and chelation. • GGT = γ-glutamyl transferase.
• Dogs with mild to moderate acute hepatic • HE = hepatic encephalopathy.
injury usually have good prognosis. • NAC = N-acetylcysteine.
FOLLOW-UP • Even dogs with nodular hepatopathy and • NSAID = nonsteroidal anti-inflammatory
PATIENT MONITORING microhepatia and ascites can respond well to drug.
• Liver enzymes initially q2–4 weeks for 8 described protocol with resolution of many • PPC = phosphatidylcholine.
weeks, then q2-4 months. histologic changes, including fibrosis. • PT = prothrombin time.
• Evaluate body weight and condition. • Good prognosis warranted if CuAH • RBC = red blood cell.
• Optimal reassessment—hepatic biopsy with detected before liver remodeling or develop • SAMe = S-adenosylmethionine.
determination of hepatic Cu concentration ment of hepatitis. • TSBA = total serum bile acid.
within 1 year of initiated treatment.
INTERNET RESOURCES
• If using zinc therapy—assess serum zinc
www.vetgen.com for genetic screening in
concentrations initially, then during first 2–3
Bedlington terriers
weeks until stable to insure values increase
but remain within nontoxic range (200– MISCELLANEOUS Suggested Reading
500 μg/dL), then q6 months; plasma zinc AGE-RELATED FACTORS Fieten H, Biourge VC, Watson AL, et al.
does not reflect liver zinc concentrations. • Health evaluations that include ALT Dietary management of Labrador retrievers
measurement help identify at-risk dogs. with subclinical hepatic copper accumula-
• Important to evaluate ALT in any dog tion. J Vet Intern Med. 2015, 29:822–827.
• Breed only Bedlington terriers without
placed on chronic NSAIDs where Cu Fieten H, Hooijer-Nouwens BD, Biourge
COMMD1 mutation; liver registry
retention appears to augment centrilobular VC, et al. Association of dietary copper and
available for Bedlington terriers proven
hepatotoxicity; measure ALT before and 2–4 zinc levels with hepatic copper and zinc
unaffected on basis of hepatic Cu concen
weeks after NSAID initiation (sooner if concentration in Labrador Retrievers. J Vet
tration <400 μg/g DWL at 1 year of age or
patient demonstrates inappetence, vomiting, Intern Med 2012, 26:1274–1280.
by gene testing.
lethargy). Hoffmann G, van den Ingh TS, Bode, P, et al.
• Other breeds noted previously may have
Cu-associated chronic hepatitis in Labrador
recognized kindred predispositions. PREGNANCY/FERTILITY/BREEDING
Retrievers. J Vet Intern Med 2006,
• Do not breed affected Bedlington terriers or
POSSIBLE COMPLICATIONS 20(4):856–861.
• d-Penicillamine can cause anorexia and
carriers.
Johnston AN, Center SA, McDonough SP,
vomiting; start at low end of dose range for • Genetics of other at-risk breeds unknown—
et al. Hepatic copper concentrations in
first week; give 1h before meals; small amount some kindred predispositions recognized.
Labrador Retrievers with and without
of food may reduce nausea but reduces SYNONYMS chronic hepatitis: 72 cases (1980–2010). J
treatment efficacy. • Bedlington hepatitis. Am Vet Med Assoc 2013, 242(3):372–380.
• d-Penicillamine can induce glycogen-type • Chronic active hepatitis. Strickland JM, Buchweitz JP, Smedley RC,
vacuolar hepatopathy and ALP activity. • Chronic Cu toxicity. et al. Hepatic copper concentrations in 546
• d-Penicillamine side effects—glomerulo • Cu toxicosis. dogs (1982-2015). J Vet Intern Med 2018,
nephritis, polyarthritis, drug-associated SEE ALSO 32:1943–1950.
hepatopathy, or autoimmune-like vesicular • Cirrhosis and Fibrosis of the Liver. Author Sharon A. Center
disease of mucocutaneous junctions that • Hepatitis, Chronic. Consulting Editor Kate Holan
resolves on drug withdrawal; note: assess urine Acknowledgment The author and book
for proteinuria before initiating therapy; rare ABBREVIATIONS editors acknowledge the prior contribution of
hepatotoxicity: indicated by escalation of ALT • ACT = activated clotting time. Sean P. McDonough.
activity; drug known to induce ALP. • ALT = alanine aminotransferase.
• Excess zinc (oral dose >200 mg/day or • APSS = acquired portosystemic shunt.
blood concentration >800 μg/dL) can cause • APTT= activated partial thromboplastin time. Client Education Handout
hemolytic anemia. • AST = aspartate transaminase. available online
Coprophagia and Pica
CAUSES
C Behavioral Causes
B ASICS • Coprophagia is considered normal maternal D IAGNOSIS
behavior; the dam or queen licks the anogenital
DEFINITION region of the neonate to stimulate elimination DIFFERENTIAL DIAGNOSIS
Pica is an abnormal ingestive behavior in and then consumes the excreta. • Coprophagia • Diagnosis is based on history and descrip
which nonfood items are consumed. may be considered a normal exploratory behavior tion of the behavior. • History should include:
Coprophagia is a form of pica in which feces in puppies; it has been postulated that high levels ⚬ Description of the problem—when and
is consumed. of deoxycholic acid in feces may contribute to where it happens. ⚬ Age of onset.
neurologic development. • It is normal for dogs ⚬ Owner’s usual response, any corrections
PATHOPHYSIOLOGY
• The pathophysiology of pica is unclear. to seek out cat feces because it is high in attempted so far, and their results. ⚬ Changes
• Coprophagia is not usually a pathologic protein—odor and taste may also be appealing. in household, schedule, diet, or health
condition. • Pica is a sign that may be • Ungulate feces is also appealing to dogs, associated with onset of problem. ⚬ Feeding
associated with a variety of different apparently due to partially digested vegetable routine of pets—when, where fed, by whom.
matter. • Dogs described as “greedy eaters” have ⚬ Any other unusual oral behaviors. ⚬ Other
conditions—any medical condition leading to
nutritional deficiencies, electrolyte imbalances, higher incidence of coprophagy; therefore a behavioral problems. ⚬ House training
gastrointestinal (GI) disturbances, poly voracious appetite may predispose to copropha status—when and where the pet eliminates.
gia. • Feces may be appetizing to some dogs, so ⚬ How the pet was house trained. ⚬ Relationships
phagia, or CNS disturbances may lead to
pica and/or coprophagia. • Severely calorie- the behavior might be self-rewarding. • Dogs that with other pets. • Environment, including daily
restricted diets or imbalanced diets leading to have been punished for eliminating in the house schedule for play, exercise, attention, or
insufficiencies may also lead to pica and/or could learn to eat their own feces in an apparent training. • Medical health should be
coprophagia. attempt to avoid punishment. • Dogs may also evaluated, including appetite and weight, any
eat their own feces as a form of “nest cleaning.” signs of nausea or GI upset such as excessive
SYSTEMS AFFECTED lip licking or surface licking, and color,
• Coprophagia may be attention-seeking behavior
GI—foreign body obstruction, GI upset consistency, and frequency of feces.
if a dog learns that it reliably leads to immediate
leading to vomiting and diarrhea; increased • Pica must be differentiated from destructive
owner attention. • Coprophagia may also develop
chance of GI parasitism with coprophagia. chewing, where items may be torn apart but
in response to anxiety or frustration. • Pica may
GENETICS occur secondary to stealing behavior when the not consumed. • Pica must also be differenti
None known. dog is highly motivated to prevent the owner ated from instances where an animal
from retrieving the stolen object or when the consumes a nonfood item because the item
INCIDENCE/PREVALENCE smells and/or tastes appealing.
• Pica—unknown. • Coprophagia—occur object has ingestive appeal. • Pica may develop as
rence has been estimated at 16–23% in dogs. a result of anxiety or frustration that leads to CBC/BIOCHEMISTRY/URINALYSIS
destruction and subsequent consumption of an • Results suggesting diabetes mellitus,
SIGNALMENT item. hyperadrenocorticism, hyperthyroidism, or
Species Medical Causes drug-induced causes of polyphagia.
Coprophagia is common in dogs but rare in • Anemia. • Malnutrition leading to poly- • Anemia or hypoproteinemia. • Results
cats. Pica is seen in both dogs and cats. phagia. • Endocrinopathies—hyperthyroid suggesting presence of a portosystemic
Breed Predilections ism, diabetes mellitus, hyperadrenocorticism. shunt—microcytosis, target cells, hypoalbu
Oriental cat breeds such as Siamese may be at • Maldigestion/malabsorption (e.g., exocrine minemia, low blood urea nitrogen (BUN),
greater risk of pica. pancreatic insufficiency). ammonium biurate crystalluria. • Peripheral
• Inflammatory bowel disease. • Small eosinophilia may occur due to gastro
Mean Age and Range
intestinal bacterial overgrowth. • CNS disease. intestinal parasitism or eosinophilic
Pica occurs more often in puppies than in
• Portosystemic shunt. • Intestinal parasitism. inflammatory bowel disease.
adult dogs. Pica in cats is most likely to begin
prior to 18 months of age. Drug-Induced Causes OTHER LABORATORY TESTS
Administration of drugs such as cortico • Trypsin-like immunoreactivity (TLI)—may
SIGNS
steroids, progestins, phenobarbital, or be low if exocrine pancreatic insufficiency
Historical Findings benzodiazepines can lead to polyphagia. exists. • Serum folate and cobalamin to
• In dogs, ingestion of inappropriate items evaluate for small intestinal bacterial
RISK FACTORS
such as rocks, clothing, and/or feces. • In cats, overgrowth and small intestinal mucosal
• Early weaning of kittens has been
ingestion of fabrics, plastic, shoelaces, string, disease. • Fecal fat and fecal trypsin may help
postulated to lead to sucking and ingestion
thread, or other inappropriate items. to evaluate for exocrine pancreatic insufficiency
of fabrics. • Cats fed low-roughage diets
Physical Examination Findings and/or not allowed access to roughage and other malabsorption/maldigestion-related
• Halitosis if coprophagia is the presenting sources such as grass. • Dogs lacking conditions. • Thyroid panel to determine if
problem. • Dental trauma if the dog targets appropriately stimulating environment, hyperthyroid. • Fecal examinations to screen
hard objects. • Pallor or weakness if anemia is adequate activity, or social interactions may for intestinal parasites; note: coprophagia can
a contributing condition. • Poor body be at risk for pica and/or coprophagia. result in false-positive tests for helminths in
condition if malabsorption or maldigestion is • Long periods of confinement, especially in dogs. • Bile acids to evaluate for presence of a
a contributing condition. • Neurologic signs a barren environment, may predispose to portosystemic shunt. • Adrenocorticotropic
if caused by neurologic disease. • May be coprophagia. • Dogs in multidog households hormone (ACTH) stimulation if hyperadren
abnormalities on abdominal palpation if may be at higher risk of demonstrating ocorticism a consideration.
gastroenteritis or foreign body. coprophagia.
(continued) Coprophagia and Pica

IMAGING DIET EXPECTED COURSE AND PROGNOSIS
Survey abdominal radiographs and/or Dietary changes may be helpful in some ∘∘ Prognosis is guarded if the condition has C
abdominal ultrasonography if indicated to cases of coprophagia. A more highly been present for a long period of time; or the
rule out foreign body obstruction. May also digestible diet or the addition of plant- owner is not willing to closely supervise the
demonstrate microhepatica if a portosystemic based enzyme supplements or meat dog when it eliminates or prevent access to
shunt is present. tenderizers is rarely successful in decreasing inappropriate items that the pet attempts to
DIAGNOSTIC PROCEDURES coprophagia. consume. • If owner is willing to supervise
• GI scoping and biopsy may be needed to CLIENT EDUCATION the dog and comply with treatment
evaluate for gastric and small bowel disease. • Owners should be counseled that copropha
recommendations, prognosis improves.
• Cultures if indicated to evaluate for small gia is, in most cases, normal canine behavior
intestinal bacterial overgrowth. and not harmful unless the dog consumes feces
containing pathogens or infective parasites.
• Owners should avoid the use of any form of M ISCELLANEOUS
direct or confrontational punishment for pica
AGE-RELATED FACTORS
or coprophagia due to the risk of increasing
T REATMENT anxiety, possibly worsening the behavior, and/
In adult or geriatric onset of pica or
APPROPRIATE HEALTH CARE coprophagia, primary underlying medical
or leading to other problem behaviors. Close
conditions should be strongly suspected.
Treatment of Pica supervision and prevention of access are the
• Prevent access to nonfood items that are best approach. PREGNANCY/FERTILITY/BREEDING
likely targets—physical barriers to prevent • Owners of wool-sucking cats should be
access or confine animal away from targeted cautioned that the behavior appears to have
nonfood items; teach dog to wear basket a breed disposition, so avoiding breeding of
this individual may be prudent and
muzzle. • Change to diet higher in fiber. M EDICATIONS responsible action. • If this behavior is
• Provide feeding toys and acceptable foraging
opportunities (e.g., green plants such as grass DRUG(S) OF CHOICE believed to be associated with a compulsive
or catnip for cats). • Teach dogs a “Drop it” If the behavior is determined to be a disorder, the animal should not be bred, as
or “Leave it” command so the owner can compulsive disorder or secondary to anxiety, compulsive disorders appear to have a
prevent consumption of inappropriate items. psychoactive drugs or anxiolytic drug therapy hereditary basis.
• If diagnosis consistent with compulsive may be indicated. SYNONYMS
disorder, see appropriate section in text for CONTRAINDICATIONS • Depraved appetite. • Wool sucking or wool
treatment. The use of any drugs that might contribute chewing in cats.
Treatment of Coprophagia to polyphagia should be avoided when SEE ALSO
• Prevent access to feces. • Walk dog on
possible. • Compulsive Disorders—Cats.
leash and pick up feces immediately. • PRECAUTIONS • Compulsive Disorders—Dogs.
Teach dog to wear basket muzzle. • Head If drugs are indicated, precautions should be • Fear, Phobias and Anxieties—Cats.
collar for increased ability to guide pet considered for the specific drug. • Fear, Phobias, and Anxieties—Dogs.
away from feces and reward “turning away” POSSIBLE INTERACTIONS ABBREVIATIONS
after defecation; dogs should then be If drugs are prescribed, interactions should be ACTH = adrenocorticotropic hormone.
•
rewarded with a tasty treat for returning to considered for the specific drug. BUN = blood urea nitrogen.
•
the owner on command. • There is no GI = gastrointestinal.
•
evidence that changing the taste or texture TLI = trypsin-like immunoreactivity.
•
of the stool helps to decrease coprophagia
or that any product marketed for the Suggested Reading
treatment of coprophagia reliably stops the F OLLOW-UP Horwitz D, ed. Blackwell’s 5 Minute Consult
behavior. • Taste aversion might be taught Clinical Companion: Canine and Feline
PATIENT MONITORING
by treating the feces with a strongly Behavior, 2nd ed. Ames, IA: Wiley-
• Client should be contacted in 1–2 weeks to
distasteful substance (e.g., hot sauce, Blackwell, 2018, pp. 436–446, 754–760.
verify compliance and determine if there is
cayenne pepper, etc.); all feces that the dog Houpt KA. Domestic Animal Behavior, 4th
improvement. • If no or minimal improve
can come in contact with must be treated ed. Ames, IA: Blackwell, 2005, pp. 321–334.
ment, further diagnostics should be
in order for this to be effective; however, Landsberg G, Hunthausen W, Ackerman L.
recommended.
even if effective, dogs can learn to recognize Behavior Problems of the Dog and Cat,
which feces are treated, and ingest untreated PREVENTION/AVOIDANCE 3rd ed. St. Louis, MO: Saunders Elsevier,
feces. • Prevent access to the items likely to be 2013, pp. 78–79, 157–158.
consumed. • Careful supervision during Author Valarie V. Tynes
ACTIVITY house training may help to prevent puppy Consulting Editor Gary M. Landsberg
• Increased mental and physical enrichment exploration of feces and reinforcement of
may help in treatment and prevention of pica coprophagia. • Administration of monthly
and coprophagia and keep the pet engaged in parasiticide to control GI parasites. Client Education Handout
alternative desirable activities. • Regular, available online
predictable schedules of interaction and POSSIBLE COMPLICATIONS
exercise can decrease anxiety and may aid in Foreign body obstruction is most common
treatment of pica and coprophagia. sequela to pica in both dogs and cats.
Corneal and Scleral Lacerations

fluorescein, forming a bright green rivulet
C (seen best with cobalt illumination).
BASICS D IAGNOSIS PATHOLOGIC FINDINGS
• Depends on wound and affected tissues.
DEFINITION DIFFERENTIAL DIAGNOSIS • Usually correlates with clinical examination
• Penetrating—a wound or foreign body • Traumatic event not observed and no findings. • Vitreal hemorrhage—may
enters but does not pass through the cornea foreign body found—consider nontraumatic organize into a fibrous band that causes
or sclera. • Perforating—a wound or foreign causes of ocular injury. • Traumatic hyphema— traction retinal detachment. • Post-traumatic
body completely passes through the cornea or generally accompanied by corneal or scleral sarcoma (cats)—may occur months to years
sclera; greater risk of vision loss than penetrating. lesions and subconjunctival or periocular after severe ocular trauma.
• Simple—only the cornea or sclera, hemorrhage. • Traumatic cataracts—
penetrating or perforating, other eye disrupted lens capsule. • Traumatic retinal
structures intact. • Complicated—perforat- detachment—accompanied by intraocular
ing, involves other ocular structures, uveal, hemorrhage.
vitreal, or retinal incarceration or prolapse CBC/BIOCHEMISTRY/URINALYSIS
TREATMENT
through the wound, traumatic cataract, Normal, or related to other injuries. APPROPRIATE HEALTH CARE
hyphema, lid lacerations. • Depends on severity. • Outpatient—if
PATHOPHYSIOLOGY integrity of globe is ensured.
• Cytologic examination and aerobic culture
• Sharp trauma—wounds by an outside-in and sensitivity of the wound and foreign NURSING CARE
mechanism. • Blunt trauma—wounds by an body—recommended even if infection is not • Sedation—consider for excited or fractious
inside-out mechanism; eye undergoes sudden apparent; specimen may be collected under patients. • When walking—apply an
changes in its equatorial and axial dimensions general anesthesia at time of surgery. • Consider Elizabethan collar (E-collar) and use a harness
and intraocular pressure (IOP); actual wound other tests (platelet count, coagulation profile, or put ipsilateral foreleg through the leash to
may be distant from point of impact; often etc.) if nontraumatic causes possible. avoid increasing IOP in affected eye.
more damaging than sharp trauma. • All or a
portion of foreign object initiating injury may IMAGING Injuries Considered for Medical
be retained in wound or eye. • Ocular ultrasonography—if ocular media Treatment
are opaque; may clarify extent and nature of • Complicated wounds, those with retained
SYSTEMS AFFECTED intraocular disease, may detect foreign body. plant material, and those caused by blunt
• Musculoskeletal—surrounding skull or • Orbital radiographs, CT, or MRI (if trauma with tissue devitalization—infection
orbital tissue. • Nervous—brain injury. nonmetallic)—may help determine common. • Bacterial endophthalmitis—
• Ophthalmic. projectile’s course; may detect foreign body. 5–7% of perforations; very rare in wounds
INCIDENCE/PREVALENCE DIAGNOSTIC PROCEDURES that only penetrate but do not perforate the
Common • Determine nature, force, and direction of cornea. • Nonperforating wounds with no
SIGNALMENT impact of object—to identify which tissues wound edge override or gape—apply an
may be involved. • Do not put pressure on E-collar; give topical antibiotic or atropine
Species eye until rupture or laceration of globe has ophthalmic solutions. • Nonperforating
Dog and cat. been ruled out. • Assess vision—menace wounds with mild wound gape or shelved
SIGNS response; aversion to bright light. • Periocular edges—apply a therapeutic soft contact lens
skin and orbit—examine for lacerations or and an E-collar; give topical antibiotic or
Historical Findings atropine ophthalmic solutions. • Simple
deformities; suspect globe involvement if lid
• Usually acute onset. • History of running full-thickness, pinpoint corneal perforation
laceration crosses eyelid margin or penetrates
through vegetation, hit by projectiles with a negative Seidel test that has a formed
orbital septum; entry sites often small and
(gunshot etc.), scratched by a cat. • Trauma anterior chamber and no uveal prolapse—
quickly seal. • Abnormal ocular motility—
may not be observed. sedentary patients; use a therapeutic soft
suggests extraocular muscle trauma, orbital
Physical Examination Findings hemorrhage or edema, retained foreign contact lens and an E-collar; give topical
• Varies with tissues affected. • Corneal, bodies, or peripheral nerve or CNS damage. antibiotic or atropine ophthalmic solutions;
scleral, or eyelid deformity, edema, or • Scleral rupture—consider if subconjunctival reexamine a few hours after applying the lens
hemorrhage. • May see retained foreign body. hemorrhage, especially if anterior chamber is and at 24 and 48 hours.
• Often rapidly seals; may appear only as deep or shallow, there is vitreal hemorrhage, ACTIVITY
subconjunctival hematoma. • May also see iris or eye is abnormally soft. • Pupils—assess • Usually confined indoors (cats) or limited to
defects, pupil distortion, hyphema, cataract, size, shape, symmetry, direct and consensual leash walks until healing is complete. • A harness is
vitreal hemorrhage, retinal detachment, and light reflexes. • Detailed ophthalmoscopy— preferred to a collar to reduce pressure on the neck
exophthalmia. assess clarity of ocular media and fundus and the risk of increased IOP and wound leaks.
CAUSES integrity, rule out intraocular foreign body.
• Seidel test—if any question of corneal or CLIENT EDUCATION
Blunt or sharp trauma. Warn client that the full extent of the injury
scleral leaking; use a dry to slightly moist
RISK FACTORS fluorescein strip to paint a thin coat of (cataracts, retinal detachment, infection) may
• Preexisting visual impairment. • Young, fluorescein over the surface of the defect; not be apparent until days or weeks after the
naïve, or highly excitable animals. • Hunting or leaking aqueous combines with the orange injury and that long-term follow-up is
running through heavy vegetation. • Fighting. necessary.
(continued) Corneal and Scleral Lacerations

SURGICAL CONSIDERATIONS control of inflammation is mandatory to POSSIBLE COMPLICATIONS
Injuries Requiring Surgical Exploration preserve the eye. • Loss of eye or vision. • Chronic ocular C
Mydriatics inflammation or pain. • Post-traumatic sar-
or Repair coma—may develop in cat eyes following trauma.
• Full-thickness corneal lacerations with a 1% atropine ophthalmic solution q6–12h—
positive Seidel test. • Full-thickness when there is significant miosis. EXPECTED COURSE AND PROGNOSIS
wounds with iris incarceration or prolapse. Analgesics • Most eyes with corneal lacerations or a
• Full-thickness scleral or corneoscleral • Topical atropine may provide sufficient pain retained corneal foreign body are salvageable.
lacerations. • Suspected retained foreign relief. • Carprofen 2.2 mg/kg PO q12h or • The more posterior the injury, the poorer the
body or posterior scleral rupture. • Simple 4.4 mg/kg PO q24h. • Tramadol—2–5 mg/kg prognosis for retention of vision. • Poor
nonperforating wound with edges that are PO q12h. prognosis—scleral or uveal involvement, no
moderately or overtly gaping and that are light perception, perforating injuries involving
long or more than two-thirds the corneal CONTRAINDICATIONS the lens or with significant vitreal hemorrhage
• Topical ophthalmic ointments—avoid in or retinal detachment. • Penetrating injuries
thickness.
Seidel-positive perforations until wound closed. usually better prognosis than perforating
Injuries Considered for Surgical • Systemic ciprofloxacin—avoid in young dogs. injuries. • Blunt trauma carries poorer
Exploration or Repair PRECAUTIONS prognosis than sharp trauma.
• Small full-thickness corneal lacerations with • Aminoglycosides—topical application may be
a negative Seidel test and no uveal prolapse. irritating and may impede reepithelization if used
• Large conjunctival lacerations. • Partial- frequently or at high concentrations; possibility
thickness corneal or scleral lacerations in an for renal toxicity. • Topical solutions may be
active patient. M ISCELLANEOUS
preferable to ointments if corneal integrity is
questionable. • Atropine—may exacerbate ASSOCIATED CONDITIONS
keratoconjunctivitis sicca and glaucoma. • Topical Depends on nature and extent of
or systemic NSAIDs—use cautiously with injury.
M EDICATIONS hyphema; unknown safety in cats. PREGNANCY/FERTILITY/BREEDING
POSSIBLE INTERACTIONS • Systemic corticosteroids—may complicate
DRUG(S) OF CHOICE
Systemic NSAIDs—may potentiate nephro pregnancy. • Systemic ciprofloxacin—should
Antibiotics be avoided during pregnancy.
toxicity of aminoglycosides; ensure good
• Penetrating—topical antibiotics alone (e.g.,
hydration and adequate renal function. SEE ALSO
neomycin, polymyxin B, and bacitracin) or
gentamicin solution q6–8h; usually sufficient. ALTERNATIVE DRUG(S) • Cataracts.
• Perforating wounds with negative Seidel Topical ciprofloxacin ophthalmic solution— • Hyphema.
test—systemic ciprofloxacin (dogs: 10–20 mg/kg may be used instead of combination of • Keratitis—Ulcerative.
PO q24h); topical cefazolin (add injectable topical cefazolin and fortified aminoglycoside; • Proptosis.
cefazolin to artificial tears to concentration of some streptococcus are resistant. • Retinal Detachment.
33 mg/mL) and either topical ophthalmic ABBREVIATIONS
ciprofloxacin or ofloxacin; both drugs q4–6h. • E-collar = Elizabethan collar.
• Perforating wounds with positive Seidel • IOP = intraocular pressure.
test—systemic ciprofloxacin (dogs: FOLLOW-UP • NSAID = nonsteroidal anti-inflammatory
10–20 mg/kg PO q24h); topical antibiotics as drug.
noted above, only after defect has been made PATIENT MONITORING
• Deep or long penetrating wounds that have Suggested Reading
watertight. Ledbetter EC, Gilger BC. Diseases and
not been sutured and perforating wounds—
Anti-Inflammatories recheck q24–48h for first several days to surgery of the canine cornea and sclera. In:
• Topical 1% prednisolone acetate or 0.1% ensure integrity of globe, to monitor for Gelatt KN, Gilger BC, Kern TJ, eds.,
dexamethasone solution q6–12h; as soon as infection, and to check control of ocular Veterinary Ophthalmology, 5th ed. Ames,
wound is sutured or has epithelialized inflammation. • Superficial penetrating IA: Wiley-Blackwell, 2013, pp. 976–1049.
(becomes fluorescein stain negative), as long wounds—usually recheck at 3–5-day intervals Maggs DJ. Diseases of the Cornea and Sclera.
as infection is not present. • Systemic until healed. • Antibiotic therapy—alter In: Maggs DJ, Miller PE, Ofri R, eds.,
prednisone 0.5–1 mg/kg PO q12–24h; for according to culture and sensitivity. Slatter’s Fundamentals of Veterinary
sutured or epithelialized wounds when Ophthalmology, 6th ed. St. Louis, MO:
inflammation is severe, when lens or posterior PREVENTION/AVOIDANCE Elsevier, 2018, pp. 213–253.
structures are involved, or when wound is • Take care when introducing new puppies to Author Paul E. Miller
infected or not epithelialized and control of households with cats. • Minimize running Consulting Editor Kathern E. Myrna
inflammation is mandatory to preserve the through dense vegetation; owner should consider
eye. • Topical nonsteroidal anti-inflammtory having bottle of saline eyewash to irrigate foreign
drugs (NSAIDs)—flurbiprofen or others; if debris from eye. • Minimize visually impaired Client Education Handout
topical corticosteroids are contraindicated and dog’s exposure to dense vegetation. available online
Corneal Opacities—Degenerations and Infiltrates

homogeneous; varies in size depending on CONTRAINDICATIONS/POSSIBLE
C severity; indistinct margins; can retain COMPLICATIONS
fluorescein stain if corneal erosion/ulceration • Topical corticosteroids—not recom-
B ASICS present. • Corneal ulcer—ocular pain, retains mended, may worsen severity; contraindi-
OVERVIEW fluorescein stain, varying degrees of edema cated with corneal ulceration. • Topical
Acquired corneal disorder characterized by lipid around the lesion. • Inflammatory cell atropine—contraindicated with KCS,
or calcium deposition. May be unilateral or infiltrates—ocular pain, gray to tan to yellow glaucoma, lens luxations.
bilateral, have distinct margins, and occur with indistinct margins; cytologic examination
secondary to other ocular or systemic disorders. of cornea reveals white blood cells,
microorganisms.
SIGNALMENT
Primarily in dogs, uncommon in cats. Lipid CBC/BIOCHEMISTRY/URINALYSIS FOLLOW-UP
deposition most common in geriatric dogs. • Systemic tests only necessary if hyperlipidemia is
May be associated with systemic hyperlipo- suspected; no systemic tests necessary for most cases. PATIENT MONITORING
proteinemia. • Lipid—evaluate fasting cholesterol, triglycer- Monitor serum cholesterol and triglycerides
ide, blood glucose concentrations. • Calcium— to assess efficacy of dietary management in
SIGNS hyperlipidemic patients; monitor treatment of
evaluate ionized calcium concentration.
• Lipid deposits—gray-white or crystalline; primary disease if present.
band-shaped, irregular, or circular. • Calcium OTHER LABORATORY TESTS
deposits—dense white to crystalline; irregular, Endocrinopathy testing—thyroid function, EXPECTED COURSE AND PROGNOSIS
adrenocorticotropic hormone (ACTH) • Corneal ulceration—associated with worsening
punctate to band-shaped lesions in the
superficial stroma. • Frequently associated with stimulation test. of disease. • Vision—may be affected in
inflammatory disorders such as keratitis or advanced disease; may be severe if primary
DIAGNOSTIC PROCEDURES ocular disease (e.g., uveitis) present. • Deposits
uveitis. • Corneal vascularization, edema, and Fluorescein staining—may retain dye around
pigmentation often present. • With progres- may recur following superficial keratectomy.
margins of deposit if raised.
sion the cornea may develop a roughened
appearance; disruption of epithelium can lead
to ulceration. • Associated ocular conditions
that may lead to corneal degeneration—cor- MISCELLANEOUS
neal scars, keratoconjunctivitis sicca (KCS), TREATMENT
• Treat primary ocular disease if present. SEE ALSO
exposure keratitis, chronic uveitis, episcleritis,
• Corneal deposits causing patient discom- • Corneal Opacities—Dystrophies.
phthisis bulbi, chronic topical steroid therapy,
fort or impaired vision may benefit from • Keratitis—Ulcerative.
limbal neoplasia. • When lipid deposition
occurs secondary to hyperlipoproteinemia, corneal debridement or superficial keratec- ABBREVIATIONS
perilimbal annular ring may form with clear tomy followed by medical treatment; deposits • ACTH = adrenocorticotropic hormone.
zone between affected cornea and limbus; likely to recur if underlying cause not • EDTA = ethylene diamine tetra-acetate.
often bilateral but may be asymmetric; corrected. • Hyperlipoproteinemia may • KCS = keratoconjunctivitis sicca.
vascularization is variable. resolve with low-fat diet and treatment of
INTERNET RESOURCES
systemic disease if present; both may slow or
CAUSES & RISK FACTORS https://www.columbiaeye.org/education/
stop progression of ocular disease.
• Lipid—hyperlipoproteinemia may increase digital-reference-of-ophthalmology/
risk or worsen existing deposits; can be cornea-external-diseases/degenerations
secondary to hypothyroidism, diabetes Suggested Reading
mellitus, hyperadrenocorticism, diet, Crispin SM, Barnett KC. Dystrophy,
pancreatitis, nephrotic syndrome, liver MEDICATIONS degeneration and infiltration of the canine
disease, hyperlipidemia of miniature DRUG(S) OF CHOICE cornea. J Small Anim Pract 1983,
schnauzers. • Calcium—hypercalcemia, • Topical broad-spectrum antibiotics (i.e., 24:63–83.
hyperphosphatemia, hypervitaminosis D, triple antibiotic) for ulcerated cornea; Author Kathern E. Myrna
hyperadrenocorticism, uremia. • Lipid and frequency depends on severity; usually Consulting Editor Kathern E. Myrna
calcium deposits are frequently seen together. uncomplicated ulcers treated q8–12h. Acknowledgment The author and book
• Topical nonsteroidal anti-inflammatory editors acknowledge the prior contribution of
drug q8–12h—indicated if uveitis noted. Amber L. Labelle
• Topical 0.2% cyclosporine—to improve
DIAGNOSIS tear film quality, reduce inflammation.
• Topical 1% atropine q8–24h—indicated to
DIFFERENTIAL DIAGNOSIS reduce pain if uveitis or ulceration is present.
• Corneal scar—nonpainful lesion, gray to • Topical ethylene diamine tetra-acetate
white; fluorescein negative; relatively smooth (EDTA) solution 0.5–3% q6h; may help
corneal surface; distinct margins. • Corneal minimize calcium deposits; usually used
stromal dystrophies—bilateral, often following debulking procedure to improve
symmetric foci of gray to white deposition, efficacy. • Artificial tear ointment q6–12h;
distinct margins; heritable, not associated may prevent or reduce frequency of
with ocular inflammation; do not retain secondary corneal ulceration; provides
fluorescein stain; often occur away from the lubrication and improves comfort when
limbus. • Edema—bluish to gray; usually corneal surface is irregular.
Corneal Opacities—Dystrophies
paracentral or peripheral cornea. • Vision—
usually not affected; visual deficit possible C
with advanced or diffuse disease.
B ASICS MEDICATIONS
Endothelial
OVERVIEW • Asymptomatic in early stages. • Edema of DRUG(S) OF CHOICE
• Primary, inherited (or familial), bilateral, temporal or inferio-temporal cornea that usually • Corneal ulceration—topical antibiotics and
and often symmetric condition of the cornea progresses to entire cornea after months to years. possibly atropine (see Keratitis—Ulcerative).
that is not associated with other ocular or • Corneal epithelial bullae (bullous keratopathy) • Epithelial—1–2% cyclosporine in oil or
systemic diseases. • Three types based on and subsequent corneal erosion ulceration may 0.2% ointment q8–24h to relieve clinical
anatomic location—epithelial: characterized develop; erosions or ulceration may cause signs. • Endothelial—topical 5% sodium
by dyskeratotic and necrotic epithelial cells, blepharospasm due to pain. • Vision—may be chloride ointment; palliative treatment; does
focal absence of epithelial basement mem- impaired with advanced disease. not markedly clear cornea, but may prevent
brane, and cell infiltrate in anterior corneal progression and rupture of corneal epithelial
stroma; stromal: lipid deposition within CAUSES & RISK FACTORS bullae.
• Epithelial—result of degenerative or
corneal stroma; endothelial: characterized by CONTRAINDICATIONS/POSSIBLE
abnormal, dystrophic endothelial cells. innate abnormalities of corneal epithelium
and/or basement membrane. • Stromal— INTERACTIONS
SIGNALMENT innate abnormality or localized error in Topical corticosteroids—no benefit to lipid
Usually dogs; rare in cats. corneal lipid metabolism; may be affected by (stromal) dystrophy, of questionable benefit
Epithelial hyperlipoproteinemia (may increase opacity). to other forms of dystrophy.
Shetland Sheepdogs—age of onset 6 • Endothelium—degeneration of endothelial
months–6 years; slow progression. cell layer; subsequent loss of endothelial cell
pump function results in corneal edema.
Stromal
• Usually young adult dogs at age of onset. FOLLOW-UP
• Affected breeds—Afghan hound, Airedale • Reexamination—necessary only if
terrier, Alaskan Malamute, American cocker ocular pain or corneal ulceration develops.
spaniel, beagle, bearded collie, bichon frisé, DIAGNOSIS • Corneal opacity—may wax and wane
cavalier King Charles spaniel, German with lipid dystrophy; unlikely to resolve.
shepherd, Lhasa apso, mastiff, miniature • Corneal ulceration—may accompany
• Epithelial, stromal—other causes of corneal
pinscher, rough collie, Samoyed, Siberian progression of epithelial or endothelial
opacity: corneal degenerations, ulcers, scars,
husky, Weimaraner, whippet, and others; dystrophy. • Vision—not substantially
inflammatory cell infiltrates. • Endothelial—
inheritance pattern identified in few breeds. affected except in advanced cases.
other causes of diffuse corneal edema: uveitis
Endothelial and glaucoma.
• Dogs—primarily Boston terriers, Chihuahuas, CBC/BIOCHEMISTRY/URINALYSIS
and dachshunds; may affect other breeds; Epithelial, stromal—high concentrations of
typically middle-aged or older at onset of cholesterol and triglyceride levels may modify MISCELLANEOUS
clinical signs; female predilection suggested. course of disease, but are not the cause. SEE ALSO
• Cats—affects young animals; described most • Corneal Opacities—Degenerations and
often in domestic shorthairs; a similar condition DIAGNOSTIC PROCEDURES
• Stromal—usually does not retain fluores- Infiltrates.
without endothelial disease is inherited as an • Keratitis—Ulcerative.
autosomal recessive disorder in Manx. cein stain. • Epithelial or endothelial—may
retain fluorescein stain, often in multifocal Suggested Reading
SIGNS punctate areas, particularly with advanced Crispin SM, Barnett KC. Dystrophy,
All cause some degree of opacity in cornea. disease. • Tonometry—to eliminate glaucoma degeneration and infiltration of the canine
Epithelial as cause of corneal edema. cornea. J Small Anim Pract 1983,
• Can be asymptomatic or have blepharospasm; 24:63–83.
multifocal white or gray circular to irregular Author Ellison Bentley
opacities or rings; sometimes associated with Consulting Editor Kathern E. Myrna
multifocal corneal erosions. • Vision usually TREATMENT
not affected. • Advanced epithelial or endothelial disease
Stromal with ulceration—may require treatment for
• Usually asymptomatic without inflamma- ulcerative keratitis. • Stromal—usually none
tion. • Central—most common; gray, white, required; may perform superficial keratec
or silver oval to circular opacity of central or tomy to remove lipid deposits if severe, but
paracentral cornea; with magnification may usually unnecessary and deposits may recur.
note multiple fibrillar to coalescing opacities • Inform client that some corneal dystrophies
that have crystalline or ground-glass are inherited. • Advanced endothelial
appearance (crystalline corneal dystrophy). dystrophy—may use therapeutic soft contact
• Diffuse—affects Airedales; more diffuse, lens with or without debridement of
dense opacity than with central dystrophy. redundant corneal epithelial tags, conjunctival
• Annular—commonly affects Siberian flap surgery, or thermal cautery of cornea.
huskies; doughnut-shaped opacity of
Corneal Sequestrum—Cats
• Fluorescein stain.
C • Tear film breakup time (TBUT)—normal
time to breakup of fluorescein-stained tear
B ASICS film is 21 seconds; TBUT may be decreased FOLLOW-UP
OVERVIEW in cats with sequestra or FHV-1 due to mucin PATIENT MONITORING
• A focal, light brown to black, plaque-like tear film deficiency or secondary to corneal • If managing medically, examine as needed
area of stromal coagulation necrosis usually disease. to monitor progression and for complications
located axially. • Corneal histopathology—confirm diagnosis associated with sloughing of sequestrum.
• Usually caused by chronic corneal ulcer- and evaluate completeness of excision. • If managed by keratectomy, examine q5–7
ation, trauma, or exposure. • PCR for FHV-1— limited value. days until corneal defect has reepithelialized
• Synonym—keratitis nigrum. • Conjunctival biopsy—goblet cell numbers (usually 7–14 days).
SIGNALMENT may decrease with conjunctival inflammation • Sequestra may recur or occur in contra
• Cats—any breed, age.
or FHV-1. lateral eye; recurrence more likely in cats with
• Brachycephalic breeds, Siamese predisposed. low Schirmer tear tests, full-thickness lesions,
• Colorpoints may be genetically or in cases in which keratectomy did not
predisposed. result in complete excision of pigmented
TREATMENT corneal tissue or predisposing cause was not
SIGNS addressed.
• Unilateral or bilateral, focal round to oval, • Lesion depth, degree of ocular pain, and
variably sized areas of corneal discoloration cost are important factors. POSSIBLE COMPLICATIONS
ranging from translucent golden-brown • Medical—supportive care, wait for Corneal perforation may occur if sequestrum
(early) to opaque black (chronic). sequestrum to spontaneously slough; ocular sloughs, leaving full-thickness defect, or if
• Often with chronic nonhealing corneal pain may persist for months and sloughing of sloughing results in deep stromal corneal
ulcer. sequestrum may lead to deep corneal ulcer that becomes malacic or infected.
• Corneal vascularization and edema. ulceration or perforation.
• History of feline herpesvirus-1 (FHV-1) Surgical Considerations
keratoconjunctivitis. • Lamellar keratectomy—if performed early,
• Blepharospasm or ocular discharge. can relieve ocular pain, promote corneal MISCELLANEOUS
• Conjunctival hyperemia and chemosis. healing, and may prevent lesion from
• Miotic pupil. ASSOCIATED CONDITIONS
involving deeper corneal stroma.
• May be static for long periods or may • Corneal ulceration—cats.
• Corneal grafting should be performed if
rapidly progress. • Eyelid conformational abnormalities
≥50% of corneal stroma has been excised;
• With chronicity, corneal vascularization (trichiasis, entropion, etc.).
options include conjunctival pedicle grafting,
may extrude plaque. grafting with synthetic, autogenous, or ABBREVIATIONS
CAUSES & RISK FACTORS heterologous biomaterials, and corneoscleral • FHV-1 = feline herpesvirus-1.
• Thought to involve chronic mechanical transposition. • KCS = keratoconjunctivitis sicca.
corneal irritation or ulceration with corneal • Diamond burr debridement may be used to • TBUT = tear film breakup time.
necrosis and desiccation. remove superficial sequestra. Suggested Reading
• Risk factors include chronic corneal • Postoperative management—broad- Featherstone HJ, Sansom J. Feline corneal
ulceration, chronic trichiasis or entropion, spectrum topical antibiotic, atropine sequestra: a review of 64 cases (80 eyes)
brachycephalic conformation, lagophthalmia, ointment, and tear supplement. from 1993 to 2000. Vet Ophthalmol 2004,
keratoconjunctivitis sicca (KCS), qualitative 7(4):213–227.
tear film disorders (lipid or mucin deficiency), Stiles J. Feline ophthalmology. In: Gelatt KN,
FHV-1 infection, topical corticosteroids, and Gilger BC, Kern TJ, eds., Veterinary
iatrogenic trauma (grid keratotomy). MEDICATIONS Ophthalmology, 5th ed. Ames, IA: Wiley,
2013, pp. 1495–1496.
DRUG(S) OF CHOICE Author Anne J. Gemensky Metzler
• Topical oxytetracycline with polymyxin B
Consulting Editor Kathern E. Myrna
or bacitracin-neomycin-polymyxin B q6–8h
D IAGNOSIS (prophylactic).
DIFFERENTIAL DIAGNOSIS • Topical 1% atropine sulfate ointment
• Corneal perforation/iris prolapse—protrud- q12–24h (improve ocular comfort).
ing iris is fleshy and yellow to light brown. • Topical lubricants (e.g., carboxymethylcel-
• Corneal foreign body. lulose gel) q6–8h (reduce mechanical
• Corneal pigmentation—rare in cats. irritation and corneal desiccation); may
• Corneal neoplasia—melanocytoma occurs prevent progression of nonulcerated
at limbus and is typically nonpainful. sequestra.
• Topical or systemic antiviral therapy in cats
CBC/BIOCHEMISTRY/URINALYSIS with history or clinical signs of FHV-1
No specific abnormalities. infection.
OTHER LABORATORY TESTS CONTRAINDICATIONS/POSSIBLE
• Schirmer tear test—very low values suggest
INTERACTIONS
KCS, but some normal cats have low values.
Topical antibiotics (neomycin) may be
• Corneal culture and cytology to rule out
irritating and cause chemical conjunctivitis.
corneal infection.
Cough
structures involved in dogs (i.e., honking RISK FACTORS
cough is typical of tracheal collapse, harsh Breed
C
sonorous cough followed by terminal retch • Toy and miniature breeds at risk for
BASICS characterizes cough of tracheal or bronchial tracheal collapse. • Terrier breeds at risk for
DEFINITION origin, faint moist cough is heard in moderate pulmonary fibrosis. • Husky, Rottweiler,
• A sudden and often repetitively occurring to severe pneumonia). • Cough can be Labrador, and Jack Russell terrier at risk for
defense reflex that helps clear large airways of described as dry or moist, productive, honking, eosinophilic bronchopneumopathy. • Giant
excess secretions, irritants, foreign particles, short or harsh, faint or sonorous, followed by breeds at risk for dilated cardiomyopathy.
and microbes, or clear foreign material from gagging or retching. • Cough can be elicited • Labrador retriever, large breeds at risk for
upper airways. • The cough reflex consists of by traction on the collar (laryngeal or tracheal laryngeal paralysis. • Siamese cats at risk for
three phases: inhalation, forced exhalation origin), aggravated by exercise or excitation feline bronchitis syndrome.
against a closed glottis, and violent expulsion (tracheal collapse), or can occur after a period
of air from the lungs following opening of the of rest (cough due to heart failure). • Can be Environmental Factors
glottis, usually accompanied by a sudden accompanied by stertor or stridor (laryngeal, Longhaired cats that are infrequently
noise. Coughing can happen voluntarily as tracheal origin) or dyspnea (many areas). groomed will periodically retch, cough, and
well as involuntarily, although in dogs and cats vomit up mats of hair.
it is presumed to be essentially involuntary. CAUSES
Drugs
Coughing should not be confused with other Upper Respiratory Tract Diseases Potassium bromide in cats.
airway sounds (cf differential diagnosis). • A variety of sinonasal conditions cause
Geographic Area (or Travel History)
PATHOPHYSIOLOGY extension of inflammation and/or secretions
Certain diseases are common in specific areas
• A physiologic reflex in healthy animals that
into the pharynx and/or larynx and can lead
(e.g., dirofilariasis, angiostrongylosis).
protects the lower airways from inhalation of to the upper airway cough syndrome (UACS),
foreign particles and helps clear particles that previously referred to as postnasal drip
have been entrapped in the mucus; acts in syndrome. • Laryngeal and/or pharyngeal
conjunction with the mucociliary clearance disease (inflammation, paralysis, tumor,
mechanism. • The cough pathway includes granuloma, collapse). • Tracheal disease DIAGNOSIS
cough receptors, which are made up of sensory (inflammation, infection, foreign body, DIFFERENTIAL DIAGNOSIS
nerves in the airways, the vagus nerve, the central collapse, stenosis, tumor). • Similar signs. • Coughing may be confused
cough center, and effector muscles. • The cough Lower Respiratory Tract Diseases with other signs such as sneezing, reverse
pathway can be stimulated by mechanical or (Tracheobronchial or Bronchopulmonary sneezing, gagging, panting, retching, and
chemical factors; endogenous triggers include vomiting; presence of terminal retch is often
Disease)
airway secretions and inflammation; exogenous misinterpreted as vomiting. • Honking noise
• Inflammatory (feline bronchitis syndrome;
triggers include smoke and aspirated foreign coughing in case of severe tracheal collapse
dogs: chronic bronchitis, eosinophilic broncho-
material. • Cough receptors include rapidly can be descried by owners as severe stertor.
pneumopathy). • Infectious—bacterial, viral
adapting stretch receptors (sensitive to CBC/BIOCHEMISTRY/URINALYSIS
(dog: distemper, kennel cough; cat: feline
mechanical stimuli) that are located within the Minimum database may suggest acute
leukemia virus [FeLV], feline immuno
mucosa of the tracheobronchial tree (especially bacterial infection (leukocytosis with left
deficiency virus [FIV], feline infectious
larynx and trachea), and pulmonary/bronchial shift) or eosinophilic airway disease (periph-
peritonitis [FIP], calicivirus, herpesvirus),
C-fibers, which are more sensitive to chemical eral eosinophilia).
parasitic (dog: Filaroides spp., Angiostrongylus
stimulation; coughing mechanisms and
vasorum, Capillaria aerophilia, Crenosoma OTHER LABORATORY TESTS
pathways are very complex and are not fully
vulpis; cat: Aerulostrongylus abstrusus; dog, cat: • Filter test for microfilaria and/or heartworm
understood, even in humans.
Paragonimus kellicotti, Dirofilaria immitis), antigen serology—for heartworm disease.
SYSTEMS AFFECTED protozoal (cat: toxoplasmosis; dog: pneumo • Serum antibody titer—toxoplasmosis, FIV,
• Respiratory—cough of any origin can be an cystosis), fungal (blastomycosis, histoplasmosis, FIP, distemper, Angiostrongylus vasorum.
inciting factor for aggravation or precipitation coccidiomycosis, cryptococcosis, aspergillosis). • Coagulation profile—for any patient that
of signs associated with tracheal collapse in • Neoplastic (primary, metastatic, compression presents with cough associated with either
susceptible breeds. • Cardiovascular— due to enlarged lymph nodes). • Chemical or epistaxis or hemoptysis. • Feces examination
enlargement or impaired function of the right traumatic (aspiration, near drowning, noxious (Baermann test: identification of
ventricle can result from a respiratory disorder fumes, foreign body, trauma, hemorrhage). Angistrongylus (dogs), Aerulostrongylus (cat),
causing tissue damage, hypoxic injury, and/or • Chronic disorders of unknown origin or other parasites (Filarial, Crenosoma).
chronic hypoxic pulmonary vasoconstriction (interstitial pulmonary fibrosis). • PCR diagnosis available for several
(cor pulmonale). microorganisms. • Tests for evaluation of
Other Diseases
SIGNALMENT • Cardiovascular diseases (pulmonary edema, possible hyperadrenocorticism (potentially
• Dogs and cats of all ages and breeds. • Much left atrial enlargement, heart-base tumor, causing pulmonary thromboembolism).
more common clinical sign in dogs than in embolism). • Gastroesophageal reflux. IMAGING
cats. • Cough of tracheal origin is less common • Compression of respiratory structures by • Thoracic radiographs are first step prior to any
in cats than in dogs. • Age, breed, and sex adjacent organs (cardiomegaly, megaesophagus, additional test—provide essential information
predispositions vary with inciting cause. hilar lymph node enlargement). about intrathoracic airways, lung parenchyma,
SIGNS • Noncardiogenic pulmonary edema (multiple pleural space, mediastinum, and cardiovascular
• Cough must be differentiated from similar causes). • Passive smoking inhalation. • Adverse system. • Thoracic computed tomography is
signs such as reverse sneezing, gagging, drug reaction—potassium bromide in cats. being more and more often used for
retching. • Description of the cough and/or identification of respiratory intrathoracic
smartphone recording of suspect sounds are problems. • Fluoroscopy—helpful to investigate
helpful in identification of the anatomic diseases in which dynamic obstruction is
Cough (continued)
suspected (tracheal collapse, bronchial collapse, Antitussives POSSIBLE COMPLICATIONS

C bronchomalacia). • Echocardiography—helpful • Hydrocodone (dog only)—0.2–0.3 mg/kg • Aggravation of tracheal collapse. • Progression
when heart failure or dysfunction is suspected. PO q 6–12h. • Butorphanol (dog only)— toward chronic bronchitis, chronic obstructive
• Thoracic ultrasonography—in case of pleural 0.25–1.1 mg/kg every 8–12h. • No pulmonary disease, lung emphysema, irrevers-
effusion or when a pulmonary or mediastinal antitussive available for cats. • In humans, ible bronchial and parenchymal remodeling,
mass is suspected. gabapentin (neuromodulator) recently bronchiectasis. • Acute severe cough might lead
DIAGNOSTIC PROCEDURES described to treat refractory chronic cough. to syncope, rib fracture, or pneumothorax.
• Gabapentin in dogs, 2–5 mg/kg by mouth • Right heart dysfunction.
• Endoscopy allows visualization of both static
(tumor, granuloma, abnormal mucosa, every 8h, but unestablished efficacy.
excessive secretions) and dynamic (laryngeal Bronchodilators
paralysis, dynamic airway collapse) airway Theophylline (for Dogs and Cats)
abnormalities. • When bronchial and/or • Pharmacokinetics are form and species MISCELLANEOUS
alveolar infiltrates are present—samples from dependent; slow-release formulations exist. AGE-RELATED FACTORS
lower airways can be obtained for diagnostic • Beneficial effects of theophylline include • In dogs with anatomic disorders of inherited
purpose (cytology, bacterial/mycologic cultures) relaxation of bronchial smooth muscle, (e.g., primary ciliary dyskinesia) or congenital
by bronchoalveolar lavage or tracheal wash. improved diaphragmatic contraction, and origin, signs might start early in life. • Puppies
• Transthoracic (fine-needle aspiration) biopsy probably some anti-inflammatory effects and kittens more likely to suffer from
or thoracoscopy—allows biopsy sample when but primary antitussive action not infectious disease. • Inflammatory disorders
interstitial infiltration is prominent. demonstrated. • Side effects are related to affect middle-aged adults. • Heart failure and
• Thoracocentesis—allows sampling of inotropic and chronotropic effects, as well tumors more frequent in older animals.
pleural fluid, can be performed under ultra- as to an increase in blood pressure; can also
sonographic guidance. • Pulse oximetry and cause nausea, diarrhea, arrhythmias, and PREGNANCY/FERTILITY/BREEDING
blood gas determination. • Pulmonary CNS excitation. • Dogs affected with primary ciliary
function tests—require sophisticated material dyskinesia. • Possible decreased fertility (in
and/or experienced technicians, not readily Beta-2 Agonists (Cats Only) male and female dogs) as cilia from urogenital
• Delivered mostly via a meter dose inhaler tract and flagellated cells can be affected.
available in private practice.
(MDI); administered IV in emergency • Proven hereditary in some breeds (Old
situations. Short-acting (salbutamol, English sheepdog; carrier test detection exists).
terbutaline, fenoterol) or long-acting
(salmeterol, formoterol) drugs. • May be SEE ALSO
TREATMENT administered temporarily to cause immediate • Asthma, Bronchitis—Cats.
• Usually treated as outpatient. • Most and temporary relief, but not as long-term • Bronchitis, Chronic.
successful management of cough involves management; have limited effect. • Side effects • Congestive Heart Failure, Left-Sided.
treatment and resolution of underlying cause include dry mouth, tachycardia, nausea; • Hypoxemia.
rather than use of medications that suppress regular inhalation of racemic and S-albuterol • Nasal Discharge.
signs. • If chronic cough is related to acute or (but not R-albuterol) induces airway • Pneumonia, Bacterial.
chronic inflammation, anti-inflammatory inflammation in both healthy and asthmatic cats. • Pneumonia, Eosinophilic.
therapy preferred to cough suppressant therapy. • Respiratory Parasites.
Expectorants • Sneezing, Reverse Sneezing, Gagging.
• Use of cough suppressant therapy must be
Guafenesin—included in some preparations • Tracheal Collapse.
limited to cases in which the cause of the
but benefit not extensively studied or proven.
cough can neither be treated medically nor ABBREVIATIONS
resolved, and in which excessive coughing leads CONTRAINDICATIONS • FeLV = feline leukemia virus.
to exhaustion of the patient or insomnia of the Antitussive agents are strictly contraindicated • FIP = feline infectious peritonitis.
owners, as well as aggravation of the disease. when cough is needed to clean the airways, • FIV = feline immunodeficiency virus.
i.e., in infectious or inflammatory airway • UACS = upper airway cough syndrome.
disease.
Suggested Reading
PRECAUTIONS Ferasin L. Coughing. In Ettinger SJ, Feldman
MEDICATIONS See side effects of respective drugs. EC, Côté E. Textbook of Veterinary Internal
DRUG(S) OF CHOICE POSSIBLE INTERACTIONS Medicine, 8th ed. St. Louis, MO: Elsevier,
Theophylline—clearance may be inhibited by 2016, 107–111.
Antimicrobial Therapy Rozanski AE, Rush JE. Acute and chronic
other drugs such as fluoroquinolones,
Indicated for tracheo-broncho-pulmonary increasing risk of theophylline toxicity. cough. In: Ettinger SJ, Feldman EC, eds.,
disease of bacterial origin. Better selected Textbook of Veterinary Internal Medicine,
based in culture and antimicrobial suscepti- 6th ed. St. Louis, MO: Elsevier, 2005,
bility testing. pp. 189–195.
Anti-inflammatory Therapy Author Cécile Clercx
• Indicated in feline bronchitis syndrome,
FOLLOW-UP Consulting Editor Elizabeth Rozanski
canine chronic bronchitis, or canine PATIENT MONITORING Acknowledgment The author and book
eosinophilic bronchopneumopathy. • Oral • Acute cough must be adequately treated in editors acknowledge the prior contribution of
prednisolone 0.5 mg/kg q12h in dogs and order to avoid chronic cough, leading to Dominique Peeters.
cats, then taper the dose progressively to possibly irreversible lesions. • Conditions
q48h. • Nebulized fluticasone or budesonide leading to chronic cough sometimes can only
100–200 μg q12h with metered dose inhaler be alleviated but not cured; communicate Client Education Handout
including spacer with face mask and inspira- with client to ensure successful management available online
tory valve. of cough.
Craniomandibular Osteopathy
OTHER LABORATORY TESTS EXPECTED COURSE AND PROGNOSIS
Serology—rule out fungal agents; indicated in • Pain and discomfort may diminish at C
atypical cases. skeletal maturity (10–12 months of age);
B ASICS exostoses may regress. • Prognosis—depends
OVERVIEW IMAGING on involvement of bones surrounding TMJ.
• Skull radiography—reveals uneven, bead-like • Elective euthanasia may be necessary.
• A non-neoplastic, noninflammatory
proliferative disease of the bones of the head. osseous proliferation of the mandible or
• Primary bones affected—mandibular rami; tympanic bullae (bilateral); extensive, periosteal
occipital and parietal; tympanic bullae; zygomatic new bone formation (exostoses) affecting one
portion of the temporal. • Bilateral symmetric or more bones around the TMJ; may show MISCELLANEOUS
involvement most common. • Affects musculo- fusion of the tympanic bullae and angular
process of the mandible. • CT—may help SYNONYMS
skeletal system. • Lion jaw. • Craniomandibular osteoarthropathy.
evaluate osseous involvement of TMJ.
SIGNALMENT • Craniomandibular osteodystrophy. • Mandibular
• Scottish, Cairn, and West Highland white DIAGNOSTIC PROCEDURES periostitis. • Westie jaw. • Scotty jaw.
terrier breeds—most common. • Labrador Bone biopsy and culture (bacterial and
ABBREVIATIONS
retrievers, Great Danes, Boston terriers, fungal)—necessary only in atypical cases; rule
• ALP = alkaline phosphatase.
Doberman pinschers, Irish setters, English out neoplasia and osteomyelitis.
bulldogs, bullmastiffs, Shetland sheepdogs, and PATHOLOGIC FINDINGS drug.
boxers—may be affected. • Usually growing • Bone biopsy—reveals normal lamellar bone • TMJ = temporomandibular joint.
puppies 4–8 months of age. • No gender being replaced by enlarged coarse-fiber bone and
predilection. • Neutering may increase incidence. Suggested Reading
osteoclastic osteolysis of periosteal or subperiosteal Franch J, Cesari JR, Font J. Craniomandibular
SIGNS region. • Bone marrow—replaced by vascular osteopathy in two Pyrenean mountain dogs.
Historical Findings
fibrous-type stroma. • Inflammatory cells— Vet Record 1998, 142(17):455–459.
• Usually relate to pain around the mouth
occasionally seen at periphery of bony lesion. Huchkowsky SL. Craniomandibular
and difficulty opening the mouth progres- osteopathy in a bullmastiff. Can Vet J 2002,
sively worsening. • Difficulty in prehension 43(11):883–885.
and mastication—may lead to starvation. LaFond E, Breur GJ, Austin CC. Breed
Physical Examination Findings TREATMENT susceptibility for developmental orthopedic
• Palliative only. • Surgical excision of diseases in dogs. J Am Anim Hosp Assoc
• Temporal and masseter muscle atrophy—
exostoses—results in regrowth within weeks. 2002, 38(5):467–477.
common. • Palpable irregular thickening of
• High-calorie, protein-rich gruel diet—helps McConnell JF, Hayes A, Platt SR, Smith KC.
mandibular rami and/or temporomandibular
maintain nutritional balance. • Surgical Calvarial hyperostosis syndrome in two
joint (TMJ) region. • Inability to fully open jaw,
placement of pharyngostomy, esophagostomy, bullmastiffs. Vet Radiol Ultrasound 2006,
even under general anesthesia. • Intermittent
or gastrostomy tube—considered to help 47(1):72–77.
pyrexia. • Bilateral exophthalmos.
maintain nutritional balance. Padgett GA, Mostosky UV. The mode of
CAUSES & RISK FACTORS inheritance of craniomandibular osteopathy
• Believed to be hereditary—occurs in certain in West Highland White terrier dogs. Am J
breeds and families. • West Highland white Med Genet 1986, 25(1):9–13.
terriers—autosomal recessive trait. • Scottish Pastor KF, Boulay JP, Schelling SH, Carpenter
terriers—possible predisposition. • Young MEDICATIONS JL. Idiopathic hyperostosis of the calvaria in
terrier with periosteal long bone disease— DRUG(S) OF CHOICE five young bullmastiffs. J Am Anim Hosp
monitor for disease. • Analgesics and anti-inflammatory Assoc 2000, 36(5):439–445.
drugs—palliative use warranted. Taylor SM, Remedios A, Myers S.
• Nonsteroidal anti-inflammatory drugs Craniomandibular osteopathy in a Shetland
(NSAIDs)—inhibit cyclooxygenase sheepdog. Can Vet J 1995, 36(7):437–439.
DIAGNOSIS enzymes. • Deracoxib (1–2 mg/kg PO Watson ADJ, Adams WM, Thomas CB.
q24h, chewable). • Carprofen (2.2 mg/kg Craniomandibular osteopathy in dogs. Compend
DIFFERENTIAL DIAGNOSIS PO q12h or 4.4 mg/kg q24h). • Meloxicam Contin Educ Pract Vet 1995, 17:911–921.
• Osteomyelitis—bones not symmetrically (load 0.2 mg/kg PO, then 0.1 mg/kg PO Author Steven M. Cogar
affected; generally not as extensive; lysis; lack q24h, liquid). • Grapiprant (2 mg/kg PO Consulting Editor Mathieu M. Glassman
of breed predilection; history of penetrating q24h). • Firocoxib (5 mg/kg PO q24h).
wound. • Traumatic periostitis—bones not
symmetrically affected; generally not as
extensive; history of trauma. • Neoplasia—
mature patient; not symmetrically affected;
more lytic bone reaction; metastatic disease. • FOLLOW-UP
Calvarial hyperostosis—young patient: frontal, PATIENT MONITORING
parietal, and occipital bones; does not involve Frequent reexaminations—mandatory to ensure
mandible; may have long bone involvement. adequate nutritional balance and pain control.
CBC/BIOCHEMISTRY/URINALYSIS PREVENTION/AVOIDANCE
• Serum alkaline phosphatase (ALP) and • Do not repeat dam–sire breedings that
inorganic phosphate—may be high. • May resulted in affected offspring. • Discourage
note hypogammaglobulinemia or breeding of affected animals.
α2-hyperglobulinemia.
Cruciate Ligament Disease, Cranial

of age. • West Highland white terrier—over- injury. • Osteochondritis dissecans of femoral
C represented affected small breed. condyle. • Neoplasia (e.g., synovial sarcoma,
osteosarcoma, chondrosarcoma). • Traumatic
BASICS Mean Age and Range fractures or avulsions. • Caudal cruciate
• Incidence increases with age >5 years. ligament rupture—uncommon and generally
DEFINITION
• Large- to giant-breed dogs may present only seen with significant trauma.
The acute or progressive failure of the
earlier in life; approx. 2 years of age.
cranial cruciate ligament (CrCL), which CBC/BIOCHEMISTRY/URINALYSIS
results in partial to complete instability of Predominant Sex N/A
the stifle joint. Female—neutered.
PATHOPHYSIOLOGY SIGNS N/A
• Function of the CrCL includes passive
General Comments IMAGING
constraint of the stifle joint by limiting
Severity of lameness—related to degree of
internal rotation of the tibia, hyperextension Radiography
rupture (partial vs. complete), mode of
of the stifle, and cranial displacement of the • Verify secondary intra-articular changes such
rupture (acute vs. chronic), occurrence of
tibia relative to the femur. • Two distinct as DJD and rule out other differentials.
meniscal injury, and severity of inflammation
bands—craniomedial band is taut on both • Common findings—joint effusion with
and DJD. Condition and therefore lameness
flexion and extension of the joint (primary capsular distention and effacement of
may be bilateral.
check) and caudolateral band is taut in infrapatellar fat pad; periarticular osteophytes;
extension and lax in flexion (secondary check). Historical Findings enthesiophytes; CrCL avulsion fractures;
• Types of injury: • Athletic or traumatic events—generally calcification of CrCL and/or menisci. • Cats
⚬ Avulsion—skeletally immature animals precede acute injuries. • Normal activity commonly have mineralized menisci present
in which acute load results in avulsion of resulting in acute lameness—suggests (incidental finding). • Necessary for preopera-
the origin or insertion of the ligament. degenerative rupture. • Subtle to marked tive planning with osteotomy procedures.
⚬ Acute (traumatic) rupture—result of intermittent lameness (for weeks to months)—
consistent with partial tears that are progress- Alternative Diagnostic Imaging
hyperextension, limb overloading, or
ing to complete rupture. Ultrasound and MRI—facility and operator
internal rotation; mid-substance tear of the
dependent.
CrCL; most common cause in cats. Physical Examination Findings
⚬ Progressive (chronic) degeneration • Varying degrees of lameness and joint DIAGNOSTIC PROCEDURES
pathogenesis remains elusive; decreases in effusion, pain, and/or crepitus; affected limb • Arthrocentesis—rule out sepsis or immune-
elasticity, stress/strain energy, failure to generally held in partial flexion while mediated disease. • Arthroscopy—gold
maintain collagen fiber organization, and standing. • Cranial drawer test—diagnostic standard; direct visualization and magnifica-
chondroid metaplasia—most common for rupture; test in flexion, normal standing tion of cruciate ligaments, menisci, and other
cause in dogs. angle, and extension. • Tibial compression intra-articular structures.
• Repetitive subclinical injury may be due to test—cranial movement of tibia relative to PATHOLOGIC FINDINGS
neuromuscular incoordination, aging, femur when tightening gastrocnemius by • Varying degrees of synovitis, cartilage
conformational abnormalities (excessive tibial flexing hock. • Medial periarticular thicken- fibrillation, and erosion. • Periarticular
plateau angle (TPA), medial luxating patella, ing (medial buttress). • Presence of click or osteophyte formation. • Meniscal damage.
narrow intercondylar notch), breed variations, pop—63% accurate in detecting meniscal • Ruptured fibers of CrCL—hyalinization;
poor muscle tone related to sedentary habits injury. • Hind limb muscle atrophy—espe- fibrous tissue invasion; necrosis; loss of
or limb immobilization, and possibly immune- cially quadriceps muscle group. • False- parallel orientation of ligament bundles.
mediated damage. • Complete and partial negative drawer or compression tests with
tears exist in varying degrees. • Untreated chronic or partial tears and in painful or
instability leads to degenerative osteoarthritic anxious patients that are not sedated or
changes within a few weeks; severe within a anesthetized. • Earliest sign of partial rupture
few months. • Medial meniscal (caudal horn) TREATMENT
is pain on hyperextension of stifle.
damage occurs in 33.2–77% of cases—due to APPROPRIATE HEALTH CARE
shearing force during drawer. CAUSES • Stabilization surgery—recommended; speeds
• Trauma. • Repetitive microinjury;
SYSTEMS AFFECTED rate of recovery; reduces degenerative changes;
excessive stifle loading. • Progressive enhances function. • Conservative manage-
Musculoskeletal, ± neurologic. degeneration. ment—diet, nonsteroidal anti-inflammatory
GENETICS RISK FACTORS drugs (NSAIDs), physical rehabilitation,
Suspected • Obesity. • Patella luxation. • Conformati weight loss; approx. 66% of patients have
INCIDENCE/PREVALENCE onal abnormalities. • Excessive caudal slope improved function over course of >1 year;
Most common cause of hind limb lameness of tibial plateau. • Narrowed intercondylar DJD is progressive; not generally recommended.
in dogs; major cause of degenerative joint notch. NURSING CARE
disease (DJD) in the stifle joint. Postsurgery—restricted activity with physical
SIGNALMENT rehabilitation (e.g., ice packing, range-of-
motion exercises, massage, and muscle
SPECIES
Dog and cat. DIAGNOSIS electrical stimulation); important for
improving mobility and strength.
Breed Predilections DIFFERENTIAL DIAGNOSIS
• Puppy laxity—positive drawer motion that ACTIVITY
• All susceptible. • Rottweiler and Labrador
stops abruptly as CrCL is stretched taut. Restricted—duration depends on method of
retriever—increased incidence when <4 years
• Patella luxation (medial or lateral). • Collateral treatment and progress of patient.
ligament injury, long digital extensor tendon
(continued) Cruciate Ligament Disease, Cranial

DIET PREGNANCY/FERTILITY/BREEDING
• Weight control—important for decreasing N/A C
load and thus stress on stifle joint. • Joint-health SEE ALSO
diets rich in omega-3 fatty acids and chondro- MEDICATIONS
• Arthritis (Osteoarthritis).
protectants may support overall joint health. DRUG(S) OF CHOICE • Patellar Luxation.
CLIENT EDUCATION NSAIDs—minimize pain; decrease inflamm-
ation. ABBREVIATIONS
• Regardless of treatment, DJD is common • CrCL = cranial cruciate ligament.
and progressive. • Return to full athletic CONTRAINDICATIONS
• DJD = degenerative joint disease.
function is possible, but requires early surgical Avoid concurrent use of corticosteroids with
intervention and rehabilitation. • Rupture of NSAIDs.
drug.
contralateral CrCL can occur in 37–48% of PRECAUTIONS • TPA = tibial plateau angle.
patients. NSAIDs—gastrointestinal irritation or renal/ • TPLO = tibial plateau leveling osteotomy.
SURGICAL CONSIDERATIONS hepatic toxicity may preclude use in some patients.
Suggested Reading
• No one technique has proven consistently POSSIBLE INTERACTIONS
Aragon CL, Budsberg SC. Applications of
superior, clinically or radiographically. • Recent N/A
evidence-based medicine: cranial cruciate
force plate studies show slight differences ALTERNATIVE DRUG(S) ligament injury repair in the dog. Vet Surg
between common techniques; dogs with tibial • Chondroprotective drugs (polysulfated 2005, 34:93–98.
plateau leveling osteotomy (TPLO) procedure glycosaminoglycans, glucosamine, and Balzter WI, Smith-Ostrin S, Warnock JJ, Ruaux
achieve normal limb loading faster than with chondroitin sulfate) may help reduce cartilage CG. Evaluation of the clinical effects of diet
extracapsular procedure. damage and improve regeneration. and physical rehabilitation in dogs following
Extra-articular Methods • Omega-3 fatty acid supplementation to tibial plateau leveling osteotomy. J Am Vet
• Wide variety of techniques that use an reduce inflammation is recommended. Med Assoc 2018, 252:686–700.
implant to mimic CrCL and restore stability; Christopher SA, Beetem J, Cook JL.
these techniques rely on periarticular fibrosis Comparison of long-term outcomes
for long-term stability. • Alternative method associated with three surgical techniques for
includes fibular head transposition to realign FOLLOW-UP treatment of cranial cruciate ligament
and tension lateral collateral ligament in order disease in dogs. Vet Surg 2013,
to restrict internal rotation and cranial drawer. PATIENT MONITORING 42(3):329–334.
Most techniques require 2–4 months of Comerford EJ, Smith K, Hayashi K. Update
Intra-articular Methods rehabilitation.
Designed to replace CrCL anatomically with on the aetiopathogenesis of canine cranial
PREVENTION/AVOIDANCE cruciate ligament disease. Vet Comp
autografts (patellar ligament, fascia), allografts,
Avoid breeding animals with conformational Orthop Traumatol 2011, 24:91–98.
xenografts, and synthetic materials.
abnormalities. Krotscheck U, Nelson SA, Todhunter RJ,
Osteotomy Procedures POSSIBLE COMPLICATIONS et al. Long-term functional outcome of
Cranial Tibial Closing Wedge Osteotomy • Subsequent meniscal injury can occur in Tibial Tuberosity Advancement vs. Tibial
• Levels TPA by removing cranially based 6–22% of patients. • Incisional and/or Plateau Leveling Osteotomy and extracap-
wedge of bone from proximal tibia and implant-related infection. • Tibial tuberosity sular repair in a heterogenous population of
eliminates cranial thrust. • Held in place with avulsion and/or fractures. • Patellar luxation. dogs. Vet Surg 2016, 45(2):261–268.
bone plate and screws. • Can potentially • Delayed bone healing (osteotomy proce- Wucherer KL, Conzemius MG, Evans R,
shorten tibia and alter stifle biomechanics. dures). • Pivot shift—unknown clinical Wilke VL. Short-term and long-term
significance <2% (self-limiting). outcomes for overweight dogs with cranial
TPLO cruciate ligament rupture treated surgically
• Rotational osteotomy of proximal tibia to level EXPECTED COURSE AND PROGNOSIS
Regardless of surgical technique, success rate or nonsurgically. J Am Vet Med Assoc 2013,
TPA and neutralize cranial tibial thrust. • Held 242:1364–1372.
in place with bone plate and screws. • Can better than 85%.
Author Marian E. Benitez
accomplish correction for angular and torsional Consulting Editor Mathieu M. Glassman
deformities.
Tibial Tuberosity Advancement
• Tibial crest osteotomy; crest is held in MISCELLANEOUS Client Education Handout
advanced position with cage and plate; bone ASSOCIATED CONDITIONS available online
graft fills defect. • Active control of cranial Meniscal damage.
tibial displacement improved, which helps
stabilize stifle. • Can combine technique with AGE-RELATED FACTORS
lateral transposition of tibial tuberosity to See Pathophysiology.
correct concurrent medial luxating patella. ZOONOTIC POTENTIAL
N/A
Cryptococcosis
SIGNS infectious peritonitis (FIP), other infections
C Historical Findings (fungal, Toxoplasma).
B ASICS • Lethargy. • Varies depending on organ CBC/BIOCHEMISTRY/URINALYSIS
systems involved. • May have signs/problems • Mild anemia in some cats. • Eosinophilia
DEFINITION for weeks to months. occasionally seen. • Chemistry usually normal.
A localized or systemic fungal infection
caused by the environmental yeast Dogs OTHER LABORATORY TESTS
Cryptococcus spp., most commonly • Neurologic—seizures, ataxia, paresis. • Latex agglutination or ELISA—detect
C. neoformans and C. gattii. • Ocular signs—periorbital swelling, blind- cryptococcal capsular antigen in serum or
ness, uveitis, hyphema. • Skin ulceration. cerebrospinal fluid (CSF); highly sensitive
PATHOPHYSIOLOGY • Lymphadenopathy. • Respiratory—upper assay; most infected animals have measurable
• C. neoformans—grows in bird droppings respiratory signs, labored breathing, coughing. capsular antigen titers; magnitude of titer
and decaying vegetation; soil disturbance • Vomiting, diarrhea, and anorexia. correlates with extent of infection. • May be
increases risk of infection. • Dogs and cats less sensitive in dogs. • May be positive with
inhale the yeast and a focus of infection is Cats
• Nasal discharge and ocular signs.
colonization alone; antigen titers 1 : 32 or
established, usually in nasal passages; greater seen with fungal invasion.
smaller dried, shrunken organisms may • Neurologic signs—seizures, disorientation,
reach the terminal airways (uncommon). vestibular signs. • Granulomatous tissue seen IMAGING
• There may be colonization or subclinical at the nares. • Firm swellings over the bridge • Nasal radiographs (cats)—soft tissue density
infection of nasal passages that spontane- of the nose. • Lymphadenopathy. • Respiratory material in nasal passage; bone destruction of
ously resolves. • Stomach and intestinal abnormalities less commonly noted. nasal dorsum. • Contrast-enhanced CT or
infections suggest that primary gastrointes- Physical Examination Findings MRI best for identifying brain and nasal
tinal entry can occur. • Dissemination— • Mild fever—<50% of patients. • Dogs—
lesions. • Thoracic radiographs—can identify
hematogenously spread via macrophages nasal discharge, multifocal CNS abnormali- lower respiratory tract disease.
from nasal passages to brain, eyes, lungs, ties, ataxia, anterior uveitis. DIAGNOSTIC PROCEDURES
and other tissues; by extension to skin of • Cats—respiratory noise (stertor), nasofacial Dogs
nose, eyes, retro-orbital tissues, and draining swelling, ulcerated crusting skin lesions on the Neurologic disease—additional procedures:
lymph nodes. head, lymphadenopathy, neurologic abnor- cytologic examination and culture of CSF,
SYSTEMS AFFECTED malities (behavior change, circling, vestibular other CSF infectious disease testing,
• Cats—mainly respiratory (nose, nasophar- signs, ataxia), ocular abnormalities (blindness, measurement of CSF capsular antigen.
ynx, and sinuses), skin (nasal planum), optic neuritis, retinal detachment).
Cats
nervous, ophthalmic, and lymphatic. CAUSES • Cytology of impression smears or aspirates of
• Dogs—mainly skin (over nose and sinuses), Exposure to cryptococcal organisms and mucoid material from nasal passages, or biopsy
respiratory (nasal passages, occasionally inability of immune system to prevent of granulomatous tissue protruding from
lungs), nervous (brain), lymphatic, and colonization and tissue invasion. nares—characteristic yeast with large nega-
ophthalmic.
RISK FACTORS tively- staining (clear) capsule. • Aspirates of
INCIDENCE/PREVALENCE • Exposure to disrupted soil. • Infection with lymph nodes or subcutaneous swellings often
• Dogs—rare in United States; prevalence feline leukemia virus (FeLV) or feline immuno- high yield. • Sedated oropharyngeal exam—in
0.00013%. • Cats—7–10 times more deficiency virus (FIV). patients with upper respiratory obstruction/
common than in dogs; most common systemic noise: may identify granuloma in nasopharynx
mycoses of cats. (spay hook or endoscope to expose the mass).
GEOGRAPHIC DISTRIBUTION • Biopsy—skin lesions. • Cultures—confirm
diagnosis; determine drug susceptibility.
• Worldwide. • Some areas of southern DIAGNOSIS
California and Australia have an increased PATHOLOGIC FINDINGS
incidence and an outbreak has occurred on DIFFERENTIAL DIAGNOSIS
• Gross lesions—gray, gelatinous mass produced
Vancouver Island in British Columbia, Dogs by polysaccharide capsule; in nose, sinuses, and
Canada. • C. gattii grows well around • Other causes of focal or diffuse neurologic nasopharynx of cats; skin lesions usually
eucalyptus trees. disease—distemper, inflammatory menin- ulcerative. • Neurologic lesions—more common
SIGNALMENT goencephalomyelitis, infectious meningoen- in dogs; diffuse or focal CNS granulomas.
cephalitis (bacterial, rickettsial, protozoal), • Chorioretinitis with or without retinal detach-
Species neoplasia, fungal diseases (depending on ment or optic neuritis. • Histologic response—
Dog and cat. geography). • Nasal lesions, especially at usually pyogranulomatous; inflammatory cell
Breed Predilections mucocutaneous junction—immune-medi- infiltrate may be mild as polysaccharide capsule
• Dogs—American cocker spaniels (United ated, neoplasia (squamous cell carcinoma). interferes with neutrophil migration; organism
States), Doberman pinschers and German • Lymphadenopathy—lymphoma, fungal characterized by capsulate yeast with narrow-
shepherd dogs (Australia) may be overrepre- disease. • Chorioretinitis and optic neuritis— neck budding.
sented. • Cats—Siamese may be at increased fungal infections, distemper, neoplasia.
risk. Cats
Mean Age and Range • Nasal disease—nasal tumors, chronic
• Most commonly cats and dogs <6 years of rhinitis, chronic sinusitis. • Ulcerative skin TREATMENT
age. • Can occur at any age. changes—bacterial infection, trauma, neoplasia
(squamous cell carcinoma). • Ocular and APPROPRIATE HEALTH CARE
Predominant Sex • Outpatient if stable. • Neurologic signs—
neurologic abnormalities—lymphoma, feline
• Dogs—none. • Cats—males may be may initially require inpatient supportive care.
overrepresented.
(continued) Cryptococcosis
NURSING CARE dermatitis (differentiate from skin lesions of AGE-RELATED FACTORS
Cats—nasal obstruction influences appetite; cryptococcosis); new skin lesions after disease N/A C
encourage to eat by offering warmed, palatable is much improved should be considered a ZOONOTIC POTENTIAL
food. drug reaction. • Amphotericin B—nephro- • Not considered zoonotic, but possibility of
ACTIVITY toxicity; caution if patient is azotemic, but transmission through bite wounds. • Inform
N/A not absolute contraindication if life-threaten- client that organism was acquired from the
ing infection. • Terbinafine—monitor for environment and that he or she could be at
DIET hepatic toxicity and anorexia.
Patients treated with itraconazole—give increased risk, especially if immunosuppressed.
medication in fatty food (e.g., canned food) ALTERNATIVE DRUG(S) PREGNANCY/FERTILITY/BREEDING
to improve absorption. Cryptococcal organisms are prone to Azole drugs can be teratogenic and should be
becoming resistant to antifungal treatment. used in pregnant animals only if the potential
CLIENT EDUCATION
• Inform client that this is a chronic disease
benefit justifies the potential risk to offspring.
that requires months of treatment. • Reassure ABBREVIATIONS
client that infection is not zoonotic. • CSF = cerebrospinal fluid.
FOLLOW-UP • FeLV = feline leukemia virus.
PATIENT MONITORING • FIP = feline infectious peritonitis.
Remove granulomatous masses in nasophar-
• Monitor liver enzyme activities monthly • FIV = feline immunodeficiency virus.
ynx to reduce respiratory difficulties.
(especially early in treatment) in patients receiving Suggested Reading
triazole antifungal agent. • Improvement in O’Brien CR, Krockenberger MB, Martin P,
clinical signs, resolution of lesions, improvement et al. Long-term outcome of therapy for 59
in wellbeing, and return of appetite measure cats and 11 dogs with cryptococcosis. Aust
MEDICATIONS response to treatment. • Capsular antigen Vet J 2006, 84:384–392.
DRUG(S) OF CHOICE titers—after 2–3 months of treatment, titers O’Brien CR, Krockenberger MB, Wigney
• Fluconazole—preferred for ocular or CNS should decrease if treatment is effective; if DI, et al. Retrospective study of feline and
disease (water soluble and better penetrates ineffective, try terbinafine, because organism may canine cryptococcosis in Australia from
CNS); cats: 50 mg/cat PO q12–24h; dogs: become resistant. • Continue monitoring antigen 1981 to 2001: 195 cases. Med Mycol 2004,
5 mg/kg PO q12h; most economical drug titers every 1–2 months during treatment and 42:449–460.
choice. • Itraconazole—cats: 10 mg/kg PO after discontinuing treatment. • Ideally treat until Pennisi MG, Hartmann K, Lloret A, et al.
q24h; dogs: 5 mg/kg PO q12h; pellets in cryptococcal antigen titers reach zero (may take Cryptococcosis in cats: ABCD guidelines
capsule can be mixed with fatty food; >2 years). on prevention and management. J Feline
itraconazole liquid has better absorption on PREVENTION/AVOIDANCE Med Surg 2013, 15:611–618.
empty stomach and compounded itraconazole The organism is ubiquitous and cannot be Sykes JE, Hodge G, Singapuri A, et al. In
is not recommended. • Amphotericin B may avoided. vivo development of fluconazole resistance
have some advantage in severe disease at a in serial Cryptococcus gattii isolates from a
dosage of 0.25 mg/kg IV q48h, given slowly POSSIBLE COMPLICATIONS
cat. Med Mycol 2017, 55:396–401.
over 3–4h, up to a total cumulative dose of Patients with neurologic disease may have
Trivedi SR, Sykes JE, Cannon MS, et al.
4–16 mg/kg; monitor renal function closely. seizures and permanent neurologic deficits.
Clinical features and epidemiology of
• Terbinafine (5 mg/kg PO q12h, 10 mg/kg EXPECTED COURSE AND PROGNOSIS cryptococcosis in cats and dogs in
PO q24h) effective for treatment of cats with Treatment—anticipated duration 4 months California: 93 cases (1988–2010). J Am Vet
resistant infections. • Flucytosine—25–50 mg/ to ≥1 year; patients with CNS disease may Med Assoc 2011, 239:357–369.
kg PO q6h; synergistic with amphotericin B, require lifelong maintenance; median time of Author Daniel S. Foy
may allow lower doses and decrease renal successful treatment with fluconazole 4 Consulting Editor Amie Koenig
toxicity. Do not use as single agent. months; median time for itraconazole
CONTRAINDICATIONS treatment 8 months.
Caution with concurrent steroid use (immuno-
available online
suppression).
PRECAUTIONS
• Triazoles—hepatotoxicity; anorexia signals MISCELLANEOUS
problems; monitor liver enzyme activities ASSOCIATED CONDITIONS
monthly initially. • Itraconazole—ulcerative N/A
Cryptorchidism
C
B ASICS DIAGNOSIS FOLLOW-UP
OVERVIEW DIFFERENTIAL DIAGNOSIS Migration of testes into the scrotum after 4
• Incomplete scrotal descent of one or both • Bilateral—previously castrated patient.
months is unlikely; rare after 6 months.
testes; most common testicular congenital • Unilateral—remaining abdominal or inguinal
anomaly. testis after removal of single scrotal testis.
• Abdominal or inguinal location for
undescended testis or testes.
Transrectal prostate exam—intact males have MISCELLANEOUS
• Diagnosis usually made at 2 months of age
pronounced prostate; prostate of larger breeds ASSOCIATED CONDITIONS
(i.e., descent to scrotal position should occur
may be beyond reach. • Inguinal or umbilical hernia.
before this time), with some exceptions of full
descent occurring between 2 and 6 months of OTHER LABORATORY TESTS • Hip dysplasia.
age. • Human chorionic gonadotropin (hCG) • Patellar luxation.
• Abdominally retained testicles typically lack or gonadotropin-releasing hormone • Penile and preputial defects (e.g.,
spermatozoa and have only Sertoli cells in the (GnRH) stimulation test (differentiate hypospadias).
seminiferous tubules; estradiol (E2) and cryptorchidism from castrated)—collect SEE ALSO
testosterone (T) can be present in normal blood sample for baseline T analysis; • Seminoma.
systemic concentrations in affected animals. administer 750 IU hCG IV or 50 μg • Sertoli Cell Tumor.
• Unilaterally cryptorchid animals are GnRH IM; repeat sample collection for T • Sexual Development Disorders.
typically fertile. analysis in 2–3 hours; twofold increase in
ABBREVIATIONS
T from baseline indicates presence of
SIGNALMENT • E2 = estradiol.
testicular tissue.
• Cats—purebred cats have higher incidence. • hCG = human chorionic gonadotropin.
• Canine anti-Müllerian hormone concentra-
• Dogs—toy and miniature breeds at 2.7 • GnRH = gonadotropin-releasing hormone.
tion—increased level indicates testicular
times greater risk than large breeds of being • PMDS = persistent Mullerian duct
Sertoli cells present.
affected; high rates in miniature schnauzers syndrome.
with persistent Müllerian duct syndrome IMAGING • T = testosterone.
(PMDS). Ultrasonography—highly sensitive for
identification of inguinal or abdominal testes.
Suggested Reading
• Incidence—rates up to 24.1% in some
Feldman EC, Nelson RW. Canine and Feline
purebred dogs (compared to 2.1% in overall Endocrinology and Reproduction.
population) with 50% incidence in dogs with Philadelphia, PA: Saunders, 1987, pp.
PMDS; in cats observed rates range from 1.3 697–699.
to 6.2%. TREATMENT Felumlee AE, Reichle JK, Hecht S, et al. Use
• Unilateral more common than bilateral;
• Identification and removal of undescended of ultrasound to locate retained testes in
right testis retained twice as often in dogs, but testis or testes. dogs and cats. Vet Radiol Ultrasound 2012,
with equal frequency in cats. • Orchiopexy—surgical tacking of retained 53(5):581–585.
• Genetics—estimated medium level of
testis into scrotum; results in misrepresentation Khan FA, Gartley CJ, Khanam A. Canine
heritability with multifactorial genetic basis; of individual’s true phenotype and genotype. cryptorchidism: an update. Reprod Dom
females act as genetic carriers for the trait. • hCG or GnRH—little controlled evidence Anim 2018, 53(6):1263–1270.
SIGNS establishing efficacy or protocol; ethical Little S. Feline reproduction: problems and
• Absence of one, or both, testicles from the concerns same as with orchiopexy. clinical challenges. J Feline Med Surg 2011,
scrotum in a patient without history of • Failure to remove retained testis—increased 13:508–515.
castration. risk of testicular neoplasia (13.6 times Author Candace C. Lyman
• Cats—strong urine odor, tom cat marking greater), spermatic cord torsion; 53% of Consulting Editor Erin E. Runcan
behavior, presence of penile spines. Sertoli cell tumors and 36% of seminomas Acknowledgment The author and book
• Abdominal pain, lameness, vomiting— occur in retained testes. editors acknowledge the prior contribution of
increased risk exists for spermatic cord torsion Carlos R.F. Pinto.
of neoplastic, retained testes.
• Feminizing paraneoplastic syndrome—
estrogen-secreting Sertoli cell tumors produce
feminizing signs including gynecomastia,
MEDICATIONS
symmetric alopecia of trunk and flanks, DRUG(S) OF CHOICE
hyperpigmentation of inguinal skin, To possibly induce descent of retained
pendulous preputial sheath, prostatic testicle:
squamous metaplasia. • hCG (dogs)—100–1,000 IU IM 4 times in
2-week period before 16 weeks of age.
• GnRH (dogs)—50–750 μg IM 1–6 times
• Affected males or carriers (i.e., females or
between 2 and 4 months of age.
nonaffected males of cryptorchid littermates)
• Buserelin (GnRH analogue; dogs)—10 μg,
present in breeding lines.
once weekly, for 3 doses.
• Carriers produce increased number of males
per litter and increased litter size; efforts to
eliminate cryptorchidism difficult in these
circumstances.
Cryptosporidiosis
• Metabolic—hypoadrenocorticism, • Tylosin—11 mg/kg PO q12h for 28 days;
hyperthyroidism (cats). reported effective in cat with concurrent C
• Infiltrative diseases—e.g., inflammatory lymphocytic duodenitis.
B ASICS bowel disease, intestinal lymphoma. • Nitazoxanide (Alinia®)—25 mg/kg PO
OVERVIEW • Dietary indiscretion or intolerance. q24h for 7–28 days; reduces oocyst shedding
• Cryptosporidium spp.—apicomplexan • Toxicities—medications, lead, etc. in cats; associated with vomiting (responsive
protozoan causing gastrointestinal disease; CBC/BIOCHEMISTRY/URINALYSIS to antiemetics); used in limited number of
ubiquitous in nature with worldwide Usually normal, can reflect underlying disease. cats.
distribution.
• Infection—sporulated oocysts are ingested, DIAGNOSTIC PROCEDURES
sporozoites are released and penetrate • Sugar and zinc sulfate centrifugal flotation—
intestinal epithelial cells; after asexual specific gravity = 1.18–1.3; concentrates fecal
reproduction, merozoites released to infect oocysts (oocysts are 5 μm, routine salt flotation FOLLOW-UP
often fails); oocysts best seen with modified • Treatment efficacy based on clinical
other cells, sexual reproduction follows, then
acid-fast stain, may have slight pink color. improvement.
oocyst shedding.
• Fecal antigen detection test (ProSpecT • Monitor oocyst shedding in feces 2 weeks
• Prepatent period—5–10 days (cats).
Cryptosporidium Microtiter Assay, Color-Vue after treatment completion or if signs persist.
• Immunocompetent animals—intestinal
Cryptosporidium) available for humans. • Prognosis excellent if underlying disease
disease.
• Fluorescent antibody assay—veterinary treated.
• Immunocompromised animals—intestinal,
liver, gallbladder, pancreatic, respiratory diagnostic laboratories.
infection. • PCR—commercial laboratories; more
• Dogs—prevalence 0.5% worldwide; sensitive for diagnosis than other techniques.
2–17% in the United States. • Submitting feces to laboratory—laboratory- MISCELLANEOUS
• Cats—prevalence 0–29% worldwide; specific protocols; can mix 1 part 100%
formalin with 9 parts feces to inactivate oocysts ZOONOTIC POTENTIAL
2–15% in the United States. Possible—transmission of infection from dogs
and decrease health risk to laboratory personnel.
SIGNALMENT and cats to humans possible; in general,
• No sex or breed predilection.
PATHOLOGIC FINDINGS transmission from pets to people rare.
• Gross lesions—enlarged mesenteric lymph
• Dogs—virtually all clinical cases in Disinfection
immunocompromised animals or animals <6 nodes, hyperemic intestinal (especially ileal)
mucosa; fix specimens in Bouin’s or formalin • 10% formaldehyde solution or 5%
months of age; older dogs can excrete oocysts ammonia solution will kill oocysts, but
without clinical signs. solution within hours of death; autolysis causes
rapid loss of intestinal surface with organisms. requires 18 hours of exposure; 50% ammonia
• Cats—more common in immuno solution kills oocysts in 30 minutes.
• Microscopic lesions—villous atrophy,
compromised cats or kittens <6 months of age. • Resistant to commercial bleach (5.25%
reactive lymphoid tissue, inflammatory
SIGNS infiltrates in lamina propria; parasites sodium hypochlorite) and chlorination of
• Most infections subclinical. throughout intestines, most numerous in drinking water.
• Principally small bowel diarrhea; large distal small intestine. • Moist heat (steam or pasteurization,
bowel diarrhea reported. >55 °C), freezing and thawing or thorough
drying also effective.
• C. canis (dogs), C. felis (cats)—ingestion of Suggested Reading
Lucio-Forster A, Griffiths JK, Cama VA, et al.
contaminated water or feces. TREATMENT Minimal zoonotic risk of cryptosporidiosis
• Morphologically, intestinal Cryptosporidium • Outpatient.
species very similar. from pet dogs and cats. Trends Parasitol
• In immunocompetent animals—diarrhea
• Some species are host specific (C. canis, C. 2010, 26:174–179.
usually mild and self-limiting; withhold food
felis); others (C. parvum, C. muris) infect Authors Matt Brewer and Jeba R.J. Jesudoss
for 24–48h to control diarrhea; oral glucose-
multiple species. Chelladurai
electrolyte solution if mild diarrhea;
• Immunosuppression—major risk factor; Consulting Editor Amie Koenig
parenteral fluids (isotonic with potassium
common causes feline leukemia virus, canine added) if severe diarrhea.
distemper virus, canine parvovirus, intestinal
lymphoma.
• Immunocompetent animals—usually asympto
matic infection with fecal oocyst shedding.
MEDICATIONS
DRUG(S) OF CHOICE
• No drugs currently labeled for animal use
in United States.
DIAGNOSIS • Paromomycin (Humatin®)—125–165 mg/
DIFFERENTIAL DIAGNOSIS kg PO q12h for 5 days; aminoglycoside
• Parasites—giardiasis, trichuriasis. effective in humans with acute intestinal
• Infectious agents—parvovirus, coronavirus, symptoms; may cause nephropathy in young
feline infectious peritonitis, Salmonella, animals with damaged gastrointestinal barrier;
Campylobacter, Rickettsia, Histoplasma. monitor urine for casts during therapy.
Crystalluria
SIGNS • Large numbers in serial samples raises
C None, or those caused by concomitant suspicion of abnormality in bilirubin
urolithiasis. metabolism.
BASICS • Usually associated with underlying diseases
CAUSES
DEFINITION in cats.
Appearance of crystals in urine. This finding In Vivo Variables
• Concentration of crystallogenic substances
Calcium Oxalate Monohydrate
may be normal, clinically significant or
in urine (in turn influenced by rate of and Calcium Oxalate Dihydrate
artifactual.
excretion and urine concentration). Crystalluria
PATHOPHYSIOLOGY • Urine pH (struvite and calcium phosphate • May be observed in apparently healthy
• Identification of crystals formed in vitro most common in neutral-to-alkaline urine; dogs and cats and in dogs and cats with
does not justify therapy. ammonium urate, sodium urate, calcium uroliths primarily composed of calcium
• Crystals form only in urine that is, or recently oxalate, cystine, and xanthine crystals most oxalate.
has been, supersaturated with crystallogenic common in acid-to-neutral urine). • Calcium oxalate monohydrate crystals most
substances; thus in vivo crystalluria represents • Solubility of crystallogenic substances in commonly associated with ethylene glycol
risk factor for urolithiasis. urine. toxicity, but calcium oxalate dihydrate may be
• Certain crystal types such as cystine, urate, • Excretion of diagnostic agents (e.g., radio- observed, or ethylene glycol toxicity may
or 2,8-dihydroxyadenine may indicate paque contrast agents) and medications (e.g., occur without crystalluria.
underlying disease; proper identification and sulfonamides).
interpretation of urine crystals important in Calcium Phosphate Crystalluria
• Dietary influence—hospital diet may differ • Large numbers of crystals presumed to be
formulation of medical protocols to dissolve from home diet; timing of sample collection
uroliths. composed of calcium phosphate have been
(fasting vs. postprandial) may influence observed in apparently healthy dogs, dogs
• Crystalluria in individuals with anatomi- evidence of crystalluria.
cally and functionally normal urinary with persistently alkaline urine, dogs with
tracts usually harmless because crystals In Vitro Variables calcium phosphate uroliths, and dogs with
eliminated before they grow large enough • Temperature. uroliths composed of mixture of calcium
to interfere with normal urinary function; • Evaporation. phosphate and calcium oxalate.
however, they represent a risk factor for • pH changes following sample collection. • Small numbers of calcium phosphate
urolithiasis. • Technique of specimen preparation— crystals may occur in association with
• Crystals that form following elimination or centrifugation versus noncentrifugation, infection-induced struvite crystalluria.
removal of urine from the patient often are of volume of urine examined. • May be observed in dogs and cats with
little clinical importance; in recent studies • Important in vitro changes that occur primary hyperparathyroidism, and renal
following time and temperature changes, following urine collection may enhance tubular acidosis.
crystals formed in 28% of dog and cat formation or dissolution of crystals; when Struvite Crystalluria
samples that were initially free of crystals. knowledge of in vivo urine crystal type and • Observed in many dogs and cats that are
• Detection of some types of crystals (e.g., quantity especially important, examine fresh healthy and as an artifact.
cystine and ammonium urate) in clinically specimens, ideally at body temperature; if not • Observed in dogs and cats with urinary
asymptomatic patients or detection of any form possible, they should be at room temperature, tract disease without uroliths.
of crystals in fresh urine collected from patients not refrigeration temperature. • Observed in dogs and cats with infection-
with confirmed urolithiasis may have diagnostic, • Collection container—spurious crystals induced struvite uroliths, sterile struvite
prognostic, or therapeutic importance. may be contaminants from unclean collection uroliths, nonstruvite uroliths, and uroliths of
• Drug crystals detected in patients admin containers. mixed composition (e.g., nucleus composed
istered high doses of medications such as RISK FACTORS of calcium oxalate and shell composed of
allopurinol, sulfadiazines, or fluoroquinolones See preceding discussion. struvite).
should prompt therapy changes due to risk
for formation of drug-containing uroliths. Cystine Crystalluria
Observed in dogs and cats with inborn
SYSTEMS AFFECTED errors of metabolism characterized by
Renal/urologic/hepatic. DIAGNOSIS abnormal transport of cystine and other
SIGNALMENT DIFFERENTIAL DIAGNOSIS dibasic amino acids; this metabolism defect
• Calcium oxalate in miniature schnauzer, can also lead to dilated cardiomyopathy
bichon frisé, Yorkshire terrier, Lhasa apso, Ammonium Urate, Sodium Urate, in cats.
miniature poodle dogs; Burmese, Himalayan, and Amorphous Urate Crystalluria
• Uncommonly seen in apparently healthy
Uric Acid Crystalluria
Persian cats. • Uncommon in dogs and cats.
• Cystine in dachshunds, English bulldogs, dogs and cats.
• Importance as described for ammonium
Newfoundlands, and others. • Frequently seen in dogs and occasionally in
cats with portal vascular anomalies, with or and amorphous urates.
• Ammonium urate in Dalmatians and
English bulldogs. without concomitant ammonium urate Xanthine Crystalluria
• Struvite in any dog with concomitant uroliths. • Suggests administration of excessive dosages
urinary tract infection (UTI). • Observed in some dogs and cats with urate of allopurinol in conjunction with consumption
• Struvite in cats not typically associated uroliths caused by disorders other than portal of relatively high amounts of dietary purine
with UTIs. vascular anomalies, such as canine breeds precursors.
• Xanthine in cavalier King Charles spaniels. identified as carriers of hyperuricosuria gene. • Primary xanthinuria has been observed in
• 2,8-dihydroxyadenine in North American Bilirubin Crystalluria cavalier King Charles spaniels.
indigenous dogs and wolves. • Primary xanthinuria and xanthine uroliths
• Observed in highly concentrated urine
from some healthy dogs. occur in cats.
(continued) Crystalluria
Miscellaneous Crystalluria OTHER LABORATORY TESTS where appropriate, and in some instances
• Uric acid monohydrate crystals from • Struvite crystalluria is not synonymous with modifying pH. C
melamine/cyanuric acid toxicosis. infection and may be the result of normal in
• Cholesterol crystals—observed in humans vivo or in vitro factors; when accompanied by
with excessive tissue destruction, nephrotic elevated pH, bacteriuria, or pyuria on cysto-
syndrome, and chyluria; observed in centesis, UTI should be considered; imaging
apparently healthy dogs. must be performed to assess for stones.
MEDICATIONS
• Hippuric acid crystals—apparently rare in • Dogs and cats with ammonium urate DRUG(S) OF CHOICE
dogs and cats; importance unknown. crystalluria and portosystemic shunts often See comments on urate crystalluria and
• Leucine crystals in dogs—importance not have high serum bile acid levels and hyper- cystinuria.
determined; may occur in association with ammonemia.
cystinuria. • Ammonium urate and amorphous urate
• Tyrosine crystals—occur in association crystals are insoluble in acetic acid;
with severe liver disease in humans; addition of 10% acetic acid to urine
uncommonly observed in dogs and cats
FOLLOW-UP
sediment containing these crystals often
with liver disorders; sodium urate needle- yields uric acid and sometimes sodium PATIENT MONITORING
like appearance commonly misinterpreted urate crystals. • Recheck urinalysis to determine if
as tyrosine needles. • Dogs and cats with calcium oxalate crystalluria is persistent.
• 2,8-dihydroxyadenine—a genetic disorder, monohydrate crystalluria secondary to • Re-radiograph or ultrasound, depending on
the result of metabolic abnormality due to ethylene glycol poisoning have detectable crystal type, to determine if crystalluria has
deficiency of enzyme adenine phosphoribosyl levels of ethylene glycol in serum and urine clinical significance or not.
transferase (APRT). up to 48 hours after ingestion. • See specific urolith types for monitoring
• Cystine crystals are insoluble in acetic acid urolithiasis.
Drug-Induced Crystalluria
• May be observed following administration while struvite crystals are soluble; a urine POSSIBLE COMPLICATIONS
of radiopaque contrast agents. nitroprusside test is positive for cystine. • Persistent crystalluria may contribute to
• May be observed following treatment with • Sulfonamide crystalluria may be associated formation of uroliths.
sulfadiazine, fluoroquinolones, xanthine with a positive lignin test. • Crystalluria may solidify crystalline-matrix
oxidase inhibitors, and tetracycline. IMAGING plugs as in male pugs and cats, resulting in
• Crystalluria may be associated with urethral obstruction.
LABORATORY FINDINGS radiographically or ultrasonographically
Drugs That May Alter Laboratory detectable uroliths.
Results • Abdominal radiographs should include the
• Urinary acidifiers (e.g., d-, l-methionine entire urethra. MISCELLANEOUS
and ammonium chloride). • 25% of radiopaque stones are not seen on
ultrasound. SEE ALSO
• Urinary alkalinizers (e.g., sodium bicarbo-
• Nephrolithiasis.
nate and potassium citrate). DIAGNOSTIC PROCEDURES • Urolithiasis, Calcium Oxalate.
CBC/BIOCHEMISTRY/URINALYSIS • Empirical therapy for struvite urolithiasis if • Urolithiasis, Calcium Phosphate.
• Bilirubin crystals may be associated with stone identified on radiographs and concur- • Urolithiasis, Cystine.
bilirubinemia and other laboratory abnor- rent UTI caused by urease-producing bacteria. • Urolithiasis, Pseudo (Dried Blood, Ossified
malities of hepatic disorders. • Basket retrieval, voiding urohydropropul- Material).
• Most dogs and cats with calcium oxalate sion, or aspiration through a transurethral • Urolithiasis, Struvite—Cats.
and calcium phosphate crystalluria are catheter to retrieve small urocystoliths. • Urolithiasis, Struvite—Dogs.
normocalcemic; some are hypercalcemic; • Urolithiasis, Urate.
calciuria may be used as a future index for • Urolithiasis, Xanthine.
calcium oxalate stone formation and treatment
ABBREVIATIONS
evaluation. TREATMENT • APRT = adenine phosphoribosyl
• Some dogs and cats with calcium oxalate • Manage clinically important in vivo transferase.
crystalluria may be acidemic. crystalluria by managing underlying cause(s) • UTI= urinary tract infection.
• Serially examine fresh specimens for or associated risk factors. Author Ewan D.S. Wolff
knowledge of in vivo urine crystals. • Minimize clinically important crystalluria Consulting Editor J.D. Foster
• Definitive identification of crystal by increasing urine volume, encouraging Acknowledgment The author and book
composition depends on one or more of complete and frequent voiding, modifying editors acknowledge the prior contributions
optical crystallography, infrared spectroscopy, diet, appropriate drug therapy, neutering of Carl A. Osborne and Lisa K. Ulrich.
X-ray diffraction, and electron microprobe
analysis.
Cutaneous Drug Eruptions

reaction to topical ear medications (in ear
C canals and on concave pinnae).
• Eosinophilic dermatitis with edema—
BASICS strong association with concurrent acute MEDICATIONS
OVERVIEW gastrointestinal disease. DRUG(S) OF CHOICE
• A wide spectrum of diseases and clinical • Pemphigus foliaceus—may be triggered by Most conditions respond to immunosuppres-
signs that vary markedly in clinical specific topical flea and tick control products; sive therapy if withdrawal of offending drug
appearance. lesions may include “splash zone” where alone is insufficient (controversial in case of
• Mild eruptions may go unnoticed or product was applied. SJS/TEN).
unreported; incidence rates for specific drugs CONTRAINDICATIONS/POSSIBLE
are unknown.
INTERACTIONS
SIGNALMENT Avoid offending drug or any other drug in
• Dogs and cats. DIAGNOSIS same class or family.
• May have a familial basis (e.g., rabies DIFFERENTIAL DIAGNOSIS
vaccine reactions in canine littermates). • Pruritus, macular/papular rashes, and
SIGNS urticaria/angioedema—allergic and parasitic
• Pruritus. diseases (atopic diseases, contact hypersensi-
• Macular and papular rashes—commonly tivity, flea-bite hypersensitivity, scabies, FOLLOW-UP
accompany pruritus as nonspecific sign of stinging insects).
inflammation. PATIENT MONITORING
• Exfoliative erythroderma—epitheliotropic
• Exfoliative erythroderma—diffuse Inpatient—if debilitated.
lymphoma in old dogs and cats.
erythematous response caused by vasodila- • Vasculitis—infectious, neoplastic, autoim- POSSIBLE COMPLICATIONS
tion; often leads to exfoliation (diffuse mune disease and idiopathic. • Secondary infection.
scaling). • EM/SJS/TEN—respiratory infections, • Electrolyte and plasma protein depletion
• Urticaria/angioedema—immediate (type I) herpes virus, parvovirus, bacterial infection (SJS/TEN).
hypersensitivity; requires prior sensitization; (noncutaneous), and internal neoplasia; EXPECTED COURSE
increased vascular permeability leads to fluid idiopathic/chronic form of EM occurs in
leakage. AND PROGNOSIS
older adult dogs.
• Hypersensitivity vasculitis—type III • Some reactions appear to activate self-
• Pemphigus/pemphigoid—consider drug
response; inflammation of cutaneous perpetuating immune responses.
reaction whenever these diseases diagnosed;
vasculature; results in poor blood flow and • Some drug metabolites may persist for
however, spontaneously occurring disease
anoxic injury to recipient tissue. days to weeks and provoke continued
more common.
• Eosinophilic dermatitis with edema response.
CBC/BIOCHEMISTRY/URINALYSIS • TEN—prognosis poor.
(Wells-like syndrome) of dogs—deeply
Potential for concurrent hepatic, renal, • Vasculitis—prognosis guarded when
erythematous plaques or macules (may be
and gastrointestinal disease with cases of systemic complications.
targetoid) accompanied by marked edema;
vasculitis.
localized, regional, or generalized distribu-
tion; clinical appearance of lesions may be OTHER LABORATORY TESTS
indistinguishable from vasculitis and • Dogs with vasculitis—rickettsial serology.
erythema multiforme (EM). • Cats with vasculitis—feline immunodefi- MISCELLANEOUS
• EM—erythematous macules or plaques ciency virus (FIV) and feline leukemia virus
(FeLV) serology, rule out feline infectious ABBREVIATIONS
expand peripherally and may clear in
peritonitis (FIP). • EM = erythema multiforme.
center (targetoid); multiple shapes/forms
• Bacterial and fungal cultures with vasculitis • FeLV = feline leukemia virus.
noted.
or pyogranulomatous inflammation. • FIP = feline infectious peritonitis.
• Stevens-Johnson syndrome (SJS)—similar
to toxic epidermal necrolysis (TEN) with less DIAGNOSTIC PROCEDURES • SJS = Stevens-Johnson syndrome.
extensive epidermal detachment (<30%) and Skin biopsy—mandatory for diagnosis of • TEN = toxic epidermal necrolysis.
often involvement of oral mucosa. most drug-induced diseases.
• TEN—extensive (>30%) necrosis and Suggested Reading
sloughing of epidermis in sheets; results PATHOLOGIC FINDINGS Helton Rhodes KA, Werner A. Blackwell’s
in moist and intensely inflamed skin Determined by specific disease process. Five-Minute Veterinary Consult: Clinical
surface. Companion: Small Animal Dermatology,
• Drug-induced pemphigus/pemphigoid— 3rd ed. Hoboken, NJ: Wiley-Blackwell,
least common drug reaction in animals; can 2018.
closely mimic autoimmune (spontaneous) Author Daniel O. Morris
TREATMENT Consulting Editor Alexander H. Werner
disease; symptoms may persist after drug • Discontinue use of offending or suspect
withdrawal. Resnick
drug.
CAUSES & RISK FACTORS • SJS/TEN—intensive supportive care and
• Any drug. fluid/nutritional support because of fluid and
• Can occur after first dose or after weeks to protein exudation and risk of sepsis.
months of administration. • Pain relief when indicated—minimal drug
• Exfoliative erythroderma—most often use recommended when drug eruption
associated with shampoos and dips; also suspected.
Cuterebriasis
• Dermatologic—mature warble unmistak- • Application of monthly heartworm
able, young warble may present as pustule or preventatives (avermectin-containing C
papule. products), flea development control products
BASICS (lufenuron-containing products), or topical
OVERVIEW Eosinophilia may be present, otherwise no flea and tick treatments may either prevent
• Flies of the genus Cuterebra are found in specific findings. the maggots from developing, or may kill
the Americas, where they are obligatory them before they access an orifice for entry.
parasites of rodents and lagomorphs. Adult OTHER LABORATORY TESTS However, based on anecdotal information,
flies lay eggs on blades of grass or in nests; N/A some cats and dogs on these products still
they hatch and crawl onto the skin of IMAGING develop warbles with maggots.
passing host. The small maggots enter a CT, MRI—may show intracranial lesions in
body orifice, migrate through various cats. ZOONOTIC POTENTIAL
internal tissues, and ultimately over several The maggots in the dog or cat pose no
DIAGNOSTIC PROCEDURES zoonotic threat.
weeks to months make their way to the skin,
N/A
where they establish a warble. The mature Suggested Reading
maggots, which may be an inch long, then Bordelon JT, Newcomb BT, Rochat MC.
drop out of the rodent or rabbit host and Surgical removal of a Cuterebra larva from
pupate in the soil. the cervical trachea of a cat. J Am Anim
• Dogs and cats become infected when they TREATMENT Hosp Assoc 2009, 45:52–54.
contact a blade of grass upon which an egg • Can remove maggots from subcutaneous Edelmann ML, Lucio-Forster A, Kern TJ, et al.
containing an infective maggot is stimulated lesions, eyes, or nares (see Web Video 1). Ophthalmomyiasis interna anterior in a dog:
to hatch and attach onto the passing animal. • Manifestations of lung migration may be keratotomy and extraction of a Cuterebra sp.
The maggots then crawl around on the cat or alleviated by corticosteroids. larva. Vet Ophthalmol 2014, 17:448–453.
dog until they find an orifice in which to • Neurologic disease has poor prognosis. Thawley VJ, Suran, JN, Boller EM. 2013
enter. Presumptive central nervous system
• Dogs and cats can develop maggots in cuterebriasis and concurrent protein-losing
warbles or can develop signs associated with nephropathy in a dog. J Vet Emerg Crit
larvae migrating within their tissues. Care 2013, 23:335–339.
• Dogs and cats can present with respiratory MEDICATIONS
Author Dwight D. Bowman
signs, neurologic signs, ophthalmic lesions, or DRUG(S) OF CHOICE Consulting Editor Amie Koenig
maggots in their skin. • Ivermectin 0.2 mg/kg SC should kill
SIGNALMENT migrating maggots; can be administered either
• Dogs and cats—all ages. to alleviate signs caused by maggots suspected
• In northern United States, most cases occur of migrating in lungs, or to kill larvae in other
in late summer and early autumn, based on tissues, including CNS; pretreatment with
time of emergence of adult egg-laying females corticosteroids may mitigate inflammatory
in spring and early summer. reaction to dying worms.
• Products containing isoxazolines (i.e.,
SIGNS afoxolaner, fluralaner, lotilaner, andsarolaner),
• Dermatologic—warble containing bot with when routinely given to cats and and dogs,
protruding spiracles. may prevent migration and warble formation
• Neurologic—ataxia, circling, paralysis, by Cuterebra spp. Efficacy and potential side
blindness, recumbency. effects in patients with migrating maggots has
• Ophthalmic lesions—larva in conjunctiva. not been reported.
• Respiratory—eosinophilic respiratory
disease.
• Dogs and cats with access to outdoors,
FOLLOW-UP
where they contact eggs and larvae. Good return of function following ivermectin
• Neonatal cats have been infected, presum-
treatment is possible.
ably with larvae carried on queen’s fur.
MISCELLANEOUS
DIAGNOSIS • In northern United States disease is
DIFFERENTIAL DIAGNOSIS seasonal, with most cases occurring in late
• Respiratory—allergies, lungworms, summer and early fall when adult flies are
migrating ascarids or hookworms. active; seasonality is less demarcated in areas
• Neurologic—rabies, distemper, angio- where warmer temperatures and active flies
strongylosis. occur through longer periods of the year.
• Ophthalmic lesions—larval Hypoderma or • Does not appear to result in prolonged
Oestrus. immunity; the same animal can develop skin
lesions several years in a row.
Cyanosis
see, with exception of discolored paw pads in neoplasia; foreign body; trauma; hypoplasia.
C cats with arterial thromboembolism. • Lower airway and parenchyma—pneumonia
• Differential cyanosis—with reverse shunting (viral, bacterial, fungal, eosinophilic, myco-
BASICS PDA, head and neck receive oxygenated blood bacteria, aspiration); chronic bronchitis;
DEFINITION via brachiocephalic trunk and left subclavian hypersensitivity bronchial disease or asthma;
A bluish discoloration of the skin and mucous artery, which arise from aortic arch; rest of the bronchiectasis; neoplasia; foreign body;
membranes owing to an increase in the body receives desaturated blood through parasites (Filaroides, Paragonimus, Pneumocystis
amount of reduced, or deoxygenated, ductus located in descending aorta. jiroveci, toxoplasmosis, Aelurostrongylus spp.);
hemoglobin within the blood. SYSTEMS AFFECTED pulmonary contusion or hemorrhage;
• Central—all systems affected.
noncardiogenic edema (smoke inhalation,
PATHOPHYSIOLOGY
• Peripheral—may diminish or abolish
snake bite, electric shock); near drowning.
• Concentration of deoxygenated
neuromuscular function of affected limb(s). • Pleural space—pneumothorax; infectious
hemoglobin—must be >5 g/dL to detect
(bacterial, fungal, feline infectious peritonitis
condition; thus anemia may obscure recognition SIGNALMENT [FIP]); chylothorax; hemothorax; pyothorax;
of cyanosis. • Central—associated with systemic • Right-to-left cardiac shunts in association with neoplasia; trauma. • Thoracic wall or
arterial hypoxemia or hemoglobin abnormalities. high pulmonary vascular resistance and diaphragm—congenital (pericardial,
• Peripheral—limited to one or more extremities pulmonary hypertension (Eisenmenger diaphragmatic hernia); trauma (diaphragmatic
of the body; associated with diminished physiology)—dogs: Keeshond, English bulldog, hernia, fractured ribs, flail chest); neuromuscular
peripheral blood flow; arterial oxygen tension klee kai, and beagle; some cats; generally young disease (tick bite paralysis, coonhound
and saturation typically normal. animals. • Tracheal collapse—usually young or paralysis).
Arterial Hypoxemia middle-aged small-breed dogs (e.g., Pomeranian,
Yorkshire terrier, poodles). • Acquired laryngeal Cardiovascular System
• Low partial pressure of inspired oxygen
paralysis—most common in old large-breed • Congenital defects—Eisenmenger
(e.g., high altitude). • Hypoventilation due to
dogs (e.g., retrievers). • Hypoplastic trachea— physiology (right-to-left shunting PDA, VSD,
primary neurologic disorders affecting brain,
identified in young English bulldogs; ASD); tetralogy of Fallot; truncus arteriosus;
cervical spinal cord, or lower motor neuron;
occasionally other breeds. • Brachycephalic double outlet right ventricle; anomalous
centrally acting respiratory depressant drugs;
airway syndrome—dogs: English and French pulmonary venous return; atresia of aortic or
chest wall injuries; pleural space diseases;
bulldogs, Pekinese, pugs, Boston terrier, and tricuspid or pulmonary valves. • Acquired
upper airway obstructions. • Ventilation–
other brachycephalic breeds. • Asthma—cats: disease—mitral valve disease; cardiomyopathy.
perfusion mismatching resulting in impaired
higher incidence reported in Siamese. • Pericardial effusion—idiopathic disease;
gas exchange (e.g., pulmonary parenchymal or
neoplasia. • Pulmonary thromboembolic
thromboembolic diseases). • Diffusion SIGNS disease—hyperadrenocorticism; immune-
impairment fromthickening of alveolar barrier
Historical Findings mediated hemolytic anemia; protein-losing
through which oxygen must pass to reach red
• Central—stridor; respiratory distress; nephropathy; dirofilariasis; severe, acute
blood cells (RBCs); interstitial lung disease
cough; voice change; episodic weakness; pancreatitis. • Pulmonary hypertension—
may cause this. • Addition of deoxygenated
syncope; exposure to oxidizing substances or idiopathic; right-to-left cardiac shunts.
venous blood to arterial circulation—
drugs causing methemoglobinemia. • Peripheral vascular disease—arterial
congenital right-to-left shunting cardiac
• Peripheral—limb paresis or paralysis. thromboembolism (feline cardiomyopathies);
defects (e.g., tetralogy of Fallot, transposition
Physical Examination Findings venous obstruction; reduced cardiac output;
of great vessels); reversed shunting cardiac
• Heart murmur or splitting of second heart
shock, arteriolar constriction.
defects caused by high pulmonary vascular
resistance (e.g., right-to-left shunting patent sound—with cardiac disease or pulmonary Neuromusculoskeletal System
ductus arteriosus [PDA], atrial septal defect hypertension. • Pulmonary crackles or • Brainstem dysfunction—encephalitis;
[ASD], ventricular septal defect [VSD]). wheezes—with pulmonary edema or trauma; hemorrhage; neoplasia; drug-induced
respiratory disease. • Muffled heart sounds— depression of respiratory center (morphine,
Abnormal Hemoglobin
owing to pleural space or pericardial disease. barbiturates). • Cervical spinal cord
• Methemoglobin—most common abnormal
• Upper airway stridor with laryngeal paralysis. dysfunction—edema; trauma; vertebral
heme pigment; unable to bind oxygen;
• Honking cough—typical of tracheal fractures; disk prolapse. • Neuromuscular
normally formed at low rate in erythrocytes;
collapse; often induced by tracheal palpation. dysfunction—overdose of paralytic agents
cats with significant exposure to acetaminophen
• Dyspnea—may be inspiratory, expiratory, or (succinylcholine, pancuronium); tick bite
will appear cyanotic. • Nicotinamide adenine
a combination (see Differential Diagnosis). paralysis; botulism; tetanus; acute polyradiculo-
dinucleotide dependent methemoglobin
• Limbs—may be cyanotic, cool, pale, painful, neuritis (coonhound paralysis);
reductase (NADH-MR)—intracellular
and edematous; can lack a pulse in conditions dysautonomia; myasthenia gravis.
reductive enzyme; maintains methemoglobin :
causing peripheral cyanosis. • Weakness—can Methemoglobinemia
hemoglobin ratio at <2%; deficiency and/or
be generalized and persistent with severe • Congenital—NADH-MR deficiency (dogs).
exposure to oxidizing agents causes methemo
cardiac diseases; can be episodic and especially • Ingestion of oxidant chemicals—acetami-
globinemia. • Hypoxia—when >20–40% of
noticeable with exercise or excitement. nophen; nitrates; nitrites; phenacetin; sulfona-
hemoglobin has been oxidized to
• Posterior paresis or paralysis—can be seen mides; benzocaine; aniline dyes; dapsone.
methemoglobin.
with distal aorta arterial thromboembolism;
Other differentiated from primary neuromuscular
• Peripheral cyanosis—results from increased disease by absence (or near absence) of pulses.
oxygen extraction from arterial supply to an
CAUSES
area (e.g., a limb); caused by severe DIAGNOSIS
vasoconstriction, poor peripheral blood flow, Respiratory System
• Larynx—paralysis (acquired or congenital); DIFFERENTIAL DIAGNOSIS
obstruction to flow associated with arterial • Generalized—systemic hypoxemia or heme
thromboembolism, or stagnation or collapse; spasm; edema; trauma; neoplasia;
granulomatous disease. • Trachea—collapse; abnormality. • Peripheral only—reduced
obstruction of venous blood flow; difficult to
(continued) Cyanosis
blood flow to extremities. • Caudal body— required to characterize bronchopulmonary changes in depth and rate of respiration; color
right-to-left shunting PDA. • Cardiac versus diseases. • Thoracocentesis—required for of mucous membranes (should return to C
respiratory causes—differentiation can be diagnosis and treatment of pleural space normal pink color if cause is not anatomic
difficult; cardiac murmur may suggest disorders. • Electrocardiography—may reveal shunt and patient has adequate reserves);
cardiac disease, but murmurs are often heard heart enlargement changes; unreliable; pulse oximetry or arterial blood analysis.
in older patients with primary respiratory echocardiography better. • Lung biopsy—can be • Instruct client to monitor mucous
disease; higher hematocrit may make necessary for diagnosis of interstitial lung disease. membrane color and respiratory effort, and
murmurs harder to hear; thoracic radiography advise immediate veterinary care if cyanotic
and echocardiography useful for differentiation. condition returns.
• Central or peripheral neurologic signs—
should prompt concern for arterial hypoxemia
owing to primary neuromuscular disease.
TREATMENT Advanced pulmonary or airway disease and
• Inpatient—immediate diagnostic testing severe cardiac disease—poor long-term
Breathing Pattern and treatment. • Stabilization therapy (e.g., prognosis.
• May help define cause. • Inspiratory oxygen, thoracocentesis, tracheostomy)—
effort—often associated with obstructive usually instituted before aggressive diagnostics.
upper airway or pleural space disease; • Specific therapy—depends on ultimate
stridor frequently localizes problem to diagnosis; usually exercise restriction and
larynx or cervical trachea. • Expiratory
MISCELLANEOUS
dietary modification required. • Surgical
effort—generally seen with obstructive treatment—depends on primary disease ASSOCIATED CONDITIONS
lower airway disease. • Rapid shallow process and extent of cardiac or respiratory • Obesity—can complicate or exacerbate
(restrictive)—may be associated with involvement. • Warn the client when underlying respiratory or cardiac diseases.
pleural space disease or neuromuscular admitting the patient that diseases associated • Ascites—can complicate or exacerbate
abnormalities of thoracic wall. with cyanosis can have dire outcomes. respiratory effort and reduce lung capacity
due to cranial displacement of diaphragm.
• Color of blood—may be darkened; AGE-RELATED FACTORS
chocolate brown with methemoglobinemia. Congenital cardiac abnormalities—usually
• Polycythemia—often accompanies MEDICATIONS the cause in young patients.
congenital heart disease; may occur with PREGNANCY/FERTILITY/BREEDING
chronic hypoxemia owing to severe respiratory DRUG(S) OF CHOICE
• Oxygen therapy—provide as soon as • Advanced pregnancy may exacerbate signs
disease. • Proteinuria—accompanies protein- because of pressure on diaphragm and
losing nephropathies, which may result in possible. • Additional drug therapy depends
on final diagnosis. • Furosemide—aggressive reduced lung expansion. • Fetuses likely to be
secondary pulmonary thromboembolism. harmed or aborted by hypoxemia associated
• Panhypoproteinemia—accompanies use indicated with suspected cardiogenic
pulmonary edema. • Methemoglobinemia as with cyanosis.
protein-losing enteropathies, which may lead
to pulmonary thromboembolism. result of ingestion of oxidizing substances SEE ALSO
(acetaminophen)—give acetylcysteine as soon • Dyspnea and Respiratory Distress.
OTHER LABORATORY TESTS as possible (140 mg/kg PO/IV; then 70 mg/ • Panting and Tachypnea.
• Co-oximetry to estimate percent of kg q4h for five treatments); cimetidine • Stertor and Stridor.
methemoglobin or carboxyhemoglobin. (10 mg/kg PO; then 5 mg/kg PO q6h for
• Arterial blood gas analysis. • Urine ABBREVIATIONS
48h) is useful adjunct to acetylcysteine;
protein : creatinine ratio—with suspected • ASD = atrial septal defect.
ascorbic acid (30 mg/kg PO q6h for seven
pulmonary thromboembolism secondary to • FIP = feline infectious peritonitis.
treatments) may be of some value, but do not
protein-losing nephropathy. • NADH-MR = nicotinamide adenine
use as sole agent; methylene blue given IV
dinucleotide dependent methemoglobin
IMAGING followed by oral supplementation reported as
reductase.
• Radiography—essential for determining successful treatment modality in dogs.
• PDA = patent ductus arteriosus.
cause. • Echocardiography—aids in • Sildenafil citrate—phosphodiesterase type 5
diagnosis of congenital or acquired cardiac inhibitor used to treat pulmonary arterial
• VSD = ventricular septal defect.
disease, pulmonary hypertension, and hypertension at 1–3 mg/kg PO q8–12h.
Author Sean B. Majoy
pulmonary thromboembolism. • CT/ CONTRAINDICATIONS Consulting Editor Elizabeth Rozanski
angiography—can further define obstructive Avoid using paralytic agents (succinylcholine, Acknowledgment The author and book
nasal, pulmonary, or pleural space disease; pancuronium) and agents that cause editors acknowledge the prior contribution of
gold standard for diagnosing pulmonary profound depression of respiratory center Ned F. Kuehn.
embolism in humans. (morphine, barbiturates).
• Pulse oximetry to estimate oxygen saturation; Client Education Handout
inaccurate when carboxyhemoglobin or available online
methemoglobin present. • Laryngoscopic FOLLOW-UP
examination—evaluate laryngeal structure and
arytenoid function. • Bronchoscopy—often PATIENT MONITORING
useful in diagnosis of airway and pulmonary • Patients in an oxygen cage should be
diseases. • Transtracheal wash, bronchoalveolar disturbed as infrequently as possible for
lavage, or fine-needle lung aspirate—often monitoring. • Assess efficacy of therapy—
Cyclic Hematopoiesis
• Signs and symptoms of FeLV in cats.
C CAUSES & RISK FACTORS
BASICS • Inherited disease in purebred or crossbred FOLLOW-UP
collie dogs.
OVERVIEW • FeLV infection in cats. PATIENT MONITORING
• Cyclic hematopoiesis in color-dilute gray Owner advised to watch for signs of
collie pups, also known as gray collie infection.
syndrome, is characterized by frequent PREVENTION/AVOIDANCE
episodes of infection with failure to thrive Dogs should not be boarded with other
and early death. Systems affected are hemato- DIAGNOSIS
animals.
poietic, ocular, respiratory, gastrointestinal, DIFFERENTIAL DIAGNOSIS
and skin. Pups may appear normal for the • Coat color dilution and nasal epithelial POSSIBLE COMPLICATIONS
first 4–6 weeks and then develop diarrhea, color dilution are always present in collies or Infections can be life threatening if
conjunctivitis, gingivitis, pneumonia, skin collie mixed breeds with cyclic hematopoiesis. untreated.
infections, joint pain, and fever. • Coat color dilution as a result of dilute gene EXPECTED COURSE
• Episodes of illness, varying from inactivity expression is also observed in collies. These AND PROGNOSIS
accompanied by fever to life-threatening dogs have blue or lilac coat color with normal Intermittent infections are expected.
infection, repeat at 11–14-day intervals. color intensity on nose and do not develop Prognosis is guarded.
• Affected pups are usually smaller than their cyclic hematopoiesis.
littermates at birth, weak, and often pushed • Trapped neutrophil syndrome is another
aside by their mothers. autosomal recessive inherited neutropenia in
SIGNALMENT border collie pups who present with recurrent
• Cyclic hematopoiesis in the collie breed is infections and musculoskeletal disease, MISCELLANEOUS
present only in the color-dilute pups. The usually between 6 and 12 weeks of age. PREGNANCY/FERTILITY/BREEDING
color dilution and bone marrow disorder are Unlike cyclic neutropenia, affected pups have Carriers or affected collies should not be
inherited as an autosomal recessive trait. This persistent neutropenia. A DNA test for this bred.
condition has also been reported in crossbred disease is available.
SEE ALSO
collie/beagle pups. • Cats will present with signs and symptoms
• Neutropenia.
• Clinical signs occur as early as 1–2 weeks of age consistent with FeLV infection.
• Thrombocytopathies.
and are always apparent by 4–6 weeks of age. CBC/BIOCHEMISTRY/URINALYSIS
Affected dogs rarely live beyond 2–3 years of age. ABBREVIATIONS
• CBC—severe neutropenia, lasting 2–5 days,
• An apparently similar disease was reported • FeLV = feline leukemia virus.
followed by neutrophilia, and occurring at
in normal-colored pups in two border collie • G-CSF = granulocyte colony-stimulating
11–14-day intervals with mild normocytic to
litters in the UK. Cyclic hematopoiesis has factor.
microcytic anemia in dogs; slight to moderate
also been reported in Pomeranians, Cocker normocytic or macrocytic anemia in cats. Suggested Reading
Spaniels, and a Basset Hound, but the disease • Local swelling, redness, and systemic signs of Harvey JW. Veterinary Hematology: A
is not well characterized in these breeds. infection usually occur during first days of Diagnostic Guide and Color Atlas. St.
• Cyclic hematopoiesis has been observed in neutrophilic phase of disease cycle; therefore, on Louis, MO: Elsevier Health Sciences,
two cats with feline leukemia virus (FeLV) initial CBC examination, neutrophilia with 2012, p.148.
infection. moderate monocytosis is usually observed. Author June C. Huang
SIGNS OTHER LABORATORY TESTS Consulting Editor Melinda S. Camus
Historical Findings A DNA mutation test is available for canine Acknowledgment The author and book
• Weakness. cyclic hematopoiesis from Animal Genetics. editors acknowledge the prior contribution of
• Failure to thrive. Alan H. Rebar.
• Conjunctivitis.
• Gingivitis.
• Diarrhea. TREATMENT
• Pneumonia. • Recombinant G-CSF or lentivirus-medi-
• Skin infections. ated G-CSF can be administered to shorten
• Joint pain. period of neutropenia and reduce infections.
• Coagulopathies. • Antibiotics and supportive therapy to treat
Physical Examination Findings or relieve symptoms.
• Dilute coat color with color dilution of • Bone marrow transplantation eliminates
nasal epithelium. cyclic hematopoiesis and can be curative.
• Smaller and weaker than normal-colored
littermates.
• Fever.
• Watery eyes, reddened gums, tonsillitis, and
diarrhea nearly always present during phase of
MEDICATIONS
hematopoietic cycle when clinical signs are DRUG(S) OF CHOICE
evident; other signs vary depending on Antibiotics and intravenous fluids as
presence of infection in various body systems. indicated for infections.
Cylindruria
dehydration, and after diuresis. • Waxy casts
usually seen with chronic kidney disease. C
• Epithelial casts formed from degeneration
BASICS of renal tubular epithelial cells; most FOLLOW-UP
OVERVIEW commonly seen with acute tubular injury. PATIENT MONITORING
• Increased number of casts in urine • White blood cell (WBC) casts indicate • Physical examination including patient’s
sediment. • Occasional hyaline and granular renal inflammation (e.g., pyelonephritis). weight to assess hydration status. • Blood
casts can be found in clinically normal • Red blood cell (RBC) casts indicate renal pressure monitoring. • CBC/chemistry/
animals. • High numbers of casts indicate hemorrhage. • Fatty casts suggest renal urinalysis monitoring.
tubular pathology, but do not correlate with tubular injury. • Chemistry profile may show
degree of damage. • Can develop with azotemia and hyperphosphatemia. • CBC
Avoid or correct risk factors (e.g., exposure
primary renal disease or systemic disorders may show anemia, erythrocytosis, leukocyto-
to toxins, infectious disease prevention,
that secondarily affect kidneys. • Absence of sis, and/or thrombocytopenia depending on
etc.).
casts does not exclude possibility of renal underlying pathology.
tubular disease. • Systems affected—renal/ POSSIBLE COMPLICATIONS
urologic. Irreversible renal disease, depending on
• Determine urine protein : creatinine ratio
underlying cause of cylindruria.
SIGNALMENT to evaluate magnitude of proteinuria.
Dog and cat. • Perform urine culture to rule out urinary
tract infection in patients with pyuria or
WBC casts. Also consider ultrasound ±
Nephrotoxicosis radiography to assess for pyelonephritis, MISCELLANEOUS
• Toxins—ethylene glycol, grape/raisin nephroliths, etc. • Test for systemic infections ZOONOTIC POTENTIAL
ingestion (dogs), lily ingestion (cats), as indicated. • If thrombocytopenic or RBC Possible in patients with leptospirosis. Use
hypercalcemia. • Nephrotoxic drugs—e.g., casts are present, perform coagulation studies safety precautions when handing urine.
aminoglycosides, amphotericin B, cisplatin, to rule out consumptive coagulopathy such as
nonsteroidal anti-inflammatory drugs, disseminated intravascular coagulation. SEE ALSO
angiotensin-converting enzyme inhibitors, Nephrotoxicity, Drug-Induced.
Disorders That May Alter Laboratory
radiocontrast agents. ABBREVIATIONS
Results
Renal Ischemia • RBC = red blood cell.
• Delayed processing of urinalysis and
• Dehydration. • Low cardiac output. • Renal • WBC = white blood cell.
examination of urine sediment may result
vessel thrombosis. • Hemoglobinuria. in disappearance of casts; ideally should be Suggested Reading
• Myoglobulinuria. examined within 30 minutes of collection. Latimer K. Duncan and Prasse’s Veterinary
Renal Inflammation • Alkaline urine can cause dissolution of Laboratory Medicine Clinical Pathology,
Infectious diseases (e.g., pyelonephritis, casts. • Low speed centrifugation necessary to 5th ed. Ames, IA: Wiley-Blackwell, 2011,
leptospirosis, feline infectious peritonitis, prevent cast destruction. pp. 264–272.
tick/vector-borne disease). Valid If Run in Human Laboratory?
Sink C, Weinstein N. Practical Veterinary
Yes Urinalysis. Ames, IA: Wiley-Blackwell,
Glomerular Disease 2012, pp. 69–84.
• Glomerulonephritis. • Amyloidosis. DIAGNOSTIC PROCEDURES Stockham S, Scott M. Fundamentals of
Consider renal biopsy if kidney disease Veterinary Clinical Pathology, 2nd ed.
persists or progresses and cause cannot be Ames, IA: Wiley-Blackwell, 2008, pp.
determined from routine diagnostic tests. 472–473.
DIAGNOSIS Author Tracie D. Romsland
Consulting Editor J.D. Foster
DIFFERENTIAL DIAGNOSIS Acknowledgment The authors and book
• Cylindruria with azotemia and adequately editors acknowledge the prior contributions
concentrated urine (specific gravity >1.030 in TREATMENT of Allyson C. Berent and Cathy E.
dogs and >1.040 in cats)—consider prerenal • Manage as outpatient unless patient is
Langston.
disorders such as dehydration. • Cylindruria dehydrated or has decompensated kidney failure.
with azotemia and inadequately concentrated • Acute kidney injury and chronic kidney
urine—consider renal failure. • Cylindruria disease should be managed according to
with leukocytosis—consider pyelonephritis or standard recommendations. • If patient
other infectious and inflammatory disorders. cannot maintain hydration, administer
• Cylindruria with glucosuria and proteinuria— parenteral fluid therapy. • Consider dialysis if
consider renal tubular necrosis. • Transient toxin exposure or leptospirosis infection.
hyaline and/or granular casts can be seen after
strenuous exercise.
• Casts classified by appearance and MEDICATIONS
quantified per low power field. • Granular CONTRAINDICATIONS/POSSIBLE
casts (fine or coarse) associated with tubular INTERACTIONS
degeneration, inflammation, or necrosis. Avoid nephrotoxic drugs.
• Hyaline casts can be seen with proteinuria,
Cytauxzoonosis
• Moderate hyperbilirubinemia and
C bilirubinuria.
• Mild hyperglycemia.
BASICS • If present, anemia is believed to be FOLLOW-UP
OVERVIEW secondary to hemolysis. EXPECTED COURSE AND PROGNOSIS
• Infection with the protozoan Cytauxzoon OTHER LABORATORY TESTS • With aggressive supportive care and
felis. • Fresh blood smear—Cytauxzoon erythro- treatment, expect 3–7 days of hospitalization
• Affects vascular system of lungs, liver, cytic form; 1–3 μm in diameter; shape of with severe illness.
spleen, kidneys, and brain; bone marrow and signet ring or safety pin. • Some cats develop pleural effusion and
developmental stages of red blood cells • Schizont-infected monocyte/macrophages require thoracocentesis.
(RBCs) affected as well. may be observed on feathered edge of thin • Cats that survive will return to normal
• Uncommon in most regions, but common blood smears. within 2–4 weeks of discharge and appear
during the spring and summer in endemic • Splenic, lymph node, liver, or bone marrow immune to reinfection.
regions. aspirate—best suited to demonstrate extra- • Some cats remain persistently infected with
• Affects feral and domestic cats in south- erythrocytic schizont forms. the intraerythrocytic form without overt
central, southeastern, and mid-Atlantic • PCR assay is commercially available. signs.
United States; range appears to be expanding • Blood type in all cats prior to transfusion. • Without treatment, most cats with acute
towards eastern and northeastern United cytauxzoonosis have died within 5 days of
States. IMAGING presentation.
• Related Cytauxzoon spp. have been identified Radiographs or ultrasound may assist in
in Europe and Asia, but have not been identifying pleural effusion or pulmonary
associated with classic Cytauxzoonosis (see edema.
Signs) as seen in North America. DIAGNOSTIC PROCEDURES
N/A MISCELLANEOUS
SIGNALMENT
• Domestic cats of all ages. PATHOLOGIC FINDINGS ZOONOTIC POTENTIAL
• Wild felids are also at risk. Organisms inside myeloid cells in bone • No known risk to humans.
• No breed or sex predilection, although marrow aspirate and in dramatically enlarged • Cannot be directly transmitted to another
most cases are diagnosed in young cats that myeloid cells in vessels of multiple organs cat except by blood or tissue inoculation.
have access to outdoors. including lung, liver, spleen, kidney, and ABBREVIATIONS
SIGNS brain. • RBC = red blood cell.
• Most cats have severe illness at presentation. Suggested Reading
• Pale mucous membranes. Cohn LA, Birkenheuer AJ, Brunker JD, et al.
• Depression. Efficacy of atovaquone and azithromycin or
• Anorexia. TREATMENT imidocarb dipropionate in cats with acute
• Dehydration. • Inpatient with aggressive supportive therapy cytauxzoonosis. J Vet Intern Med 2011,
• High fever. including supplemental oxygen. 25(1):55–60.
• Icterus. • Blood transfusion. Reichard MV, Thomas JE, Arther RG, et al.
• Splenomegaly. • Feeding tube for medication and nutri- Efficacy of an imidacloprid 10%/flumethrin
• Hepatomegaly. tional support. 4.5% collar (Seresto®, Bayer) for preventing
• Some cats may be infected but the transmission of Cytauxzoon felis to
asymptomatic. domestic cats by Amblyomma americanum.
CAUSES & RISK FACTORS Parasitol Res 2013, 112(Suppl. 1):11–20.
• Bite of infected tick (primarily Amblyomma Author Adam J. Birkenheuer
MEDICATIONS Consulting Editor Amie Koenig
americanum or Dermacentor variabilis).
• Roaming in areas shared by reservoir hosts DRUG(S) OF CHOICE
(bobcats). • Combination of atovaquone (15 mg/kg PO
• Living in same household/region as cat q8h with a fatty meal) and azithromycin
diagnosed with cytauxzoonosis. (10 mg/kg PO q24h) and supportive care is
associated with survival rates of 60%.
• Imidocarb dipropionate—5 mg IM two
injections 14 days apart has been recom-
mended, but is associated with survival rates
DIAGNOSIS of approximately 27%.
• Heparin (100–300 U/kg SC q8h or
• Other causes of pancytopenia such as sepsis
300–900 U/kg/day as IV CRI) until time of
and panleukopenia. discharge (longer if significant thrombosis
• Other causes of fever and jaundice such as
such as pulmonary thromoboembolism is
pancreatitis, hepatitis, and cholangitis. present).
• Bicytopenia or pancytopenia are the most INTERACTIONS
common findings; thrombocytopenia is N/A
almost always present.
Deafness
(20% if white) in UK; English setter: 8% in • Chronic otitis externa, media, or interna.
United States; English cocker spaniel: 7% in • Use of ototoxic drugs.
United States; border collie: 2–3% in UK; • General anesthesia.
BASICS purebred white cats: 20% in United States D
DEFINITION and Germany; non-purebred white cats: 50%
• Partial or complete hearing loss. in UK and United States.
• Two forms: GEOGRAPHIC DISTRIBUTION
◦ Sensorineural deafness—caused by Prevalence for different breeds varies between DIAGNOSIS
damage to receptors in cochlea, cochlear countries. DIFFERENTIAL DIAGNOSIS
nerve, or auditory pathways in CNS. • Early age of onset—suggests congenital
◦ Conduction deafness—caused by SIGNALMENT
• Breed-related congenital cochlear degenera- causes in predisposed breeds.
inability to conduct sound vibration • Use of ototoxic drugs, recent anesthesia, or
through external to inner-ear structures. tion described in >90 breeds of dogs. Most
breeds have a large amount of white pigmen- chronic ear disease—suggests acquired causes.
PATHOPHYSIOLOGY tation associated with merle or piebald genes, • Evaluate for brain disease.
Sensorineural Deafness except for Doberman pinscher, puli, CBC/BIOCHEMISTRY/URINALYSIS
• Hereditary—breed-related cochlear Shropshire terrier. Congenital sensorineural Usually normal.
degeneration closely associated with the deafness present by 6 weeks of age, although OTHER LABORATORY TESTS
recessive alleles of the piebald locus and the has late onset in border collie (5 years) and • Bacterial culture and sensitivity of ear canal
dominant allele of the merle locus in dogs Rhodesian ridgeback (4–12 months). if otitis externa.
and with the dominant allele of the white • No association with gender. Dogs with blue
• Myringotomy with culture of aspirates if
locus in cats. These genes alter the ability of iris color have a higher incidence of congeni- otitis media.
neural crest melanocytes to populate regions tal deafness.
of the body including skin, hair, iris, ocular • Mixed-breed cats with white hair coat and IMAGING
tapetum, and portions of the cochlea. The blue irises—high incidence of deafness. • Tympanic bullae and skull radiographs—
absence of melanocytes in the stria vascularis Purebred white cats that carry the Siamese may show soft tissue opacity and bone
of the cochlea is associated with early gene for blue eyes have a lower incidence of remodeling of tympanic bulla; often unre-
postnatal degeneration of this structure. Can congenital deafness. markable in cases with otitis media/interna.
also be non-pigment-associated and in some • Acquired deafness may occur in any breed • Ultrasound of tympanic bullae—may show
cases also affect the vestibular system, such as or age of dog and cat. anechoic content in cases with otitis media/
in Doberman pinschers (associated with a interna, but low sensitivity.
SIGNS • CT/MRI—higher sensitivity for middle–
mutation in the PTPRQ gene). • Unilateral deafness often goes unnoticed.
• Acquired—cochlear degeneration due to inner ear disease and intracranial pathology.
Rarely, dogs have difficulty localizing sound.
chronic infection, ototoxicity, neoplasia, • With bilateral disease, animals do not DIAGNOSTIC PROCEDURES
chronic exposure to loud noises, anesthesia- respond to auditory cues such as calling their • Brainstem auditory evoked response
associated, or age-related loss of hair cells and name or rattling food dish. Often they are (BAER)—gold standard test for evaluation of
spiral ganglion cells (presbycusis). easily startled. Commonly have heightened hearing. Measures electrical response of cochlea
Conduction Deafness response to vibration and visual cues. and auditory pathways in the brain to an
• Congenital defects in external ear canal, auditory stimulus; reliable to identify dogs
CAUSES with unilateral disease or partial hearing loss.
tympanic membrane, or ossicles that transmit
vibration in middle ear are rare. Hereditary Sensorineural Deafness Bone conduction stimulation can be useful to
predisposition in primary secretory otitis • Genetic etiology likely in neonates. distinguish sensorineural from conduction
media in the cavalier King Charles spaniel. • Acquired cochlea and cochlear nerve deafness. Can be used to determine the
• Acquired defects resulting in stenosis/ damage—infectious (otitis interna), neoplasia hearing threshold.
obstruction of external ear canal, rupture of of bony labyrinth or nerve, trauma (physical • Otoacoustic emissions (OAEs)—low-level
tympanic membrane, or fusion of bony or noise), systemic or topically applied drugs sounds produced by inner ear as part of the
ossicles; most commonly associated with or toxins (antibiotics: aminoglycosides, normal hearing process that can be measured
chronic otitis or middle ear polyps. polymyxin, erythromycin, vancomycin, by placing a probe containing a microphone
chloramphenicol; antiseptics: ethanol, in the external ear canal. Two forms have been
SYSTEMS AFFECTED chlorhexidine, cetrimide; antineoplastics: used in dogs for assessment of sensorineural
Nervous—inner ear. cisplatin, carboplatin; diuretics: furosemide; deafness—transient evoked OAEs (TEOAEs)
GENETICS heavy metals: arsenic, lead, mercury; and distortion product OAEs (DPOAEs).
Genetics of congenital deafness not fully miscellaneous: ceruminolytic agents, OAE is best suited for cases with congenital
understood, although strong association with propylene glycol, salicylates), presbycusis, deafness, as it tests outer hair cell function and
the piebald and the merle locus in dogs and anesthesia-induced. is not affected by inner hair cell, synapse, or
dominant white locus in cats (pigment-associ- Conduction Deafness cochlear nerve deficiencies. DPOAEs may
ated genes related to coat color). • Otitis externa and other external ear canal show benefits in assessing age-related and
INCIDENCE/PREVALENCE disease (e.g., stenosis of canal, foreign bodies, noise-induced hearing loss and may reduce
Prevalence of congenital deafness in one or neoplasia, or ruptured tympanum). cost and testing times in congenital sensori-
both ears available for the following breeds— • Otitis media, middle-ear polyps, primary neural deafness compared to BAER.
Dalmatian: 30% in United States, 18% in secretory otitis media. PATHOLOGIC FINDINGS
UK, 17% in Switzerland, 20% in Germany; RISK FACTORS • Congenital deafness—degeneration of the
Jack Russell terrier: 4% in United States; • Merle, piebald gene, or white coat color; stria vascularis with subsequent collapse of
Australian cattle dog: 15% in United States, blue eye color. membranous labyrinth structures. Bony
10% in Australia; English bull terrier: 11% labyrinth remains intact.
Deafness (continued)
• Acquired deafness—related to primary • Cochlear implants can be used in dogs with POSSIBLE COMPLICATIONS
disease such as otitis or neoplasia. moderate to profound deafness, but only Deaf dogs need protected environments and
• Ototoxicity—degeneration of otic hair preliminary data available and very expensive. training to be functional pets.
D cells, cochlear nerve degeneration, and loss of
stria vascularis.
MEDICATIONS MISCELLANEOUS
DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING
TREATMENT • None for congenital deafness. Dogs homozygous for recessive merle gene
CLIENT EDUCATION • Treat otitis based on culture and sensitivity can be blind and sterile.
Deaf animals may be functional pets, but results.
ABBREVIATIONS
require patience, specialized training, and PRECAUTIONS • BAER = brainstem auditory evoked
extra protection from traffic. • Aminoglycosides or other ototoxic drugs— response.
SURGICAL CONSIDERATIONS use with caution. • DPOAE = distortion product OAE.
• Directed toward acquired causes; congenital • Topical treatment of external ear canal— • OAE = otoacoustic emission.
deafness irreversible. avoid if tympanic membrane is ruptured. • TEOAE = transient evoked OAE.
• Otitis externa, media, or interna—medical Author Rita Gonçalves
or surgical approaches depend on culture and
sensitivity test results, response to antibiotics,
and imaging findings. Conduction may FOLLOW-UP C
lient Education Handout
improve as otitis externa or media resolves. PATIENT MONITORING available online
As needed for management of otitis.
Deciduous Teeth, Persistent (Retained)

CAUSES & RISK FACTORS erupted in an abnormal position, full root
• Cause is unknown, but is suspected to have extraction of the deciduous tooth is necessary.
a genetic basis. • Small-breed dogs are • If the deciduous root has undergone
BASICS predisposed. resorption, it may not need to be extracted. D
OVERVIEW
• A persistent (retained) deciduous tooth is
one that is still present when the permanent
tooth begins to erupt or has fully erupted. DIAGNOSIS MEDICATIONS
• Numerous factors influence the exfoliation
of deciduous teeth—lack of a permanent DIFFERENTIAL DIAGNOSIS DRUG(S) OF CHOICE
successor; ankylosis of the deciduous crown • Supernumerary teeth. • Gemination of the • Topical oral antimicrobial rinse prior to
or root to the alveolus; failure of the developing crown. extraction. • Pain management prior to,
permanent crown to contact the deciduous CBC/BIOCHEMISTRY/URINALYSIS during, and following extraction.
root, preventing resorption of the deciduous N/A CONTRAINDICATIONS/POSSIBLE
root during eruption. INTERACTIONS
IMAGING
SIGNALMENT N/A
Intraoral Radiography
• More common in dogs than cats. • More
• Distinguish between permanent tooth and
common in small-breed dogs (e.g., Maltese,
deciduous tooth. • Provide evidence or extent
poodle, Yorkshire terrier, Pomeranian, etc.).
of root resorption of the deciduous tooth.
• Occurs during permanent tooth eruption FOLLOW-UP
• Identify dental abnormalities prior to
phase, which begins at 3 months of age for
extraction, including persistent deciduous PATIENT MONITORING
incisors and 5–7 months of age for canine
tooth with no permanent successor, retained • After surgery, restrict activity for the rest of
teeth and molars. • Persistent deciduous teeth
root with crown missing, and unerupted the day. • Analgesia (nonsteroidal anti-inflam-
may not be detected or diagnosed until later
permanent tooth. • Identify relationship of matory drug [NSAID]) for 24–36 hours
in life. • No sex predilection.
deciduous root and permanent crown prior to postop. • Soft diet for 3 days—canned food or
SIGNS extraction. moistened dry kibble. • No chew toys for
General Comments DIAGNOSTIC PROCEDURES 3 days; no “tug of war” for 1 week. • Oral
• Persistent deciduous teeth can cause the • Complete oral examination—chart oral chlorhexidine rinse for 3–5 days. • Continue
permanent teeth to erupt in an abnormal cavity to indicate presence of persistent daily tooth brushing after 24 hours.
position resulting in a malocclusion; early deciduous teeth, malpositioned teeth, missing PREVENTION/AVOIDANCE
recognition and intervention are essential. teeth, soft tissue trauma, and other oral May be prevalent in certain breeds and
• Maxillary canine teeth erupt mesial (rostral) abnormalities. • Appropriate preoperative lines—avoid similar breeding.
to the persistent deciduous canine teeth; this diagnostics prior to procedure to include
can result in a diastema (space) between the intraoral radiography. POSSIBLE COMPLICATIONS
maxillary canine tooth and the third incisor • Malocclusion that results after full eruption
PATHOLOGIC FINDINGS of permanent teeth may require treatment.
that is too narrow to accommodate the crown N/A
zcanine position is referred to as mesiover- • Linguoversion of one or both mandibular
sion. • Mandibular canine teeth erupt canine teeth. • Mesioversion of one or both
lingual to the persistent deciduous teeth; this maxillary canine teeth.
can result in a narrow space between the EXPECTED COURSE AND PROGNOSIS
lower canines resulting in impingement on TREATMENT • Once extracted, there should be no further
the soft tissue of the hard palate. The problems. • Resulting malocclusion needs
mandibular canine position is referred to as Client Education
further evaluation. • Gingiva generally heals
linguoversion. • All permanent incisors • Persistent deciduous teeth may be prevalent
uneventfully.
erupt lingual to the persistent deciduous in certain breeds. • Start looking at teeth
incisors; this can result in a rostral crossbite. from the first puppy or kitten visit. • Inform
owners that you will be evaluating for
Physical Examination Findings exfoliation of deciduous teeth as well as for
• Presence of a deciduous tooth with the proper eruption of permanent teeth. MISCELLANEOUS
permanent tooth erupting or fully erupted.
• Abnormal position of the permanent tooth Surgical Considerations SEE ALSO
due to persistence of the deciduous tooth. • Extract the deciduous tooth as soon as the Malocclusions—Skeletal and Dental.
• Oral malodor from accumulation of debris permanent tooth has erupted through the
gingiva. • Pain management - local/regional ABBREVIATIONS
and plaque due to crowding of the permanent • NSAID = nonsteroidal anti-inflammatory drug.
tooth and the persistent deciduous tooth. and systemic. • Intraoral radiographs.
• Local gingivitis and periodontal disease due to • General anesthesia with endotracheal tube INTERNET RESOURCES
plaque accumulation from crowding. in place and cuff inflated. • Elevation of http://www.avdc.org/avdc-nomenclature
• Oronasal fistula from linguoversion of the deciduous tooth. • Careful, gentle elevation Suggested Reading
permanent mandibular canine teeth. • Deciduous is critical; excessive force or pressure can Lobprise HB, Dodd JR eds. Wiggs’s Veterinary
tooth crown is usually smaller than the permanent damage the developing permanent tooth (and Dentistry: Principles and Practice, 2nd.
tooth. • Deciduous tooth might not have an other underlying structures). • A fractured or Hoboken, NJ, Wiley-Blackwell; 2019.
underlying permanent tooth, and will often retained root may need to be removed with a Author Randi Brannan
remain intact and vital. gingival flap. • If a permanent tooth has Consulting Editor Heidi B. Lobprise
Deep Cutaneous Mycoses

SIGNALMENT • Yeast form in the mammal host causes
Cryptococcosis disseminated infection.
D BASICS • Young dogs and cats; more common in Coccidioidomycosis
cats. • Dimorphic saprophytic fungi.
DEFINITION • Siamese, Birman, and ragdoll cats • Found in sandy, alkaline soils with high
• Fungal infections that may secondarily • Doberman pinscher, German shepherd environmental temperature.
disseminate by hematogenous route to the dogs, and cocker spaniels. • Main infectious species Coccidioides immitis
skin. and C. posadasi.
• Most often caused by cryptococcosis, Blastomycosis
blastomycosis, and coccidioidomycosis. • Young dogs (1–3 years); rare in cats. RISK FACTORS
• Doberman pinscher. • Immunosuppressed hosts are more predis-
PATHOPHYSIOLOGY • Increased incidence in male dogs posed to develop cryptococcosis caused by C.
Cryptococcosis Coccidioidomycosis neoformans.
Main route of infection is inhalation and • Living in or visiting endemic areas increases
• Young dogs; rare in cats.
colonization of nasal mucosa, followed by • Boxer and Doberman pinscher predisposed.
risk of cryptococcosis (C. gattii), blasto
hematogenous spread to lymph nodes, skin, • Increased incidence in males.
mycosis, and coccidioidomycosis.
bones, and CNS.
SIGNS
Blastomycosis
• Infection by inhalation of spores Historical Findings
produced from mycelial growth in the • Nonspecific clinical signs (asthenia, weakness, DIAGNOSIS
environment. anorexia, weight loss), respiratory signs, or the DIFFERENTIAL DIAGNOSIS
• Spores settle in airways, transform into appearance of skin lesions in the animal. • Deep staphylococcal pyoderma.
yeast forms, and establish a primary infection • Upper respiratory signs—cryptococcosis
• Nocardiosis.
of the lungs, followed by dissemination via and blastomycosis. • Actinomycosis.
blood and lymphatic vessels. • Lameness—coccidioidomycosis.
• Mycobacterial infections.
• Colonize lymph nodes, skin, eyes, bones, Physical Examination Findings (Skin) • Pseudomycetoma (cat).
CNS, and testes. • Chromoblastomycosis.
Cryptococcosis
Coccidioidomycosis • Cat—multiple papules, nodules, abscesses, • Pheohyphomycosis.
• Infection by inhalation of arthroconidia. and ulcers; bridge of nose/dorsal muzzle • Hyalohyphomycosis.
• In the lungs, arthroconidia transform into (primary site) or any skin ara; lesions may • Leishmaniasis.
spherules filled with endospores, which drain a serous exudate. • Sterile nodular panniculitis.
disseminate by hematogenous routes to • Dog—papules, dermal-subcutaneous • Sterile pyogranuloma syndrome.
bones, skin, eyes, heart, testes, CNS, liver, nodules or ulcers; located on any portion of • Eosinophilic granuloma.
and kidneys, among others. the integument, lips, tongue, or claw beds. CBC/BIOCHEMISTRY/URINALYSIS
SYSTEMS AFFECTED Blastomycosis • Generally nonspecific—nonregenerative
Systemic infections via inhalation with Dog—draining tracts and abscesses in anemia, leukocytosis, monocytosis,
hematogenous dissemination to multiple one-third of cases; Planum nasale, face, and eosinophilia.
organs—skin, lymph nodes, eyes, bones, claw bed most frequent locations. • Serum biochemical profile may reflect
CNS, testes. specific organ involvement; hypoalbumine-
Coccidioidomycosis mia and hyperglobulinemia common.
GENETICS Dog—dermal nodules that progress to
N/A abscesses and ulcers, or draining tracts over OTHER LABORATORY TESTS
INCIDENCE/PREVALENCE sites of infected bone; Coccidioides infection Cryptococcosis
• Uncommon diseases, may also be asymptomatic. • Detection of cryptococcal polysaccharide
• Incidence depends on geographic location; CAUSES capsular antigen in serum using a latex
can be very high (e.g., coccidioidomycosis in agglutination technique.
Cryptococcosis • Organism can be cultured in Sabouraud
areas of Arizona).
• Dimorphic fungi.
agar from skin lesions.
GEOGRAPHIC DISTRIBUTION • Filamentous form in the environment.
• Yeast phase in mammalian tissues. Blastomycosis
Cryptococcosis
• Genus Cryptococcus includes 40 species— Measuring antibodies in serum (agar gel
• C. neoformans worldwide distribution.
most infections in dogs and cats caused by immunodiffusion [AGID], ELISA) assists in
• C. gattii associated with tropical and
C. neoformans and C. gattii. diagnosis of blastomycosis when organisms
subtropical climates.
• C. neoformans often found in soils cannot be specifically identified in cytologic
• Recognized also in North America and
associated with bird excrement. or histologic specimens.
British Columbia (Vancouver Island).
• C. gattii found in soils, especially in those Coccidioidomycosis
Blastomycosis covered with leaves of some tree species • Conclusively diagnosed by cytologic or
Areas of the United States and Canada (eucalyptus), and in the bark of some trees histologic visualization of the organism.
surrounding the Ohio and Mississippi River (oak, maple, cedar). • Detection of antibodies (AGID, ELISA)
valleys, the Great Lakes, and the Saint commonly used when the organism cannot be
Lawrence River. Blastomycosis
• Dimorphic fungus. demonstrated in cytology or biopsy samples.
Coccidioidomycosis • Mycelial form lives in moist soil and in • Coccidioides grows in common culture
Southwestern United States, Mexico, and decomposing organic matter such as wood media.
areas of Central and South America. and leaves.
(continued) Deep Cutaneous Mycoses

• Exposure to mycelial growth in cultures a PREVENTION/AVOIDANCE
potential hazard to humans—organism Avoid visiting areas where these infections are
should not be cultured outside of qualified endemic.
laboratories with proper warning of the MEDICATIONS D
differential diagnosis. DRUG(S) OF CHOICE N/A
IMAGING Cryptococcosis
• Radiographs-- evaluate for the presence • Itraconazole (5 mg/kg PO q12–24h).
• Prognosis is guarded; depends on the
of lesions in the upper airways, lungs, • Fluconazole (10 mg/kg PO q12–24h).
affected organs.
and bones. • Treatment maintained for 6–18 months—
• Poor prognosis with CNS involvement in
• Ultrasound imaging—to evaluate for the until resolution of clinical disease.
cryptococcosis.
presence of lesions in the abdominal cavity. • Some authors recommend continued
antifungal therapy until the cryptococcal
antigen is zero.
• Cytologic evaluation of all cutaneous
lesions (papules, nodules, abscesses) by Blastomycosis
fine-needle aspirate of solid lesions or • Itraconazole (5 mg/kg PO q12–24h).
MISCELLANEOUS
impression smears of exudates. • Fluconazole (10 mg/kg PO q12–24h). ASSOCIATED CONDITIONS
• Cytologic preparations usually reveal a • Treatment continued for at least 60 days N/A
pyogranulomatous exudate with the presence and at least 1 month after all signs of disease ZOONOTIC POTENTIAL
of the causal organism. have resolved. • Cryptococcosis, blastomycosis, and
• Cryptococcosis—number of organisms is Coccidioidomycosis coccidioidomycosis are not considered
very high and they are easily detected. • Fluconazole (10 mg/kg PO q12–24h). zoonoses.
• Blastomycosis and coccidioidomycosis— • Itraconazole (5 mg/kg PO q12–24h). • Infected dogs and cats pose no public
detection of the fungal elements more • Treatment is prolonged—treat for at least health threat because infective forms are not
difficult. If cytologic preparations are 1 year and/or until resolution of clinical produced in tissues.
inconclusive, a skin biopsy for histopatho- disease. • Handling mycelial cultures of the organism
logic examination should be obtained. in the laboratory is dangerous.
• Histologically, these diseases are character- PRECAUTIONS
ized by a nodular to diffuse pyogranuloma- N/A PREGNANCY/FERTILITY/
tous dermatitis and panniculitis, with the POSSIBLE INTERACTIONS BREEDING
presence of the causal organisms. Azole antifungals, especially ketoconazole, are • Vertical transmission of cryptococcosis and
inhibitors of cytochrome P450 (CYP) and blastomycosis has been reported in humans—
PATHOLOGIC FINDINGS
can increase serum levels of other drugs that considered extremely rare and not reported in
Chronic pyogranulomatous reaction with the
are metabolized by this route (e.g., cyclosporine). dogs and cats.
presence of organisms in tissues.
• Intrauterine transmission of coccidioidomy-
ALTERNATIVE DRUG(S) cosis not likely to occur because of the large
Cryptococcosis size of the spherules.
Amphotericin B and flucytosine for CNS SYNONYMS
TREATMENT and/or resistant infection. • Cryptococcosis—torulosis, European
APPROPRIATE HEALTH CARE Blastomycosis blastomycosis.
Outpatient medical management, unless Amphotericin B for resistant infection. • Blastomycosis—Gilchrist disease, Chicago
severe internal lesions (meningoencephalitis, Coccidioidomycosis
disease.
severe kidney disease). • Ketoconazole (5–10 mg/kg PO q12–
• Coccidioidomycosis—valley fever, San
NURSING CARE 24h)—if fluconazole or itraconazole is not Joaquín Valley fever.
N/A available. ABBREVIATIONS
ACTIVITY • Side effects more common and more severe • AGID = agar gel immunodiffusion.
Normal activity. with ketoconazole than with the other two INTERNET RESOURCES
azoles in cats. https://www.cdc.gov/fungal
DIET
N/A CONTRAINDICATIONS Suggested Reading
• Ketoconazole is hepatotoxic and should not Greene CG. Infectious Diseases of the Dog and
CLIENT EDUCATION be prescribed to patients with liver damage.
Owners should be informed of the risk Cat, 4th ed. St. Louis, MO: Elsevier, 2012.
• Amphotericin B is nephrotoxic and is Helton Rhodes KA, Werner A. Blackwell’s
involved in visiting areas where these contraindicated in patients with kidney damage.
infections are endemic. Five-Minute Veterinary Consult
Clinical Companion: Small Animal
SURGICAL CONSIDERATIONS Dermatology, 3rd ed. Hoboken, NJ:
Surgical excision of large tissue masses infected Wiley-Blackwell, 2018.
with Cryptococcus (skin nodules, lymph nodes, Author Lluís Ferrer
nasopharyngeal masses) when possible. FOLLOW-UP Consulting Editor Alexander H. Werner
PATIENT MONITORING Resnick
The frequency of monitoring depends on the
severity and location of the lesions.
Demodicosis
<5 lesions. • Generalized—both young and Cats
old animals. • D. cati may be more common • Allergic dermatitis. • Dermatophytosis.
in middle-aged or older cats; D. gatoi seems • Any cause of alopecia or pruritus.
D BASICS to be more common in younger cats and CBC/BIOCHEMISTRY/URINALYSIS
DEFINITION kittens, but any age can be affected. Normal unless there is an underlying
An inflammatory parasitic disease of dogs and process.
cats characterized by an increased number of SIGNS
demodectic mites in the hair follicles and on Dogs
the epidermis. • Feline leukemia virus (FeLV) and FIV
• Patchy alopecia—most common site is the
face, especially around the perioral and serology. • Fecal samples—rare finding of
PATHOPHYSIOLOGY mites in feces; more common with cats.
periocular areas and forelegs; may also be seen
Dogs DIAGNOSTIC PROCEDURES
on the trunk and feet. • Pododemodicosis—
• Three species of mites identified in the dog:
lesions localized to the feet. • Disease can • Skin scrapings diagnostic for finding mites
◦ Demodex canis—follicular mite; part of the
progress to become or begin with a general- in most cases—D. gatoi may be difficult to
normal fauna of the skin; typically present in find. • Hair plucking can be used in areas
ized distribution. • Usually not pruritic
small numbers; resides in the hair follicles and such as eyelids. • Skin biopsy—may be
unless secondarily infected. • Hair follicles
sebaceous glands of the skin, transmitted from needed when lesions are chronic, granuloma-
distended with large numbers of mites, lose
the mother to the neonate during the first 2–3 tous, and fibrotic (especially on the foot);
hair and develop secondary bacterial
days of nursing. ◦ Demodex injai—large, may be needed to diagnose demodicosis in
folliculitis, followed by rupturing of the
long-bodied mite found in the pilosebaceous the shar pei breed.
follicles (furunculosis). • With progression,
unit, mode of transmission unknown; only
the skin becomes severely inflamed, exuda-
associated with adult-onset disease, with highest
tive, and granulomatous. • D. injai may be
incidence noted in the terrier breeds often
associated with greasy seborrheic dermatitis of
along the dorsal midline (West Highland white
the dorsal trunk, comedones, erythema,
terrier and wirehaired fox terrier).◦ Demodex TREATMENT
alopecia, and hyperpigmentation.
cornei—lives in the stratum corneum of the
epidermis; mode of transmission unknown; Cats APPROPRIATE HEALTH CARE
most likely a morphologic variant of D. canis. • D. cati—partial to complete alopecia of the • Localized D. canis lesions often (90%)
• Proliferation of mites may be the result of eyelids, periocular region, head, neck, flank, resolve spontaneously. • Evaluate the health
immunologic disorder, either genetic or and ventrum. • D. gatoi—pruritus with status of patients presenting with generalized
iatrogenic. • Pruritus occurs when a dramatic scaling, erythema, and/or crusting lesions of demodicosis.
secondary bacterial infection is present. due to inflammation and self-trauma. CLIENT EDUCATION
• Ceruminous otitis externa has been • Localized—most cases resolve spontane-
Cats
reported. • D. cati often associated with ously. • Generalized—frequent manage-
• Two species of mites identified in the cat:
immunosuppressive disease. ment problem due to chronicity. Juvenile
◦ Demodex gatoi—contagious; can be asympto-
matic, but most commonly is associated with CAUSES onset considered to have an inheritable
pruritic dermatitis leading to self-trauma, • Dog—D. canis, D. injai, and D. cornei. predisposition—breeding of affected
alopecia, and barbering. ◦ Demodex cati— often • Cat—D. cati and D. gatoi. animals is not recommended.
associated with immunosuppressive and RISK FACTORS
metabolic disease; these mites cause folliculitis
and alopecia, but are rarely pruritic. Dogs
• Exact immunopathologic mechanism
SYSTEMS AFFECTED unknown. • Dogs with generalized demodi- MEDICATIONS
Skin/exocrine. cosis may have abnormal or depressed T-cell DRUG(S) OF CHOICE
GENETICS function. • Development associated with Dogs
Initial proliferation of mites may be the result oclacitinib treatment. • Genetic factors (especially
of a genetic disorder. juvenile onset), immunosuppression, and/or Isoxazolines antiparasitics
metabolic diseases may predispose animal. • Treatment of choice—excellent efficacy
INCIDENCE/PREVALENCE against demodicosis at label doses for fleas;
• Dogs—D. canis is very common. • Cats— Cats safe for avermectin-sensitive dogs. • Side
depending on geographic location, D. gatoi • D. cati—often associated with metabolic effects uncommon—vomiting, diarrhea,
may be common or rare; D. cati is rare. diseases that affect the immune system (e.g., inappetence, or neurologic signs including
SIGNALMENT feline immunodeficiency virus [FIV], hyper- seizures.
adrenocorticism, diabetes mellitus).
Species • D. gatoi—considered contagious; cats in Ivermectin
Dogs and cats. contact with other cats are at risk. • 0.3–0.6 mg/kg q24h PO very effective;
Breed Predilections initiate therapy with a test dose of 0.12 mg/
• D. canis—American Staffordshire terrier, kg q24h for first week to observe for any signs
shar-pei, Boston terrier, English bulldog, and of sensitivity. • Treat for 30–60 days beyond
West Highland white terrier. • D. injai— negative skin scrapings (average 3–8 months).
West Highland white and wirehaired fox
DIAGNOSIS • Non-FDA-approved usage—do not use in
terriers, shih tzu. • Potential increased DIFFERENTIAL DIAGNOSIS avermectin-sensitive (ABCB-1 mutation)
incidence in Siamese and Burmese cats. breeds.
Dogs
Mean Age and Range • Bacterial folliculitis/ Milbemycin Oxime
• Juvenile onset, localized—usually in dogs furunculosis. • Dermatophytosis. • Any • 1–2 mg/kg PO q24h cures 50% of cases;
<1 year of age; median 3–6 months, typically cause of inflammatory alopecia. 2 mg/kg PO q24h cures 85% of cases.
(continued) Demodicosis
• ABCB-1 mutation individuals may have for 12–36 hours after treatment. • Rare side
neurologic signs with higher doses; tolerate effects—vomiting, diarrhea, pruritus, polyuria,
milbemycin better than other drugs in this class. mydriasis, bradycardia, hypoventilation,
• Non-FDA-approved usage. hypotension, hypothermia, ataxia, ileus, MISCELLANEOUS D
Moxidectin bloat, hyperglycemia, convulsions, death. ASSOCIATED CONDITIONS
• Yohimbine at 0.11 mg/kg IV is an antidote, • Adult-onset demodicosis—sudden
• 0.3 mg/kg PO q24h or topical application
once weekly. • Non-FDA-approved usage— as is atipamezole. • Incidence and severity of occurrence is associated with internal disease,
do not use in avermectin-sensitive (ABCB-1 side effects do not appear to be proportional malignant neoplasia, and/or immunosuppres-
mutation) breeds. to dose or frequency of use. • Apply in a sive disease; approximately 25% of cases are
well-ventilated area; owners should wear idiopathic over a follow-up period of 1–2
Amitraz aprons and gloves so they do not come in years. • D. cati associated with FeLV, FIV,
• Applied in the United States as a 250 ppm contact with the dip. • Human beings can toxoplasmosis, iatrogenic immune suppres-
(0.025%) dip every 14 days and in Europe as a develop dermatitis, headaches, and respiratory sants, papillomaviral plaques, and systemic
500 ppm (0.05%) dip every 7 days. See adverse difficulty after exposure. Amitraz should not lupus erythematosus (SLE).
effects below. • Clipping the hair coat and be used by people taking monoamine oxidase
bathing with a benzoyl peroxide shampoo before AGE-RELATED FACTORS
(MAO) inhibitors (e.g., some antihistamines,
application of the rinse assist response. • Amitraz- Young dogs are often predisposed to a
antidepressants, and antihypertensives).
containing collars and spot-ons are not effective. localized form.
• Can dysregulate blood sugar in diabetics.
• Efficacy is proportional to the frequency of ZOONOTIC POTENTIAL
administration and the concentration of the rinse. Ivermectin and Milbemycin
None
• Poor compliance limits efficacy. • 11% and Signs of toxicity—salivation, vomiting,
mydriasis, confusion, ataxia, hypersensitivity to PREGNANCY/FERTILITY/BREEDING
30% of cases will not be cured; may need to try
sound, weakness, recumbency, coma, and death. Do not breed animals with the generalized
an alternative therapy or control with mainte-
form.
nance rinse every 2–8 weeks. POSSIBLE INTERACTIONS
• Amitraz—may interact with heterocyclic SYNONYMS
DRUG(S) OF CHOICE
antidepressants, xylazine, benzodiazepines, • Mange. • Red mange.
Cats and macrocyclic lactones. • Ivermectin and SEE ALSO
Isoxazoline antiparasitics milbemycin—cause elevated levels of mono- Ivermectin and Other Macrocyclic Lactones
• Treatment of choice at label doses for fleas. amine neurotransmitter metabolites, which Toxicosis.
• Side effects uncommon but include could result in adverse drug interactions with
amitraz and benzodiazepines. • Spinosad and ABBREVIATIONS
drooling, vomiting, diarrhea, inappetence, or
other drugs in that class are contraindicated • FeLV = feline leukemia virus.
neurologic signs including seizures.
with ivermectin therapy. • FIV = feline immunodeficiency virus.
2% lime sulfur • MAO = monoamine oxidase.
• Can be diluted, sponged over the cat, and • SLE = systemic lupus erythematosus.
allowed to dry without rinsing once weekly
for 6 treatments. • Malodorous, staining, and
Suggested Reading
FOLLOW-UP Sastre N, Ravera I, Villanueva S, et al.
difficult to apply to the face. • Patient should
Phylogenetic relationships in three species
be restricted from grooming after application. PATIENT MONITORING of canine Demodex mite based on partial
Alternatives Repeat skin scrapings and evidence of clinical sequences of mitochondrial 16S rDNA. Vet
Alternative but less effective options for the resolution are used to monitor progress, Derm 2012, 23(6):509–e101.
treatment of D. gatoi: generally repeated every 2–4 weeks until Author Melissa N.C. Eisenschenk
• Milbemycin oxime—1 mg/kg PO q24h. resolution, and then treatments are continued Consulting Editor Alexander H. Werner
• Doramectin—0.6 mg/kg SC weekly 1–2 months beyond negative scrapings. Resnick
• Ivermectin—0.2–0.3 mg/kg PO q24–48h. PREVENTION/AVOIDANCE Acknowledgment The author and book
Neurologic side effects such as ataxia are Do not breed animals with generalized editors acknowledge the prior contribution of
possible with ivermectin. disease. Karen Helton Rhodes.
CONTRAINDICATIONS POSSIBLE COMPLICATIONS
Do not use ivermectin in avermectin-sensitive Secondary bacterial folliculitis and Client Education Handout
breeds—collies, Shetland sheepdogs, Old furunculosis. available online
English sheepdogs, Australian shepherds,
other herding breeds, and crosses with these EXPECTED COURSE AND PROGNOSIS
breeds. Screening for the ABCB-1 mutation Prognosis is very good for elimination of the
is recommended. demodicosis with isoxazoline treatment.
Prognosis depends heavily on compliance,
PRECAUTIONS and genetic, immunologic, and underlying
Amitraz diseases. Severe, generalized cases with
• Side effects—somnolence, lethargy, underlying disease may be refractory to
depression, anorexia seen in 30% of patients treatments other than isoxazoline.
Dental Caries
• There is no reported breed, age, or gender • Deep periodontal pockets predispose to
predilection. root caries.
• Anecdotally, the author has observed a • Animals with poorly mineralized enamel,
D BASICS higher incidence of pit-and-fissure lesions in lower salivary pH, diets high in fermentable
OVERVIEW the occlusal tables of the maxillary first molar carbohydrates, and poor oral hygiene are at
• Caries is the decay of the dental hard tissues teeth in large-breed dogs such as Labrador risk of developing caries.
(enamel, cementum, and dentin) due to the retrievers and German shepherds. • Loss of enamel through any means (hypo-
effects of oral bacteria on fermentable calcification at the developmental stage,
carbohydrates on the tooth surface. SIGNS abrasive wear or attrition, traumatic fracture)
• The word “caries” is Latin for rottenness • Incipient smooth-surface caries—appears as that exposes the softer, underlying dentin may
and is both the singular and plural form. an area of dull, frosty-white enamel. increase the risk for the development of caries.
• Oral bacteria ferment carbohydrates on • Clinical caries—appears as a structural
the tooth surface, resulting in the produc- defect on the surface of the crown or root.
tion of acids leading to demineralization of • The defect is frequently filled with or lined
the hard tissues, thus allowing bacterial and by dark, soft necrotic dentin. The defect may
also trap and hold food debris.
DIAGNOSIS
leukocytic digestion of the organic matrix
of the tooth. • Affected dentin will yield to a dental DIFFERENTIAL DIAGNOSIS
• Caries has been very common in humans in explorer and can be removed with a dental • Crown fracture, abrasive wear or attrition
“westernized” society, where diets rich in excavator or curette. with exposed tertiary dentin, or extrinsic
highly refined carbohydrates are the norm. staining.
Aggressive public education and preventive CAUSES & RISK FACTORS • Enamel hypocalcification with exposed and
measures have resulted in a decline in • Caries is caused by oral bacteria fermenting stained dentin.
incidence over the past several decades. carbohydrates on the tooth surface, leading to • Tooth resorption (FORL) has been misnamed
• In humans, Streptococcus mutans is particu- the production of acids (acetic, lactic, feline caries in the past.
larly implicated in the development of caries. propionic) that demineralize the enamel, • Tooth resorption can also occur in dogs and
• For various reasons (e.g., diet lower in cementum, and dentin, followed by digestion may be mistaken for caries.
refined carbohydrates, higher salivary pH, of the organic matrix of the tooth by oral • Sound dentin is hard and will not yield to a
lower salivary amylase, conical crown shape, bacteria and/or leukocytes. dental explorer, whereas carious dentin is soft
wider interdental spacing, different indig- • There is a constant exchange of minerals and will yield to a sharp instrument.
enous oral flora), caries is not common in the between the tooth surfaces (enamel, any exposed • Root caries may be confused with external
domestic dog, but it does occur and should dentin or root cementum) and the oral fluids; if root resorption, though the distinction would
be looked for. there is a net loss of mineral, caries develops. often be academic, as either usually indicates
• A study published in the Journal of • Early (incipient) caries may be reversible the need for extraction.
Veterinary Dentistry in 1998 (see Suggested through remineralization. • The lesion should be staged as to the depth
Reading) reported that 5.3% of dogs 1 year of • Once the protein matrix collapses, the of the pathology.
age or older had one or more caries lesions, lesion is irreversible. • Table 1 is adapted from the American
with 52% having bilaterally symmetric • Any factors that allow prolonged retention Veterinary Dental College approved
lesions. of fermentable carbohydrates and bacterial nomenclature for tooth resorption as
• Caries can affect the crown or roots of the plaque on the tooth surface predispose to the published on its website.
teeth and is classified as pit-and-fissure, development of caries. CBC/BIOCHEMISTRY/URINALYSIS
smooth-surface, or root caries. • A deep occlusal pit on the maxillary first
N/A
molar is the most common place for caries to
SIGNALMENT develop. IMAGING
• Caries occurs in dogs. • Dental surfaces in close contact with an Intraoral Dental Radiography
• Reported in cats; tooth resorption (feline established caries are at risk of developing a • Areas of demineralization and tissue loss
odontoclastic resorptive lesions [FORL]) has lesion by extension. will appear as lucent areas contrasted against
sometimes been misnamed feline caries. To • Deep occlusal pits and developmental radiodense normal dental tissues.
the author’s knowledge, there are no grooves on the crown surface predispose to • If the lesion has penetrated into the pulp
published reports of true dental caries pit-and-fissure caries. chamber, there will be endodontic disease,
occurring in the domestic cat, though it is • Tight interdental contacts predispose to and periapical disease may be evident if the
theoretically possible. smooth-surface caries. lesion is sufficiently longstanding.
Table 1
Stage 1 Defect involves enamel or cementum only.

Stage 2 Defect extends into dentin but not into pulp chamber.
Stage 3 Deep dental hard tissue loss (cementum and/or enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its
integrity.
Stage 4 Extensive dental hard tissue loss (cementum and/or enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost
its integrity.
Stage 5 Majority of crown lost; root remnants remaining.
(continued) Dental Caries

• Small lesions may be difficult to demon- • Lesions that result in extensive coronal carefully (clinically and radiographically)
strate due to superimposition of normal, tissue loss (stage 4 or 5)—extraction is at any opportunity to monitor for the
radiodense tissues (dental and skeletal). typically the only treatment option. As the development of new lesions.
pulp tissue in the roots will be contami- D
DIAGNOSTIC PROCEDURES PREVENTION/AVOIDANCE
• Visual examination of the clean, dry tooth
nated, complete removal of all root remnants Avoidance of diet and treats high in refined
surface under good light and with the aid of is essential. carbohydrates may reduce the risk of the
magnification. • Root caries—if the periodontal disease
development of further caries.
• Exploration with a sharp dental explorer—
can be managed and the restoration placed
supragingivally, restoration may be possible; EXPECTED COURSE
the explorer will sink into carious dentin and
stick, providing the sensation of “tug-back” however, for most teeth with root caries, AND PROGNOSIS
upon withdrawal. extraction will be the treatment of choice. If a lesion has been properly debrided and
• If only one root of a multirooted tooth restored it should have an excellent progno-
• Subgingival exploration—reveals irregularities
in the root surface. is carious—extraction of the affected root sis. Appropriate staging and case selection,
• Caries detection dyes have been used by
with endodontic treatment of the remaining thorough removal of all carious tissues, and
human and veterinary dentists to aid in the root(s) is also an option. adherence to restorative principles are
differentiation between sound and carious • For high-risk patients—application of a essential.
dentinal tissue. However, their use may lead pit-and-fissure sealant and/or fluoride-
to false-positive results and overtreatment releasing dental bonding agent on remain-
through the removal of excess tissue. Reliance ing teeth with occlusal surfaces may be
on visual, tactile, and radiographic findings is considered.
MISCELLANEOUS
preferable.
SYNONYMS
• Cavities.
MEDICATIONS • Dental decay.
DRUG(S) OF CHOICE ABBREVIATIONS

TREATMENT • Postoperative broad-spectrum antibiotics— • FORL = feline odontoclastic resorptive
• Focus on prevention—examine the adult may be indicated if there is pulp involvement lesions.
dentition of adolescent dogs (6–8 months of necessitating endodontic treatment or INTERNET RESOURCES
age) to identify anatomically compromised extraction. • http://www.toothvet.ca/PDFfiles/
areas at risk for the development of caries. • Postoperative analgesia with nonsteroidal DentalCaries.pdf
Deep pits in the occlusal surface of the anti-inflammatory drugs and/or narcotics is • https://avdc.org/avdc-nomenclature
maxillary first molar (for example) can be indicated following endodontic or exodontic • http://www.toothvet.ca/PDFfiles/Tooth_
filled with a pit-and-fissure sealant or treatment or extensive restorative work of resorption_in_cats.pdf
fluoride-releasing dental bonding agent to vital teeth. • http://www.toothvet.ca/PDFfiles/RLs_in_
prevent caries development if identified prior Dogs.pdf
to the development of any decay. CONTRAINDICATIONS/POSSIBLE
• Incipient caries—can be arrested and Suggested Reading
INTERACTIONS Hale FA. Dental caries (cavities). In: Lobprise
possibly reversed by application of a fluoride N/A
varnish or fluoride-releasing dental bonding HB, ed., Blackwell’s Five-Minute Veterinary
agent and modification of the risk factors. Consult Clinical Companion: Small Animal
• Lesions that result in mild to moderate coronal Dentistry. Ames, IA: Blackwell, 2007, pp.
tissue loss (stage 1 or 2)—remove carious dentin 212–224.
and unsupported enamel using hand instru- Hale FA. Dental caries in the dog. J Vet Dent
FOLLOW-UP 1998, 15:79–83.
ments and power rotary dental instruments, then
restore the coronal anatomy with a bonded, PATIENT MONITORING Hale FA. Veterinary dentistry. Dental caries
composite restoration or prosthetic restoration. • Examine and radiograph treated teeth 6 in the dog. CVJ 2009, 50:1301–1304.
• Lesions that extend into pulp tissue months postoperatively, then annually or as McComb D. Caries-detector dyes—how
(stage 3)—endodontic treatment must the opportunity presents. accurate and useful are they? J Can
precede restorative treatment. Alternatively, • Evaluate the integrity of the restorations, Dent Assoc 2000, 66:195–198. http://
extraction may be indicated. As the pulp assess for further decay at the margins or www.cda-adc.ca/jcda/vol-66/issue-
tissue in the roots will be contaminated, under the restorations, assess for the develop- 4/195.html
complete removal of all root remnants is ment of endodontic disease. Author Fraser A. Hale
essential if extraction is performed. • As affected individuals frequently have Consulting Editor Heidi B. Lobprise
more than one caries, examine all teeth
Dentigerous Cyst
DIAGNOSTIC PROCEDURES Suggested Reading
Histopathologic assessment if atypical Babbitt SG, Krakowski Volker M, Luskin IR.
radiographic findings (any unerupted teeth Incidence of radiographic cystic lesions
D BASICS demonstrating radiolucency surrounding the associated with unerupted teeth in dogs. J
OVERVIEW unerupted crown should be submitted for Vet Dent 2016, 33(4):226–233.
Cyst formation originating from tissue histologic evaluation). Lobprise HB. Blackwell’s Five-Minute
surrounding the crown of an unerupted tooth. Veterinary Consult Clinical Companion:
Small Animal Dentistry. Ames, IA:
SIGNALMENT
Blackwell, 2007.
• Any breed that is at an increased risk for
TREATMENT Lobprise HB, Dodd JR. Wigg’s Veterinary
impaired eruption.
• Appropriate preoperative antimicrobial and
Dentistry: Principles and Practice, 2nd ed.
• Boxers, bulldogs—mandibular first
pain management therapy when indicated. Ames, IA: Wiley-Blackwell, 2019.
premolars, often bilateral.
• Appropriate patient monitoring and
Verstraete FJM, Zin BP, Kass PH, et al.
• Unerupted teeth at 6–7 months of age, but
support during anesthetic procedure. Clinical signs and histologic findings in
cystic development may not occur until much
• If cystic formation is present—surgical
dogs with odontogenic cysts: 41 cases
later, if at all.
extraction, complete debridement of cyst (1995–2010). J Am Vet Med Assoc 2011,
SIGNS 239(11):1470–1476.
• Cystic changes may be initially unapparent
lining, and histologic evaluation.
• If an embedded tooth has been present in a
White SC, Pharoah MJ. Oral Radiology
without diagnostic imaging. Principles and Interpretation, 5th ed. St.
• “Missing” tooth.
mature animal—assess for any cystic structure
or other pathologic changes involving the Louis, MO: Mosby, 2004, pp. 388–392.
• Formation of a soft swelling at the site of a Author Christopher J. Snyder
missing tooth, often fluctuant with fluid. tooth; continued monitoring (minimally
yearly) may be reasonable if surgical extraction Consulting Editor Heidi B. Lobprise
• Patient may present, with no previous
indication of a problem, for a pathologic would damage large amounts of bone.
• If a nonstrategic tooth can be easily
fracture of the mandible due to cystic
destruction of the surrounding bone. extracted, it would be best to do so, even if
cystic changes are not present.
Unerupted teeth.
MEDICATIONS
DIAGNOSIS DRUG(S) OF CHOICE
Postoperative analgesics, as necessary.
• Odontogenic keratocyst—cyst of the jaw
demonstrating aggressive expansion that may, INTERACTIONS
or may not, be associated with unerupted teeth. N/A
• Primordial cyst—cystic degeneration of a
tooth bud before enamel/dentin formation
(cyst without a tooth).
• Oral mass—odontoma (complex or FOLLOW-UP
compound): tooth structures (enamel, dentin,
cementum, and pulp) sometimes contained POSSIBLE COMPLICATIONS
within cystic structure, but with different • Pathologic fracture may occur if dentigerous
levels of organization. cyst is not diagnosed and treated.
• Transformation to ameloblastomas have • Fracture of mandible at time of extraction,
been reported in humans; histologic due to compromised supporting bone.
evaluation of the cyst lining is highly • Cyst development and expansion result in
recommended. weakening of the bone at that location and
may risk causing root resorption or devitaliza-
CBC/BIOCHEMISTRY/URINALYSIS tion of neighboring teeth.
• No abnormalities typically found.
• Preoperative diagnostics where appropriate EXPECTED COURSE AND PROGNOSIS
for safe administration of general anesthesia. • Extraction should be performed to avoid
risk for future cyst development.
IMAGING • Good with early detection and extraction.
• Definitive diagnosis from radiography. • Fair to guarded with extensive bone
• Radiographs are essential in any instance of destruction or pathologic fracture.
missing or unerupted teeth.
• Radiographically—radiolucent cyst
originating from the remnant enamel organ at
the neck of the tooth and encompassing the
crown (a halo). MISCELLANEOUS
• CT studies of the head should evaluate for INTERNET RESOURCES
presence of unerupted teeth. https://avdc.org/avdc-nomenclature
Dermatomyositis
• Several littermates may be affected, but the DIAGNOSTIC PROCEDURES
severity of the disease often varies significantly • Skin biopsy—may be diagnostic for
among affected dogs. dermatomyositis, although this disease can be
BASICS difficult to definitively diagnose; avoid D
DEFINITION • Waxing and waning lesions. infected and scarred lesions.
An inheritable inflammatory disease of the • Usually seen in affected dogs before 6 • Muscle biopsy—proper muscle selection
skin, muscles, and vasculature that develops months of age. can be difficult because pathologic changes
in young collies, Shetland sheepdogs, and • Begins around the eyes and lips, face, inner may be mild consisting of muscle necrosis
their crossbreeds. ear pinnae, tip of the tail, and bony promi- and atrophy.
nences—the entire face may be involved. • Electromyography (EMG)—ideally, used to
PATHOPHYSIOLOGY
• Pressure points over bony prominences, select affected muscles for biopsy; if EMG is
• The exact pathogenesis of dermatomyositis
especially the carpal and tarsal regions. not available, atrophied muscles should be
is unknown.
• Characterized by variable degrees of crusted biopsied.
• A familial predisposition has been reported
in collies and Shetland sheepdogs; however, erosions, ulcers, and alopecia, with erythema, PATHOLOGIC FINDINGS
possible triggers for the disease include scaling, and scarring. Skin Biopsy
infectious agents (especially viral), vaccines, • Foot pad and oral ulcers, as well as nail
• Scattered apoptosis or vacuolation of
drugs, malignancy, toxins, infection—as seen abnormality or loss may occur. individual and follicular basal cells; may lead
with ischemic dermatopathy in other breeds. • Scarring—often a sequela to the initial skin
to intrabasal or subepidermal clefting.
• Based on the clinical and histopathologic lesions. • Mild pigmentary incontinence.
evidence, an immune-mediated or auto- • Atrophy of the masseter and temporal
• Superficial, mild, diffuse dermal and
immune process may be involved. muscles—severe cases may have difficulty perivascular cellular infiltrates—composed of
eating, drinking, and swallowing. lymphocytes, plasma cells, and histiocytes.
SYSTEMS AFFECTED
• Stiff or high-stepping gait.
• Skin/exocrine. • Follicular atrophy and perifollicular fibrosis
• Myositis—signs may be absent or vary from
• Musculoskeletal. in chronic cases.
subtle decrease in the mass of the temporalis • Secondary epidermal ulceration and dermal
GENETICS muscles to generalized symmetric muscle scarring—may be present.
Autosomal dominant inheritance, with atrophy and stiff high-stepping gait. • Histopathologic features may be subtle and
variable expression in collies and Shetland • Dogs with megaesophagus may present
consist mostly of atrophic changes; however,
sheepdogs. with aspiration pneumonia. the combination of epidermal and follicular
INCIDENCE/PREVALENCE CAUSES basal cell degeneration, perivascular inflamm
Exact prevalence is unknown. • Hereditary in collies, Shetland sheepdogs, ation, and follicular atrophy with fibrosis is
SIGNALMENT and their crosses. highly suggestive of dermatomyositis.
• Infectious agents, toxins, malignancy,
Species Muscle Biopsy
vaccines, or drugs may be a triggering event. • Variable multifocal accumulations of
Dogs • Immune-mediated disease in other breeds.
inflammatory cells, including lymphocytes,
Breed Predilections RISK FACTORS plasma cells, macrophages, and neutrophils.
• Inheritable disease in collie, Shetland Mechanical pressure and trauma, and • Myofibril degeneration—characterized by
sheepdog and their crossbreeds, Beauceron ultraviolet light exposure may worsen fragmentation, vacuolation, atrophy, fibrosis,
shepherd, Belgian Tervuren, Rottweiler, cutaneous lesions. and regeneration.
kelpie, and Portuguese water dog.
• Similar symptoms reported in the mongrel, EMG
Welsh corgi, Lakeland terrier, chow chow, EMG abnormalities are present especially in
German shepherd dog, schipperke, and kuvasz. the muscles of the head and distal limbs;
• Dogs of other breeds with similar signs are DIAGNOSIS findings include fibrillation potentials (rapid,
classified as ischemic dermatopathy (dermato- irregular, and unsynchronized contraction of
myositis-like), and not dermatomyositis as muscle fibers) and positive sharp waves.
• Demodicosis.
previously reported. • Dermatophytosis.
Mean Age and Range • Bacterial folliculitis.
• Cutaneous lesions typically develop before • Juvenile cellulitis.
6 months, and may develop as early as 7 • Discoid lupus erythematosus. TREATMENT
weeks of age. • Systemic lupus erythematosus.
• Full extent of lesions usually present by 1 • Polymyositis.
• Most dogs treated as outpatients.
year of age, and may lessen thereafter. • Ischemic dermatopathy.
• Dogs with severe myositis and megaesopha-
• Adult-onset dermatomyositis can occur, but • Epidermolysis bullosa simplex.
gus may need hospitalization for supportive
is rare, and is usually less severe. CBC/BIOCHEMISTRY/URINALYSIS care.
Predominant Sex Serum creatine kinase may be elevated due to • Severe cases may warrant euthanasia.
None reported. muscle damage. • Assist to eat if muscles of mastication are
OTHER LABORATORY TESTS affected; feed at an elevated position if
SIGNS megaesophagus develops.
• Antinuclear antibody titers—rule out
General Comments systemic lupus erythematosus. • Nonspecific supportive therapy includes
• Clinical signs vary from subtle skin lesions • Elevated levels of immunoglobulin G and gentle bathing and soaking to remove crusts,
and subclinical myositis to severe skin lesions circulating immune complex correlated with and treatment of secondary bacterial folliculitis
with generalized muscle atrophy, abnormal disease severity. (if present).
gait, and megaesophagus.
Dermatomyositis (continued)
ACTIVITY ALTERNATIVE DRUG(S) SYNONYMS

• Avoid activities that may traumatize the N/A • Familial canine dermatomyositis.
skin. • Canine familial dermatomyositis.
D • Keep indoors during the day to avoid solar • Ischemic dermatopathy in collies and
radiation. Shetland sheepdogs.
DIET FOLLOW-UP SEE ALSO
N/A • Lupus Erythematosus, Cutaneous
CLIENT EDUCATION (Discoid).
• Do not breed affected animals.
• Lupus Erythematosus, Systemic (SLE).
• Discuss the hereditary nature of the disease. • Neuter intact animals to reduce hormonal
• Note that affected dogs should not be bred. influence on symptoms. ABBREVIATIONS
• Inform the owner that the disease is not • Minimize trauma and exposure to sunlight. • EMG = electromyography,
curable, although spontaneous resolution or electromyographic.
waxing and waning of symptoms may occur. • PT = prothrombin time.
• Secondary bacterial folliculitis.
• Discuss prognosis and possible complica- • PTT = partial thromboplastin time.
• Mildly to moderately affected dogs may
tions, especially in severely affected dogs. Suggested Reading
have residual scarring.
• Therapeutic efficacy of medical treatment
• Severely affected dogs may have trouble Bresciani F, Zagnoli L, Fracassi F, et al.
can be difficult to assess because the disease Dermatomyositis-like disease in Rottweiler.
chewing, drinking, and swallowing due to
tends to be cyclic in nature and is often Vet Dermatol 2014, 25(3):229–e62.
scarring of the masticatory and esophageal
self-limiting. Carlotti DN, Grucker S, Germain PA.
muscles.
• Megaesophagus may develop, predisposing Dermatomyositis in a four month old
the dog to aspiration pneumonia. schipperke. Pratique Medicale et
• Dogs may be lame due to damage of the Chirurgicale de l’Animal de Compagnie
MEDICATIONS muscles of the extremities. 2005, 40(3):141–144.
Gross TL, Ihrike PJ, Walder EJ, Affolter VK.
DRUG(S) OF CHOICE EXPECTED COURSE AND PROGNOSIS
Skin Diseases of the Dog and Cat, 2nd ed.
• Vitamin E 200–800 IU PO q12–24h. • Long-term prognosis—variable, depending
Oxford: Blackwell Science, 2005, pp.
• Essential fatty acid supplement. on severity of disease.
49–52, 503–505.
• Prednisolone 1–2 mg/kg PO q12–24h until • Minimal disease—prognosis good; tends to
Hargis AM, Mundell AC. Familial canine
remission, then alternate-day to twice-weekly spontaneously resolve with no evidence of
dermatomyositis. Compend Contin Educ
administration using the lowest dosage scarring.
Pract Vet 1992, 14:855–864.
possible for long-term control. • Mild to moderate disease—tends to resolve
Helton Rhodes KA, Werner A. Blackwell’s
• Nonsteroidal anti-inflammatory medication spontaneously, but residual scarring is
Five-Minute Veterinary Consult Clinical
(if steroids contraindicated). common.
Companion: Small Animal Dermatology,
• Pentoxifylline 10–20 mg/kg PO q12h. • Severe disease—prognosis for long-term
3rd ed. Hoboken, NJ: Wiley-Blackwell,
• Tetracycline (250 mg >10 kg, 500 mg survival is poor as damage to the skin and
2018.
<10 kg PO q8–12h), doxycycline (10 mg/kg muscle may be lifelong.
Levy BJ, Linder KE, Olivry T. The role of
q24h), minocycline (5 mg/kg q12h), with
oclacitinib in the management of ischemic
niacinamide (250 mg >10kg, 500 mg <10 kg
dermatopathy in four dogs. Vet Dermatol
PO q8–12h).
2019, 30(3): 201–208.
• Tacrolimus 0.1% applied q12h.
• Oclacitinib 0.4-0.6mg/kg BID.
MISCELLANEOUS Rothing A, Rufenacht S, Welle MM.
ASSOCIATED CONDITIONS Dermatomyositis in family of working
PRECAUTIONS Kelpies. Tierarztl Prax Ausg K Kleintiere
None
• Pentoxifylline—rarely causes gastric Heimtiere 2015, 43(5):331–336.
irritation; can affect clotting times (pro- AGE-RELATED FACTORS Wahl JM, Clark LA, Skalli O, et al.
thrombin time [PT]/partial thromboplastin • Initial clinical signs usually occur in dogs Analysis of gene transcript profiling and
time [PTT] prolongation and thrombocyto- younger than 6 months. immunobiology in Shetland sheepdog
penia) and dogs receiving anticoagulant • Adult onset—rare; more commonly seen in with dermatomyositis. Vet Dermatol
therapy should be monitored carefully when dogs that had subtle lesions as puppies. 2008, 19(2):52–58.
treated with this drug; possible rare seizure or ZOONOTIC POTENTIAL Author Liora Waldman
reduction of seizure threshold in epileptics. None Consulting Editor Alexander H. Werner
• Glucocorticoids—discuss possible side Resnick
effects with the owner. PREGNANCY/FERTILITY/BREEDING
• Tacrolimus can cause local irritation. • Do not breed affected dogs.
• Pregnancy may exacerbate clinical Client Education Handout
POSSIBLE INTERACTIONS symptoms.
Glucocorticoids and nonsteroidal anti-inflam- available online
• Estrus may exacerbate clinical symptoms.
matory medications can cause gastrointestinal
bleeding if used concurrently.
Dermatophilosis
Cats 10–20 mg/kg PO q12h. • Amoxicillin
• Infections—actinomycosis, nocardiosis, 10–20 mg/kg PO q12h.
sporotrichosis, cryptococcosis, opportunistic
BASICS mycobacterial granuloma, Rhodococcus D
OVERVIEW equi.• Foreign body. • Bite wound abscess.
• “Mud rash” or “mud fever.” • Caused by • Cutaneous or mucosal neoplasia.
FOLLOW-UP
Dermatophilus congolensis. • Rare crusting CBC/BIOCHEMISTRY/URINALYSIS
dermatitis (dogs). • Rare nodular subcutaneous Usually normal. PATIENT MONITORING
and oral disease (cats). • Systems affected— • Dogs—reexamine after 2 weeks of treat-
skin/exocrine. DIAGNOSTIC PROCEDURES ment to ensure complete resolution; give an
Dogs additional 7 days of systemic therapy if
SIGNALMENT indicated. • Cats—monitor biweekly for 1
• Dogs and cats. • No age, breed, or sex • Cytologic examination of exudate from
under crusts or of macerated crusts. month after apparent resolution of lesions,
predilection. depending on location.
• Biopsy—crusts contain organisms; submit
SIGNS with tissue samples. • Distinctive morphol- EXPECTED COURSE
Historical Findings ogy of organism in cytologic and histopatho- AND PROGNOSIS
• Association with cattle, sheep, or horses. logic preparations; bacterium forms branching • Dogs—excellent. • Cats—varies with the
• Occasionally free-roaming dogs. • Cats with chains of small diplococci resembling “railroad location of lesions and extent of surgical
subcutaneous disease—episode of trauma; tracks.” • Real-time quantitative polymerase debridement; complete resolution can be
existence of a foreign body; lesions generally chain reaction (RT-qPCR)—crust samples achieved with early diagnosis and medical/
chronic; no systemic clinical signs, except when and hair. surgical therapy.
internal organs or large oral lesions develop. Cats
Physical Examination Findings • Histopathologic examination—biopsy of
• Dogs—lesions: circular to coalescent, papular, nodules; procedure of choice. • Culture from
crusted skin lesions on the head and/or trunk, crusts or tissues—alert laboratory of differential;
requires use of special selective medium;
MISCELLANEOUS
lesions resemble superficial bacterial pyoderma
caused by Staphylococcus pseudintermedius; isolation is possible but usually very difficult. ZOONOTIC POTENTIAL
lesions may resemble dermatophilosis in horses • RT-qPCR—crust samples and hair. • Veterinarians and animal care workers—
(adherent thick, gray-yellow crusts that infection uncommon even with exposure to
PATHOLOGIC FINDINGS
incorporate hair and leave a circular, glistening, infected farm animals.
• Dogs—crusting and superficial pustular
shallow erosion when removed); pruritus is • Dogs and cats—very unlikely to serve as a
dermatitis; palisading of the crusts with
variable. • Cats—subcutaneous, oral, or internal source for human infection; caution is
orthokeratotic and parakeratotic hyper-
ulcerated and fistulated nodules or abscesses warranted for exposure of immunocompro-
keratosis; organism visualized within the
similar to lesions caused by other actinomycetes mised individuals.
crusts. • Cats—pyogranulomatous
in this species; superficial pyogenic crusting inflammation; central necrosis; fistulous ABBREVIATIONS
disease of the face has been reported. tract formation; organism visualized near • RT-qPCR = real-time quantitative
CAUSES & RISK FACTORS the necrotic center of granulomas, polymerase chain reaction.
• D. congolensis—causative agent; Gram-positive, especially with Gram stain. Suggested Reading
branching filamentous bacterium classified as an Frank LA, Kania SA, Weyant E. RT-qPCR
actinomycete; very common cause of crusting for the diagnosis of dermatophilosis in
dermatoses in hoofed animals; persists in the horses. Vet Dermatol 2016,
environment within crusts. • Dogs, cats, and TREATMENT 27(5):431–e112.
humans can be exposed directly from lesions • Dogs—antibacterial shampoo with gentle Hirazumi M, Tagawa Y. Isolation and
on large animals or from environmental removal of crusts: iodine or lime-sulfur may characterization of flagellar filament from
exposure. • Infectious stage—requires wetting also be used. • Cats—for pyogranulomas zoospores of Dermatophilus congolensis.
for activation; cannot penetrate intact and abscesses: surgical debridement; Vet Microbiol 2014, 173(1–2):141–146.
epithelium; minor trauma or mechanical exploration for foreign body; establishment Author Mitchell D. Song
transmission by biting ectoparasites (Amblyomma of drainage for exudate. Consulting Editor Alexander H. Werner
variegatum) may help in establishing infection. Resnick
• Deeper infections—require traumatic
inoculation of infectious material.
MEDICATIONS
DRUG(S) OF CHOICE
DIAGNOSIS • Treatment should be continued for 10–20
days. • Penicillin V (10 mg/kg PO q12h) for
DIFFERENTIAL DIAGNOSIS 10–20 days; drug of choice. • Tetracycline
Dogs (22–30 mg/kg PO q8h); doxycycline
• Staphylococcal folliculitis. • Acute moist (5–10 mg/kg PO q12h); minocycline
dermatitis. • Dermatophytosis. • Pemphigus (5–12 mg/kg PO q12h. • Ampicillin
foliaceus. • Keratinization disorder.
Dermatophytosis
Mean Age and Range • Microscopic examination of the growth for
• M. canis is more common in younger animals. microconidia and macroconidia—necessary
• Generalized dermatophytosis in older dogs to confirm pathogenic dermatophyte and to
D BASICS associated with immunosuppression. identify genus and species; helps identify
DEFINITION SIGNS source of infection.
• Cutaneous fungal infection affecting the • Positive culture—indicates presence of a
cornified regions of hair, claws, and occasion- Physical Examination Findings dermatophyte; however, organisms may be
ally the superficial layers of the skin. • Inapparent carrier state—cats. transient (i.e., geophilic dermatophytes on
• Microsporum and Trichophyton dermato- • Extreme variability of clinical signs. the feet).
phytes are most commonly isolated. • Classic lesion—slowly expanding circular
patch of alopecia with scale. Skin Biopsy
PATHOPHYSIOLOGY • Seborrheic or greasy hair coat. • Not usually required for diagnosis.
• Dermatophytes—grow in the keratinized • Papular or pustular eruptions. • Can be helpful in confirming true invasion
layers of hair, claw, and skin; do not thrive in and infection, or to diagnose suspicious cases
living tissue. CAUSES with negative fungal culture.
• Exposure to or contact with a dermato- Multiple species identified; majority of
cases caused by M. canis, M. gypseum, PCR
phyte does not necessarily result in an PCR of the dermatophyte DNA on the hair
infection. Infection may not result in clinical T. mentagrophytes, and M. persicolor
(nonfollicular). samples may be helpful. Positive PCR does
signs. not necessarily indicate active infection—
• 2–4-week incubation period. RISK FACTORS dead fungal organisms from a successfully
• Infective spores must contact the skin • Immunocompromise caused by medica- treated infection may be detected on PCR, as
surface and defeat host-protective mecha- tions or disease. will inapparent carriers.
nisms (innate immunity, normal flora, sebum, • High population density.
grooming) in order for infection to occur. • Poor management practices. PATHOLOGIC FINDINGS
• Factors that favor the development of • Folliculitis, perifolliculitis, or furunculosis.
disease—stress, trauma, ectoparasite infest- • Fungal hyphae seen in H&E-stained
ations, and immunosuppression. sections; special stains allow easier visualiza-
• Infected animals may remain as asympto- tion of the organism.
matic (inapparent) carriers for a prolonged DIAGNOSIS
period of time; some animals never become DIFFERENTIAL DIAGNOSIS
symptomatic. • Staphylococcal folliculitis.
• Demodicosis. TREATMENT
SYSTEMS AFFECTED • Allergic dermatitis.
Skin/exocrine. • Pemphigus foliaceus. APPROPRIATE HEALTH CARE
• Keratinization defect. Quarantine owing to the infective and
INCIDENCE/PREVALENCE zoonotic nature of the disease.
• Lesions may mimic many dermatologic DIAGNOSTIC PROCEDURES
conditions; overdiagnosis is likely common. CLIENT EDUCATION
Wood’s Lamp Examination • Many shorthaired cats and many dogs will
• Infection rates (inapparent and clinical) vary • Can be misleading—not all M. canis
widely, depending on the population studied. undergo spontaneous remission within 3
isolates fluoresce; most other pathogenic months.
GEOGRAPHIC DISTRIBUTION dermatophytes do not fluoresce. • Longhaired animals should be clipped to
• More common in hot, humid climates. • True positive reaction—apple-green reduce environmental contamination.
• Incidence of dermatophyte species may vary fluorescence of the hair shaft. False-positive • Decontamination of the environment
seasonally and geographically. and false-negative results commonly due to reduces the risk of false positive fungal
• M. canis—cats: UK, southern United debris on the hair and skin, inadequate cultures, which can lead to prolonged
States, Italy, and Brazil; source most often equipment, and/or poor technique. treatment and confinement.
infected cat. Microscopic Examination of Hair • Infective spores are shed into the environ-
• M. gypseum—dogs: southern United States; • Choose hairs that fluoresce under Wood’s ment, but do not multiply in the environ-
less than 1% in UK; source most often soil. lamp illumination to increase success. ment; transmission of the disease strictly
• M. persicolor—India, Brazil, and North • Hyphae and arthrospores seen invading hair from a contaminated environment (i.e., no
America; source most often associated with shafts. direct contact with an infected animal) is
rodents. extremely rare.
• T. mentagrophytes—India and UK; less common Fungal Culture with Identification
• Effective disinfectants.
in southern United States, Italy, and Brazil; source • Choose hairs that fluoresce under Wood’s
• Diluted sodium hypochlorite (0.5%)—
most often associated with rodents. lamp if possible. concentrations ranging from 1 : 10 to 1 : 100
• Pluck hairs from the periphery of an
SIGNALMENT effective with short contact times.
alopecic area or brush haircoat with a sterile • Enilconazole (0.2%)—available as a
Species toothbrush or carpet square (especially concentrated spray or fogger; 10-minute
Dog, cat, and many others. inapparent or treated patients). contact time recommended. Not available in
• Dermatophyte test media—dermatophytes
Breed Predilections the United States.
change media color to red during the early • Accelerated hydrogen peroxide—should not
• Cat—longhaired breeds (Persian and
growing phase of the culture; saprophytes be mixed with concentrated sodium hypo-
Himalayan).
cause color change after significant colony chlorite products; 10-minute contact time
• Dog—Yorkshire terrier and Manchester
growth; examine inoculated media daily. recommended.
terrier. Increased exposure in working and
• Fungal colonies are nonpigmented/white to
hunting dogs. • Washable textiles—decontaminate via
slightly yellow. Contaminants are often darker. mechanical washing; two washings on the
(continued) Dermatophytosis
longest wash cycle in a washing machine PRECAUTIONS • Decontaminate the environment.
found to be effective. Ketoconazole • Consider prophylactic treatment of exposed
• Treatment can be both frustrating and animals.
expensive, especially in multianimal house-
• Hepatopathy has been reported and can be D
severe in cats. POSSIBLE COMPLICATIONS
holds or with recurrent cases; consider referral • Inhibits endogenous production of steroid False-negative dermatophyte culture.
to a veterinary dermatologist. hormones in dogs. EXPECTED COURSE AND PROGNOSIS
Itraconazole • Many animals will “self-clear” infection
• Rare vasculitis and ulcerative skin lesions at over a period of a few months.
doses of 5 mg/kg q12h; not noted in patients • Treatment hastens clinical cure and helps
MEDICATIONS receiving 5 mg/kg q24h. reduce environmental contamination.
DRUG(S) OF CHOICE • Hepatotoxicity reported infrequently in • Some infections, particularly in longhaired
• Topical therapy and clipping— recom- dogs. cats or multianimal situations, can be
mended concurrently with systemic therapy; Terbinafine persistent.
may help prevent environmental contam- • Gastrointestinal upset, hepatotoxicity, and bone
ination. marrow suppression (pancytopenia, neutropenia).
• Lime-sulfur (1 : 16 dilution or 8 oz per • Decrease dosage with renal and/or hepatic
gallon of water), miconazole/chlorhexidine insufficiency. MISCELLANEOUS
(0.2%), or enilconazole (0.2%) applied once • Concurrent administration with Cimetidine
to twice weekly; lime sulfur is odoriferous ZOONOTIC POTENTIAL
increases blood concentration; rifampin
and can stain; enilconazole is not currently • Dermatophytosis is zoonotic.
decreases blood concentration.
approved for use in companion animals in • Considered a low-level pathogen; disease is
the United States. Shampoos containing Lime-Sulfur Solution not life-threatening, can be easily treated, but
1–2% ketoconazole, miconazole, or 0.5% Ingestion of lime-sulfur may lead to oral may cause scarring.
climbazole; a minimum of a 3-minute erosions.
PREGNANCY/FERTILITY/
contact time is recommended; little to no ALTERNATIVE DRUG(S) BREEDING
residual effect. • Lufenuron—a chitin synthesis inhibitor • Griseofulvin is teratogenic.
• Use of an Elizabethan collar, particularly in used in flea control; not effective in con- • Ketoconazole can affect steroidal hormone
cats, is recommended to prevent ingestion of trolled studies. synthesis, especially testosterone.
these products. • Fluconazole—less effective option, but less
• Itraconazole—dogs and cats: 5–10 mg/kg expensive than itraconazole. SYNONYMS
PO q24h in one-week-on, one-week-off Ringworm
schedule for minimum of 3 cycles; manufac- ABBREVIATIONS
tured drug preferred over compounded • FeLV = feline leukemia virus.
formulations due to absorption/concentration • FIV = feline immunodeficiency virus.
variability. Compounded formulations have FOLLOW-UP
been shown to be of extremely variable Suggested Reading
PATIENT MONITORING Bond R. Superficial veterinary mycoses. Clin
efficacy. • Dermatophyte culture required to monitor
• Ketoconazole—resistance reported (10 mg/
Dermatol 2010, 28(2):226–236. doi:
response to therapy; many animals clinically 10.1016/j.clindermatol.2009.12.012
kg q24h PO); not recommended in cats. improve but remain culture-positive.
• Griseofulvin—effective, but use declining
Miller WH, Griffin CE, Campbell KL.
• Continue treatment until at least two Muller & Kirk’s Small Animal Dermatology,
due to cost and requirement for monitoring. subsequent cultures are negative.
• Terbinafine—effective, may be helpful in
7th ed. Philadelphia, PA: Saunders, 2013,
• In resistant cases, cultures should be repeated pp. 5226–5241.
cases resistant to azole drugs; dogs: weekly using the toothbrush technique.
20–30 mg/kg q12–24h for 4–8 weeks; cats: Moriello KA, Coyner K, Paterson S, Mignon
• Weekly or biweekly CBC if treating with B. Diagnosis and treatment of dermatophy-
20–40 mg/kg q24–48h for 4–8 weeks; griseofulvin; periodic evaluation of liver
dermatophyte carriers: 8.25 mg/kg q24h for tosis in dogs and cats. Vet Dermatol 2017,
enzymes if treating with ketoconazole, 28(3). doi: 10.1111/vde.12440
4–8 weeks; side effects may include gastroin- itraconazole, or terbinafine.
testinal upset, hepatotoxicity, neutropenia, Authors W. Dunbar Gram and Andhika
• Depending on which systemic medications Putra
and pancytopenia. used, appropriate follow-up should be
• Antifungal vaccines have not been shown to
performed due to potential side effects. Resnick
protect against challenge exposure.
PREVENTION/AVOIDANCE Acknowledgment The authors and book
CONTRAINDICATIONS • Initiate a quarantine period and obtain editors acknowledge the previous contribu-
• Corticosteroids—can modulate inflamma- dermatophyte cultures of all animals entering tion of Sheena Narine-Reece
tion and prolong the infection. the household to prevent reinfection from
• Griseofulvin—do not administer to cats inapparent carriers.
with feline leukemia virus (FeLV) or feline • Consider exposure based on species Client Education Handout
immunodeficiency virus (FIV); teratogen. isolated. available online
Dermatoses, Depigmenting Disorders

• Immune-mediated pigmentary inconti- basement membrane zone and intercellular
nence. • Oculocutaneous albinism. spaces. • ANA—occasionally positive.
D BASICS RISK FACTORS Uveodermatologic Syndrome
• Sun exposure—DLE, SLE, and PE. • Drug • Depigmentation is a primary symptom.
DEFINITION triggered—PF, EM. • Uveitis—usually precedes dermatologic
• Pathologic or cosmetic condition involving
disease. • Cutaneous macular depigmentation
loss of pigmentation of the skin and/or hair
with inflammation on nose, lips, and eyelids.
coat, either by lack of pigmentation or by
• Striking poliosis and leukotrichia. • Biopsy
melanocyte damage. • Leukotrichia—whiten-
DIAGNOSIS of early lesions—interface dermatitis,
ing of the hair (nonspecific location). • Poliosis
pigmentary incontinence.
—whitening of hair on the head/face. DIFFERENTIAL DIAGNOSIS
• Leukoderma—whitening of the skin. Others
Mucocutaneous Pyoderma • Contact dermatitis (uncommon)—depig-
PATHOPHYSIOLOGY • Biopsy—epidermal hyperplasia with
• Melanocytes may be damaged or destroyed
mentation secondary due to chronicity;
superficial pustulation. • Depigmentation is erythema of rostral nasal planum and lips; no
by toxins (including toxic melanin precursors), secondary and develops with chronicity.
inflammatory mediators, auto-antibodies, and/ ulceration and minimal crusting; history of
• Skin lesions—affects the lips, perioral area, exposure. • Vitiligo—depigmentation often
or inhibitors of melanogenesis. • Diseases and nasal/alar folds. • Clinically similar to
may be distinguished clinically by depigmen- without inflammation; cutaneous macular
intertrigo (skinfold bacterial folliculitis). depigmentation on nose, lips, eyelids,
tation as the initial symptom versus depig- • Swelling and fissuring lead to erosions and
mentation occurring secondary to inflamm- footpads, and nails; concurrent leukotrichia.
crusts. • ++Biopsy—epidermal hyperplasia • Seasonal nasal hypopigmentation—depigmenta-
ation. with superficial pustulation. • Antibiotic tion is a primary symptom; normal black
SYSTEMS AFFECTED responsive. • Frequent recurrence if due to an coloration of nasal planum fades to light tan or
• Skin/exocrine. • Ophthalmic. underlying cause. pink; usually seasonal or slowly progressive with
SIGNALMENT Nasal Solar Dermatitis age. • Albinism—hereditary lack of pigment
• Mucocutaneous pyoderma—German • Depigmentation is secondary and develops of the skin, hair coat, and irises (not a
shepherd dog. • Systemic lupus erythemato- with chronicity. • Lesions confined primarily to depigmenting process). • Aurotrichia—
sus (SLE)—German shepherd dog. • Discoid dorsal muzzle and precipitated by sun exposure. young miniature gray schnauzers may
lupus erythematosus (DLE)—collie, Shetland • Begins in poorly pigmented skin at the junction develop idiopathic golden hair coat
sheepdog, German shepherd dog, Siberian husky; of the nasal planum and dorsal muzzle. • Negative coloration, primarily of the trunk.
may occur more often in females. • Pemphigus for direct immunofluorescence. • Solar vasculo- • Endocrinopathy may cause coat color
foliaceus (PF)—chow chow, Akita, cocker pathy may appear similar. change, mainly from black to reddish-
spaniel, dachshund, Labrador retriever. DLE brown. • Drug reaction—depigmentation is
• Uveodermatologic syndrome—Akita, • Depigmentation is a primary symptom.
often secondary; resembles many cutaneous
Samoyed, Siberian husky. • Vitiligo—dogs: • Primarily affects nasal area, eyelid margins,
disorders such as DLE, SLE, PF, and PE;
Belgian Tervuren, German shepherd dog, and lip margins. • Exacerbated by sun pruritus is variable; onset of symptoms is
Doberman pinscher, Rottweiler, German exposure. • Positive direct immunofluores- usually within 2 weeks of administration.
shorthaired pointer, Old English sheepdog, • Proliferative arteritis of the nasal philtrum—
cence at basement membrane zone.
dachshund; usually less than 3 years of age; • Biopsy—interface dermatitis.
depigmentation is secondary and develops
cats: Siamese. • Seasonal nasal hypopigmenta- with chronicity; marked focal ulceration of
SLE the nasal planum often resulting in acute,
tion—Siberian husky, Alaskan Malamute,
• Depigmentation is a primary symptom. severe hemorrhage; no additional skin
Labrador retriever, golden retriever.
• Multisystemic disease. • Skin lesions— lesions noted; this may be an idiopathic
• Epitheliotropic lymphoma (mycosis
fungoides)—typically dogs >10 years old. often involve nose, face, and mucocutaneous syndrome associated with allergy.
• Proliferative arteritis of the nasal philtrum—
junctions; multifocal or generalized. • Dermatophytosis— depigmentation is
• Antinuclear antibody (ANA)—may be secondary and develops with chronicity;
Saint Bernard, giant schnauzer. • Periocular
leukotrichia—Siamese cat. • Chediak- positive. • Positive direct immunofluores- especially develops on the dorsal muzzle
Higashi syndrome—Persian cat. cence at basement membrane zone. and face; hyperpigmentation may also
PF occur, especially with Tricophyton mentagro-
SIGNS phytes infection. • Epitheliotropic lym-
• Depigmentation develops with chronicity.
• Leukotrichia. • Leukoderma. • Lightening phoma—depigmentation is secondary and
• Initial lesions on face and ears; commonly
of the pigmentation in the skin (seen as a develops with chronicity; occurs in
“graying” or “browning” of previously involve footpads; eventually generalized.
• Biopsy—subcorneal pustules with acantholysis. mucocutaneous areas, nose, and skin. • EM
pigmented areas). • Erythema. • Erosion and in dogs—classic annular lesions with a clear
• Positive direct immunofluorescence in
ulcerations. center; depigmentation is secondary and
intercellular spaces of epidermis.
CAUSES develops with chronicity. • Zinc defi-
• Mucocutaneous pyoderma. • DLE. • SLE. PE ciency—depigmentation may be a primary
• PF. • Pemphigus erythematosus (PE). • Depigmentation is a primary symptom. or secondary symptom; zinc is required for
• Uveodermatologic syndrome. • Contact • Lesions—primarily confined to face and normal melanin synthesis. • Chediak-
hypersensitivity. • Vitiligo. • Seasonal nasal ears, nasal planum, and lip margins. Higashi syndrome—depigmentation is a
depigmentation. • Albinism. • Schnauzer • Depigmentation often precedes significant primary symptom; young Persian cats (blue
gilding syndrome. • Endocrinopathy. • Drug lesions. • Exacerbated by sun exposure. smoke color); ophthalmologic signs,
reaction. • Erythema multiforme (EM). • Biopsy—intraepidermal pustules with prolonged bleeding. • Cyclic neutropenia
• Proliferative arteritis of the nasal philtrum. acantholysis and interface dermatitis. in young silver-gray collie dogs with
• Postinflammatory depigmentation. • Positive direct immunofluorescence at light-colored nose.
(continued) Dermatoses, Depigmenting Disorders

CBC/BIOCHEMISTRY/URINALYSIS roughened edges cause abrasions. POSSIBLE COMPLICATIONS
• Usually normal. • SLE—may see hemolytic • Application of water-resistant sunblock • Sunburn in areas of depigmentation.
anemia, thrombocytopenia, or evidence of ointments or gels with an SPF/UVA and • Squamous cell carcinoma—in cases of solar
glomerulonephritis. • Hematologic abnor- UVB >30 to depigmented and sun-exposed damage and actinic keratosis of depigmented D
malities in Persian cats with Chediak-Higashi areas of skin. • Uveodermatologic syn- areas. • SLE—associated scarring with
syndrome. • Cyclic neutropenia in collie dogs drome—management by veterinary ophthal- ulcerative dermatitis.
(cyclic hematopoiesis anomalies). mologist recommended. • Appropriate
OTHER LABORATORY TESTS antibiotics—pyoderma. • Appropriate
• Fungal culture—dermatophytosis.
antifungals— dermatophytosis.
• ANA—positive in SLE. MISCELLANEOUS
DIAGNOSTIC PROCEDURES ZOONOTIC POTENTIAL
• Cytology—acantholytic cells (pemphi- Dermatophytosis—can cause infection in
MEDICATIONS
gus), neoplastic lymphocytes (epithelio- humans.
tropic lymphoma). • Joint tap—evidence of DRUG(S) OF CHOICE
• Auto-immune dermatoses—immuno SEE ALSO
polyarthritis in SLE. • Ocular examina-
suppressive therapy with prednisolone or • Cutaneous Drug Eruptions.
tion—uveitis in uveodermatologic syn-
dexamethasone and azathioprine (dogs) or • Lupus Erythematosus, Cutaneous (Discoid).
drome. • Direct immunofluorescence—
chlorambucil (cats); see specific diseases. • Lupus Erythematosus, Systemic (SLE).
deposition of immunoglobulin at the
• Topical corticosteroids—PE, DLE. • Lymphoma, Cutaneous Epitheliotropic.
basement membrane zone with DLE, SLE,
• Vitiligo and nasal depigmentation—no • Pemphigus.
and PE, and in the intercellular spaces of
treatment. • Epitheliotropic lymphoma— • Uveodermatologic Syndrome (VKH).
the epidermis with PF and PE. • Skin
biopsy. • Genetic testing for oculocutaneous multiple treatment protocols. ABBREVIATIONS
albinism. CONTRAINDICATIONS • ANA = antinuclear antibody.
Azathioprine therapy—not recommended in • DLE = discoid lupus erythematosus.
PATHOLOGIC FINDINGS
cats; may cause fatal leukopenia or • EM = erythema multiforme.
Histopathologic Examination of the Skin thrombocytopenia. • PE = pemphigus erythematosus.
• Interface dermatitis—DLE, SLE, uveoder- • PF = pemphigus foliaceus.
matologic syndrome. • Pigmentary inconti- ADVERSE REACTIONS • SLE = systemic lupus erythematosus.
nence—DLE, PE. • Intraepidermal Ketoconazole may cause lightening of the hair
pustules with acantholysis—PF and PE. coat, elevated alkaline phosphatase, and gastro- Suggested Reading
intestinal distress. Mealey KL. Pharmacotherapeutics for
• Hypomelanosis—vitiligo, uveodermato-
Veterinary Dispensing. Ames, IA: Wiley-
logic syndrome, seasonal nasal hypopigmenta- ALTERNATIVE DRUG(S) Blackwell, 2019.
tion, and Auriotrichosis. • Apoptosis • Cyclosporine, modified—5 mg/kg/day for Miller W, Griffin C, Campbell, K. Muller
(individual cell necrosis of keratinocytes)— auto-immune disorders. • Tacrolimus—0.1% and Kirk’s Small Animal Dermatology, 7th
drug reaction and EM. • Proliferation of gel applied daily to lesions in combination ed. St. Louis, MO: Elsevier, 2013.
spindle cells of dermal arteries and arteri- with or to replace corticosteroids; may sting; Morris DO, Kennis RA. Clinical dermatol-
oles—proliferative arteritis. • Infiltration of avoid licking; wear latex gloves to apply. ogy, special issue. Vet Clin Small Anim
neoplastic lymphocytes— epitheliotropic • Pimecrolimus—1% cream applied daily to Pract 2013, 43(1).
lymphoma. lesions in combination with or to replace Torres SMF, Roudebush P, eds., Advances in
corticosteroids; may sting; avoid licking; wear Veterinary Dermatology, Vol. 8. Hoboken,
latex gloves to apply. NJ: Wiley, 2017.
Author Guillermina Manigot
TREATMENT Consulting Editor Alexander H. Werner
• Outpatient, except for SLE, EM, and Resnick
cutaneous lymphoma with systemic involve- FOLLOW-UP
ment. • Reduce exposure to sunlight—DLE, PATIENT MONITORING
SLE, and PE. • Immunosuppressive therapy— Client Education Handout
• Varies with specific disease and treatment
SLE, PF, and PE. • Avoid contact with topical available online
prescribed. • Postinflammatory depigmentation
drugs. • Contact dermatitis—avoid irritant; should resolve when the cause of inflamma-
replace plastic or rubber dishes: particularly if tion is treated.
Dermatoses, Erosive or Ulcerative

superficial or deep; deep ulceration can present as Parasitic
sinuses with draining tracts, cavitated lesions with • Demodicosis—ulcerative with crusting
well-demarcated borders, or exudative crusted (especially with secondary bacterial folliculi-
D BASICS lesions. • Some specific diseases are typically tis). • Sarcoptic/notoedric mange—erosive
DEFINITION accompanied by fever and malaise, especially with crusting. • Flea bite allergy—erosive to
A heterogenous group of skin disorders auto-immune disorders and infectious etiologies. ulcerative. • Feline mosquito bite hypersensi-
characterized by disruption of the epidermis • May be associated with extracutaneous disease tivity—erosive to superficial or deep ulcerative.
(erosions) or, if the basement membrane is (e.g., superficial necrolytic dermatitis and hyper- • Pelodera and hookworm migration—deep
compromised, the epidermis and dermis (ulcers). eosinophilic syndrome of cats). ulcerative.
Congenital/Hereditary
PATHOPHYSIOLOGY CAUSES
• Canine familial dermatomyositis (predomi-
Varies widely, depending on the cause; may Autoimmune nantly in collies and Shetland sheepdogs)—
include congenital or developmental • Pemphigus foliaceus—crusting with erosion. erosive. • Epidermolysis bullosa—superficial
disorders that compromise tissue cohesion; • Pemphigus vulgaris—superficial ulcerative. ulcerative. • Cutaneous asthenia (Ehlers–
cell-mediated (inflammatory or neoplastic) • Bullous pemphigoid and epidermolysis Danlos syndrome)—skin tears easily.
injury; anoxic injury; antigen-specific bullosa acquisita—superficial ulcerative.
auto-immune disorders; and necrosis due to Metabolic
• Discoid lupus erythematosus and muco
trauma, toxins, contactants (irritants), • Superficial necrolytic dermatitis (usually
cutaneous lupus erythematosus—erosive or
microbial organisms, or parasitic migration. associated with advanced hepatic disease or
superficial ulcerative. • Exfoliative lupus
pancreatic glucagonoma)—crusting with
SYSTEMS AFFECTED (German shorthaired pointers)—scaling
erosion. • Hyperadrenocorticism—erosive to
Skin/exocrine. with erosion. • Vesicular lupus (rough collies
ulcerative when complicated by secondary
and Shetland sheepdogs)—superficial
GENETICS infections or calcinosis cutis. • Uremia
ulcerative. • Cold agglutinin disease—deep
Some diseases are likely heritable due to breed (mucous membranes)—superficial ulcerative.
ulcerative.
predilections; however, there are no genetic Neoplastic
Immune-Mediated
screening tests available for any of the diseases • Squamous cell carcinoma—erosive to
• Erythema multiforme, Stevens–Johnson
listed. ulcerative with scale or crust. • Feline
syndrome, and toxic epidermal necrolysis (may
squamous cell carcinoma in situ (Bowenoid
INCIDENCE/PREVALENCE be drug induced)—erosive to superficial
in situ carcinoma)—erosive with scale or
Rare to common, depending on the cause. ulcerative. • Vasculitis—superficial to deep
crust. • Mast cell tumors—superficial to
ulcerative (may be cavitated). • Idiopathic
SIGNALMENT deep ulcerative. • Epitheliotropic lymphoma
panniculitis—deep ulcerative (usually exudative
(mycosis fungoides)—erosive to superficial
Species with crusting). • Canine eosinophilic furunculo-
ulcerative. • Feline thymoma-associated
Dogs and cats. sis of the face (may be insect related)—ulcerative
exfoliative dermatosis—scaling with erosion.
and crusting. • Canine juvenile cellulitis (puppy
Breed Predilections • Feline paraneoplastic alopecia—erosive.
Some specific causes (see below) have strong breed strangles)—erosive to superficial or deep
predilections, e.g., lupoid disorders, familial ulcerative. • Feline indolent ulcer (rodent Nutritional
dermatomyositis, and zinc-responsive dermatosis. ulcer)—erosive to superficial or deep ulcerative. Zinc-responsive dermatosis—crusting with
Infectious erosion.
Mean Age and Range
• Surface pyoderma—acute moist pyotrau- Physical/Conformational
• Highly variable according to etiology.
• Canine juvenile cellulitis and several matic dermatitis: erosive. • Superficial
Dermatoses
congenital diseases (see below) are diagnosed staphylococcal folliculitis—erosive to
• Pressure point ulcers—deep ulcerative.
in very young animals. superficial ulcerative. • Bacterial folliculi-
• Intertrigo (skinfold pyoderma)—erosive.
tis/furunculosis—deep ulcerative.
Predominant Sex • Superficial fungal (Malassezia dermatitis, Idiopathic
Sex predispositions may vary according to dermatophytosis)—erosive to superficial • Feline dorsal neck ulcer—deep ulcerative
the disease in question. ulcerative. • Deep fungal (sporotrichosis, with crusting. • Canine and feline acne—
SIGNS cryptococcosis, histoplasmosis, blastomyco- erosive to ulcerative. • Feline plasma cell
sis, coccidioidomycosis)—deep ulcerative pododermatitis—superficial to deep
Historical Findings with or without sinuses and draining tracts. ulcerative.
• Pruritus may result in ulcers or erosions • Opportunistic mycobacteriosis—deep
due to self-trauma; especially ectoparasitism, Miscellaneous
ulcerative nodules with sinuses and draining
superficial pyoderma, and Malassezia tracts. • Actinomycetic bacteria (Nocardia Thermal (heat/cold), electrical, solar, or
dermatitis. • Exposure to caustic chemicals, spp., Actinomyces spp., Streptomyces chemical irritant/burns—depth of lesions
burns, cold stress, venomous reptiles and spp.)—deep ulcerative nodules with sinuses depends on severity of insult.
insects, etc. • Some infectious diseases (e.g., and draining tracts. • Pythiosis/lagenidiosis
pythiosis, coccidioidomycosis, feline cow and protothecosis— ulcerative, prolifera-
pox) have very restricted ranges. • Previous tive with or without draining tracts.
or concurrent systemic signs or illness. • Leishmaniasis—erosive to superficial or DIAGNOSIS
Physical Examination Findings deep ulcerative. • Feline cow pox—deep
• Lesions may be heterogenous in gross ulcerative. • Feline immunodeficiency
Depends upon presentation.
appearance; some diseases result in erythematous virus (FIV)/feline leukemia virus (FeLV)
erosions with minimal crust or scale, while others related—erosive to superficial ulcerative. CBC/BIOCHEMISTRY/URINALYSIS
cause scale or crusting that (when removed) • Feline herpesvirus-associated dermato- May be abnormal with metabolic or systemic
results in erosion. • Ulcers may be shallow/ sis—ulcerative with crusting. disease.
(continued) Dermatoses, Erosive or Ulcerative

IMAGING immune-mediated, and infectious diseases
• Rarely indicated. • Thoracic radio- listed may be teratogens.
graphs—deep/systemic fungal diseases,
feline thymoma-associated exfoliative MEDICATIONS SYNONYMS D
Superficial necrolytic dermatitis = necrolytic
dermatitis, or systemic neoplasia. DRUG(S) OF CHOICE migratory erythema, metabolic epidermal
• Abdominal ultrasound—superficial Variable by cause. necrosis, hepatocutaneous syndrome.
necrolytic dermatitis (dogs) or paraneoplas-
PRECAUTIONS SEE ALSO
tic alopecia (cats).
Side effects—associated with many antimicrobial, • Acne—Cats.
DIAGNOSTIC PROCEDURES immunosuppressive, and antineoplastic drugs. • Acne—Dogs.
• Skin scraping—ectoparasitism. • Direct • Actinomycosis & Nocardia.
impression cytology—bacteria, yeast, or • Azotemia and Uremia.
Dependent on medications administered.
acantholytic keratinocytes in pemphigus. • Blastomycosis.
• Fine-needle aspirate with cytology— indu- • Coccidioidomycosis.
rated or nodular lesions. • Culture: bacterial • Cold Agglutinin Disease.
(aerobic and anaerobic), mycobacterial, and/or • Cryptococcosis.
fungal—suspected infectious disease. • Fungal FOLLOW-UP • Demodicosis.
serology and serology for pythiosis and PATIENT MONITORING • Dermatophytosis.
lagenidiosis may be indicated on a case-by- Dependent on disease process, concurrent • Feline Herpesvirus Infection.
case basis and depending upon geographic systemic disease(s), drugs used, and potential • Feline Immunodeficiency Virus (FIV)
location. • PCR and immunohistochemistry side effects expected. Infection.
are adjuncts to the histologic diagnosis of • Feline Leukemia Virus (FeLV) Infection.
feline herpesvirus-associated dermatitis. PREVENTION/AVOIDANCE
• Incidence of many feline infectious diseases • Feline Paraneoplastic Alopecia.
PATHOLOGIC FINDINGS can be minimized by restricting outdoor • Flea Bite Hypersensitivity and Flea Control.
activity. • Some autoimmune diseases (lupus • Histoplasmosis.
Skin Biopsy
and pemphigus) are aggravated by ultraviolet • Hookworms (Ancylostomiasis).
• For cavitated lesions, the leading edge
light exposure; patients should be restricted • Hyperadrenocorticism (Cushing’s Syndrome—
(elliptical full-thickness biopsy) should be
harvested with a scalpel blade if the defect is from sun exposure during peak hours of the day. Dogs.
• Hyperadrenocorticism (Cushing’s Syndrome—
too large to be excised in total. • Punch biopsy POSSIBLE COMPLICATIONS
sufficient for diffuse erosive lesions; should Cats.
• Determined by cause. • Some diseases are • Leishmaniosis, Cutaneous.
take normal skin near a lesion and lesions that potentially life-threatening. • Some diseases • Lupus Erythematosus, Cutaneous (Discoid).
are both early and late in development. have zoonotic potential. • Infections and • Lymphoma, Cutaneous Epitheliotropic.
drug side effects are possible in cases requiring • Malassezia Dermatitis.
immunosuppression. • Mast Cell Tumors.
EXPECTED COURSE • Mycobacterial Infections.
TREATMENT AND PROGNOSIS • Notoedric Mange.
• Some infectious diseases (nocardiosis, atypical • Panniculitis/Steatitis.
APPROPRIATE HEALTH CARE • Pemphigus.
• Outpatient for most diseases. • Varies mycobacteriosis) may be controlled with chronic
antimicrobial therapy, but are generally not • Pododermatitis.
widely according to the cause. • Protothecosis.
curable if lesion progression is extensive by the
DIET time of diagnosis. • Pythiosis/lagenidiosis— • Puppy Strangles (Juvenile Cellulitis).
• Nutritional support may be necessary in prognosis is extremely poor for response to • Pyoderma.
debilitated animals, especially those with therapy and survival when lesions are extensive. • Pythiosis.
superficial necrolytic dermatitis. • Correcting • Sarcoptic Mange.
dietary deficiencies is the only treatment for • Sporotrichosis.
generic dog-food dermatosis. • Supple- • Squamous Cell Carcinoma, Skin.
mentation of zinc is necessary for zinc- • Superficial Necrolytic Dermatitis.
responsive dermatosis. MISCELLANEOUS • Vasculitis, Cutaneous.
CLIENT EDUCATION ZOONOTIC POTENTIAL ABBREVIATIONS
Variable by diagnosis; most important with • Sarcoptic acariasis. • Dermatophytosis. • FeLV = feline leukemia virus.
suspected or confirmed zoonotic disease. • Sporotrichosis. • Mycelial phase of some • FIV = feline immunodeficiency virus.
fungi (e.g., Coccidioides immitis, Blastomyces
SURGICAL CONSIDERATIONS dermatitidis), when grown on culture media, Suggested Reading
• Indicated as curative treatment for feline can be infectious to humans through Mason IS. Erosions and ulcerations. In:
thymoma-associated exfoliative dermatitis. inhalation. In-clinic fungal culturing (other Ettinger SH, Feldman EC, eds., Textbook
• May be curative for nonmetastatic than for dermatophytes) is not advised. of Veterinary Internal Medicine, 7th ed. St.
pancreatic or hepatobiliary tumors causing Louis, MO: Saunders Elsevier, 2010, pp. 79–83.
paraneoplastic alopecia. • Radical surgical PREGNANCY/FERTILITY/BREEDING Author Daniel O. Morris
excision of nodules and draining tracts may • Due to the potential severity of clinical Consulting Editor Alexander H. Werner Resnick
be an adjunct to antimicrobial therapy of signs and syndromes, any patient diagnosed
infections caused by rapid-growing with an erosive/ulcerative disease that occurs
Mycobacteria spp. and Nocardia spp. in cats with moderate to strong breed predilections Client Education Handout
and pythiosis or lagenidiosis in dogs. should not be used for breeding. • Many available online
drugs used to treat the auto-immune,
Dermatoses, Exfoliative
scaling, crusting, and erythema around the • Nutritional disorders—malnutrition and
eyes, ears, feet, lips, and external orifices; two generic dog food dermatosis; auto-immune
syndromes: young adult dogs (mainly dermatoses—pemphigus complex: may
D BASICS Siberian husky and Alaskan Malamute) and appear exfoliative; vesicles become scaly and
DEFINITION rapidly growing large-breed puppies; crusty; cutaneous and systemic lupus
Excessive or abnormal shedding of epidermal nutritionally responsive. erythematosus: cutaneous signs often appear
cells resulting in the clinical presentation of • Ectodermal defects—follicular dysplasias; as areas of alopecia and scaling.
cutaneous scaling. color mutant or dilution alopecia; represent • Neoplasia—primary epidermal neoplasia
anomalies in melanization of the hair shaft (epitheliotropic lymphoma): with alopecia
PATHOPHYSIOLOGY
and structural hair growth; keratinization and scaling as epidermal structures are
• An increase in the production, an increase
defects theorized as causative for several damaged by infiltrating lymphocytes;
in the desquamation, or a decrease in the
syndromes; Doberman pinscher, Irish setter, preneoplastic conditions (actinic keratosis):
cohesion of keratinocytes results in abnormal
dachshund, chow chow, Yorkshire terrier, initially appear exfoliative.
shedding of epidermal cells individually (fine
poodle, Great Dane, whippet, saluki, and • Miscellaneous—any disease process may
scale) or in sheets (coarse scale).
Italian greyhound; failure to regrow blue or result in excessive scale formation due to a
• Primary exfoliative disorders—keratiniza-
fawn hair with normal “point” hair growth, metabolic disorder or to cutaneous
tion defects: genetic control of epidermal cell
excessive scaliness, comedone formation, inflammation.
proliferation and maturation is abnormal.
secondary pyoderma. • Exfoliative disorders—rare in cats: tail
• Secondary exfoliative disorders—disease
• Idiopathic nasodigital hyperkeratosis— gland hyperplasia, feline thymoma-associated
alters the normal maturation and prolifera-
excessive build-up of scale and crusts on the exfoliative dermatitis.
tion of epidermal cells.
nasal planum and footpad margins; possibly a
• Anomalies in sebaceous or apocrine gland
senile change; generally asymptomatic;
function may be present or causative.
spaniels and retrievers; cracking and
SYSTEMS AFFECTED secondary bacterial infection can cause pain.
Skin/exocrine.
DIAGNOSIS
• Sebaceous adenitis—inflammatory disease
targeting sebaceous glands and ducts causing DIFFERENTIAL DIAGNOSIS
SIGNALMENT
patchy or diffuse hair loss and excessive scaling; Based on signalment and history (breed-associ-
• Dog and cat.
tightly adherent follicular casts; standard ated vs. age of onset), presence/absence of
• Primary—apparent by 2 years of age;
poodle, Akita, Samoyed, German shepherd, pruritus (hypersensitivity vs. secondary infection),
characteristic in affected breeds.
Havanese, Bernese Mountain dog, and vizsla. and concurrent signs (endocrinopathy).
• Secondary—any age; any breed of dog or
cat. • Ichthyosis—rare and severe congenital CBC/BIOCHEMISTRY/URINALYSIS
disorder of keratinization; West Highland • Normal with primary keratinization
SIGNS white terrier, golden retriever, cavalier King disorders.
Physical Examination Findings Charles spaniel, and Norfolk terrier; • Mild, nonregenerative anemia and
• Dry or greasy collections of fine or coarse generalized accumulations of scale and crusts hypercholesteremia are consistent with
scale located diffusely throughout the hair at an early age; secondary infections (bacterial hypothyroidism.
coat or focally in keratinaceous plaques. and yeast) common. • Neutrophilia, monocytosis, eosinopenia,
• Oily skin and hair. • Primary seborrhea in Persian kittens. lymphopenia, elevated serum alkaline
• Malodor. phosphatase, hypercholesterolemia, and
• Comedones. Secondary hyposthenuria suggest hyperadrenocorticism.
• Follicular casts. • Cutaneous hypersensitivity—with pruritus,
secondary skin trauma, and irritation. OTHER LABORATORY TESTS
• Candle wax–like deposits on hair.
• Ectoparasitism—scabies, demodicosis, and Thyroid hormone levels and adrenal
• Silver scales, mostly affecting nose, face,
cheyletiellosis; with inflammation and function tests if an endocrinopathy is
and ears.
exfoliation. suspected; see specific chapters for test
• Alopecia.
• Bacterial folliculitis—bacterial enzymatic recommendations. Serology, PCR, cytology,
• Pruritus.
disadhesion with increased exfoliation of and histopathology for Leishmaniasis; see
• Secondary bacterial folliculitis and/or
keratinocytes. specific chapter.
Malassezia dermatitis.
• Dermatophytosis—increased exfoliation as IMAGING
CAUSES a skin mechanism in resolving infection. Thoracic radiographs—feline thymoma-
Primary • Cutaneous Leishmaniasis in endemic regions associated exfoliative dermatitis.
• Primary idiopathic seborrhea (primary of the world; systemic signs might be present.
keratinization disorder)—primary cellular • Endocrinopathy—hypothyroidism:
• Skin scraping.
defect; accelerated epidermopoiesis and abnormalities in keratinization, failure to
• Skin biopsy—rule out particular differential
hyperproliferation of the epidermis, regrow hair, and excessive sebum production;
diagnoses; strongly recommended for most
follicular infundibulum, and sebaceous hyperadrenocorticism: abnormal keratiniza-
cases.
gland; cocker and springer spaniel, West tion and decreased follicular activity; excessive
• Intradermal allergy test.
Highland white terrier, basset hound, scaling and secondary pyoderma common in
• Restricted ingredient food trial.
Doberman pinscher, Irish setter, and both syndromes; other hormonal abnormali-
• Cytology of skin surface.
Labrador retriever. ties may also be associated with excessive
• Microscopic examination of plucked
• Vitamin A–responsive dermatosis—young scaling.
hairs—macromelanosomes and structural
cocker spaniels; clinically similar to severe • Age—dull, brittle, and scaly hair coat due
anomalies in follicular dysplasia and color
idiopathic seborrhea; identified by response to alterations caused by natural changes in
dilution alopecia.
to oral vitamin A supplementation. epidermal metabolism associated with age; no
• Zinc-responsive dermatosis—alopecia, dry specific defect identified.
(continued) Dermatoses, Exfoliative

• Systemic antibiotics—secondary pyoderma. ZOONOTIC POTENTIAL
• Retinoids—varied success for idiopathic or • Dermatophytosis and several ectoparasites
primary seborrhea; reports of individual have zoonotic potential.
TREATMENT response in refractory cases; isotretinoin • Leishmaniasis is a reportable disease. D
• Frequent and adequate topical therapy. (1 mg/kg PO q12–24h); if response is seen,
• Diagnose and control treatable primary and PREGNANCY/FERTILITY/BREEDING
taper dosage (1 mg/kg q48h or 0.5 mg/kg Systemic retinoids and vitamin A in
secondary diseases. q24h); difficult to dispense due to strict
• Recurrence of secondary infections may therapeutic dosages—extreme teratogen; do
prescription procedures. not use in intact females because of severe and
require repeated therapy and further • Cyclosporine (modified) 5 mg/kg/day until
diagnostics. predictable teratogenicity and extremely long
controlled, then decreased to minimal withdrawal period; women of childbearing
• Maintaining control is often lifelong. effective maintenance dosage for individual
• Prioritize restoration of epidermal barrier age should not handle these medications.
cases of keratinization disorder associated
integrity and function. with hypersensitivity, sebaceous adenitis, SYNONYMS
epidermal dysplasia, ichthyosis, and/or • Keratinization disorder, seborrhea,
Malassezia dermatitis. idiopathic seborrhea, keratinization defect,
dyskeratinization.
PRECAUTIONS • Eczema, psoriasis, dandruff—incorrect
MEDICATIONS • Corticosteroids—use judiciously to
human terms.
control the inflammation resulting from • Sebopsoriasis—correct term to describe
DRUG(S) OF CHOICE exfoliative disorders; may mask signs of similarities between some human and canine
Shampoos pyoderma and prevent accurate diagnosis of keratinization defects.
• Contact time—5–15 minutes required; >15 primary disease.
minutes discouraged, may result in epidermal • Vitamin A and D analogues—side effects SEE ALSO
maceration, loss of barrier function, and can be severe; patients should be referred to a • Atopic Dermatitis.
excessive epidermal drying and irritation. dermatologist before being treated with these • Demodicosis.
• Relative keratolytic activity—hypoaller- drugs; teratogenic. • Hyperadrenocorticism (Cushing’s
genic < sulfur/salicylic acid < benzoyl Syndrome)—Cats.
peroxide. • Hyperadrenocorticism (Cushing’s
• Ethyl lactate—less keratolytic/less drying; Syndrome)—Dogs.
useful for moderate bacterial folliculitis and • Hypothyroidism.
dry scale. FOLLOW-UP • Leishmaniosis
• Chlorhexidine—antimicrobial; mildly • Malassezia Dermatitis.
PATIENT MONITORING
drying; useful for moderate bacterial • Pyoderma.
• Antibiotics and topical therapy—monitor
folliculitis and Malassezia dermatitis. • Sarcoptic Mange.
response every 3 weeks; patients may
• Tar—keratolytic, keratoplastic, and respond differently to the various topical Suggested Reading
antipruritic; useful for moderate scale therapies. Gross TL, Ihrke PJ, Walder EJ, Affolter V.
associated with pruritus. • Development of additional diseases and Skin Diseases of the Dog and Cat:
Moisturizers/Barrier Restoration recurrence of pyoderma—reevaluation critical Clinical and Histopathologic Diagnosis,
• Restore skin hydration and increases to determine if new factors are involved and if 2nd ed. Oxford: Blackwell Science,
effectiveness of subsequent shampoos. changes in therapy are necessary. 2005.
• Humectants—enhance hydration of the • Endocrinopathy—specific laboratory Miller W, Griffin C, Campbell, K. Muller
stratum corneum by attracting water from the testing for disease management. and Kirk’s Small Animal Dermatology,
dermis; at high concentrations may be keratolytic. • Selective autoimmune disorders—clinical 7th ed. St. Louis, MO: Elsevier, 2013.
• Propylene glycol spray (50–75% dilution evaluation and laboratory monitoring Torres SMF, Roudebush P, eds., Advances
with water) applied frequently. frequent initially; based on diagnosis and in Veterinary Dermatology, Vol. 8.
• Microencapsulation—may improve residual treatment protocols. Hoboken, NJ: Wiley, 2017.
activity of moisturizers by allowing sustained • Retinoid drugs—serum chemistries, Author Guillermina Manigot
release after bathing. including triglycerides, and Schirmer tear Consulting Editor Alexander H. Werner
• Emollients—coat the skin; smooth the tests. Resnick
roughened surfaces produced by excessive
scaling; usually combined with occlusives to
promote hydration of the epidermis. Client Education Handout
• Barrier restoration—phytosphingosines, available online
MISCELLANEOUS
ceramides.
AGE-RELATED FACTORS
Systemic Therapy Skin aging might be related to increase in
• Specific disease (e.g., thyroxine replacement exfoliative disorders or relapses.
for hypothyroidism).
Dermatoses, Neoplastic
• The most frequently reported cutaneous or SIGNS
subcutaneous tumors in cats are basal cell General Comments
tumor, squamous cell carcinoma, mast cell
D BASICS tumor, and fibrosarcoma. • Skin tumors in
Most common clinical sign is a cutaneous or
subcutaneous nodule; some tumors have an
DEFINITION cats are more frequently malignant; skin ulcerated surface; others may result in
• Neoplastic proliferation of cells derived from tumors in dogs are more frequently benign. excessive scaling or in the formation of
the skin or migrating to the skin. • Epidermal cutaneous plaques.
tumors include those arising from keratinocytes,
Geographic regions near the equator, with Historical Findings
melanocytes, Merkel cells, and Langerhans
high altitude, or with sand or other reflective • Tumors are most often slow growing; the
cells, and epitheliotropic lymphoma. • Adnexal
surfaces, have a higher incidence of solar- owner may find them during petting,
tumors include those arising from hair follicles,
induced neoplastic dermatoses. bathing, or grooming of the pet. • Tumors
sebaceous glands, and sweat glands. • Dermal
and subcutaneous skin tumors include those of may be rapidly growing and appear (or
SIGNALMENT increase in size) quickly (e.g., histiocytoma).
mesenchymal origin and tumors of round cell
origin. • Secondary or metastatic skin tumors Species Physical Examination Findings
result from the proliferation of cells from Dogs and cats. • Nodules—cutaneous or subcutaneous.
primary neoplasms of other organs in the skin. Breed Predilections • Cutaneous ulcers. • Excessive scaling.
PATHOPHYSIOLOGY • Canine breeds with the highest overall • Cutaneous papillomas. • Cutaneous
• Neoplasia develops as a result of changes in incidence of skin tumors include boxer, plaques.
genes controlling cell proliferation and Scottish terrier, bullmastiff, basset hound, CAUSES
homeostasis. • More than 100 cancer-related Weimaraner, Kerry blue terrier, and • Genetic (gene mutations). • Environmental
genes have been identified. • Oncogenes Norwegian elkhound. • Feline breeds with (e.g., ultraviolet light, radiation exposure).
encode proteins that promote cell growth; the highest overall incidence of skin tumors • Viruses (e.g., papillomaviruses, feline
tumor-suppressor genes encode proteins that include Siamese and Persian. • Certain leukemia virus, feline immunodeficiency virus).
restrict cell proliferation and differentiation. breeds are predisposed to specific types of • Toxins (e.g., tars). • Drugs (e.g., immuno
• Mutations in p53, a tumor-suppressor gene, tumors (see Suggested Reading). • Dog— suppressive agents, chemotherapeutic agents).
are found in approximately 50% of cancers in breeds associated with the most common ◦ Epidermal neoplasms: ◦ Keratinocytes—
humans and have also been found in many cutaneous neoplasms: ◦ Lipoma—cocker papillomas, squamous cell carcinoma, basal
tumors affecting dogs and cats. • Ultraviolet spaniel, dachshund, Doberman pinscher, cell carcinoma, basosquamous carcinoma.
light promotes tumor development by Labrador retriever, miniature schnauzer, ◦ Melanocytes—melanoma. ◦ Merkel
damaging DNA and suppressing the immune Weimaraner. ◦ Sebaceous gland tumor— cells—Merkel cell carcinoma. ◦ Langerhans
system. • Many viruses promote tumor growth beagle, cocker spaniel, dachshund, Irish cells—histiocytoma and malignant
through stimulating cell proliferation and/or setter, Lhasa apso, Malamute, miniature histiocytosis. ◦ Epitheliotropic lymphoma—
suppressing the immune system. • Reports of schnauzer, poodle, shih tzu, Siberian husky. T lymphocytes. • Adnexal neoplasms: ◦ Hair
specific cutaneous neoplasia associated with ◦ Mast cell tumor—American Staffordshire follicles—trichofolliculoma, trichoepithelioma,
medications and/or vaccinations. terrier, beagle, Boston terrier, boxer, bull infundibular keratinizing acanthoma,
terrier, dachshund, English bulldog, fox tricholemmoma, pilomatrixoma, trichoblastoma.
SYSTEMS AFFECTED terrier, golden retriever, Labrador retriever, ◦ Sebaceous glands—sebaceous adenoma,
Skin/exocrine. pug, shar-pei, Weimaraner. ◦ Histiocytoma— sebaceous epithelioma, sebaceous
GENETICS American Staffordshire terrier, Boston terrier, adenocarcinoma, perianal gland epithelioma,
• Breed predispositions have been reported
boxer, cocker spaniel, dachshund, Doberman perianal gland carcinoma. ◦ Sweat glands—
for specific tumors, but the mode of pinscher, English springer spaniel, Great apocrine cystadenoma, apocrine secretory
inheritance in these breeds has not been Dane, Labrador retriever, miniature adenoma/adenocarcinoma, apocrine ductal
determined. Mutations in oncogenes and/or schnauzer, Rottweiler, Scottish terrier, adenoma/carcinoma, eccrine carcinoma.
tumor-suppressor genes (e.g., p53) are present shar-pei, Shetland sheepdog, West Highland • Dermal and subcutaneous neoplasms:
in many types of skin tumors. white terrier. ◦ Papilloma—cocker spaniel, ◦ Mesenchymal origin—soft tissue
Kerry blue terrier. • Cat—breeds associated sarcoma: fibroma/fibrosarcoma, myxoma/
INCIDENCE/PREVALENCE with the most common cutaneous myxosarcoma, hemangiopericytoma,
• The combined incidence rate for skin neoplasms: ◦ Basal cell tumor—Persian, lymphangioma/lymphangiosarcoma,
tumors has been reported as 728/100,000 Himalayan (basal cell carcinoma—Siamese). hemangioma/hemangiosarcoma, lipoma/
(0.728%) for dogs and 84/100,000 (0.084%) ◦ Squamous cell carcinoma—no predisposed liposarcoma, neurofibrosarcoma, leiomyoma/
for cats. • The skin is the most common site breed reported. ◦ Mast cell tumor—Siamese. leiomyosarcoma, synovioma/synovial
of occurrence of neoplasia in the dog (30% of ◦ Fibrosarcoma—no predisposed breed sarcoma, rhabdomyoma/rhabdomyosarcoma.
total tumors) and the second most common reported. ◦ Round cell origin—transmissible venereal
site in the cat (20% of total tumors). tumor, mast cell tumor, plasmacytoma,
Mean Age and Range
• Canine skin tumors are approximately 55% lymphoma, histocytoma, and histocytic tumors.
• The median age for cutaneous neoplasia is
mesenchymal, 40% epithelial, and 5% • Secondary or metastatic skin tumors result
10.5 years in dogs and 12 years in cats. • The
melanocytic. • The most frequently from the metastasis or primary neoplasms in
peak age period for cutaneous neoplasia in
reported cutaneous or subcutaneous tumors other organs to the skin.
dogs and cats is 6–14 years.
in descending order for dogs are lipoma,
sebaceous gland adenoma, mast cell tumor, Predominant Sex RISK FACTORS
papilloma, and histiocytoma. • Feline skin • Females have a higher incidence of tumors • Hair coat color and length (e.g., hairless
tumors are approximately 50% epithelial, in dogs (56%). • Males have a higher breeds, white hair coat, lightly pigmented
48% mesenchymal, and 2% melanocytic. incidence of tumors in cats (56%). skin—increased risk for squamous cell
carcinoma). • Age (e.g., young animals
(continued) Dermatoses, Neoplastic

highest risk for viral infections, older ACTIVITY AGE-RELATED FACTORS
animals at highest risk for environment- Varies with tumor type and location. Vary with tumor type and location.
associated neoplasia). • Sunlight exposure
(e.g., dogs and cats that sunbathe or spend
DIET ZOONOTIC POTENTIAL D
Diets high in omega-3 fatty acids, arginine, None
time outdoors on reflective surfaces have and protein may be beneficial in boosting the
higher risk of ultraviolet light–induced PREGNANCY/FERTILITY/BREEDING
immune response and preventing cancer- Varies with tumor type; some may have a
skin tumors). • Genetics—certain breeds associated cachexia.
have higher risk of developing specific types genetic predisposition.
of tumors (see above and Suggested CLIENT EDUCATION SYNONYMS
Reading). Varies with tumor type and location. N/A
SURGICAL CONSIDERATIONS SEE ALSO
• Vary with tumor type and location—wide • Adenocarcinoma, Skin (Sweat Gland,
margins may be needed to prevent Sebaceous).
DIAGNOSIS reoccurrence of infiltrative tumors. • Basal Cell Tumor.
• Pretreatment with antihistamines approp
DIFFERENTIAL DIAGNOSIS • Fibrosarcoma, Bone.
riate when excising mast cell tumors. • Lipoma, Infiltrative.
• Cyst. • Abscess. • Inflammatory nodule/
granuloma/plaque—sterile granulomatous and • Malignant Fibrous Histiocytoma.
pyogranulomatous disease, sterile panniculitis, • Mast Cell Tumors.
fungal infection, mycobacterial infection, • Papillomatosis.
foreign body. • Trauma/self-induced skin MEDICATIONS • Squamous Cell Carcinoma, Skin.
ulceration. • Hamartoma/nevus. DRUG(S) OF CHOICE INTERNET RESOURCES
CBC/BIOCHEMISTRY/URINALYSIS Vary with tumor type—chemotherapy • http://www.oncolink.org/types/section.
N/A protocols are useful in some cases. cfm?c=22&s=69
• http://www.vetcancersociety.org
OTHER LABORATORY TESTS CONTRAINDICATIONS
• Cytology (fine-needle aspirate or impression Vary with tumor type and presence of Suggested Reading
smear). • Regional lymph node aspirate (for concurrent disease. Campbell KL, ed. Small Animal Dermatology
staging). Secrets. Philadelphia, PA: Hanley & Belfus,
PRECAUTIONS
2004, pp. 385–458.
IMAGING Vary with tumor type and location.
Goldschmidt MH, Shofer FS. Skin Tumors of
Thoracic radiographs and abdominal ultra- POSSIBLE INTERACTIONS the Dog and Cat. Oxford: Butterworth
sonography useful for staging (evaluate for Vary with tumor type and location. Heinemann, 1992.
metastatic disease or underlying primary Gross TL, Ihrke PJ, Walder EJ, et al. Skin
neoplasia). ALTERNATIVE DRUG(S)
Vary with tumor type and location. Diseases of the Dog and Cat: Clinical and
DIAGNOSTIC PROCEDURES Histopathologic Diagnosis, 2nd ed. Oxford:
• Cytology. • Biopsy with histopathologic Blackwell, 2005, pp. 561–893.
examination. • Immunohistochemistry (useful Martin PD, Argyle DJ. Advances in the
in confirming certain types of tumors). management of skin cancer. Vet Dermatol
PATHOLOGIC FINDINGS
FOLLOW-UP 2013, 24:173–180.
PATIENT MONITORING Miller WH, Griffin CE, Campbell KL, eds.
Varies with tumor type; see specific tumors
Varies with tumor type and location. Muller & Kirk’s Small Animal Dermatology,
for additional information.
7th ed. Philadelphia, PA: Elsevier, 2013, pp.
PREVENTION/AVOIDANCE 774–843.
• Varies with tumor type and location. Shearer D, Dobson J. An approach to nodules
• Minimize exposure to ultraviolet light to and draining sinuses. In: Foster A, Foil C,
TREATMENT help prevent some types of tumors. BSAVA Manual of Small Animal
APPROPRIATE HEALTH CARE POSSIBLE COMPLICATIONS Dermatology, 2nd ed. Gloucester: BSAVA,
• Varies with tumor type. • Observation is Vary with tumor type and location. pp. 55–65.
appropriate for some benign tumors. Author Karen L. Campbell
EXPECTED COURSE AND PROGNOSIS Consulting Editor Alexander H. Werner
• Surgical excision, cryosurgery, radiation Vary with tumor type and location.
therapy, and/or tumor-specific chemotherapy Resnick
or immunotherapy may be curative or
palliative.
NURSING CARE MISCELLANEOUS
• Varies with tumor type and location. • Traumatized ASSOCIATED CONDITIONS
tumors may become secondarily infected. Vary with tumor type and location.
Dermatoses, Papulonodular
• Metabolic—cutaneous xanthomatosis, ACTIVITY
calcinosis circumscripta. No specific alteration of activity
• Hypersensitivity—feline eosinophilic recommended.
D BASICS dermatitis. DIET
DEFINITION • Neoplasia.
No specific alteration of diet recommended.
• Diseases whose primary lesions manifest as RISK FACTORS
papules and nodules. CLIENT EDUCATION
• Bacterial folliculitis, dermatophytosis, and
• Papule—solid, elevated lesion of the skin • For fungal infections, treatment may be
demodicosis—any disease or medication that expensive and prognosis can be guarded for
less than 1 cm in diameter. causes immune compromise or interferes with
• Nodule—solid, elevated lesion of the skin deep/systemic fungal infections.
the barrier function of the skin. • For immune-mediated processes, treatment
more than 1 cm in diameter that extends into • Pelodera dermatitis—may be associated with
deeper layers of the skin. may be for the duration of the patient’s life.
contact with decaying organic debris (straw or
PATHOPHYSIOLOGY hay) containing Pelodera strongyloides. SURGICAL CONSIDERATIONS
• Papules—usually the result of tissue Rarely necessary unless neoplasia is diagnosed.
infiltration by inflammatory cells; accompanying
intraepidermal edema or epidermal hyperplasia
and dermal edema. DIAGNOSIS
• Nodules—usually the result of a massive MEDICATIONS
infiltration of inflammatory or neoplastic cells DIFFERENTIAL DIAGNOSIS
into the dermis or subcutis. Determined by cause. DRUG(S) OF CHOICE
SYSTEMS AFFECTED CBC/BIOCHEMISTRY/URINALYSIS Bacterial Folliculitis
Skin/exocrine. Usually normal—determined by cause. • Superficial pyoderma—appropriate
OTHER LABORATORY TESTS antibiotics based on bacterial culture and
GENETICS susceptibility testing for at least 3–4 weeks, or
Determined by cause; specific diseases may be Determined by cause.
1 week beyond resolution of clinical signs.
more commonly seen in certain breeds. IMAGING • Deep pyoderma—appropriate antibiotics
INCIDENCE/PREVALENCE N/A based on bacterial culture and susceptibility
Determined by cause. DIAGNOSTIC PROCEDURES testing for at least 6–8 weeks, or 2 weeks
GEOGRAPHIC DISTRIBUTION • Skin scraping—parasites. beyond resolution of clinical signs.
• Dermatophyte cultures—dermatophytes. • Identify and control underlying cause to
Determined by cause.
• Pustule (if present) impression smear prevent recurrence.
SIGNALMENT cytology—bacteria and degenerative • See Pyoderma for additional recomm-
Species neutrophils compatible with bacterial endations.
Dogs and cats. folliculitis; eosinophils can be compatible Sebaceous Adenitis
Breed Predilection
with hypersensitivity and/or with rupturing • Appropriate antibiotics if secondary
Determined by cause. folliculitis or furunculosis; acantholytic bacterial infection present.
keratinocytes consistent with an inflamma • Propylene glycol and water (50–75%
Mean Age and Range tory folliculitis or pemphigus disease. dilution) once daily as a spray to affected
Determined by cause. • Culture from tissue (fungal, bacterial, myco- areas helpful in mild cases.
Predominant Sex bacterial)—identify deep/systemic infection; • Essential fatty acid dietary supplements
Determined by cause. possible susceptibility report for treatment. (omega-3 and omega-6 PO).
• Aspirate and cytology from nodule—identify • Topical therapy—antiseborrheic shampoos,
SIGNS cellular infiltrate; presence of organisms.
• Papules and/or nodules with distribution
emollient rinses (baby oil), and humectants.
• Skin biopsy— determine definitive • Cyclosporine, modified (5 mg/kg PO q24h).
characteristic of the cause. diagnosis; especially if baseline diagnostic • Vitamin A (10,000–30,000 IU PO daily or
• Accompanying crusting, inflammation, procedures are normal and/or initial empiric
pigmentation changes, and hair coat changes 1000 IU/kg PO daily).
treatment is ineffective. • Refractory cases—isotretinoin (1 mg/kg
often noted; also characteristic of the cause.
PATHOLOGIC FINDINGS PO q12–24h); if response is seen, taper
CAUSES Depends upon underlying disease process. dosage (1 mg/kg q48h or 0.5 mg/kg q24h);
• Superficial and deep bacterial folliculitis the synthetic retinoids have become
(e.g., Staphylococcus). difficult to dispense due to strict prescrip
• Other bacterial—mycobacterial, actinomy tion procedures.
cosis, nocardiosis, abscess. • Most cases are refractory to corticosteroids.
• Fungal—dermatophytosis (including
TREATMENT
• See Sebaceous Adenitis, Granulomatous for
pseudomycetoma/kerion), histoplasmosis, APPROPRIATE HEALTH CARE additional recommendations.
cryptococcosis, coccidiomycosis, sporo • Outpatient for nearly all causes (except
trichosis, blastomycosis, phaeohyphomycosis. some cases of neoplasia). Canine and Feline Acne
• May resolve without therapy in mild cases.
• Sebaceous adenitis, granulomatous. • Generalized demodicosis with secondary
• Warm water soaks or Epsom salt solution
• Canine and feline acne. sepsis requires hospitalization.
• Parasitic—demodicosis, Leishmaniasis, flea
(2 T/quart or 30 m/L of water) for 5–10 min.
NURSING CARE • Chlorhexidine-based pads, or acetic acid/
bite hypersensitivity, sarcoptic mange, pelodera Depends upon underlying issue.
dermatitis. boric acid pads/wipes, or benzoyl peroxide
• Sterile nodular—sterile pyogranulomatous
gels used daily or alternated daily; topical
dermatitis and panniculitis, reactive histiocytosis. ceramide/EFA preparations may be helpful.
(continued) Dermatoses, Papulonodular

• Topical creams/ointments—mupirocin 2% PRECAUTIONS • Repeat fungal culture—monitor therapy in
ointment: topical antibiotic; apply q24h; • Side effects more common and more severe patients with dermatophytosis (see
should not be used in cats with deep lesions; with ketoconazole than with other azoles in cats. Dermatophytosis).
metronidazole, 0.05% Vitamin A acid cream, • Cats can be sensitive to the irritant effects • Resolution of lesions—monitor progress of D
clindamycin are alternative options. of benzoyl peroxide. sebaceous adenitis, actinic conditions, and all
• Secondary bacterial infection—systemic • Fatty acids—use with caution in dogs with other diseases.
antibiotics. inflammatory bowel disease or recurrent POSSIBLE COMPLICATIONS
• Underlying cause(s) should be determined pancreatitis. Dependent upon specific disease.
and treated accordingly. • Isotretinoin—may cause keratoconjunctivi
• Refractory cases—isotretinoin (1–2 mg/kg tis sicca, hyperactivity, pinnal pruritus,
PO q24h); oral synthetic retinoids have erythematous mucocutaneous junctions,
become difficult to dispense due to strict swollen tongue, lethargy with anorexia or
prescription procedures; prednisolone PO vomiting, abdominal distension, or collapse; MISCELLANEOUS
(1–2 mg/kg/day for 10–14 days and taper) CBC and chemistry screen abnormalities ASSOCIATED CONDITIONS
may reduce scar tissue formation. include high platelet count, hypertriglyceri N/A
• See Acne—Cats and Acne—Dogs for demia, hypercholesterolemia, and high
additional recommendations. alanine transaminase; teratogen. AGE-RELATED FACTORS
• Cyclosporine—may cause vomiting and N/A
Pelodera Dermatitis
• Remove and destroy bedding. diarrhea, gingival hyperplasia, B lymphocyte ZOONOTIC POTENTIAL
• Wash kennels, beds, and cages and treat hyperplasia, hirsutism, papillomatous skin • Dermatophytosis—incidence in humans
with a premise insecticide or flea spray. eruptions, and increased incidence of reported in 30–50% of cases of Microsporum
• Bathe affected animal and remove crusts. infection; decreased glucose homeostasis; canis, but possible with all dermatophytosis cases.
• Parasiticidal dip or ivermectin as recom potential toxic reactions rare and include • Fungal infections—potential depends upon
mended for sarcoptic mange. nephrotoxicity and hepatotoxicity. organism.
• Corticosteroids as needed for inflammation. • Azathioprine, mycophenolate mofetil, and • Sarcoptic mange.
• Severe infection—may require use of chlorambucil—potential for bone marrow
antibiotics. suppression, gastrointestinal upset;
• Synthetic retinoids—teratogens; do not use in
azathioprine can cause hepatotoxicity and
Sterile Nodular Dermatoses pregnant animals, animals intended for
possibly pancreatitis.
• Attempt to identify underlying cause. reproduction, or intact female animals; should
• Cyclosporine, modified 5 mg/kg PO q24h. POSSIBLE INTERACTIONS not be handled by women of childbearing age.
• Tetracycline (250 mg <10 kg, 500 mg • Cyclosporine and corticosteroids interact • Corticosteroids—avoid use in pregnant animals.
>10 kg q8–12h), doxycycline (10 mg/kg with several medications; an appropriate • Cyclosporine—avoid during pregnancy
q24h), or minocycline (5 mg/kg q12h) with drug formulary should be consulted prior unless necessary; dosages two to five times
niacinamide (250 mg <10 kg, 500 mg >10 kg to usage. normal have been fetotoxic and embryotoxic
q8–12h). • Referral to a veterinary dermatologist in rats and rabbits.
• Corticosteroids at immunosuppressive should be considered if the etiology remains • Antifungal agents should be avoided in
doses and taper according to response. undetermined and/or prior to prescribing pregnant animals.
• Chemotherapeutic drugs (chlorambucil or unfamiliar medications. • All drugs should be used with caution in
azathioprine or mycophenolate mofetil). ALTERNATIVE DRUG(S) pregnant and breeding animals.
Other N/A SEE ALSO
• Dermatophytosis—itraconazole, • Acne—Cats.
ketoconazole, or terbinafine; see • Acne—Dogs.
Dermatophytosis. • Demodicosis.
• Kerion—see Dermatophytosis. • Dermatophytosis.
FOLLOW-UP
• Demodicosis/sarcoptic mange—see • Pyoderma.
Demodicosis, Sarcoptic Mange. PATIENT MONITORING • Sebaceous Adenitis, Granulomatous.
• Other bacterial infection—antibiotics • CBC, chemistry screen, urinalysis, and
urine cultures—monitor periodically in Suggested Reading
dependent upon culture and sensitivity Helton Rhodes KA, Werner A. Blackwell’s
results. patients receiving immunosuppressive
medications; monitoring will depend upon Five-Minute Veterinary Consult Clinical
• Deep/systemic fungal infection. Companion: Small Animal Dermatology, 3rd
• Feline eosinophilic dermatitis—look for medication and dosage.
• CBC, chemistry screen, and urinalysis—
ed. Hoboken, NJ: Wiley-Blackwell, 2018.
underlying cause. Author Karen A. Kuhl
• Neoplasia—see Dermatoses, Neoplastic. monitor monthly for 4–6 months in patients
receiving synthetic retinoid therapy. Consulting Editor Alexander H. Werner
CONTRAINDICATIONS • Tear production—monitor monthly for
Resnick
Corticosteroids and immunosuppressive 4–6 months, then every 6 months in patients
medications should be avoided with receiving synthetic retinoid therapy or
folliculitis, dermatophytosis, kerion, and sulfonamide-containing antibiotics. Client Education Handout
demodicosis. • Skin scraping—monitor therapy in patients
available online
with Demodicosis (see Demodicosis).
Dermatoses, Sterile Nodular/Granulomatous

• Cutaneous xanthoma—high-fat treats or inflammation that can extend from the dermis
diet, diabetes mellitus, hyperlipidemia. to the panniculus; differentiated from infectious
diseases by obtaining negative cultures.
D BASICS • Canine eosinophilic granuloma—accumu-
DEFINITION lation of eosinophils with edema, possible
Sterile diseases with primary lesions of mucin, and collagen degeneration.
DIAGNOSIS • Calcinosis cutis—diffuse calcium deposi-
nodules and/or plaques.
DIFFERENTIAL DIAGNOSIS tion of the dermal collagen and adnexa that
PATHOPHYSIOLOGY • Sterile nodular dermatoses must be may extend into the deeper tissue.
• Nodules/plaques—usually result from an differentiated from deep bacterial and fungal • Calcinosis circumscripta—focal to multi-
infiltration of inflammatory cells into the infections and dermal neoplasia. focal deposits of mineral that efface the soft
dermis and subcutis; may be secondary to • Diagnosis by histopathology and deep tissue.
endogenous or exogenous stimuli. tissue cultures. • Reactive histiocytosis (cutaneous and
• Inflammation is typically, but not always, • Immunohistochemistry—differentiating systemic)—markedly angiocentric infiltrate of
granulomatous to pyogranulomatous. histiocytic conditions. histiocytes that do not form granulomas or
SYSTEMS AFFECTED • Immunohistochemical staining and PCR pyogranulomas.
Skin/exocrine. testing—diagnose Leishmaniasis and myco- • Malignant histiocytosis (disseminated histio-
GENETICS bacterial infections. cytic sarcoma)—dense pleomorphic cell
Oligogenic transmission is proposed for CBC/BIOCHEMISTRY/URINALYSIS proliferation of spindle or round cells that
histiocytic sarcoma for Bernese mountain • Amyloidosis—possible changes in efface normal tissue architecture; tumors from
dogs. biochemistry and/or urinalysis if internal other spindle and round cell tumors differenti-
organs are affected. ated by immunohistochemistry; see specific
SIGNALMENT • Malignant histiocytosis—pancytopenia. chapters.
• Collagenous nevi—German shepherd dogs • Calcinosis cutis—changes characteristic of • Sterile nodular panniculitis—neutrophilic
3–5 years old. hyperglucocorticoidism. to pyogranulomatous inflammation that
• Calcinosis circumscripta—German • Cutaneous xanthomas—may have affects the deep dermis and panniculus
shepherd dogs <2 years old. glucosuria, hyperglycemia, and/or lipid predominantly; adipocytes may be necrotic or
• Systemic histiocytosis and malignant histiocyto- profile abnormalities. may be infiltrated by foamy macrophages;
sis—Bernese mountain dogs (primarily), • Sterile panniculitis—possible biochemistry differentiated from infectious diseases by
Rottweilers, and retrievers (golden and Labrador). changes associated with pancreatitis, hepatic obtaining negative cultures.
• Eosinophilic granuloma—Siberian huskies disease, or systemic lupus erythematosus. • Collagenous nevi—focal but often subtle
<3 years, males. dermal thickening of normal collagen
IMAGING bundles.
SIGNS Radiology and ultrasonography—involvement • Cutaneous xanthoma—diffuse granu-
• Characterized by single to multiple dermal of internal organs in amyloidosis and histiocy- lomatous inflammation composed of large
to subcutaneous nodules and/or plaques. tosis; areas of dystrophic calcification and/or foamy macrophages; lakes of extracellular
• Firm to fluctuant. adrenal enlargement or tumor in dogs with amorphous lipid deposits and cholesterol
• Occasionally painful. calcinosis cutis; renal or uterine tumors in clefts.
• Overlying epidermis may be normal to German shepherd dogs with collagenous nevi.
ulcerated.
CAUSES DIAGNOSTIC PROCEDURES
• Amyloidosis. • Skin biopsy for histopathology and cultures
(fungal, aerobic, anaerobic, and mycobacterial).
• Foreign body reaction.
• Biopsies should be excisional and taken
TREATMENT
• Spherulocytosis.
• Idiopathic sterile granuloma and from an intact or early (nondraining) nodule APPROPRIATE HEALTH CARE
if possible. • Most of these disorders can be treated on an
pyogranuloma.
• Canine eosinophilic granuloma. • Culture samples should be taken from outpatient basis.
nodular tissue, not exudates. • Neoplastic or metabolic disorders may
• Calcinosis cutis.
• Calcinosis circumscripta. • Special histopathologic stains for bacteria, require hospitalization and supportive care.
• Reactive (cutaneous, systemic) or malignant mycobacteria, and fungi. NURSING CARE
histiocytosis (disseminated histiocytic sarcoma). PATHOLOGIC FINDINGS Gentle bathing and soaking to clean the skin
• Sterile nodular panniculitis. • Amyloidosis—accumulation of amorphous and remove debris.
• Collagenous nevi (nodular dermatofibrosis). eosinophilic deposits that may extend into the DIET
• Cutaneous xanthoma. subcutis; deposits stain apple green with Animals with xanthoma should be on a
Congo red in polarized light. low-fat diet.
RISK FACTORS • Foreign body reaction—suppurative to
• Foreign body reaction—induced by pyogranulomatous inflammation that affects CLIENT EDUCATION
exposure to any irritating material. the dermis, subcutis, and occasionally the • Malignant histiocytosis, amyloidosis,
• Calcinosis cutis—increased risk with underlying muscle. collagenous nevi of German shepherd dogs,
exposure to high doses of exogenous or • Spherulocytosis—histiocytes surrounding and systemic reactive histiocytosis are almost
endogenous glucocorticosteroids. thin-walled parent bodies filled with homo always fatal.
• Panniculitis—increased risk with vitamin geneous eosinophilic spherules. • Prognoses for cutaneous reactive histiocytic
E–deficient diet. • Idiopathic sterile granuloma and pyogranu- disease, sterile panniculitis, and sterile
loma—granulomatous to pyogranulomatous pyogranuloma are guarded since they may
(continued) Dermatoses, Sterile Nodular/Granulomatous

require long-term immunosuppressive ◦ Cyclosporine, modified (5–10 mg/kg • Many of the other conditions have a
therapy; a few of these cases will not respond 24h) can be used together with predniso- guarded prognosis; many require lifelong
to therapy at all. lone or as an alternative to glucocorticos- immunosuppressive therapy to remain in
teroid therapy if the patient is steroid remission. D
intolerant or steroids are not sufficiently
effective.
◦ Tetracycline (250 mg <10 kg, 500 mg
MEDICATIONS >10 kg q8–12h), doxycycline (10 mg/kg
MISCELLANEOUS
q24h), or minocycline (5 mg/kg q12h)
DRUG(S) OF CHOICE
with niacinamide (250 mg <10 kg, 500 mg ASSOCIATED CONDITIONS
• Amyloidosis—no known therapy, unless
>10 kg q8–12h) can also be used as an • Calcinosis cutis—hyperglucocorticoidism,
the lesion is solitary and can be surgically
alternative to glucocorticoid therapy; this is chronic renal failure, and diabetes mellitus.
removed.
effective only in mild cases. • Calcinosis circumscripta—(occasionally)
• Spherulocytosis—only effective treatment is
• Collagenous nevi—no therapy for most hypertrophic osteodystrophy and idiopathic
surgical removal.
cases since cystadenocarcinomas are usually polyarthritis.
• Idiopathic sterile granuloma and
bilateral; for rare unilateral case of cystadeno- • Collagenous nevi—renal cystadenoma/
pyogranuloma:
carcinoma or cystadenoma, removal of single cystadenocarcinoma and uterine, leiomyoma/
◦ Prednisolone (2.2–4.4 mg/kg divided
affected kidney may be helpful; ovariohyster- leiomyosarcoma.
PO q12h) is the first line of therapy;
ectomy should be performed in intact females • Cutaneous xanthoma—diabetes mellitus
continue steroids for 7–14 days after
to remove leiomyomas. and hyperlipoproteinemia.
complete remission, then taper dose.
• Cutaneous xanthoma—correction of
◦ Azathioprine (2.2 mg/kg q48h) or SEE ALSO
underlying diabetes mellitus or hyperlipopro-
cyclosporine (modified, 5–10 mg/kg q24h) • Adenocarcinoma, Renal.
teinemia usually curative.
added as a steroid-sparing drug. • Amyloidosis.
• Foreign body reactions—removal of the CONTRAINDICATIONS • Hyperadrenocorticism (Cushing’s
offending substance; secondary deep bacterial Corticosteroids and other immunosuppressive Syndrome)—Dogs.
infections require treatment with both topical drugs should be avoided, if possible, in any
and systemic antibiotics. animal with secondary bacterial folliculitis. ABBREVIATIONS
• Canine eosinophilic granuloma—predniso- • DMSO = dimethyl sulfoxide
PRECAUTIONS
lone (1.1–2.2 mg/kg PO q24h) usually DMSO—handle with care; monitor serum INTERNET RESOURCES
effective. calcium levels if used to treat calcinosis cutis. http://www.histiocytosis.ucdavis.edu
• Cutaneous/systemic or malignant histiocy-
Suggested Reading
tosis—no effective long-term therapy; see
Helton Rhodes KA, Werner A. Blackwell’s
Histiocytosis, Cutaneous.
Five-Minute Veterinary Consult Clinical
• Calcinosis cutis—underlying disease must
FOLLOW-UP Companion: Small Animal Dermatology,
be controlled if possible; most cases require
3rd ed. Hoboken, NJ: Wiley-Blackwell,
antibiotics to control secondary bacterial PATIENT MONITORING 2018.
infections; hydrotherapy and frequent • Patients on long-term immunosuppressive O’Kell AL, Inteeworn N, Diaz SF, et al.
bathing in antibacterial shampoos minimize therapy should have CBC, chemistry screen, Canine sterile nodular panniculitis:
secondary infection; topical dimethyl urinalysis, and urine culture performed at retrospective study of 14 cases. J Vet Intern
sulfoxide (DMSO) is useful (applied to no least every 6 months. Med 2010, 24:278–284.
more than one-third of the body once daily • Dogs treated with DMSO for calcinosis Santoro D, Prisco M, Ciaramella P.
until lesions resolve); if lesions are extensive, cutis should have calcium levels checked every Cutaneous sterile granulomas/pyogranulo-
serum calcium levels should be monitored 7–14 days for first month of therapy if large mas, leishmaniasis and mycobacterial
closely while using DMSO. areas are affected. infections. J Small Anim Pract 2008,
• Calcinosis circumscripta—surgical
POSSIBLE COMPLICATIONS 49:552–561.
excision.
Long-term use of immunosuppressive therapy Schissler J. Sterile pyogranulomatous
• Sterile nodular panniculitis:
(especially glucocorticosteroids) may make dermatitis and panniculitis. Vet Clin Small
◦ Single lesions can be removed surgically.
patients more susceptible to other dermatoses Anim 2019, 49:27–36.
◦ Prednisolone (2.2–4.4 mg/kg PO q24h or
such as bacterial folliculitis, demodicosis, and Author Dawn E. Logas
divided PO q12h) treatment of choice;
dermatophytosis, as well as systemic side effects. Consulting Editor Alexander H. Werner
administer until lesions regress, then taper;
Resnick
some dogs remain in long-term remission, EXPECTED COURSE AND PROGNOSIS
others require prolonged alternate-day therapy. • Systemic amyloidosis, malignant histiocyto-
◦ Azathioprine (2.2 mg/kg q48h) can be sis, systemic reactive histiocytosis, and
used together with prednisolone as a nodular dermatofibrosis—invariably fatal. Client Education Handout
available online
corticosteroid-sparing agent.
Dermatoses, Sun-Induced
CAUSES & RISK FACTORS kg PO tapering dosage; discontinue when
• White-haired and lightly haired individuals possible.
with poorly pigmented skin. • Imiquimod 5% cream—induces local
D BASICS • History of sunbathing. immune response; for individual lesions, esp.
OVERVIEW • Outdoor housing. actinic keratosis; apply q48h until resolution.
The hair coat and epidermal pigmentation • Regions with greater sun exposure, high • Cryosurgery—actinic keratosis, SCC.
protect the skin from damage caused by UV altitudes; usually occurs in summer, but also • Antibiotics—control secondary pyoderma
light radiation. Excessive UV exposure in winter as result of reflection from snow. (see Pyoderma).
damages keratinocytes (producing mutation), CONTRAINDICATIONS/POSSIBLE
causes inflammation, and decreases cutaneous
INTERACTIONS
immune system surveillance. UVA (320–400 nm)
Firocoxib—gastrointestinal upset; elevated
penetrates more deeply than UVB (290– DIAGNOSIS liver enzymes.
320 nm). Prolonged and repeated damage
leads to preneoplastic changes and eventual DIFFERENTIAL DIAGNOSIS
neoplasia. Prolonged sun exposure in darkly • Dermatophytosis.
pigmented individuals may cause thermal • Demodicosis.
burn. UV exposure may exacerbate • DLE. FOLLOW-UP
symptoms of pemphigus erythematosus (PE), • PE. • Patients should be regularly screened for
discoid lupus erythematosus (DLE), systemic • Pemphigus foliaceus. development and removal of new lesions.
lupus erythematosus (SLE), and dermato- • Drug eruption. • Sun-induced dermatoses rarely metastasize.
myositis. • Contact dermatitis. • Long-term therapy necessary following
• Chemical burn. extended periods of sun damage.
SIGNALMENT
• Dogs—Dalmatian, bull terrier, boxer, DIAGNOSTIC PROCEDURES ABBREVIATIONS
bulldog, basset hound, beagle, whippet, • Biopsy/histopathology—definitive • COX2 = cyclooxygenase-2.
American Staffordshire terrier, Australian diagnosis. • DLE = discoid lupus erythematosus.
shepherd (nasal solar dermatitis). • Solar dermatitis—epidermal hyperplasia, • PE = pemphigus erythematosus.
• Cats—white cats. apoptotic keratinocytes, perivascular • SCC = squamous cell carcinoma.
inflammation, vascular dilatation, dermal • SLE = systemic lupus erythematosus.
SIGNS fibrosis and elastosis.
• Dogs—glabrous areas especially axillae, • Actinic keratosis—parakeratotic hyper-
Suggested Reading
flanks, ventral abdomen, lateral extremities. keratosis with epidermal atypia and solar Albanese F, Abramo F, Caporali C, et al.
• Cats—pinnae, nasal planum, dorsal muzzle, elastosis. Clinical outcome and cyclo-oxygenase-2
eyelids. • Hemangioma—proliferative blood-filled
expression in 5 dogs with solar dermatitis/
• Solar dermatitis—photodermatitis. vascular channels with minimal atypia or actinic keratosis treated with firocoxib. Vet
◦ Nasal—erythema and scaling at junction mitosis. Dermatol 2013, 24(6):606–e147.
of haired and hairless skin of nose; expands • Hemangiosarcoma—invasive proliferation
Burrows AK. Actinic dermatoses and sun
caudally followed by scarring. of atypical endothelial cells with areas of protection. In: Kirk’s Current Veterinary
◦ Truncal—erythema, scaling, and lichenifi- vascular space formation. Therapy XV. St. Louis, MO: Elsevier, 2014,
cation; gradual palpable thickening of white • SCC—invasion of dermis by keratinocytes;
pp. 480–482.
areas (adjacent dark areas are normal), keratin “pearls,” mitoses, atypia. Author Clarissa P. Souza
comedones; secondary deep pyoderma. • Solar-induced thermal burn—partial/full
• Actinic keratosis— premalignant epithelial thickness necrosis of the epidermis, adnexa, Resnick
dysplasia capable of becoming invasive dermis; coagulation necrosis. Acknowledgment The author acknowledges
squamous cell carcinomas (SCC); indurated, the prior contribution of Alexander H.
crusted, hyperkeratotic plaques. Werner Resnick.
• Hemangioma—well-circumscribed plaques
or nodules, firm to fluctuant, bluish to
purplish. TREATMENT
• Hemangiosarcoma—poorly circumscribed • Sun avoidance—keep indoors during day;
dermal dark red to purple, fluctuant nodules; avoid reflected sunlight; apply waterproof
may become large; commonly ulcerate and (>30 SPF) sunscreen (without zinc oxide
bleed; subcutaneous hemangiosarcomas and PABA); sun-protective clothing.
usually not solar induced. • Surgical excision of neoplastic lesions.
• SCC—proliferative and ulcerated plaques;
easily traumatized; secondary pyoderma
common; locally invasive and slow to metastasize.
• Solar-induced thermal burn (dorsal thermal
MEDICATIONS
necrosis)—alopecia, erythema, ulceration,
eschars/necrosis, and crusts on the dorsal DRUG(S) OF CHOICE
parts of the body; dogs with dark shorthair • Cyclooxygenase-2 (COX2) inhibitors—
coats at increased risk. overexpression by sun-damaged cells;
• Cutaneous horns—firm hornlike projec- inhibition of COX2 demonstrated improve-
tions, may originate from actinic keratoses, ment: firocoxib 5 mg/kg/day PO.
SCC, or other neoplasia; the base of a horn • Glucocorticoids—reduced inflammation
must be inspected for underlying cause. noted in acute cases; prednisolone 0.5–1 mg/
Dermatoses, Vesiculopustular
• Bacterial folliculitis usually secondary to a • Dermatophyte culture positive.
predisposing factor (e.g., demodicosis, • Secondary bacterial folliculitis common.
hypothyroidism, allergy, or corticosteroid • Skin biopsy—folliculitis with fungal
BASICS administration). elements. D
DEFINITION • UV light—pemphigus erythematosus,
bullous pemphigoid, SLE, DLE, and Sterile Eosinophilic Pustulosis
• Pustule—small (<1 cm), circumscribed
dermatomyositis. • Rare idiopathic dermatosis of dogs.
elevation of the epidermis filled with pus.
• Direct smears—numerous eosinophils,
• Vesicle—small (<1 cm), circumscribed
nondegenerate neutrophils, occasional
elevation of the epidermis filled with clear
acantholytic keratinocytes, and no bacteria.
fluid.
• Biopsy—eosinophilic intraepidermal
PATHOPHYSIOLOGY pustules, folliculitis, and furunculosis.
Pustules and vesicles—produced by edema,
DIAGNOSIS
• Direct immunofluorescence negative.
acantholysis (pemphigus), ballooning degenera- DIFFERENTIAL DIAGNOSIS • Rapid response to glucocorticosteroids.
tion (viral infections), proteolytic enzymes from Superficial Pyoderma Linear IgA Dermatosis
neutrophils (pyoderma), degeneration of basal • Most common cause. • Rare idiopathic dermatosis of dachshunds.
cells (lupus), or dermoepidermal separation • Readily responds to appropriate antibiotic • Tends to wax and wane.
(bullous pemphigoid). therapy if underlying cause is effectively managed. • Pustules—sterile and subcorneal.
SYSTEMS AFFECTED • Intact pustule—direct smear reveals • Direct immunofluorescence positive for IgA
Skin/exocrine. neutrophils engulfing bacteria; most often at basement membrane zone.
Staphylococcus pseudintermedius; biopsy
SIGNALMENT SLE
demonstrates intraepidermal neutrophilic
• Lupus—collies, Shetland sheepdogs, and • Multisystemic disease with variable clinical
pustules or folliculitis with bacteria.
German shepherd dogs may be predisposed. signs and cutaneous manifestations, including
• Pemphigus erythematosus—collies and Pemphigus Complex mucocutaneous ulceration.
German shepherd dogs may be predisposed. • Group of immune-mediated diseases • Direct immunofluorescence positive at the
• Pemphigus foliaceus—Akitas, chow chows, characterized histologically by disadhesion of basement membrane zone.
dachshunds, bearded collies, Labrador keratinocytes within the epidermis (acantho- • Antinuclear antibody (ANA) positive.
retrievers, Newfoundlands, Doberman lytic keratinocytes).
• Direct smears—many acantholytic
DLE
pinschers, and schipperkes may be predisposed.
• Affects only the skin; lesions usually
• Bullous pemphigoid—collies and keratinocytes, nondegenerate neutrophils,
eosinophils, and few to no bacteria. confined to the head.
Doberman pinschers may be predisposed.
• Depigmentation, erythema, and ulceration
• Dermatomyositis—young collies and • Culture of an intact pustule negative.
• Direct immunofluorescence—deposits in
of the nasal planum common.
Shetland sheepdogs.
• Skin biopsy—interface and lichenoid
• Subcorneal pustular dermatosis—schnau- the intercellular spaces of the epidermis in
approximately 50% of cases. dermatitis.
zers affected most frequently.
• Direct immunofluorescence positive at the
• Linear immunoglobulin (Ig) A dermato- • Tends to wax and wane irrespective of
antibiotic therapy; responds to immunosup- basement membrane zone.
sis—dachshunds exclusively; very rare.
• ANA negative.
• Dermatophytosis—young animals. pressive therapy.
• Pemphigus foliaceus and erythematosus— Bullous Pemphigoid
SIGNS
superficial acantholysis leading to erosions; • Ulcerative disorder of the skin and/or
N/A
face, pinnae, and footpads (foliaceus) mucous membranes.
CAUSES commonly affected; mucous membranes not • Skin biopsy—subepidermal cleft formation.
Pustules/Vesicles affected; biopsy: subcorneal acantholysis; • Direct immunofluorescence positive at the
• Superficial pyoderma—impetigo, superfi- interface and lichenoid inflammation with basement membrane zone.
cial spreading pyoderma, superficial bacterial pemphigus erythematosus. • No acantholysis.
folliculitis, canine or feline acne. • Pemphigus vulgaris—severe and deep form
• Pemphigus complex—pemphigus foliaceus, of pemphigus; characterized by erosions Dermatomyositis
pemphigus erythematosus, panepidermal rapidly leading to ulcerations of oral cavity, • Idiopathic inflammatory disease of the skin
pemphigus; pemphigus vulgaris produces mucocutaneous junctions, and skin; biopsy: and muscle of young collies and Shetland
deep clefts that rapidly erode into ulcers. suprabasal acantholysis and cleft formation. sheepdogs; seen rarely in adult animals.
• Subcorneal pustular dermatosis. • Direct immunofluorescence positive at the • Lesions affect the face, ear tips, tail tip, and
• Dermatophytosis. intercellular spaces of the deeper epidermis. pressure points of the extremities.
• Demodicosis. • Characterized by alopecia, crusting,
Subcorneal Pustular Dermatosis
• Sterile eosinophilic pustulosis. • Rare idiopathic pustular dermatosis of dogs.
pigmentation disturbances, erosions/
• Linear IgA dermatosis. • Tends to wax and wane.
ulceration, and scarring.
• Systemic lupus erythematosus (SLE). • Skin biopsy—follicular atrophy, perifolliculitis,
• Intact pustules—direct smears reveal
• Discoid lupus erythematosus (DLE). numerous neutrophils, no bacteria, and and hydropic degeneration of the basal cells.
• Bullous pemphigoid • Direct immunofluorescence negative.
occasional acantholytic keratinocytes; cultures
• Dermatomyositis. • Muscle biopsy and electromyography
negative.
• Cutaneous drug eruption. • Direct immunofluorescence negative.
(EMG)—evidence of inflammation.
• Epidermolysis bullosa. • Poor response to glucocorticosteroids and CBC/BIOCHEMISTRY/URINALYSIS
RISK FACTORS antibiotics. • Usually unremarkable.
• Drug exposure—SLE and bullous • SLE—possible anemia, thrombocytopenia,
Dermatophytosis
pemphigoid. • Common disease of both dogs and cats.
or glomerulonephritis.
Dermatoses, Vesiculopustular (continued)
• Eosinophilic pustular dermatosis—most • Sulfasalazine—10–20 mg/kg PO q8h until • Long-term sulfasalazine therapy—monitor

affected dogs have peripheral eosinophilia. remission; then as needed. tear production.
• Immunosuppressive therapy—monitor
D OTHER LABORATORY TESTS Linear IgA Dermatosis
every 1–2 weeks initially; then every 3–4
ANA titer—may be positive with SLE. • Prednisolone—2.2–4.4 mg/kg PO q24h until
remission; taper to alternate-day therapy. months during maintenance therapy.
• Dapsone—1 mg/kg PO q8h until
• Direct smear from intact pustule/vesicle.
• Culture of intact pustule/vesicle.
remission; taper and give as needed.
• Skin biopsy for histopathology. Sterile Eosinophilic Pustulosis
• Direct immunofluorescence, including IgA. Prednisolone—2.2–4.4 mg/kg PO q24h until MISCELLANEOUS
• EMG—fibrillation potentials (rapid, irregular, remission; then as needed to prevent relapses AGE-RELATED FACTORS
and unsynchronized contraction of muscle fibers) (usually long-term, alternate-day therapy N/A
and positive sharp waves in dermatomyositis. required).
ZOONOTIC POTENTIAL
• Muscle biopsy—myofibril degeneration,
PRECAUTIONS Dermatophytosis: may infect human beings
characterized by fragmentation, vacuolation,
in the household.
atrophy, fibrosis, and regeneration in dermato- Prednisolone
myositis. • Secondary infection. PREGNANCY/FERTILITY/BREEDING
• Iatrogenic Cushing’s syndrome. N/A
• Muscle wasting. SEE ALSO
• Steroid hepatopathy. • Acne—Cats.
TREATMENT • Behavioral changes. • Acne—Dogs.
• Polydipsia, polyuria. • Dermatomyositis.
APPROPRIATE HEALTH CARE • Polyphagia. • Dermatophytosis.
• Periodic bathing with an antimicrobial
Dapsone • Lupus Erythematosus, Cutaneous (Discoid).
shampoo—helps remove surface debris and • Lupus Erythematosus, Systemic (SLE).
control secondary bacterial folliculitis. • Dogs—mild anemia, mild leukopenia, and
mild elevation of alanine aminotransferase • Pemphigus.
• Usually treated as outpatient.
(ALT), not associated with clinical signs; • Pyoderma.
• SLE, pemphigus vulgaris, and bullous
pemphigoid may be life-threatening and usually return to normal when dosage is ABBREVIATIONS
require inpatient intensive care. reduced for maintenance. • ALT = alanine aminotransferase.
• Rare fatal thrombocytopenia or severe • ANA = antinuclear antibody.
leukopenia. • DLE = discoid lupus erythematosus.
• Occasional vomiting, diarrhea, or pruritic • EMG = electromyography.
skin eruption. • Ig = immunoglobulin.
MEDICATIONS • Cats—more susceptible to dapsone toxicity; • SLE = systemic lupus erythematosus.
DRUG(S) OF CHOICE hemolytic anemia and neurotoxicity reported. Suggested Reading
See specific disease chapters for more Sulfasalazine Helton Rhodes KA, Werner A. Blackwell’s
information. Keratoconjunctivitis sicca. Five-Minute Veterinary Consult Clinical
Bacterial Folliculitis Azathioprine and Chlorambucil Companion: Small Animal Dermatology,
• Empiric choices—cephalexin (22 mg/kg Potential for bone marrow suppression, number="3">3rd ed. Hoboken, NJ:
PO q12h); clindamycin (11 mg/kg PO gastrointestinal upset; azathioprine can cause Wiley-Blackwell, 2018.
q24h); amoxicillin–clavulanic acid (12.5– hepatotoxicity and possibly pancreatitis. Nuttall T, Eisenschenk M, Heinrich NA,
15 mg/kg PO q12h). Harvey RG. Skin Diseases of the Dog and
• Appropriate antibiotic choice based on Cyclosporine Cat, 3rd ed. London: CRC Press, 2018.
cultures from intact pustules. May cause vomiting and diarrhea, gingival Author Guillermina Manigot
hyperplasia, B-lymphocyte hyperplasia, hirsutism, Consulting Editor Alexander H. Werner Resnick
Pemphigus Complex/Bullous Pemphigoid papillomatous skin eruptions, and increased Acknowledgment The author and book
Immunosuppressive/combination therapy: incidence of infection; decreased glucose editors acknowledge the prior contribution of
• Corticosteroids—prednisolone 2.2–4.4 mg/ homeostasis; potential toxic reactions rare and Karen Helton Rhodes.
kg PO tapering dosage; see Pemphigus. include nephrotoxicity and hepatotoxicity.
• Azathioprine—2 mg/kg PO q48h to twice
weekly. POSSIBLE INTERACTIONS
N/A C
lient Education Handout
• Chlorambucil—2 mg/m2 PO q48h.
available online
• Tetracycline—250 mg <10 kg, 500 mg ALTERNATIVE DRUG(S)
>10 kg PO q8–12h. N/A
• Doxycycline—10 mg/kg PO q24h.
• Minocycline—5 mg/kg PO q12h with
niacinamide: 250 mg <10 kg, 500 mg >10 kg
PO q8–12h.
• Cyclosporine, modified—5 mg/kg PO q24h.
FOLLOW-UP
Subcorneal Pustular Dermatosis PATIENT MONITORING
• Dapsone—monitor hemogram, platelet
• Dapsone—1 mg/kg PO q8h until remission;
tapered to 1 mg/kg q24h or twice weekly. count, and ALT every 2 weeks initially and if
any clinical side effects develop.
Dermatoses, Viral (Non-Papillomatosis)

• Dogs—zinc deficiency syndromes,
hepatocutaneous syndrome, nasal hyper
keratosis. • Neoplasia—with extensive
BASICS crusting and ulceration; squamous cell FOLLOW-UP D
OVERVIEW carcinoma, mast cell tumor, epitheliotropic PATIENT MONITORING
• Dermatoses caused by viral infection within lymphoma. Varies based on viral infection and presence
keratinized structures. • Viral replication may CBC/BIOCHEMISTRY/URINALYSIS or absence of systemic involvement.
cause cytosuppressive effects or upregulate Nonspecific PREVENTION/AVOIDANCE
keratinization, resulting in hyperplastic or Prevent hunting behavior and exposure to
crusted conditions. OTHER LABORATORY TESTS
• Skin biopsy—necessary to prove viral origin potentially infectious materials and infected
SIGNALMENT of skin lesions; not always conclusive; if animals.
• Young to young adult dogs. • Cats of any age. considering herpesvirus dermatitis, inform EXPECTED COURSE
SIGNS pathologist of suspicion. • Virus isolation. AND PROGNOSIS
• Facial involvement or involvement of head • Serology—confirms FeLV, FIV, or other • Skin lesions may not respond to therapy.
is common. • Lesions often asymmetric in viral infection. • Systemic signs may eventually develop as
distribution. • Paws and/or foot pads may DIAGNOSTIC PROCEDURES result of viral infection. • Dependent on
be affected as well as mucocutaneous • Skin scrapings, trichograms—parasitic causal virus, animals may self-cure. • In cats,
junctions. • Acute or gradual onset; lesions infestations. • Dermatophyte culture—fungal papillomavirus infection may progress to
may be associated with bite wound or fight. infections. • Epidermal cytology—bacterial bowenoid in situ carcinoma.
• Variable pruritus; can progress to self- folliculitis. • Skin biopsy is definitive
mutilation. • Crusts. • Abscess. diagnostic test. • Immunohistochemical
• Paronychia. • Poor wound healing. staining for viral particles. • Viral serology
• Seborrhea. • Exfoliative dermatitis. and/or PCR.
• Cutaneous horns. • Gingivitis/stomatitis. MISCELLANEOUS
• Cutaneous or oral ulceration. • Nasodigital PATHOLOGIC FINDINGS
AGE-RELATED FACTORS
hyperkeratosis. • Pigmented macules or • Irregular hyperplasia. • Ballooning
Dependent on viral cause.
plaques. • Progression to bowenoid in situ degeneration. • Hydropic interface dermati-
tis. • Syncytial-type giant cell formation ZOONOTIC POTENTIAL
carcinoma (feline immunodeficiency virus
within epidermis and/or outer root sheath of Feline cowpox virus and contagious viral
[FIV], papillomavirus). • Multiple mast cell
hair follicle with associated apoptotic pustular dermatitis (parapoxvirus) can be
tumors (FIV). • Systemic signs of illness may
keratinocytes. • Keratinocyte inclusion transmitted to other dogs, humans, and
be present. • Signs consistent with upper
bodies. • Epidermal ulceration with dermal cats.
respiratory infection may or may not be
present prior to development of skin lesions. necrosis, necrosis of epitrichial sweat glands, SEE ALSO
neutrophilic and/or eosinophilic • Canine Distemper.
CAUSES & RISK FACTORS inflammation. • Feline Herpesvirus Infection.
• Feline leukemia virus (FeLV). • FIV.
• Feline Immunodeficiency Virus (FIV)
• Feline cowpox virus infection. • Feline
Infection.
infectious peritonitis. • Feline papillomavirus.
• Feline Leukemia Virus (FeLV) Infection.
• Canine papillomavirus. • Canine distem-
per. • Contagious viral pustular dermatitis TREATMENT ABBREVIATIONS
(orf [parapoxvirus]). • Pseudorabies • Usually outpatient, except for systemically • FeLV = feline leukemia virus.
(α-herpesvirus). • Feline rhinotracheitis ill patients. • Prevent exposure to other • FIV = feline immunodeficiency virus.
infection (α-herpesvirus-1). • Feline animals that could become infected.
Suggested Reading
calicivirus infection. • Fighting or hunting Helton Rhodes KA, Werner A. Blackwell’s
behavior, multiple animal households, Five-Minute Veterinary Consult Clinical
exposure to infected animals, and/or ingestion Companion: Small Animal Dermatology, 3rd
of infected material increases risk of exposure.
MEDICATIONS ed. Hoboken, NJ: Wiley-Blackwell, 2018.
Author Elizabeth R. Drake
DRUG(S) OF CHOICE Consulting Editor Alexander H. Werner
• Supportive care and treatment of
Resnick
secondary infections. • Cats—herpesvirus:
DIAGNOSIS L-lysine 200–500 mg/cat q12h (questionable
DIFFERENTIAL DIAGNOSIS efficacy); interferon-α 30 units/cat/day PO;
• Crusting diseases—drug eruption, actinic famcyclovir 125 mg q12h or 40–90mg/kg
keratoses, pemphigus foliaceus, systemic q12h, use of topical acyclovir reported.
lupus erythematosus, other causes for • Cats—bowenoid in situ carcinoma:
exfoliative dermatitis. • Allergic disorders— imiquimod. • Dogs—individual papillomas:
usually pruritic: atopy, fleas, food. • Feline surgical excision; imiquimod.
herpesvirus dermatitis lesions can mimic CONTRAINDICATIONS/POSSIBLE
lesions of eosinophilic granuloma complex.
• Parasitic diseases—canine and/or feline
INTERACTIONS
scabies, demodicosis, cheyletiellosis. Immunosuppressive therapies.
• Infectious diseases—superficial and deep
bacterial and fungal infections, leishmaniasis.
Destructive and Scratching Behavior—Cats

CBC/BIOCHEMISTRY/URINALYSIS Phobias, and Anxieties—Cats; Compulsive
Usually normal. Disorders—Cats.
D BASICS OTHER LABORATORY TESTS Pheromones and Nutraceuticals
As indicated to rule out medical conditions (T4). • Feline interdigital pheromone applied to
OVERVIEW scratching posts to encourage scratching. • F3 facial
• Behavior that causes damage to an owner’s IMAGING
As indicated to rule out medical conditions. pheromone, cat-appeasing pheromone, alpha-
home or belongings. • Primary destructive casozepine, and l-theanine may reduce anxiety.
behaviors are normal feline behaviors that occur DIAGNOSTIC PROCEDURES
during exploration and play; scratching may be For chewing/ingestive behavior, attention to
part of normal nail maintenance and communi- oral cavity and scoping if indicated to rule out
cation with visual and scent marks. • Secondary gastrointestinal causes. FOLLOW-UP
destructive behavior may be a sign of other
PATIENT MONITORING
behavioral conditions and disease states.
Weekly follow-up to support owners.
Systems Affected
TREATMENT PREVENTION/AVOIDANCE
• Gastrointestinal—damage to teeth;
• Destructive behavior is normal and self-reward-
vomiting, diarrhea, obstruction if items Treat underlying disease.
ing. • Frequency may be reduced through client
ingested. Primary Destructive Behavior education during the first well-care visit,
• Ingestion of toxic material could affect any • Keep claws trimmed. • Supervise/confine until regardless of the age of the patient. • Provide
organ system. appropriate behavior patterns have been information on suitable outlets for scratching,
SIGNALMENT established; provide food, litter, toys, and chewing, exploration, play, and enrichment.
• Any breed or gender; may be genetic basis scratching posts in confinement area. • Prevent
access to potential targets. • Provide acceptable POSSIBLE COMPLICATIONS
for sucking or chewing fabric in Siamese,
• Owners become frustrated, resulting in
Burmese, and Birman. • Primary destructive scratching substrate such as sisal, cardboard, and
loosely woven carpet in locations and orientation declawing or relinquishment. • Punishment can
behavior is more common in young cats.
(horizontal or vertical) based on cat’s preference. trigger fear or aggression. • Obstruction due to
SIGNS foreign body, including string foreign body.
• Apply feline interdigital pheromone to
Primary Destructive Behavior scratching posts. • Provide climbing towers, EXPECTED COURSE AND PROGNOSIS
• No specific environmental trigger. interactive play, feeding stations at different levels, • Resolution of normal exploratory behavior
• Common targets for scratching are food-dispensing toys, and multiple small meals. usually within weeks. • Anxiety-based
furniture, door frames, carpet, speakers. • Reward appropriate behavior. • Reduce appeal conditions and compulsive disorders often
• Curtains and furniture may be damaged of target areas and objects—e.g., double-sided require long-term management, including
when cats climb to explore or play. • May sticky tape. • Provide indoor grass gardens. psychotropic medication.
chew houseplants. • Items resembling string, • Declawing is banned in a number of countries
including thread, shoelaces, and rubber and jurisdictions for ethical and humane reasons;
bands, are often chewed and ingested; small where still legally permissible it should be a last
items that are batted about may be acciden- resort after owners have been counseled on all MISCELLANEOUS
tally swallowed. alternative options. • While behavior modifica-
tion is being implemented, plastic claw covers AGE-RELATED FACTORS
Secondary Destructive Behavior Rule out medical conditions in adult onset.
• Attention-seeking—destructive behavior in may be applied to prevent further damage.
presence of owner. • Separation-related Secondary Destructive Behavior PREGNANCY/FERTILITY/BREEDING
distress—destructive behavior in absence of the • Attention-seeking behavior—provide Preparturient destructive behavior (nesting).
owner. • Compulsive behavior—licking, owner-initiated interactions. • Separation- SEE ALSO
chewing, sucking, or ingesting nonfood items. related distress—provide opportunities for • Compulsive Disorders—Cats.
• Scratching may occur secondary to household independent play and exploration. • Fears, Phobias, and Anxieties—Cats.
conflict. • Compulsive disorder—identify and reduce • Kitten Behavior Problems.
CAUSES & RISK FACTORS sources of anxiety; offer appropriate outlets INTERNET RESOURCES
• Lack of suitable outlets for scratching, climbing, for play, chewing, and food-filled toys; some • https://fearfreehappyhomes.com/category/
perching, play, and resting. • Inadequate cats will chew rawhide; prevent access to explore/exercise-enrichment • https://catvets.
supervision, particularly in young cats. target items. • Reduce household conflict. com/guidelines/practice-guidelines/
environmental- needs-guidelines • https://
indoorpet.osu.edu/cats
Suggested Reading
MEDICATIONS Heath S. Canine and feline enrichment in the home
DIAGNOSIS DRUG(S) OF CHOICE and kennel: a guide for practitioners. Vet Clin
DIFFERENTIAL DIAGNOSIS • Medication is not indicated for primary North Am Small Anim Pract 2014, 44:427–449.
• Rule out medical conditions, especially if onset destructive or attention-seeking behaviors. Landsberg G, Hunthausen W, Ackerman L.
in mature cat. • Conditions affecting digestion, • Medication may be indicated in combina- Behavior Problems of the Dog and Cat, 3rd
absorption, and appetite, including recent diet tion with behavior management and ed. Philadelphia, PA: Elsevier Saunders, 2013.
change. • Gastrointestinal disease and medical modification for anxiety-based conditions Author Ellen M. Lindell
conditions associated with pain or anxiety. and compulsive disorders. • See Fear, Consulting Editor Gary M. Landsberg
Destructive Behavior—Dogs
SIGNS • Cognitive dysfunction syndrome—
• Destructive behavior is a clinical sign rather destructive behavior related to agitation,
than a diagnosis. anxiety, and abnormal repetitive behaviors
BASICS • Dogs may use their teeth or claws to damage with onset or progression in patients 7 years D
DEFINITION floors, furniture, walls, or frames of doors and or older; other signs of cognitive dysfunction
• Behavior that causes damage to an owner’s windows or dig at fencing. Some dogs chew or are typically present.
home, property, or belongings. even ingest small personal items. CBC/BIOCHEMISTRY/URINALYSIS
• Primary destructive behavior is normal • Clients may ascribe the underlying motiv- No pathology expected.
behavior that includes exploratory and play- ation to spite or suggest a diagnosis such as
based behavior. separation anxiety. Though barriers are often OTHER LABORATORY TESTS
• Secondary destructive behavior is a clinical targeted in association with separation-related As indicated to rule out medical conditions.
sign of another behavior condition. distress or territorial behavior, no focus of DIAGNOSTIC PROCEDURES
damage is pathognomonic. As indicated to rule out medical conditions.
PATHOPHYSIOLOGY
• Knowledge of the contexts in which
• Dogs normally explore and engage with PATHOLOGIC FINDINGS
destructive behavior occurs is critical for
their environment. When access to appropri- N/A except lesions secondary to self-trauma.
diagnosis.
ate outlets and enrichment is not readily
• Physical examination findings—fractured
available and in the absence of supervision and
teeth; excoriations on nose; broken front
guidance, owner’s property may be targeted.
claws; digital pain.
• Insufficient opportunities for social
interactions can contribute to destructive CAUSES TREATMENT
behavior. • Primary destructive behavior: APPROPRIATE HEALTH CARE
• Dogs may dig for comfort or cooling, and ◦ Inadequate supervision provides access to • Traumatic injuries are typically minor and
to escape confinement. Digging can be self-rewarding behavior. can be managed with outpatient care.
triggered by sounds of burrowed animals and ◦ Lack of access to preferred chewable and/ Traumatic dental injuries and GI foreign
scents of food sources. or interactive toys. bodies may require surgical intervention.
• Though manipulating the environment ◦ Insufficient cognitive enrichment. • Behavioral treatment protocols include
results in property damage, it may be self- ◦ Inadequate social enrichment. behavior modification to address frustration
rewarding and self-soothing. • Secondary destructive behavior: or anxiety; determination of safe methods for
• Conditions causing distress, including pain, ◦ Confinement in presence of an inciting supervision, confinement; and customized
fear, anxiety, and frustration, can contribute trigger. enrichment protocol based on patient
to destructive behavior. ◦ Confinement frustration. preferences and owner lifestyle.
◦ Separation-related distress—inadequate • All toys carry a potential risk of injury to
SYSTEMS AFFECTED
habituation to absence of owner. the patient, including inadvertent ingestion
• Behavioral—frustration or anxiety.
◦ Noise phobia. and dental injury.
• Gastrointestinal (GI)—damage to teeth or
◦ Territorial behavior. • Environmental management:
oral mucosa; pharyngitis or esophagitis;
◦ Unintentional reinforcement by owner. ◦ Prevent or supervise access to potential
vomiting, diarrhea, or obstruction if ingested.
◦ Medical conditions associated with pain. targets of destruction.
• Musculoskeletal—trauma caused by
RISK FACTORS ◦ Provide thermoregulation options (kiddie
scratching, chewing, or digging.
• Skin—excoriation, nail damage secondary Early environmental experiences including prior pool, dog house) to reduce digging.
emotional trauma are risk factors for develop- • Behavior modification may include:
to trauma.
ment of fear and anxiety-related conditions. ◦ Providing for and reinforcing alternative
• Ingestion of toxic material could affect any
organ system. desirable activities and outlets.
◦ Relaxation exercises to reduce inadvertent
GENETICS reinforcement of undesirable behavior.
None ◦ Habituation to crate or gate confinement.
INCIDENCE/PREVALENCE DIAGNOSIS • Environmental enrichment:
Normal canine behavior—problem reported DIFFERENTIAL DIAGNOSIS ◦ Preference testing of appropriate toys and
by approximately 12% of owners. • Pathologic conditions—index of suspicion chew items.
for underlying medical condition should be ◦ Provide acceptable substrate and location
GEOGRAPHIC DISTRIBUTION for digging—treats and toys can be buried
None high in adult patients with sudden onset of
destructive behavior in absence of notable to encourage digging in area.
SIGNALMENT environmental changes. • Design a schedule for provision of exercise,
• Species—dog. • GI disease—if pica accompanies destructive cognitive enrichment, social enrichment, and
• Breed predilections—certain breeds are by chewing: rule out conditions affecting reward-based training.
nature more active and, if insufficient outlets digestion, absorption, and polyphagia, • Design a behavioral log to record progress
for exploratory and/or social engagement, including recent diet changes that can affect and preferences.
may engage in destructive behavior. Northern satiety; licking of surfaces such as floors, NURSING CARE
breeds may dig for resting and thermoregula- carpet, and nonfood items may be associated Behavioral appointments can be scheduled
tion. Some terrier and hound breeds may dig with upper GI disease. with veterinarian or trained nursing staff.
when burrowing for prey. • Separation-related distress.
• Mean age and range—primary destructive • Noise phobia, storm phobia—distress in
ACTIVITY
behavior most often seen in puppies and • Aerobic exercise schedule should consider
response to stimulus.
young dogs; secondary destructive behavior • Territorial behavior—destructive behavior
the patient’s physical health. Healthy dogs
seen at any age. related to presence of triggers; window frames may benefit from two half-hour exercise
• Predominant sex—N/A. and doorways are damaged. sessions each day.
Destructive Behavior—Dogs (continued)
• Cognitive stimulation may be provided • Medication complements behavior POSSIBLE COMPLICATIONS

with reward-based training and food modification and may provide more rapid Without adequate support, owners may
puzzles. resolution when treating anxiety-based become frustrated, resulting in relinquish-
D • Provide opportunities for dogs to engage conditions. ment of the dog. Owners may seek advice
in breed-typical normal behaviors, including Selective Serotonin Reuptake Inhibitors from individuals offering “quick fixes” that
sniffing and “hunting” (tracking, nosework). could ultimately jeopardize the patient.
(SSRIs)
DIET Fluoxetine—0.5–2 mg/kg PO q24h. XPECTED COURSE AND PROGNOSIS
E
• Some patients benefit from feeding via Prognosis is excellent. Resolution of normal
puzzles and food-stuffed toys. Tricyclic Antidepressants (TCAs) exploratory behavior is usually rapid.
• Food toys may not be appropriate for pets Clomipramine—1–3 mg/kg PO q12h.
that exhibit possessive or food-related For Situational Anxiety (Alone or
aggression. Together with SSRI or TCA)
CLIENT EDUCATION • Alprazolam—0.01–0.1 mg/kg PO prior to MISCELLANEOUS
• Clients should take an active role in event.
• Trazodone—3–10 mg/kg PO prior to event. ASSOCIATED CONDITIONS
managing destructive behavior.
• Clonidine—0.01–0.05 mg/kg PO prior to Destructive behavior is often associated with
• Preadoption counseling provides an
event. attention-seeking behavior.
opportunity to educate clients regarding
providing for pets’ needs, including social CONTRAINDICATIONS AGE-RELATED FACTORS
and exploratory play and safe toys. TCAs—contraindicated in animals with Young dogs are at increased risk for normal
• Provide a plan for supervision and cardiac conduction disturbances or glaucoma. destructive behavior.
enrichment. ZOONOTIC POTENTIAL
• Teach clients to communicate expectations PRECAUTIONS
Benzodiazepines may disinhibit aggression— None
by reinforcing desired behaviors and
preventing access to undesirable behaviors, use with caution in dogs with a history of PREGNANCY/FERTILITY/BREEDING
including dog proofing and confinement aggressive behavior. Preparturient destructive behavior (nesting).
training. POSSIBLE INTERACTIONS SEE ALSO
• Provide references for local trainers who • SSRIs, TCAs, and trazodone should not be • Cognitive Dysfunction Syndrome.
support positive reinforcement rather than used with monoamine oxidase inhibitors, • Marking, Roaming, and Mounting
confrontation. including amitraz and selegiline. Behavior—Dogs.
• Combining drugs that increase serotonin • Puppy Behavior Problems.
Aversive Products and Punishment
• Application of nontoxic bitter-tasting
(e.g., SSRI or TCA with trazodone) should be • Separation Anxiety Syndrome.
products to targeted objects is sometimes done with caution to avoid serotonin • Thunderstorm and Noise Phobias.
used to manage primary destructive behavior syndrome. • Unruly Behaviors: Jumping, Pulling,
in conjunction with supervision. ALTERNATIVE DRUGS Chasing, Stealing—Dogs.
• It is essential that, upon discovering an Dog-appeasing pheromone, nutraceuticals ABBREVIATIONS
unpleasant taste, the dog has immediate containing L-theanine or alpha-casozepine, or • GI = gastrointestinal.
access to an appropriate item; it is more a calming probiotic may be used to reduce • SSRI = selective serotonin reuptake inhibitor.
effective and appropriate to supervise and mild anxiety. The safety margin is wide. • TCA = tricyclic antidepressant.
quietly guide dogs toward appropriate items.
INTERNET RESOURCES
• Punishment is not an accepted tool for
• fearfreehappyhomes.com
managing destructive behavior; it does not
• https://indoorpet.osu.edu/dogs/
address the underlying motivation and can
lead to fear, anxiety, or aggression.
FOLLOW-UP environmental_enrichment_dogs
PATIENT MONITORING Suggested Reading
Weekly calls to confirm compliance and Heath S. Canine and feline enrichment in the
N/A
adjust enrichment based on patient prefer- home and kennel: a guide for practitioners.
ences. Most patients benefit from one-on-one Vet Clin North Am Small Anim Pract 2014,
behavior modification sessions every 2 weeks. 44:427–449.
PREVENTION/AVOIDANCE Horwitz D, ed. Blackwell’s 5 Minute Consult
MEDICATIONS Client education during the first visit, Clinical Companion: Canine and Feline
DRUG(S) OF CHOICE regardless of the age of the patient. Provide Behavior, 2nd ed. Hoboken, NJ: Wiley,
• Medication is not indicated for treating information on suitable outlets for chewing, 2018, pp. 745–753, 767–773.
primary destructive behaviors or attention- digging, exercise, reward training, and the Author Ellen M. Lindell
seeking behavior. importance of both cognitive and social Consulting Editor Gary M. Landsberg
enrichment.
Diabetes Insipidus
Pyometra is a surgical emergency and should
be removed as soon as the patient is
BASICS DIAGNOSIS stabilized. D
DEFINITION DIFFERENTIAL DIAGNOSIS
Diabetes insipidus (DI) is a disorder of water Polyuric Disorders
metabolism characterized by polyuria (PU), • Hyperadrenocorticism.
urine of low specific gravity or osmolality • Diabetes mellitus. MEDICATIONS
(so-called insipid, or tasteless, urine), and • Renal disease.
polydipsia (PD). DRUG(S) OF CHOICE
• Hyperthyroidism—cats. • CDI—DDAVP (1–2 drops of intranasal
PATHOPHYSIOLOGY • Hyperadrenocorticism. preparation in conjunctival sac q12–24h to
• Central DI (CDI)—deficiency in the • Liver disease—portosystemic shunt. control PU/PD); alternatively, intranasal
secretion of antidiuretic hormone (ADH). • Pyometra. preparation may be given SC (2–5 μg,
• Nephrogenic DI (NDI)—renal insensitivity • Pyelonephritis. q12–24h). Oral preparation of DDAVP is
to ADH. • Hypercalcemia. available in 0.1–0.2 mg tablets, with each
• Primary PD. 0.1 mg comparable to 1 large drop of
SYSTEMS AFFECTED
• Endocrine/metabolic. CBC/BIOCHEMISTRY/URINALYSIS intranasal preparation.
• Renal/urologic. • Usually normal; hypernatremia in patients • NDI—hydrochlorothiazide (2–4 mg/kg
with excessive free water loss. PO q12h), in addition to treatment of any
INCIDENCE/PREVALENCE • Urinary specific gravity low (<1.006, underlying cause.
• Primary CDI—rare. hyposthenuria).
• Primary NDI—rare.
CONTRAINDICATIONS
OTHER LABORATORY TESTS None
SIGNALMENT Plasma ADH (not commercially available). PRECAUTIONS
Species IMAGING Overdose of DDAVP can cause water
Dog and cat. • MRI or CT scan if pituitary tumor is intoxication.
Breed Predilections suspected.
• Abdominal radiographs or ultrasound may
None
help rule out other polyuric disorders.
Mean Age and Range
• Congenital forms <1 year.
DIAGNOSTIC PROCEDURES FOLLOW-UP
• ADH supplementation trial—preferred to
• Acquired forms, any age. PATIENT MONITORING
water deprivation test; therapeutic trial with
• Adjust treatment according to patient’s
SIGNS synthetic ADH (desmopressin [DDAVP]);
signs; ideal dosage and frequency of DDAVP
• PU. positive response (water intake decreases by
administration based on water intake.
• PD. 50% in 5–7 days).
• Laboratory tests such as PCV, total solids,
• Incontinence—occasional. • Modified water deprivation test (see
and serum sodium concentration, and patient
• Signs of intracranial mass if due to pituitary Appendix II for protocol)—not routinely
weight to detect dehydration (inadequate
tumor. recommended due to risk of complications.
DDAVP replacement).
• Dehydration and weakness in animals with • Rule out all other causes of PU/PD before
uncompensated free water loss. considering primary CDI. PREVENTION/AVOIDANCE
Circumstances that might increase water loss.
CAUSES PATHOLOGIC FINDINGS
Degeneration and death of neurosecretory POSSIBLE COMPLICATIONS
Inadequate Secretion of ADH neurons in neurohypophysis (primary CDI). Anticipate complications of primary disease
• Congenital defect. (e.g., pituitary tumor).
• Idiopathic.
• Trauma. EXPECTED COURSE AND PROGNOSIS
• Neoplasia. • CDI usually permanent, except in patients
TREATMENT in which condition was trauma induced.
Renal Insensitivity to ADH • NDI usually resolves with treatment of
• Congenital—defect in aquaporin (renal APPROPRIATE HEALTH CARE underlying disorder.
tubular channel that allows free water • Patients should be hospitalized for modified • Prognosis generally good, depending on
reabsorption). water deprivation test; the ADH trial is often underlying disorder.
• Secondary to drugs (e.g., lithium, performed as an outpatient procedure. • Without treatment, dehydration can lead to
demeclocycline). • Animals with NDI should have underlying stupor, coma, and death.
• Secondary to endocrine and metabolic disease diagnosed and treated.
disorders (e.g., hyperadrenocorticism, ACTIVITY
hyponatremia, hypercalcemia). Not restricted.
• Secondary to renal disease or infection (e.g.,
pyelonephritis, chronic kidney disease,
DIET MISCELLANEOUS
Normal, with free access to water.
pyometra). AGE-RELATED FACTORS
CLIENT EDUCATION • Congenital CDI and NDI usually manifest
• Review dosage of DDAVP and admini before 6 months of age.
stration technique. • CDI related to pituitary tumors usually
• Importance of having water available at all seen in dogs >5 years old.
times.
Diabetes Insipidus (continued)
SYNONYMS • DI = diabetes insipidus. Author Patty A. Lathan

• Cranial diabetes insipidus. • NDI = nephrogenic diabetes insipidus. Consulting Editor Patty A. Lathan
• ADH-responsive diabetes insipidus. • PD = polydipsia. Acknowledgment The author and book
D • PU = polyuria. editors acknowledge the prior contribution
SEE ALSO
Hyposthenuria Suggested Reading of Rhett Nichols.
ABBREVIATIONS Feldman EC, Nelson RW, Reusch CE,

• ADH = antidiuretic hormone.
Scott-Moncrieff JCR. Canine and Feline
• CDI = central diabetes insipidus.
Endocrinology, 4th ed. Philadelphia, PA:
available online
Saunders, 2015.
Diabetes Mellitus With Hyperosmolar Hyperglycemic State
SIGNALMENT • Myxedema coma—manifestation of severe

Species hypothyroidism with similar clinical signs
without hyperosmolarity or hyperglycemia;
BASICS Dog and cat (more frequent).
low total thyroxine and elevated thyroid- D
DEFINITION Breed Predilections stimulating hormone present.
• The hyperosmolar hyperglycemic state N/A
(HHS) is a complicated form of diabetes Mean Age and Range • Hyperglycemia—blood glucose concen
mellitus (DM) characterized by severe hyper- Most common in middle-aged dogs (mean 9 tration frequently exceeds 600 mg/dL and
glycemia and dehydration that produces a years) and cats (mean 12 years). severe hyperglycemia (1500–2000+ mg/dL)
marked elevation in serum osmolarity. Unlike exists in some patients. • Azotemia—elevated
Predominant Sex
diabetic ketoacidosis (DKA), ketone production blood urea nitrogen (BUN) and serum
N/A
and metabolic acidosis are not major features of creatinine concentrations are common, usually
HHS. • Specific guidelines for HHS diagnosis SIGNS prerenal, but renal azotemia occurs in some
are lacking in dogs and cats, but serum effective Historical Findings patients. • Sodium—hypo- or hypernatremia
osmolarity >320 mOsm/L, glucose • All patients have DM; in some, diagnosis of may be observed; hyperosmolarity is most
concentration >600 mg/dL, and bicarbonate DM occurs prior to HHS. • Some patients severe with concurrent hyperglycemia and
concentration >18 mEq/L, along with minimal have concurrent chronic illness. • Signs hypernatremia. • Potassium—hypokalemia is
ketonuria, are criteria in humans. caused by DM—may not be appreciated after common; hyperkalemia is associated with
PATHOPHYSIOLOGY HHS onset: ◦ Polydipsia. ◦ Polyuria. acute kidney injury or reduced urine output.
• Hyperglycemia is due to insulin deficiency ◦ Polyphagia. ◦ Weight loss. • Signs caused • Acidosis—metabolic acidosis is less severe
from DM; insulinopenia reduces tissue glucose by HHS: ◦ Weakness/lethargy. ◦ Vomiting. than DKA; hypobicarbonemia and
utilization and increases hepatic glucose ◦ Reduced appetite. ◦ Neurologic complaints— hyperlactatemia occur secondary to
production, leading to increased extracellular abnormal responsiveness, coma. hypovolemia or renal failure. • Glucosuria—
glucose concentrations; the magnitude of Physical Examination Findings present; mild ketonuria possible. • Urine
hyperglycemia in HHS is usually greater than • Findings associated with dehydration and
specific gravity (USG) variable; may be
in DKA. • Hyperosmolarity develops hypovolemia: ◦ Decreased skin turgor. misleading due to glucosuria, which increases
secondary to hyperglycemia and is exacerbated ◦ Prolonged capillary refill time. ◦ Reduced
USG.
by dehydration and reduced extracellular fluid pulse pressure. ◦ Tachycardia. ◦ Hypothermia. OTHER LABORATORY TESTS
volume; the contribution of glucose to total • Findings associated with hyperosmolarity: • Blood and urine osmolarity—serum
plasma osmolarity is significant in HHS. ◦ Lethargy, depressed mentation, stupor, or osmolarity >320 mosm/L consistent with
• Dehydration and volume deficit are typically coma. ◦ Seizure. • Findings associated with DM: HHS; urine osmolality elevated due to
severe and are caused by several factors, ◦ Low body condition score. ◦ Cataracts (dogs). glucosuria. • Serum osmolarity can be
including reduced water intake and volume estimated from routine serum chemistry results:
losses via gastrointestinal and renal systems. CAUSES
• Develops in patients with DM and severe
2 ([Na+]+[K+]) + [BUN]/2.8 + [Glucose]/18; if
• Reduced plasma volume decreases results are in IU, equation is modified: 2
glomerular filtration rate and urine dehydration/volume loss. • Reduced water
intake may precede onset of HHS. ([Na+]+[K+]) + [BUN] + [Glucose].
production, leading to azotemia; in HHS,
severe volume contraction with reduced • Comorbid conditions common. IMAGING
urinary glucose excretion results in severe RISK FACTORS N/A
hyperglycemia and plasma hyperosmolarity. Risk for HHS may be higher in diabetic DIAGNOSTIC PROCEDURES
• Hyperketonemia and ketonuria are not animals with concurrent disorders, including N/A
major features of HHS; lactic acidosis heart disease, renal insufficiency, hyperadren- PATHOLOGIC FINDINGS
secondary to volume depletion, tissue ocorticism, acute pancreatitis, and neoplasia. • Pancreas—consistent with DM: islet
hypoperfusion, and impaired glucose
atrophy and loss (dogs and cats) and islet
metabolism is the major cause of acidosis in
amyloid (cats). • Brain—changes not specific
patients with HHS.
for HHS; evidence of CNS edema.
SYSTEMS AFFECTED DIAGNOSIS
• Endocrine. • Renal/urologic—prerenal
azotemia due to decreased extracellular fluid DIFFERENTIAL DIAGNOSIS
• DM—may be uncomplicated to complicated,
volume; urine production usually maintained
by glucose-induced diuresis unless volume including DKA and HHS; all have similar TREATMENT
deficit is severe or acute kidney injury is clinical signs and laboratory findings, but can APPROPRIATE HEALTH CARE
present. • Cardiovascular—hypovolemia; be subcategorized based on magnitude of Life-threatening medical emergency
metabolic acidosis and electrolyte abnormalities hyperglycemia and hyperketonemia. requiring inpatient treatment. After HHS
• Hypernatremia—severe hypernatremia resolution, patients require treatment and
may contribute to hypotension and poor
myocardial contractility. • Nervous— produces CNS signs similar to HHS, but follow-up for DM.
hyperosmolarity promotes intracellular with sodium as major osmole; polyuria and
polydipsia may be present, particularly if NURSING CARE
dehydration and neuronal dysfunction. • Correction of fluid deficits—major
hypernatremia develops secondary to diabetes
GENETICS insipidus. • Hyperosmolarity of any cause— treatment goal, begin prior to insulin
N/A may produce similar CNS abnormalities; toxins replacement; IV fluid replacement indicated
INCIDENCE/PREVALENCE (e.g., ethylene glycol or alcohol) or CNS for ill patients; enteral water can assist with free
Uncommon lesions (e.g., causing adipsia) may cause water replacement in patients that tolerate oral
hyperosmolarity. • CNS disease—primary intake. • Fluid type and rate depend on
GEOGRAPHIC DISTRIBUTION CNS disorders may produce clinical signs of patient’s hydration and volume status and
N/A HHS; marked fluid deficits are not expected. magnitude of metabolic derangements; fluid
Diabetes Mellitus With Hyperosmolar Hyperglycemic State (continued)
deficit is estimated using the equation: kg/24h (some protocols recommend 1.1 U/ POSSIBLE COMPLICATIONS
%volume depletion * body weight(kg) = fluid kg/24h dose in cats) added to 250 mL of 0.9% • Hypoglycemia or electrolyte disturbances
deficit (L). • Hypo- and normonatremic NaCl; prior to beginning CRI, 50 mL of may develop during treatment. • Severe
D patients—isotonic crystalloid solution is solution should pass through plastic neurologic signs, including coma and death,
appropriate for initial volume replacement; administration tubing and be discarded may occur. • Dehydration and shock can
replacement of volume deficit should occur (insulin binds to some plastics); CRI started at precipitate acute kidney injury. • Death due to
over 12–24h; patients with hypotension or 5 mL/h (cat) or 10 mL/h (dog) and infusion shock or coma may occur in untreated animals.
shock due to hypovolemia should receive fluid rate adjusted as needed to reduce hyperglycemia EXPECTED COURSE AND PROGNOSIS
bolus of 20–25% of estimated blood volume at desired rate and maintain target glucose • Hydration and blood pressure should improve
(dog: 80 mL/kg; cat: 50 ml/kg), which can be concentration. • Once HHS is resolved and within a few hours of initiating fluid therapy and
repeated until blood pressure is adequate; once patient stable, discontinue insulin CRI and resolve over 12–24h; hyperglycemia is corrected
blood pressure is restored, the remaining deficit transition to longer-acting insulin to be used over 6–12h once insulin therapy started.
is replaced over 12–24h. • Hypernatremic for chronic DM management. • Electrolyte derangements must be managed to
patients—hypernatremia implies a free water CONTRAINDICATIONS avoid osmotic complications secondary to
deficit and its occurrence with hyperglycemia N/A sodium fluctuations, and to avoid hypo-/
in HHS may result in life-threatening hyperkalemia, hypophosphatemia, or hypo
hyperosmolarity; isotonic (0.9%) saline PRECAUTIONS
• Brain edema may occur when hyperosmolarity magnesemia. • Depending on patient response,
solution appropriate for initial volume prognosis is guarded; worse if severe neurologic
replacement in hypernatremic patients with is corrected too rapidly; patients with edema
develop worsening neurologic status during compromise or renal failure is present.
hypovolemic hypotension; if hypernatremia
persists after blood pressure and urine output treatment; minimizing rapid decreases in glucose
are restored, use of hypotonic (0.45%) saline and sodium during treatment lowers edema risk.
solution indicated to replace free water and • Insulin administration can result in hypokalemia;
reduce sodium, unless oral water intake electrolytes should be monitored frequently MISCELLANEOUS
possible; recommended that serum sodium (q4–6h) until stable.
concentration reduction should not exceed POSSIBLE INTERACTIONS • DKA and HHS have significant overlap in
12 mEq/day (see Hypernatremia). • Electrolyte N/A clinical signs and laboratory abnormalities.
replacement—potassium deficiency is • Patients with HHS should be evaluated for
expected, and should be replaced unless ALTERNATIVE DRUG(S)
• Ultrashort-acting insulins (insulin aspart or concurrent conditions (cardiac or renal
hyperkalemia is present; dosage based on failure, pancreatitis, neoplasia, etc.).
magnitude of hypokalemia; potassium insulin lispro) may be substituted for regular
replacement by IV infusion should not exceed insulin in CRI protocols. • Protocol for SYNONYMS
0.5 mEq K+/kg/h and fluids with supplemented intermittent IM use of regular insulin (when • Diabetic coma. • Hyperosmolar nonketotic
K+ should be avoided during rapid volume CRI not available)—0.2 U/kg IM initially, syndrome.
infusion; supplementation of other electrolytes followed by 0.1 U/kg IM q1h until glucose
SEE ALSO
(e.g., magnesium, phosphorous) may also be <250 mg/dL; subsequent doses 0.5–1.0 U/kg
• Diabetes Mellitus With Ketoacidosis.
necessary. • Glucose supplementation—some IM q4–6h to maintain glucose concentration
• Diabetes Mellitus Without Complication—
protocols recommend using dextrose infusion between 150 and 250 mg/dL.
Cats. • Diabetes Mellitus Without
to prevent hypoglycemia during insulin Complication—Dogs. • Hyperglycemia.
therapy; 2.5–5% dextrose CRI used as needed • Hyperosmolarity.
to maintain blood glucose concentrations
ABBREVIATIONS
between 150 and 250 mg/dL. FOLLOW-UP • BUN = blood urea nitrogen. • DKA =
ACTIVITY PATIENT MONITORING diabetic ketoacidosis. • DM = diabetes mellitus.
N/A • Volume and hydration status—monitor • HHS = hyperosmolar hyperglycemic state.
DIET heart rate, pulse quality, capillary refill time, • USG = urine specific gravity.
N/A blood pressure, bodyweight, and urine Suggested Reading
output. • Blood glucose—monitor q1–2h to Koenig A, Drobatz KJ, Beale AB, King LG.
CLIENT EDUCATION guide insulin therapy; aim for gradual
• Patients frequently have a serious concurrent Hyperglycemic, hyperosmolar syndrome in
reduction of serum glucose (50–100 mg/ feline diabetics: 17 cases (1995–2001). J Vet
disorder(s) that affects prognosis. • Permanent dL/h) to 150–250 mg/dL without hypo
DM is expected and survivors will require Emerg Crit Care 2004, 14:30–40.
glycemia. • Monitor serum Na+ and K+ O’Brien MA. Diabetic emergencies in small
lifelong treatment for DM. concentrations, especially during correction animals. Vet Clin North Am Small Anim
SURGICAL CONSIDERATIONS of hypernatremia or K+ supplementation; Pract 2010, 40:317–333.
N/A magnesium and phosphorous should be Rand JS. Diabetic ketoacidosis and hyperos-
monitored, especially after start of insulin mola hyperglycemia in cats. Vet Clin North
therapy. • After stabilization, long-term Am Small Anim Pract 2013, 43:367–379.
monitoring appropriate for DM is indicated. Trotman, TK, Drobatz KJ, Hess RS.
MEDICATIONS PREVENTION/AVOIDANCE Retrospective evaluation of hyperosmolar
• Adequate insulin therapy and monitoring hyperglycemia in 66 dogs (1993–2008). J
DRUG(S) OF CHOICE of glycemia in patients with DM may reduce Vet Emerg Crit Care 2013, 23:557–564.
• CRI of regular insulin is recommended for risk of HHS. • Early recognition and Author Thomas Schermerhorn
initial glucose control; insulin therapy should effective treatment of new-onset DM may Consulting Editor Patty A. Lathan
be started 2–6h after starting fluid therapy so reduce risk of DKA or HHS. Acknowledgment The author and book
initial decrease in serum glucose is not extreme. editors acknowledge the prior contribution of
• CRI preparation—regular insulin at 2.2 U/
Deborah S. Greco.
Diabetes Mellitus With Ketoacidosis

• Unkempt haircoat. • ECG and blood pressure monitoring
• Thin body condition. indicated for patients with shock or
• Ketone odor on breath. electrolyte abnormalities.
BASICS • Icterus. D
PATHOLOGIC FINDINGS
DEFINITION • Dandruff.
Pancreatic islet cell atrophy.
A medical emergency secondary to absolute or CAUSES
relative insulin deficiency, characterized by • Diabetes mellitus.
hyperglycemia, ketonemia, metabolic acidosis, • Infection (e.g., pyoderma, pneumonia,
dehydration, and electrolyte depletion. urinary tract infection, prostatis, pyelo
nephritis, pyometra).
TREATMENT
PATHOPHYSIOLOGY
• Insulin deficiency causes an increase in • Concurrent disease (e.g., heart failure, APPROPRIATE HEALTH CARE
lipolysis, resulting in excessive ketone body pancreatitis, renal insufficiency or failure, • If the animal is bright, alert, and well hydrated,
production and metabolic acidosis; an inability asthma, neoplasia, acromegaly). intensive care and IV fluid administration are
to maintain fluid and electrolyte homeostasis • Estrus. not required; start SC administration of insulin
causes dehydration, prerenal azotemia, • Idiopathic. (short- or intermediate-acting insulin), offer
electrolyte disorders, obtundation, and death. • Medication noncompliance. food, and supply constant access to water;
• Many patients with diabetic ketoacidosis • Stress. monitor closely for signs of illness (e.g., anorexia,
(DKA) have underlying conditions such as • Surgery. lethargy, vomiting).
infection, inflammation, or heart disease that • Treatment of animals with DKA that are
RISK FACTORS
cause stress hormone (e.g., glucagon, cortisol, systemically ill requires intensive inpatient
• Any condition that leads to absolute or
growth hormone, epinephrine) secretion; this care; goals are to correct depletion of water
relative insulin deficiency.
probably contributes to development of insulin and electrolytes, reverse ketonemia and
• History of corticosteroid or beta blocker
resistance and DKA by promoting lipolysis, acidosis, and increase rate of glucose use by
administration.
ketogenesis, gluconeogenesis, and glycogenolysis. insulin-dependent tissues.
• Dehydration and electrolyte abnormalities NURSING CARE
result from osmotic diuresis, promoting the • Fluids—necessary to ensure adequate
loss of total body water and electrolytes. cardiac output and tissue perfusion and to
DIAGNOSIS maintain vascular volume; also reduce blood
SYSTEMS AFFECTED
• Endocrine/metabolic. DIFFERENTIAL DIAGNOSIS glucose concentration.
• Gastrointestinal. • Hyperosmolar hyperglycemic state. • IV administration of isotonic crystalloid
• Hematologic (cats). • Acute hypoglycemic coma/insulin overdose. supplemented with potassium is initial fluid
• Uremia/azotemia due to renal disease or of choice; volume and rate determined by
GENETICS postrenal obstruction. fluid replacement needs plus maintenance
None • Other cause of metabolic acidosis (e.g., requirements; replace over 24–48h.
INCIDENCE/PREVALENCE lactic acidosis, ethylene glycol intoxication, ACTIVITY
Unknown renal tubular acidosis). N/A
GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS DIET
None • Leukocytosis with mature neutrophilia.
Following stabilization, diet should be
• Hyperglycemia—blood glucose concen
SIGNALMENT adjusted to account for patient’s diabetes,
tration usually >250 mg/dL. concurrent disease, and body condition.
Species • High liver enzyme activity.
Dog and cat. High-fiber diets are not recommended in
• Hypercholesterolemia and lipemia. underweight pets.
Breed Predilections • Azotemia.
• Dog—miniature poodle and dachshund. • Hypochloremia. CLIENT EDUCATION
• Cat—none. • Hypokalemia. Serious medical condition requiring lifelong
• Hyponatremia. insulin administration in most patients.
Mean Age and Range • Hypophosphatemia. Confirm that client is prepared to inject twice
• Dog—mean age 8.4 years. • Hypomagnesemia. daily insulin prior to treatment of DKA.
• Cat—median age 11 years (range: 1–19 years). • High anion gap—anion gap = (sodium + SURGICAL CONSIDERATIONS
Predominant Sex potassium) – (chloride + bicarbonate); normal N/A
• Dogs—females 1.5 times more prevalent is 16 ± 4.
than males. • Glucosuria and ketonuria.
• Cats—males 2 times more prevalent than • Variable urinary specific gravity with active
females. or inactive sediment.
SIGNS • Hyperproteinemia. MEDICATIONS
• Heinz body anemia (cats).
• Shock. DRUG(S) OF CHOICE
• Dehydration. OTHER LABORATORY TESTS
Insulin
• Hypothermia. • Metabolic acidosis—HCO3– <15 mEq/L
• Regular insulin is the insulin of choice until
• Polyuria. (total CO2 estimates HCO3–).
eating; lispro insulin may also be considered.
• Polydipsia or adipsia. • Hyperosmolarity (>330 mOsm/kg).
• Initial dosage—0.2 U/kg IM (or SC if
• Anorexia. • Bacterial culture of urine and blood.
• Weakness.
hydration normal).
DIAGNOSTIC PROCEDURES • Subsequent dosage 0.1–0.2 U/kg IM given
• Vomiting. • Abdominal and thoracic radiography and
• Lethargy. 3–6h later—may be given hourly if patient is
ultrasound may be necessary to identify closely monitored; response to previous insulin
• Tachypnea. comorbid diseases.
• Muscle wasting and weight loss. dosage should be considered when calculating
Diabetes Mellitus With Ketoacidosis (continued)
subsequent dosages; ideally, glucose • Recheck blood gas or serum total carbon • Diestrus.
concentration should drop by 50–100 mg/dL/h. dioxide (TCO2) before further supplementation. • Bacterial infection.
• Regular insulin can also be administered as • Electrolyte depletion.
D CRI via designated catheter. Dogs: 2.2 units/kg
Phosphorus Supplementation
• Pretreatment serum phosphorus is usually AGE-RELATED FACTORS
in 250 mL of 0.9% NaCl; Cats: 1.1 units/kg in normal; however, treatment of ketoacidosis N/A
250 mL 0.9% NaCl. Then, allow 50 mL of reduces phosphorus, and serum concen
dilute insulin to flow through IV tubing and ZOONOTIC POTENTIAL
trations should be checked q12–24h once N/A
discard. If blood glucose >250 mg/dL, supplementation is initiated.
administer at 10 mL/h; if blood glucose • Dosage—0.01–0.03 mmol/kg/h for 6–12h PREGNANCY/FERTILITY/BREEDING
200–250 mg/dL, administer at 7 mL/h; if blood in IV fluids (may need to increase dose to • Risk of fetal death may be relatively high.
glucose 150–200 mg/dL, administer at 5 mL/h; 0.06 mmol/kg/h). Remember to account for • Glucose regulation is often difficult in
if blood glucose 100–150 mg/dL, administer at additional potassium in potassium phosphate pregnant animals.
5 mL/h and add 2.5% dextrose to IV crystalloid if supplemented.
fluids; if blood glucose <100 mg/dL, discontinue SYNONYMS
IV insulin infusion and continue 2.5–5% CONTRAINDICATIONS N/A
dextrose in IV crystalloid infusion. If the patient anuric or oliguric or if blood SEE ALSO
• Check blood glucose q1–3h using auto- potassium concentration >5 mEq/L, do not • Diabetes Mellitus Without Complication—
mated test strip analyzer (Accu-Chek® III, supplement potassium until urine flow is Cats.
Alpha Trak® II glucometer), corrected for established or potassium concentration decreases. • Diabetes Mellitus Without Complication—
patient’s PCV as indicated. PRECAUTIONS Dogs.
• Monitor urine or serum ketones daily. • Use bicarbonate with caution in patients ABBREVIATIONS
• Administer longer-acting insulin once without normal ventilation (cannot excrete • DKA = diabetic ketoacidosis.
patient is eating, drinking, and ketosis is carbon dioxide created during treatment). • TCO2 = total carbon dioxide.
resolved; the dosage is based on that of • Acidosis results in falsely elevated blood
short-acting insulin given in hospital. Suggested Reading
ionized calcium concentrations; calcium Behrend E, Holford A, Lathan P, et al. 2018
Potassium Supplementation should be rechecked as acidosis resolves and AAHA diabetes management guidelines for
• Total body potassium is depleted and supplemented as necessary. dogs and cats. J Am Anim Hosp Assoc
treatment (e.g., fluids and insulin) will POSSIBLE INTERACTIONS 2018, 54:1–21.
further lower serum potassium. None Difazio J, Fletcher DJ. Retrospective
• If possible, check potassium concentration comparison of early- versus late-insulin
before initiating insulin therapy to guide ALTERNATIVE DRUG(S) therapy regarding effect on time to
supplementation; if extremely low, insulin None resolution of diabetic ketosis and ketoacido
therapy may need to be delayed (hours) until sis in dogs and cats: 60 cases (2003–2013).
serum potassium concentration increases. J Vet Emerg Crit Care 2016, 26:108–115.
• Refractory hypokalemia may indicate Hume DZ, Drobatz KJ, Hess RS. Outcome
hypomagnesemia, requiring magnesium FOLLOW-UP of dogs with diabetic ketoacidosis: 127 dogs
replacement at 0.75–1 mEq/kg/24h IV as (1993–2003). J Vet Intern Med 2006,
PATIENT MONITORING 20(3):547–555.
magnesium chloride or magnesium sulfate.
• Attitude, hydration, cardiopulmonary Kerl ME. Diabetic ketoacidosis: pathophysiology
• Supplementation of potassium should start
status, urine output, and bodyweight. and clinical and laboratory presentation. Comp
at 0.2 mEq/kg/h, which can be adjusted to
• Blood glucose q1–3h initially; q6h once stable. Cont Educ Pract Vet 2001, 23:220–228.
max 0.5 mEq/kg/h. Potassium concentration
• Electrolytes q4–8h initially; q24h once stable. Kerl ME. Diabetic ketoacidosis: treatment
should be measured q6-8h until stabilized.
• Acid-base status q8–12h initially; q24h recommendations. Comp Cont Educ Pract
Dextrose Supplementation once stable. Vet 2001, 23:330–339.
• Because insulin is required to correct the Malerba E, Mazzarino M, Del Baldo F, et al.
ketoacidotic state, the supplementation of Use of lispro insulin for treatment of
Appropriate insulin administration.
dextrose allows continuous insulin admini diabetic ketoacidosis in cats. J Fel Med Surg
stration without hypoglycemia. POSSIBLE COMPLICATIONS 2019, 21:115–123.
• Whenever blood glucose <200 mg/dL, 50% • Hypokalemia. Sieber-Ruckstuhl NS, Klev S, Tschuor F, et al.
dextrose should be added to fluids to produce • Hypoglycemia. Remission of diabetes mellitus in cats with
2.5% dextrose solution (increase to 5% dextrose • Hypophosphatemia. diabetic ketoacidosis. J Vet Intern Med
if glucose <100 mg/dL). Discontinue dextrose • Cerebral edema. 2008, 22:1326–1332.
once glucose is maintained above 250 mg/dL. • Pulmonary edema/heart failure. Author Katherine Gerken
• Insulin therapy is continued as long as • Renal failure. Consulting Editor Patty A. Lathan
blood glucose >100 mg/dL Acknowledgment The author and book
EXPECTED COURSE AND PROGNOSIS editors acknowledge the prior contribution of
Bicarbonate Supplementation Guarded Deborah S. Greco.
• Controversial; consider if patient’s venous
blood pH <7.0 or HCO3– <11 mEq/L; of
little benefit if pH >7.0. Client Education Handout
• Dosage—bodyweight (kg) × 0.3 × base available online
MISCELLANEOUS
deficit (base deficit = normal serum bicarb
onate – patient’s serum bicarbonate); slowly ASSOCIATED CONDITIONS
administer ¼ to ½ of dose IV and give • Pancreatitis.
remainder in fluids over 3–6h. • Hyperadrenocorticism.
Diabetes Mellitus Without Complication—Cats

• Polyuria (PU)/PD, polyphagia, weight DIAGNOSTIC PROCEDURES
loss, generalized muscle wasting, poor Liver fine-needle aspiration—if concern for
coat quality. hepatic lipidosis.
BASICS • Signs suggesting a complication—anorexia, D
PATHOLOGIC FINDINGS
DEFINITION lethargy, depression, vomiting, jaundice. • Usually no gross necropsy changes;
• Disorder of carbohydrate, fat, and protein Physical Exam Findings pancreatic weight may be increased.
metabolism caused by an absolute or relative Hepatomegaly, dehydration, plantigrade • Histopathology—normal, more likely to
insulin deficiency, resulting in the hallmark stance (diabetic neuropathy). reveal islet amyloidosis, vacuolar or hydropic
abnormality of persistent hyperglycemia. degeneration of the islets of Langerhans;
• The most common form in cats resembles CAUSES
• Genetic susceptibility. lymphoplasmacytic pancreatic infiltration
Type II or non-insulin-dependent diabetes rare in cats.
mellitus (DM) of humans. • Islet amyloid deposition.
• Pancreatitis.
PATHOPHYSIOLOGY • Diseases causing insulin resistance (e.g.,
• Insulin resistance impairs the ability of hyperadrenocorticism and acromegaly).
tissues (especially muscle, adipose tissue, and • Drugs (e.g., glucocorticoids and TREATMENT
liver) to use carbohydrates, fats, and proteins. progestogens).
• Impaired systemic glucose utilization APPROPRIATE HEALTH CARE
coupled with ongoing hepatic gluconeogen- RISK FACTORS • Compensated cats can be managed as
esis causes persistent hyperglycemia, which • Obesity. outpatients if they are alert, hydrated, and
directly impairs insulin secretion by reducing • Advanced age. eating and drinking without vomiting.
functional beta cell mass (“glucose toxicity”). • For decompensated patients, see Diabetes
• Initial beta cell dysfunction progresses to Mellitus With Ketoacidosis.
irreversible failure of insulin production as NURSING CARE
reactive oxidative species, inflammatory DIAGNOSIS Fluid therapy—in decompensated patients.
cytokines, and amyloid deposition perpetuate
beta cell injury and loss. DIFFERENTIAL DIAGNOSIS ACTIVITY
• Stress hyperglycemia—no PU/PD or Strenuous activity may lower insulin require-
SYSTEMS AFFECTED weight loss; blood glucose concentration ments; consistent daily activity level is helpful.
• Endocrine/metabolic—electrolyte normal if sample taken when cat is not
depletion, metabolic acidosis. DIET
stressed; normal fructosamine concentration. Ultra-low-carbohydrate (<12% metabolizable
• Hepatobiliary—chronic pancreatitis, • Renal glucosuria—absence of
hepatic lipidosis. energy) and high protein (>40% metabolizable
hyperglycemia; usually does not cause PU/PD energy) canned diets may improve glycemic
• Neuromuscular—muscle wasting, or weight loss.
peripheral neuropathy. control, and increase the likelihood of
• Renal/urologic—osmotic diuresis with
CBC/BIOCHEMISTRY/URINALYSIS diabetic remission in newly diagnosed
• Mild normocytic, normochromic anemia diabetic cats.
compensatory polydipsia (PD); urinary tract
infection. possible. CLIENT EDUCATION
• Glucose >150 mg/dL.
• Discuss maintaining a consistent daily
GENETICS • High alkaline phosphatase (ALP), alanine
Genetic susceptibility suspected in certain feeding and medication schedule, home glucose
aminotransferase (ALT), and aspartate monitoring, signs of hypoglycemia and what to
breeds (e.g., European Burmese cats). aminotransferase (AST) activities. do, and when to seek veterinary assistance.
INCIDENCE/PREVALENCE • Hypercholesterolemia, hyperbilirubinemia,
• Clients are encouraged to chart pertinent
Reported at between ~1 : 250 (0.4%) to and hypertriglyceridemia. daily information about the pet, such as any
~1 : 100 (1.2%) cats. • Total CO2 or HCO3 low with ketoacidosis
home-obtained glucose readings or patterns
or severe dehydration. of exhibited clinical signs (e.g., PU/PD or
GEOGRAPHIC DISTRIBUTION • Glucosuria, ketonuria uncommon in
N/A appetite).
uncomplicated DM.
SIGNALMENT • Isosthenuria, proteinuria. SURGICAL CONSIDERATIONS
Intact females should have ovariohysterectomy
Species OTHER LABORATORY TESTS when stable; progesterone secreted during
Cat • Fructosamine >350 μmol/L—confirms
diestrus makes management of DM difficult.
Breed Predilections
persistence of hyperglycemia.
• Feline pancreas-specific lipase >3.50 μg/L—
Breeds with possible increased susceptibility
include Burmese (Europe, Australia, and identifies presence of pancreatitis.
• Urine culture—positive in 10–15% of
New Zealand), Maine Coon, Russian Blue,
Siamese, and Norwegian Forest cats. newly diagnosed DM. MEDICATIONS
IMAGING DRUG(S) OF CHOICE
Mean Age and Range
• Thoracic and abdominal radiography— to • Insulin is treatment of choice and should be
Over 80% of cases are 7 years or older at
evaluate for concurrent or underlying disease initiated at 1–2 units per cat SC q12h; based
diagnosis; range: 1–19 years.
(e.g., neoplasia, cystic or renal calculi, on routine monitoring, some cats may
Predominant Sex emphysematous cystitis, or cholecystitis). eventually be reduced to once-daily dosing.
Males are overrepresented, but common in • Abdominal ultrasonography—in selected • Two U-40 insulin formulations are FDA-
both sexes. patients, particularly those with jaundice, to approved for use in cats—protamine zinc (PZI)
SIGNS evaluate for hepatic lipidosis, cholangio and porcine zinc lente insulin suspension.
Historical Findings
hepatitis, and pancreatitis.
• Obesity often present prior to diagnosis.
Diabetes Mellitus Without Complication—Cats (continued)
• Most consensus recommendations support are normal and weight stable to increasing, AGE-RELATED FACTORS
the use of PZI or glargine (U-100) as disease is likely to be regulated. Congenital and juvenile forms of DM are rare
first-choice insulin therapy for cats. • Glucose curves—ideally generated by the (<3% of cases are under 2 years of age) and
D owner at home. Perform 5–14 days after may be more difficult to manage.
PRECAUTIONS
Glucocorticoids, megestrol acetate, and starting insulin or after any dose adjustments ZOONOTIC POTENTIAL
progesterone cause insulin resistance. If until controlled, then again at 1 month, and None
steroid therapy is necessary, use oral every 3–6 months thereafter.
• Fructosamine—maintain <400 μmol/L. PREGNANCY/FERTILITY/BREEDING
methylprednisolone. Avoid injectable steroids. • Insulin requirements should be monitored
Recheck monthly during initial regulation,
POSSIBLE INTERACTIONS then every 3–6 months as part of routine closely during pregnancy as they are expected
• Drugs that may increase insulin sensitivity— monitoring visits. to fluctuate.
angiotensin-converting enzyme inhibitors, • Urinary monitoring—useful for identifying • Severe maternal hypoglycemia can negatively
sulfonamides, tetracycline, beta blockers, ketones in chronically unregulated patients or impact fetal viability and neonatal neurologic
monoamine oxidase inhibitors, salicylates. persistently negative glucose in cats likely function, therefore should be avoided during
• Drugs that increase insulin resistance— entering remission. gestation.
glucocorticoids, estrogen supplements, • Flash glucose monitoring system (FreeStyle SYNONYMS
furosemide, thiazide diuretics, and calcium Libre®)—24-hour glucose monitoring system N/A
channel blockers. that measures blood glucose BG every 5
• Always consult a new medication’s product minutes for up to 14 days; use reported in SEE ALSO
insert. dogs, but not cats. Anecdotal evidence • Diabetes Mellitus With Ketoacidosis.
suggests the device is not 100% accurate, but • Diabetes Mellitus With Hyperosmolar
ALTERNATIVE DRUG(S) Hyperglycemic State.
• Oral sulfonylureas (e.g., glipizide)—only helpful in assessing BG trends in cats in
considered when insulin therapy is not which a BG curve is not possible. ABBREVIATIONS
possible (e.g., owner considering euthanasia PREVENTION/AVOIDANCE • ALP = alkaline phosphatase.
instead of injections). Initial does of 2.5 mg Prevent or correct obesity; avoid unnecessary • ALT = alanine aminotransferase.
PO q12h can be used and monitored use of glucocorticoids or megestrol acetate. • AST = aspartate aminotransferase.
similar to insulin. If DM is not controlled • BG = blood glucose.
after 2 weeks, dose of 5 mg PO q12h may POSSIBLE COMPLICATIONS • DM = diabetes mellitus.
be tried; however, response is seen in <40% • Seizure, blindness, or coma with insulin • PU/PD = polyuria and polydipsia.
of cats and often not sustained long term. overdose. • PZI = protamine zinc insulin.
Potential side effects are hypoglycemia, • Diabetic ketoacidosis or hyperglycemic
hyperosmolar syndrome. INTERNET RESOURCES
hepatic enzyme alterations, icterus, and https://www.aaha.org/guidelines/diabetes_
vomiting. EXPECTED COURSE AND PROGNOSIS guidelines/default.aspx
• Acarbose—an alpha-glucosidase • Prognosis with treatment and monitoring is
inhibitor used to limit intestinal glucose good; most animals have a normal lifespan. Suggested Reading
absorption. Often used in combination • Some cats may recover insulin-secreting Behrend E, Holford A, Lathan P, et al. 2018
with diet and insulin at a starting dose of ability (“diabetic remission”), typically if AAHA diabetes management guidelines for
12.5 mg PO q12h; diarrhea is most glycemic control is achieved within 6 months dogs and cats. J Am Anim Hosp Assoc
common side effect. of diagnosis; however, relapse is common (~30%). 2018, 54:1–21.
• Drugs warranting further study for utility • Reported remission rates vary greatly Sparkes A, Cannon M, Church D, et al.
in managing feline DM include once-weekly (0–100%); however, studies surveying general ISFM consensus guidelines on the practical
injected glucagon-like peptide 1 analogues practitioners have suggested ~25–30% is management of diabetes mellitus in cats. J
and oral renal tubular transporter inhibitors. reasonable expectation. Feline Med Surg 2015, 17:235–250.
Author Andrew C. Bugbee
Consulting Editor Patty A. Lathan
editors acknowledge the prior contribution
FOLLOW-UP MISCELLANEOUS of Deborah S. Greco.
PATIENT MONITORING ASSOCIATED CONDITIONS
• Owner-assessed clinical signs (PU/PD, Urinary tract infection, chronic pancreatitis. Client Education Handout
appetite, attitude) and bodyweight—if signs available online
Diabetes Mellitus Without Complication—Dogs

Breed Predilections (e.g., glomerulonephropathy, liver
• Samoyed, Tibetan terrier, Cairn terrier, dysfunction, gastrointestinal disease) will
golden retriever (United States only) lower fructosamine level for given average
BASICS overrepresented. • Keeshond, poodle, blood glucose. ◦ Best used for ongoing D
DEFINITION dachshund, miniature schnauzer, beagle may management of relatively stable diabetic
• Fasting hyperglycemia of sufficient have increased predisposition. • Boxer, patients; fructosamine concentration in upper
magnitude to result in characteristic clinical German shepherd, golden retriever (UK only) third of reference range reflects excellent
signs including weight loss with normal or underrepresented. diabetic control; concentration in lower third
increased appetite, polydipsia (PD), and Mean Age and Range is more suggestive of overzealous diabetic
polyuria (PU) caused by glucosuria. Mean ~8 years; range: 4–14 years (excluding control and possible increased risk of
• Disorder of carbohydrate, fat, and protein rare juvenile form). hypoglycemia. • Plasma insulin concen
metabolism caused by absolute or relative trations not particularly helpful—while low
insulin deficiency. • Generally canine Predominant Sex insulin concentration suggests insulin
diabetes mellitus (DM) is characterized by Female deficiency, may be reflection of reversible islet
loss of insulin-secreting ability through SIGNS exhaustion (persistent hyperglycemia can
presumed immune-mediated destruction of • PU/PD, polyphagia with weight loss. impair insulin secretory activity, even if
pancreatic beta cells. • Far less frequently, • Hepatomegaly. • Cataracts common functional beta cells present).
canine DM may develop as result of finding—approximately 80% of dogs with IMAGING
combination of relative insulin-deficient DM for >12 months will have cataracts • Radiography—useful to look for
state with concurrent peripheral insulin regardless of level of control. • Lethargy, comorbidities (e.g., cystic or renal calculi,
resistance. depression, inappetence, anorexia, and emphysematous cystitis, cholecystitis,
PATHOPHYSIOLOGY vomiting may occur in animals with keto- pancreatitis). • Ultrasonography—indicated
• Absolute or relative insulin deficiency acidosis. in selected patients, particularly those with
results in accelerated tissue catabolism, CAUSES jaundice, to evaluate for presence of
impaired ability to maintain carbohydrate, • Immune-mediated isletitis. • Disorders that obstructive hepatopathy or pancreatitis.
lipid, and protein homeostasis, as well as predispose to secondary immune-mediated DIAGNOSTIC PROCEDURES
insulin resistance. • Reduced insulin- isletitis—pancreatitis, viral illness. Liver biopsy (percutaneous)—indicated in
secreting ability, peripheral insulin resistance, RISK FACTORS some jaundiced patients to evaluate other
and continued hepatic gluconeogenesis result • Diestrus. • Genetic susceptibility. • Use of causes for hepatopathy.
in persistent hyperglycemia of sufficient glucocorticoids or progestins.
severity to overload renal tubular glucose PATHOLOGIC FINDINGS
resorption; leading to glucosuria, osmotic • Necropsy findings—hepatomegaly with
diuresis, PU accompanied by compensatory significant hepatic lipid accumulation.
PD. • Loss of insulin-dependent glucose- • Histopathologic findings generally reveal
mediated hypothalamic satiation signaling DIAGNOSIS dramatic reduction in size and number of
results in polyphagia. • Decreased insulin- pancreatic islets with relatively normal
DIFFERENTIAL DIAGNOSIS exocrine tissue architecture.
dependent utilization of glucose results in Renal glucosuria—not associated with hyper-
catabolic protein breakdown with weight loss glycemia, usually no weight loss or
and increased lipid mobilization (hyperlipi polyphagia.
demia, hepatic lipidosis, production of
ketoacids). • Accumulation of large amounts CBC/BIOCHEMISTRY/URINALYSIS TREATMENT
of ketone bodies leads to metabolic acidosis • Hemogram usually normal. • Glucose
(see Diabetes Mellitus With Ketoacidosis). >200 mg/dL, possible ketonemia. • High APPROPRIATE HEALTH CARE
serum alkaline phosphatase (ALP) and • Compensated dogs generally alert, well
SYSTEMS AFFECTED alanine aminotransferase (ALT) enzyme hydrated, eating and drinking without
• Endocrine/metabolic—electrolyte depletion activities, generally with greater proportionate vomiting, and can be managed as outpatients.
and metabolic acidosis. • Hepatobiliary— increase in ALP. • Hypercholesterolemia, • For management of decompensated
hepatic lipidosis. • Ophthalmic—cataracts. lipemia. • Electrolyte alterations vary; patients, see Diabetes Mellitus With
• Renal/urologic—glucosuria resulting in hypokalemia and hypophosphatemia may be Ketoacidosis.
osmotic diuresis and increased likelihood of present. • Total CO2 or HCO3 will be low
bacterial urinary tract infections, particularly DIET
with ketoacidosis or severe dehydration. • Diet should be calorically and constitutively
of upper urinary tract. • Glucosuria, ketonuria in some dogs. consistent. • Ideally glucose-lowering effects
GENETICS • Urinary specific gravity variable depending of insulin should match glucose-raising effects
Certain breeds dramatically over- and on degree of glucosuria. of the meal. ◦ Most insulins act maximally
underrepresented, suggesting inherited OTHER LABORATORY TESTS 2–4h after SC administration, and most food
susceptibility to immune-mediated “isletitis.” • Anion gap—high in patients with absorbed within 1h of consumption, so
INCIDENCE/PREVALENCE ketoacidosis. • Glycated proteins— glycemic control almost always improved if
• Prevalence varies between 1 : 400 and fructosamine or glycosylated hemoglobin: dog fed 60–90 min after q12h insulin dosing.
1 : 500. • Onset has seasonal incidence; more extent of glycosylation directly related to ◦ Animals that “graze” throughout day can be
animals diagnosed in autumn and winter. blood glucose concentration over lifespan of fed dry food ad libitum and given 2 small
protein in circulation (10–20 days for meals of canned food as above. ◦ If insulin
SIGNALMENT can only be administered once daily, feed
fructosamine, 4–8 weeks for hemoglobin).
Species ◦ Glycated protein concentration modified total daily caloric intake in 2 or 3 meals
Dog by changes in albumin or hemoglobin within first 6–8h after insulin dosing. • Feed
concentrations; accelerated albumin turnover caloric quantity appropriate for animal’s ideal
Diabetes Mellitus Without Complication—Dogs (continued)
bodyweight (~60 kcal/kg); food should be canine and porcine insulin have identical early indicator of need for reduction in dose
something dog will eat reliably and within amino acid sequence, hence Vetsulin does not in patients with well-controlled clinical signs;
short period. • Obese diabetic dogs—feed produce significant insulin antibody response, should never be used by owner to make
D restricted caloric intake to ensure ideal whereas most other commercially available independent adjustment of insulin dose;
bodyweight achieved within 2–4 months insulins do; however, no evidence the owner-measured urine glucose levels not
using high-fiber, low-calorie food; while development of insulin antibodies has any particularly useful.
high-fiber diet may improve patient satiety clinical significance. PREVENTION/AVOIDANCE
and possibly owner satisfaction, has no role in PRECAUTIONS • Neuter females; avoid unnecessary use of
improving diabetic control. • While snacks • Glucocorticoids, megestrol acetate, and megestrol acetate. • No evidence exists to
should generally be avoided, small treats given progesterone cause insulin resistance. suggest obesity increases risk of DM in
at time of injection to positively reinforce • Hyperosmotic agents (e.g., mannitol and neutered dogs.
owner–patient interaction should be radiographic contrast agents) should be
encouraged. POSSIBLE COMPLICATIONS
avoided if patient is already hyperosmolar • Cataracts can occur even with good glycemic
CLIENT EDUCATION from hyperglycemia. control. • Weakness, especially with exercise;
• Most important that insulin and feeding
ALTERNATIVE DRUG(S) seizures or coma may occur with insulin
regime are discussed and agreed with owner Oral hypoglycemic agents are generally not overdose.
and they feel comfortable with plan; effective recommended.
management requires significant owner– EXPECTED COURSE AND PROGNOSIS
patient interaction; flexibility in establishing • Dogs generally have permanent disease
best management regime is thus paramount unless affected during estrus cycle, where
and rigid “one size fits all protocols” should neutering may resolve diabetes for a period.
be avoided. • Discuss daily feeding and FOLLOW-UP • Prognosis with twice-daily insulin treatment
medication schedule, home monitoring, signs and feeding aligned with insulin’s maximum
PATIENT MONITORING
of hypoglycemia and what to do, and when to effects is good.
• Diabetic dogs require regular contact
call or visit veterinarian. • Clients encouraged between owner and veterinary team; visits
to keep chart of pertinent information about should occur every 3–4 months if animal is
pet, such as daily water consumption, weekly stable and clinical signs are controlled, or
bodyweight, current insulin dose, and more frequently if control is poor or variable. MISCELLANEOUS
amount of food consumed; use of standardized Criteria to assess control include: ◦ Clinical
clinical scoring tool should be encouraged to ASSOCIATED CONDITIONS
signs—degree of PU/PD, appetite, and • Urinary tract infection. • Cataracts.
maintain consistency across veterinary and bodyweight; if within acceptable limits,
tech teams involved in managing both dog disease likely well regulated; consider using AGE-RELATED FACTORS
and owner. standardized clinical scoring system to Juvenile DM is rare and may be more
SURGICAL CONSIDERATIONS consistently evaluate clinical phenotype. difficult to manage.
Intact females should have ovariohysterec- ◦ Glycated proteins—fructosamine or PREGNANCY/FERTILITY/BREEDING
tomy when stable; progesterone secreted glycosylated hemoglobin; see above. • DM can develop during pregnancy, in
during diestrus makes management of DM ◦ Glucose curve—provides information on which case pregnancy is difficult to maintain.
more unpredictable. insulin effectiveness, duration of action, • Exogenous insulin administration may
nadir (lowest blood glucose level achieved cause fetal oversize and dystocia. • Insulin
during dosing interval), and potential for resistance develops, making hyperglycemia
rebound hyperglycemia; results subject to difficult to control. • Pregnant bitch is prone
influence of stress (hospitalization, multiple to ketoacidosis; emergency ovariohysterectomy
MEDICATIONS blood draws) and “normal” conditions may be necessary. • Do not breed dogs
DRUG(S) OF CHOICE should be mimicked as much as possible; with DM.
• Insulin—almost always required • Vetsulin® used most effectively when establishing
(porcine-origin lente) 0.75 units/kg SC q12h initial control, changing insulin type, dose, ABBREVIATIONS
initial dose; note: U-40 insulin—must use or frequency, or problem solving for difficult • ALP = alkaline phosphatase.
with U-40 insulin syringe; availability may be diabetic; duration of curve ideally matches • ALT = alanine aminotransferase.
limited. • Humulin N—intermediate-acting, dosing interval (12 or 24 hours)—identifi • DM = diabetes mellitus.
cation of nadir (to avoid iatrogenic • PD = polydipsia.
human insulin; 0.75 units/kg SC q12h initial
dose. • Novolin N—intermediate-acting, hypoglycemia) and glucose level at time of • PU = polyuria.
human insulin; 0.75 units/kg SC q12h initial dosing are most important aspects of curve; Author David B. Church
dose. • PZI Vet® (intermediate- to longer- goal is to establish effective insulin dose Consulting Editor Patty A. Lathan
acting protamine zinc human insulin) rarely (decline in blood glucose to 100–200 mg/
used in dogs; note: U-40 insulin—must use dL) for appropriate duration (majority of
with U-40 syringe. • Detemir insulin— 12- or 24-hour dosing interval) with nadir
available online
longer-acting, synthetic insulin; part of reason >80 mg/dL and <150 mg/dL; in dogs
for its delayed release is because bound to average glucose levels for 12-hour period
albumin; unlike insulins mentioned above, overnight are lower than during daylight
starting dose should be considerably lower: period. • Home glucose monitoring using
0.1 unit/kg SC q12h initial dose. • Glargine serial blood glucose estimations or real-time
insulin—longer-acting, synthetic insulin; measures using SC glucose monitoring
0.75 units/kg SC q12h initial dose. • Species of devices—requires owner commitment,
origin of insulin may affect pharmacokinetics; compliance, and competence; most useful as
Diaphragmatic Hernia
Standard Imaging CONTRAINDICATIONS
• Three-view thoracic and abdominal Avoid nonsteroidal anti-inflammatories for at
radiography. • Horizontal beam radiography. least 24–48 hours following trauma.
BASICS • Ultrasonography. D
OVERVIEW Additional Imaging
• Protrusion of an abdominal organ through • Contrast radiography—upper gastrointestinal
an abnormal opening in the diaphragm, either positive contrast series; peritoneography. • CT. FOLLOW-UP
as an acquired injury or as a congenital defect. Imaging Findings
• Congenital—pleuroperitoneal (PIPDH) or PATIENT MONITORING
• Identification of gastrointestinal viscera • Frequent or continuous ECG monitoring.
peritoneopericardial diaphragmatic hernia within pleural space and/or absence from
(PPDH). • Traumatic—most often the result • Observation of ventilation. • Pulse
abdominal cavity makes diagnosis of oximetry. • Serial arterial blood gas
of a motor vehicle accident. • Impaired lung diaphragmatic herniation often uncomplicated.
expansion. • Myocardial trauma. • Evidence evaluation.
• Other radiographic signs include loss of
of shock. • Systems affected—respiratory, diaphragmatic outline and cardiac silhouette, POSSIBLE COMPLICATIONS
cardiovascular, gastrointestinal. displacement of lung fields, presence of • Respiratory distress—due to concurrent
SIGNALMENT gas-filled viscera, and pleural effusion.• For injury or pneumothorax. • Reexpansion
• Dogs and cats. • Acquired—no breed predil- congenital PPDH cardiac silhouette is pulmonary edema (RPE) is uncommon but
ection. • Congenital (PPDH)—Weimaraner, markedly enlarged and may have evidence of often fatal complication; to minimize risk of
Maine coon cat, and Persian cats. gas-filled structures within it. • Contrast or RPE, avoid aggressive positive-pressure
• Congenital PIPDH—golden retriever, advanced imaging is often unnecessary. ventilation following reduction of herniated
cavalier King Charles spaniel. • Young organs, and avoid aggressive evacuation of
animals at higher risk for both congenital and pleural space in postoperative period.
• Thoracocentesis for pleural effusion.
traumatic causes (median age 1.2 and 3.1 • Recurrence uncommon, but most often
• Pericardiocentesis for pericardial effusion.
years, respectively). • No sex predilection. associated with inadequate surgical repair.
SIGNS EXPECTED COURSE AND PROGNOSIS
Traumatic If animal survives for first 12–24 hours after
• Can be acute, subacute, or chronic. • Possible surgery, prognosis is excellent. Reported
TREATMENT survival rates range from 80 to 90%. Death
known history of blunt trauma. • Difficulty
breathing. • Evidence of shock (tachycardia, Emergency Inpatient Intensive Care most often due to concurrent injury.
pale mucous membranes, weak pulses). Management
• Gastrointestinal sounds ausculted in thorax. • Address shock. • Improve ventilation and
• Empty abdomen on abdominal palpation. cardiac output. • Manage concurrent injury.
• Signs may be progressive. • Gastric decompression if indicated. MISCELLANEOUS
Congenital Surgical Management ASSOCIATED CONDITIONS
• May not have clinical signs or may develop • Exploratory laparotomy. • Reduction and • Congenital PPDH may be associated with
clinical signs later in life. • Difficulty assessment of herniated abdominal viscera. other congenital midline defects. • Animals
breathing. • Gastrointestinal signs. • Signs • Surgical repair of diaphragmatic rent. suffering trauma may have significant
may be progressive. • Evidence of shock • Additional surgical procedures (e.g., splenec concurrent injuries.
(tachycardia, pale mucous membranes, weak tomy, intestinal resection and anastomosis, liver
pulses). • Evidence of cardiac tamponade. lobectomy). • Pleural space evacuation ABBREVIATIONS
• Arrhythmias. • Muffled heart sounds. (thoracostomy tube placement, thoracocentesis). • AFAST® = abdominal focused assessment
with sonography for trauma.
CAUSES & RISK FACTORS Nursing Care
• PIPDH = pleuroperitoneal diaphragmatic
Traumatic • IV fluid therapy. • Oxygen supplement
hernia.
• Motor vehicle accident. • Other blunt trauma. ation. • Pain management.
• POCUS = point-of-care ultrasound.
• Penetrating trauma (e.g., bite wounds). Surgical Considerations • PPDH = peritoneopericardial
• Anesthesia and surgery should be delayed diaphragmatic hernia.
until animal is hemodynamically stable. • RPE = reexpansion pulmonary edema.
• Emergency surgery indicated with evidence of • TFAST® = thoracic-focused assessment with
DIAGNOSIS gastrothorax, gastrointestinal entrapment, or sonography for trauma.
persistent respiratory distress. • Long lasting
DIFFERENTIAL DIAGNOSIS absorbable monofilament suture (e.g., Maxon® Suggested Reading
• Pneumothorax. • Pulmonary contusion. or PDS®) should be used to close the diaphragm Burns CG, Bergh MS, McLoughlin MA.
• Hemothorax. in a full-thickness simple continuous pattern. Surgical and nonsurgical treatment of
• Care should be taken around caval foramen, peritoneopericardial diaphragmatic hernia
esophageal hiatus, and aortic hiatus. in dogs and cats: 58 cases (1999–2008). J
Nonspecific changes due to trauma may be noted.
Am Vet Med Assoc 2013, 242:643–650.
OTHER LABORATORY TESTS Legallet C, Thieman Mankin K, Selmic LE.
Serum lactate—may be significantly elevated Prognostic indicators for perioperative
following trauma. survival after diaphragmatic herniorrhaphy
IMAGING MEDICATIONS in cats and dogs: 96 cases (2001–2013).
Point-of-Care Ultrasound (POCUS) DRUG(S) OF CHOICE BMC Vet Res 2017, 13:16.
• Thoracic-focused assessment with • Appropriate postoperative pain medications; Author Catriona M. MacPhail
sonography for trauma (TFAST®). consider local analgesia. • Antiarrhythmic Consulting Editor Elizabeth Rozanski
• Abdominal focused assessment with agents as indicated.
sonography for trauma (AFAST®).
Diarrhea, Antibiotic Responsive

CBC/BIOCHEMISTRY/URINALYSIS • Long-term administration of both tylosin
• Typically normal. • Hypoalbuminemia is and metronidazole has been found to induce
uncommon finding. long-term dysbiosis in ARD dogs, which is
D BASICS very difficult to correct; this dysbiosis is
OVERVIEW • Fecal examination for parasites should be
associated with changes in bile acid metabo-
• Defined as chronic diarrhea with no ident- performed. • Serum cobalamin levels may be lism and serum metabolome, and persists for
ifiable underlying etiology that responds to low and folate levels may be increased or over 6 months after discontinuing treatment.
antibiotic therapy. • Antibiotic-responsive decreased. • Serum trypsin-like immunoreac-
diarrhea (ARD) was previously termed tivity (measured to rule out EPI) is normal.
idiopathic (primary) small intestinal bacterial
overgrowth (SIBO); this term is no longer used IMAGING
as it was based on quantitative culture of bacteria Routine abdominal imaging (radiographs and FOLLOW-UP
in the upper gastrointestinal tract that could not ultrasound) should be performed to rule out • Clinical resolution of diarrhea is most
be confirmed by newer PCR-based methods; other causes for diarrhea. These tests are important criterion. • Weight gain may also be
secondary SIBO is a result of concurrent unremarkable in cases of ARD. seen; hypoalbuminemia (if present) should
gastrointestinal diseases (e.g., exocrine pancreatic DIAGNOSTIC PROCEDURES resolve. • Relapses usually occur when anti-
insufficiency [EPI]). • Current theories center Diagnosis depends upon ruling out all other biotics are discontinued; some dogs can be
on the possibility of immune dysregulation, causes for chronic diarrhea (especially maintained on very low doses of antibiotics long
possibly associated with abnormal CD4+ T-cells, food-responsive diarrhea) and a clinical term, however the development of antimicrobial
immunoglobulin (Ig) A plasma cells, cytokine response to an appropriate course of resistance in these dogs is a concern. • Recent
expression, and, in German shepherd dogs, antibiotic therapy. studies suggest ARD dogs have poor long-term
mutations in pattern recognition receptors. prognosis, possibly due to induction of dysbiosis;
SIGNALMENT many dogs eventually will become steroid
resistant or will be euthanized because of
Species treatment resistance.
Dog TREATMENT
• Hospitalization generally not indicated;
Breed Predilections treated on outpatient basis. • Role of diet in
Increased incidence in German shepherd, ARD is unknown; current recommendations
boxer, and Chinese Shar-Pei. are to feed low-fat, highly digestible food or MISCELLANEOUS
Mean Age and Range elimination or hydrolyzed diet.
More common in young dogs, with median SEE ALSO
age of 2 years. Small Intestinal Dysbiosis.
Predominant Sex ABBREVIATIONS
N/A MEDICATIONS • ARD = antibiotic-responsive diarrhea.
• EPI = exocrine pancreatic insufficiency.
SIGNS DRUG(S) OF CHOICE • Ig = immunoglobulin.
Historical Findings • Several options for antibiotics available— • SIBO = small intestinal bacterial overgrowth.
• Small bowel signs—inappetence or anorexia, tylosin (5–10 mg/kg PO q24h); metronida-
zole (10–15 mg/kg PO q12h); oxytetracycline Suggested Reading
vomiting, weight loss, large-volume diarrhea. Allenspach K, Culverwell C, Chan D.
• Large bowel signs—tenesmus, hematochezia, (10–20 mg/kg PO q8h). • In some cases,
combination therapy may be necessary. Long-term outcome in dogs with chronic
increased frequency of defecation. enteropathies: 203 cases. Vet Rec 2016,
• Antibiotic therapy administered for 4–6
Physical Examination Findings weeks and then discontinued. • If serum 178(15):368. doi: 10.1136/vr.103557
Weight loss, poor body condition, borboryg- cobalamin levels decreased, cobalamin German AJ, Day MJ, Ruaux CG, et al.
mus, and flatulence may be detected; hemato- supplementation should be pursued; dogs: Comparison of direct and indirect tests for
chezia may be present if there is large bowel 50 μg/kg up to max dose of 1,500 μg small intestinal bacterial overgrowth and
involvement. parenteral cobalamin; doses given as SC antibiotic-responsive diarrhea in dogs. J Vet
CAUSES & RISK FACTORS injections once weekly for 6 weeks, then once Intern Med 2003, 17:33–43.
• Genetic mutations in pattern recognition genes every other week for 6 weeks; serum Toresson L, Steiner JM, Spodsberg E, et al.
(TLR4 and TLR5) have been associated with the cobalamin levels should be reassessed at end Effects of oral versus parenteral cobalamin
disease. • Certain enteropathogenic bacteria of therapy; oral cobalamin supplementation is supplementation on methylmalonic acid
(Clostridium perfringens, Escherichia coli, and effective at dosage of 0.25–1.0 mg PO daily. and homocysteine concentrations in dogs
Lawsonia intracellularis) have been suspected but with chronic enteropathies and low
CONTRAINDICATIONS/POSSIBLE cobalamin concentrations. Vet J 2019,
not proven to be etiologic agents.
INTERACTIONS 243:8–14. doi: 10.1016/j.tvjl.2018.11.004
• Oxytetracycline may cause staining of tooth Westermarck E, Skrzypczak T, Harmoinen J,
enamel; doses should be decreased in animals et al. Tylosin-responsive chronic diarrhea
with hepatic or renal insufficiency; oxytetra- in dogs. J Vet Intern Med 2005,
DIAGNOSIS cycline has been associated with high 19:177–186.
DIFFERENTIAL DIAGNOSIS incidence of bacterial transfer of resistance Author Karin Allenspach
• Secondary SIBO. • EPI. • Parasitic genes. • Metronidazole undergoes extensive Consulting Editor Mark P. Rondeau
infection. • Inflammatory bowel disease. hepatic metabolism; dosages should be
• Food-responsive diarrhea. • Neoplasia. reduced in animals with hepatic insufficiency.
Diarrhea, Chronic—Cats
or enlarged mesenteric lymph nodes. • Rectal CBC/BIOCHEMISTRY/URINALYSIS
palpation typically unremarkable. • Eosinophilia in some cats with parasitism,
eosinophilic enterocolitis, hypereosinophilic
BASICS Large Bowel
syndrome, or neoplasia. • Macrocytosis in D
• Body condition typically unremarkable.
DEFINITION • Dehydration—uncommon. • Abdominal some cats with hyperthyroidism or FeLV
• A change in the frequency, consistency, and palpation may reveal thickened large bowel, infection. • Anemia that is variably
volume of feces for more than 3 weeks or with a foreign body, neoplastic mass, intussusception, or regenerative and may show microcytosis
pattern of episodic recurrence. • Can be either enlarged mesocolic lymph nodes. • Rectal suggests chronic GI bleeding and iron
small bowel, large bowel, or mixed in origin. palpation may reveal irregularity of rectal mucosa, deficiency. • Leukopenia in some cats with
intraluminal or extraluminal rectal masses, rectal FeLV or FIV infection.
PATHOPHYSIOLOGY
stricture, or sublumbar lymphadenopathy. • Panhypoproteinemia caused by PLE is
• High solute and fluid secretion—secretory
uncommon in cats with intestinal disease, but
diarrhea. • Low solute and fluid absorption— CAUSES can occur; hypoalbuminemia can be seen.
osmotic diarrhea. • High intestinal permeability.
Small and Large Intestinal Diseases • Biochemical profiles and urinalysis
• Abnormal gastrointestinal (GI) motility.
Primary Disease abnormalities may suggest renal disease,
• Many cases involve various combinations of
• Inflammatory bowel disease (IBD)—e.g., hypoproteinemia, hepatobiliary disease, or
these four basic pathophysiologic mechanisms.
lymphoplasmacytic enteritis, eosinophilic endocrinopathy.
SYSTEMS AFFECTED
enteritis, granulomatous enteritis. • Neoplasia— OTHER LABORATORY TESTS
• Endocrine/metabolic—fluid, electrolyte,
e.g., lymphoma, including large cell (B-cell Fecal and/or Rectal Scraping Exam
and acid-base. • Exocrine. • GI. • Lymphatic.
lymphoma) and small cell alimentary lymphoma • Direct wet prep, routine centrifugation fecal
GENETICS (T-cell), adenocarcinoma, mast cell neoplasia. flotation, fecal ELISA testing may indicate GI
N/A • Bacterial—e.g., Salmonella spp., enterotoxic
parasites. • Cytologic examination of rectal
INCIDENCE/PREVALENCE Escherichia coli, other enterobacteriaceae species, scrapings may reveal specific organisms, such as
Unknown Clostridia spp.: usually acute diarrhea. • Viral— Histoplasma, Prototheca, or Tritrichomas. • PCR
e.g., enteric coronavirus (usually acute diarrhea fecal testing should be interpreted with caution,
GEOGRAPHIC DISTRIBUTION unless combined with other viral infections or
Worldwide because positive results for toxin genes or
co-factors), feline infectious peritonitis, feline infectious agents may or may not correlate with
SIGNALMENT leukemia virus (FeLV) associated, feline clinical disease; interpret PCR results in light of
immunodeficiency virus (FIV) associated. patient signalment, history, clinical presentation,
Species
• Mycotic—e.g., histoplasmosis. • Algal—e.g.,
Cat vaccination history, and other laboratory data.
protothecosis, pythiosis. • Parasites—e.g., • PCR for Tritrichomonas—most sensitive test;
Breed Predilections Giardia, Toxocara spp., Ancylostoma, Toxascaris be certain to send fresh fecal sample, colonic
None leonina, Cryptosporidium spp., Cystoisospora spp., lavage fluid, or loop scraping for testing.
Mean Age and Range Tritrichomonas foetus. • Partial obstruction—e.g., • Culture feces if Salmonella is suspected—
Any age. foreign body, intussusception, neoplasia. special media required.
• Secondary lymphangiectasia—very rare in cats.
Predominant Sex • Intestinal microbial dysbiosis—cause vs. effect. Thyroid Function Tests
None • Short bowel syndrome. • GI ulceration—rare • High total T4 or free T4 concentration
SIGNS in cats. indicates hyperthyroidism. • If hyper
thyroidism is suspected but T4 is normal,
General Comments Maldigestion perform a T3 suppression test, repeat the T4 a
• Underlying disease process determines extent • Hepatobiliary disease—lack of bile salts
few months later, or perform a technetium
of clinical signs. • 2–3% increase of water needed for intraluminal digestion. • Exocrine scan of the thyroid glands.
content of stool results in gross description of pancreatic insufficiency (EPI).
diarrhea. • Classification of small, large, and Serologic Testing
Dietary Test for FeLV and FIV—especially if
mixed bowel types of diarrhea may have overlap • Dietary intolerance (food-responsive
of descriptive findings. hematologic abnormalities are present.
diarrhea). • Food allergy.
Historical Findings Test for Exocrine Pancreatic Function
Metabolic Disorders Feline-specific trypsin-like immunoreactiv-
• Small bowel diarrhea can include—normal to • Hyperthyroidism. • Cobalamin deficiency—
increased volume; normal to moderately ity—test of choice for diagnosis of EPI.
typically secondary to underlying IBD or
increased (2–4 times/day) defecation frequency; lymphoma. • Renal disease. • Hepatobiliary IMAGING
weight loss; polyphagia; melena; flatulence and disease. • Adverse drug reactions. • Survey abdominal radiography may indicate
borborygmus; vomiting: variable. • Large abnormal intestinal pattern, organomegaly,
bowel diarrhea can include—smaller volume; Congenital Anomalies mass, foreign body, pancreatic disease,
frequency of defecation is increased (>4 times/ • Short colon. • Portosystemic shunt.
hepatobiliary disease, urinary disease, or
day); often hematochezia and mucus; tenesmus, • Persistent pancreaticomesojejunal ligament.
abdominal effusion; low yield in most cats
urgency, dyschezia; flatulence and borborygmus: RISK FACTORS with chronic diarrhea. • Contrast radio
variable; vomiting: variable. Dietary changes, feeding poorly digestible or graphy (upper GI series or barium enema)
Physical Examination Findings high-fat diets. may indicate bowel wall thickening, intestinal
ulcers, mucosal irregularities, mass, radiolucent
Small Bowel foreign body, or stricture; procedure performed
• Poor body condition associated with malab- infrequently in cats in light of advantages of
sorption, maldigestion, and protein-losing abdominal ultrasonography. • Abdominal
enteropathy (PLE). • Variable dehydration. DIAGNOSIS
ultrasonography may demonstrate bowel wall
• Abdominal palpation may reveal segmental or DIFFERENTIAL DIAGNOSIS thickening, abnormal bowel wall layering, GI
diffusely thickened small bowel loops associated First localize the origin of the diarrhea to the or extra-GI masses, intussusception, foreign
with infiltrative disease, abdominal effusion, small or large bowel (or both) on the basis of body, ileus, abdominal effusion, hepatobiliary
foreign body, neoplastic mass, intussusception, historical signs.
Diarrhea, Chronic—Cats (continued)
disease, pancreatitis, renal disease, or DIET POSSIBLE COMPLICATIONS

mesenteric or mesocolic lymphadenopathy. • Feeding elimination diet (intact novel • Dehydration. • Lowered body condition.
protein source or hydrolyzed protein) will • Abdominal effusions as related to specific
D DIAGNOSTIC PROCEDURES
resolve diarrhea in 40–60% of cats with cause of chronic diarrhea.
If maldigestive (EPI), metabolic, parasitic,
dietary, and infectious causes have been chronic enteropathy; response should be EXPECTED COURSE AND PROGNOSIS
excluded, consider empiric dietary therapy, detected within 2–3 weeks following dietary Vary with underlying disease.
utilizing an elimination diet for 2 weeks implementation. • Repeated changes of diet
before performing endoscopy and biopsy or a made in order to maintain a symptom-free
laparotomy for definitive diagnosis. situation suggest that further testing needed.
CLIENT EDUCATION
Endoscopy/Laparoscopy
Complete resolution of signs is not always
MISCELLANEOUS
• Upper GI flexible endoscopy allows exam-
possible in cats with IBD, neoplasia, or fungal ASSOCIATED CONDITIONS
ination and biopsy of gastric and duodenal
disease despite proper treatment. N/A
mucosa; always obtain multiple (8–10) mucosal
specimens from each segment/area. • Flexible SURGICAL CONSIDERATIONS AGE-RELATED FACTORS
colonoscopy allows examination of entire rectum, Pursue exploratory laparotomy and surgical N/A
colon, cecum, and ileum; always obtain multiple biopsy if evidence of obstruction, intestinal ZOONOTIC POTENTIAL
mucosal specimens (8–10) from each segment. mass, or mid-small bowel disease unreachable • Toxoplasmosis. • Giardiasis (low zoonotic
• Visual impressions of GI mucosal detail may via endoscopic procedure. potential). • Cryptosporidiosis. • Salmonellosis.
not reflect histopathologic changes; always take • Campylobacter jejuni.
biopsies. • Endoscopic biopsies rely upon
infiltrative and inflammatory diseases being PREGNANCY/FERTILITY/BREEDING
represented in first two layers of the intestinal N/A
wall, and segments biopsied being representative
MEDICATIONS
SYNONYMS
of disease process. • Full-thickness biopsies can DRUG(S) OF CHOICE None
be obtained via laparoscopy from one or more • Disease specific. • Prednisolone (1–2 mg/
kg BID) for management of IBD; SEE ALSO
segments of small intestine (not large intestine)
chlorambucil (2 mg/cat q48–72h) should be • Cobalamin Deficiency. • Diarrhea, Antibiotic
via exteriorization of the segment(s), but are not
considered together with prednisolone in Responsive. • Exocrine Pancreatic Insufficiency.
typically necessary as most diseases can be
severe IBD cases that are refractory to • Food Reactions (Gastrointestinal), Adverse.
diagnosed endoscopically.
steroids alone or for management of small • Inflammatory Bowel Disease. • Small
Surgical Biopsy Intestinal Dysbiosis.
cell intestinal lymphoma. • Supplementation
Surgical approach beneficial if biopsies of
with cyanocobalamin at 250 ug SC per cat ABBREVIATIONS
multiple organs (small intestine, lymph
on a weekly basis for 6 consecutive weeks, • EPI = exocrine pancreatic insufficiency.
nodes, stomach, pancreas, liver) are desired.
followed by every 3 weeks for the indefinite • FeLV = feline leukemia virus. • FIV = feline
Ultrasound-Guided GI Aspiration or future. • Probiotics can be beneficial in immunodeficiency virus. • GI = gastrointestinal.
Biopsy some patients with chronic nonspecific • IBD = inflammatory bowel disease. • PLE
• Can perform ultrasound-guided fine-needle diarrhea. = protein-losing enteropathy.
aspiration on some GI mass lesions, but CONTRAINDICATIONS Suggested Reading
cytologic interpretation accuracy is subject to Anticholinergics exacerbate most types of Evans SE, Bonczynski JJ, Broussard JD, et al.
sample quality, expertise, and limitations of chronic diarrhea and should not be used for Comparison of endoscopic and full-thick-
technique; small cell alimentary lymphoma empirical treatment. ness biopsy specimens for diagnosis of
cannot be diagnosed by cytology, as cells will be inflammatory bowel disease and alimentary
small lymphocytes. • Paracentesis of peritoneal PRECAUTIONS
Opiate antidiarrheals such as diphenoxylate tract lymphoma in cats. J Am Vet Med
fluid for fluid analysis, culture, and cytology is Assoc 2006, 229(9):1447–1450.
recommended. • Concern has been expressed and loperamide can cause hyperactivity and
respiratory depression in cats and should not Sabattini S, Bottero E, Turba ME, et al.
for risk of translocation of cancer cells or Differentiating feline inflammatory bowel
infective organisms with these procedures. be used for more than 3 days.
disease from alimentary lymphoma in duodenal
PATHOLOGIC FINDINGS POSSIBLE INTERACTIONS endoscopic biopsies. J Small Anim Pract 2016,
Vary with underlying disease. N/A 57(8):396–401. doi: 10.1111/jsap.12494
ALTERNATIVE DRUG(S) Tolbert MK, Gookin JL. Tritrichomonas foetus:
N/A a new agent of feline diarrhea. Compend
Contin Educ Pract Vet 2009, 31(8):374–381.
Willard MD, Mansell J, Fosgate GT, et al.
TREATMENT Effect of sample quality on the sensitivity of
APPROPRIATE HEALTH CARE endoscopic biopsy for detecting gastric and
• Outpatient medical management most FOLLOW-UP duodenal lesions in dogs and cats. J Vet
common. • Treat underlying cause. PATIENT MONITORING Intern Med 2008, 22(5):1084–1089.
NURSING CARE • Assess changes in frequency and severity of Author Karin Allenspach
• Give fluid therapy with balanced electrolyte diarrhea and bodyweight. • Resolution Consulting Editor Mark P. Rondeau
solution as needed. • Correct electrolyte and usually occurs within 2–3 weeks following Acknowledgment The author and book
acid-base imbalances. successful implementation of dietary therapy; editors acknowledge the prior contribution of
consider reevaluating diagnosis if diarrhea Mark E. Hitt.
ACTIVITY does not resolve.
No restriction.
PREVENTION/AVOIDANCE Client Education Handout
N/A available online
Diarrhea, Chronic—Dogs
enteropathy (PLE). • Variable dehydration. RISK FACTORS
• Abdominal palpation may reveal thickened Small Bowel
small bowel loops (diffuse or segmental) • Large-breed, younger, and less severely
BASICS associated with infiltrative disease, abdominal affected dogs have higher risk of food-
D
DEFINITION effusion, foreign body, neoplastic mass, responsive diarrhea. • Yorkshire terrier, West
• A change in the frequency, consistency, and intussusception, or enlarged mesenteric lymph Highland white terrier, Rottweiler, soft-coated
volume of feces for more than 3 weeks. • Can nodes. • Rectal palpation typically unremarkable. wheaten terrier predisposed to lymphang
be small bowel, large bowel, or mixed. Large Bowel iectasia secondary to IBD.
PATHOPHYSIOLOGY • Body condition more typically normal. Large Bowel
• Secretory diarrhea. • Osmotic diarrhea. • Dehydration—uncommon. • Abdominal • Dietary changes or indiscretion, stress, and
• Increased permeability. • Abnormal palpation may reveal thickened large bowel, psychological factors may play a role.
gastrointestinal (GI) motility. • Many cases foreign body, neoplastic mass, intussusception, • Granulomatous colitis (invasive adherent E.
involve combinations of these pathophysio or enlarged mesocolic lymph nodes. • Rectal coli–associated)—boxer, French bulldog <3
logic mechanisms. palpation may reveal irregularity of colorectal years old. • Pythiosis more common in
mucosa, intraluminal or extraluminal rectal large-breed dogs that spend more time
SYSTEMS AFFECTED
masses, rectal stricture, or sublumbar outside (roaming, hunting).
• Endocrine/metabolic. • Exocrine.
lymphadenopathy.
• Cardiovascular (fluid balance). • GI.
• Lymphatic. CAUSES
GENETICS Small Bowel
DIAGNOSIS
N/A Primary Small Intestinal Disease
• Inflammatory bowel disease (e.g., lympho DIFFERENTIAL DIAGNOSIS
plasmacytic enteritis, eosinophilic enteritis, First localize the origin to the small or large
Unknown
granulomatous enteritis, immunoproliferative bowel (or both).
GEOGRAPHIC DISTRIBUTION enteropathy of Basenjis). • Primary or secondary CBC/BIOCHEMISTRY/URINALYSIS
Pythiosis occurs often in young, large-breed dogs lymphangiectasia. • Neoplasia. • Bacterial • Eosinophilia may be associated with
living in rural areas, with a higher incidence in (Campylobacter jejuni, Salmonella spp., invasive parasitism, eosinophilic enterocolitis, hypo
states bordering the Gulf of Mexico. adherent or enterotoxic Escherichia coli, other adrenocorticism, paraneoplastic causes, or
SIGNALMENT enterobacteriaceae species). • Mycotic (e.g., pythiosis. • Lymphopenia and hypocholestero
histoplasmosis). • Algal (e.g., protothecosis, lemia may be associated with lymphangiectasia.
Species
pythiosis). • Parasites (e.g., Giardia, Toxocara • Anemia and microcytosis suggest chronic GI
Dog
spp., Ancylostoma, Toxascaris leonina, bleeding and iron deficiency. • Panhypopro
Breed Predilections Cryptosporidium spp., Cystoisospora spp.). teinemia resulting from PLE associated with
• Yorkshire terrier, West Highland white • Partial obstruction (e.g., foreign body, infiltrative small bowel disorders and lymphangi
terrier, Rottweiler, soft-coated wheaten intussusception, neoplasia). • Antibiotic- ectasia. • Biochemical profiles and urinalysis
terrier—lymphangiectasia secondary to responsive diarrhea (ARD; intestinal microbial abnormalities may suggest renal disease,
inflammatory bowel disease (IBD). • Boxer dysbiosis). • Short bowel syndrome. hepatobiliary disease, or endocrinopathy.
and French bulldog—granulomatous colitis.
Maldigestion OTHER LABORATORY TESTS
Mean Age and Range • Exocrine pancreatic insufficiency (EPI).
Fecal and/or Rectal Scraping Exam
Any age. • Hepatobiliary disease—lack of intraluminal bile.
• Direct wet-prep examination, fecal ELISA
Predominant Sex Dietary testing, and zinc sulfate centrifugation (for
None • Food-responsive enteropathy. • Food allergy. Giardia) may indicate GI parasites; multiple
SIGNS Metabolic Disorders samples may be required for whipworm
• Hepatobiliary disease. • Hypoadrenocorticism. infestations. • Cytologic examination of rectal
General Comments scrapings may reveal specific organisms, such as
• Disease processes determine extent of • Uremic gastroenteritis. • Toxins—entero
toxins, aflatoxins, exotoxins, food poisoning. Histoplasma or Prototheca. • PCR fecal testing
clinical signs. • 2–3% increase of water can be helpful when screening for uncommon
content of stool results in gross description of • Adverse drug reactions.
or difficult to diagnose infections; interpret
diarrhea. • Classification of small, large, and Large Bowel with caution as many of the microorganisms
mixed bowel types of diarrhea may have Primary Large Intestinal Disease can be found in healthy, nondiarrheic animals
overlap of descriptive findings. • Inflammatory bowel disease (e.g., lympho (e.g., viral enteritis, cryptosporidiosis, Giardia,
Historical Findings plasmacytic colitis, eosinophilic colitis, Salmonella, C. perfringens enterotoxin gene, C.
• Small bowel diarrhea can include—normal to granulomatous colitis). • Neoplasia. difficile, Campylobacter jejuni); PCR testing
increased volume; normal to moderately • Infection (e.g., histoplasmosis, adherent should be interpreted in light of patient
increased (2–4 times/day) defecation frequency; invasive E. coli [granulomatous colitis], signalment, history, clinical presentation,
weight loss; polyphagia; melena; flatulence and Prototheca, pythiosis). • Parasites (e.g., vaccination history, and other laboratory data.
borborygmus; vomiting—variable. • Large Trichuris vulpis, Giardia intestinalis, Entamoeba • Culture feces if Campylobacter or Salmonella
bowel diarrhea can include—smaller volume; histolytica, Balantidium coli). • Ileocolic suspected—special media required; check with
frequency of defecation increased (>4 times/ intussusception and cecal inversion. laboratory prior to submission.
day); often hematochezia and mucus; tenesmus, Dietary Tests of Exocrine Pancreatic Function
urgency, dyschezia; flatulence and borborygmus— • Diet—dietary indiscretion, diet changes, Canine-specific trypsin-like immunoreactivity
variable; vomiting—variable. food-responsive enteropathy, foreign material (TLI)—test of choice for confirming EPI.
Physical Examination Findings (e.g., bones, plastic, wood, hair). • Fiber- Tests for Malabsorption
Small Bowel responsive large bowel diarrhea. • Serum folate—low serum folate may be
• Poor body condition associated with Miscellaneous associated with proximal small intestinal
malabsorption, maldigestion, and protein-losing Irritable bowel syndrome. malabsorption. • Cobalamin—low serum
Diarrhea, Chronic—Dogs (continued)
cobalamin may be associated with EPI or ileal PLE—serum proteins, cholesterol, and
malabsorption; primary cobalamin deficiency clinical signs (ascites, subcutaneous edema,
syndromes are rare (border collie, giant pleural effusion). • Resolution of diarrhea
D schnauzer). TREATMENT usually gradual with treatment; if does not
Tests for Metabolic Disease APPROPRIATE HEALTH CARE resolve, reevaluate diagnosis.
• Resting cortisol—value <2.0 μg/dL should • Outpatient medical management most PREVENTION/AVOIDANCE
be followed up with adrenocorticotrophic common. • Treat underlying cause. N/A
hormone stimulation test to evaluate for NURSING CARE POSSIBLE COMPLICATIONS
hypoadrenocorticism. • Fasting and 2-hour • Fluid therapy with balanced electrolyte • Dehydration. • Lowered body condition.
postprandial serum bile acids—test if solutions as needed. • Correct electrolyte and • Abdominal effusions as related to specific
hepatobiliary disease suspected; significantly acid-base imbalances. cause of chronic diarrhea. • Ascites, subcutan-
increased values suggest hepatic dysfunction eous edema, and/or pleural effusion with
ACTIVITY
or portosystemic shunting. hypoalbuminemia from PLE.
No restrictions.
IMAGING EXPECTED COURSE AND PROGNOSIS
DIET
• Survey abdominal radiography may indicate Vary with underlying disease.
• Therapy with elimination diets or hydrolyzed
abnormal intestinal pattern, organomegaly, mass,
diets can be beneficial in up to 75% of dogs
foreign body, pancreatic disease, hepatobiliary
with uncomplicated chronic enteropathies.
disease, urinary disease, or abdominal effusion.
• Feeding lower-fat, novel (for the patient)
• Contrast radiography (upper GI series or
barium enema) may indicate bowel wall
protein source, highly digestible, or fiber- MISCELLANEOUS
supplemented diets for 3–4 weeks may resolve ASSOCIATED CONDITIONS
thickening, intestinal ulcers, mucosal
diarrhea due to dietary intolerance or allergy; N/A
irregularities, mass, radiolucent foreign body, or
repeated changes of diet to maintain symptom-
stricture; utility of contrast radiography has been AGE-RELATED FACTORS
free situation suggests further testing needed.
replaced with ultrasound in most patients. N/A
• Abdominal ultrasonography may demonstrate CLIENT EDUCATION
bowel wall thickening, abnormal bowel wall Complete resolution of signs is not always ZOONOTIC POTENTIAL
layering, GI or extra-GI masses, intussusception, possible in dogs with severe IBD, lymphangi • Giardiasis (low risk of transmission).
foreign body, ileus, abdominal effusion, hepato- ectasia, intestinal neoplasia, and pythiosis. • Salmonellosis. • Campylobacter jejuni.
biliary disease, or mesenteric or mesocolic • Ascaridiasis.
lymphadenopathy. Pursue laparotomy and biopsy if evidence of PREGNANCY/FERTILITY/BREEDING
DIAGNOSTIC PROCEDURES obstruction, intestinal mass, or mid-small bowel N/A
If maldigestive (EPI), metabolic, parasitic, dietary, disease unreachable via ultrasound-guided SYNONYMS
and infectious causes have been excluded, then procedure, or if diagnosis based on endoscopic N/A
consider dietary trial using elimination diet biopsy or ultrasound-guided procedure is SEE ALSO
(novel, single protein source) or hydrolyzed diet questioned because of poor response to therapy. • Colitis, Histiocytic Ulcerative. • Diarrhea,
for 2 weeks in stable dogs prior to performing Antibiotic Responsive. • Fiber-Responsive
advanced diagnostics (endoscopy or laparotomy Large Bowel Diarrhea. • Food Reactions
and biopsy). Up to 75% of dogs in referral (Gastrointestinal), Adverse. • Inflammatory
practices have been shown to be diet responsive. MEDICATIONS Bowel Disease. • Lymphangiectasia. • Protein-
Endoscopy/Laparoscopy DRUG(S) OF CHOICE Losing Enteropathy. • Small Intestinal Dysbiosis.
• Upper GI flexible endoscopy allows • Disease-specific. • Prednisone (2 mg/kg BID for ABBREVIATIONS
examination and biopsy of gastric and duodenal 2 weeks, with slow tapering over 6 weeks) for IBD. • ARD = antibiotic-responsive diarrhea.
mucosa; always obtain multiple (8–10) mucosal • Cyclosporine has shown to rescue dogs with • EPI = exocrine pancreatic insufficiency.
specimens from each segment. • Flexible steroid-refractory IBD. • Need for cyanocobala • GI = gastrointestinal. • IBD = inflammatory
colonoscopy allows examination of rectum, min supplementation must be assessed in all dogs bowel disease. • PLE = protein-losing
colon, cecum, and ileum; always obtain with chronic enteropathy. • Probiotics beneficial in enteropathy. • TLI = trypsin-like immuno-
multiple mucosal specimens (8–10) from each some dogs with chronic enteropathy. reactivity.
segment. • Gross appearance of mucosa does
not always correlate with histopathology; always CONTRAINDICATIONS Suggested Reading
take biopsies. • Endoscopic biopsies rely upon Anticholinergics can exacerbate the situation Allenspach K, Culverwell C, Chan D.
diseases being represented in first two layers of with many causes of chronic diarrhea; they Long-term outcome in dogs with chronic
intestinal wall and segments biopsied being are sometimes used to relieve cramping enteropathies: 203 cases. Vet Rec 2016,
representative of others not reached. • Full- associated with irritable bowel syndrome. 178(15):368. doi: 10.1136/vr.103557
thickness biopsies not indicated as most diseases PRECAUTIONS Willard MD, Mansell J, Fosgate GT, et al.
can be diagnosed endoscopically. • Surgical N/A Effect of sample quality on the sensitivity of
approach can be advantageous if biopsies of endoscopic biopsy for detecting gastric and
POSSIBLE INTERACTIONS duodenal lesions in dogs and cats. J Vet
multiple organs (e.g., small intestine, lymph N/A
nodes, stomach, pancreas, liver) are desired Intern Med 2008, 22(5):1084–1089.
ALTERNATIVE DRUGS Author Karin Allenspach
Ultrasound-Guided GI Aspirates N/A Consulting Editor Mark P. Rondeau
• Ultrasound-guided fine-needle aspiration of GI Acknowledgment The author and book
mass lesions can be helpful for diagnosing mast editors acknowledge the prior contribution of
cell tumors, carcinomas, and large-cell lymphoma. Mark E. Hitt.
• Seeding of neoplastic cells is a concern.
FOLLOW-UP
Capsule Endoscopy
Capsule endoscopy procedures can help identify PATIENT MONITORING Client Education Handout
• Frequency and consistency of stool, available online
location of bleeding ulcers in the jejunum.
appetite, and bodyweight. • In dogs with
Digoxin Toxicity
all patients with concentrations >1.5 ng/mL
have signs of toxicity; some with values in the
normal range have signs of toxicity, especially
BASICS if hypokalemic. To minimize the risk of FOLLOW-UP D
toxicity, the author aims to achieve a digoxin • Inform owner that reduction in appetite is
OVERVIEW
Not uncommon in patients treated with level between 0.5 and 1 ng/mL. an early indication of digoxin toxicity.
digoxin due to digoxin’s narrow therapeutic • Monitor renal function and electrolytes
IMAGING frequently in patients receiving digoxin; lower
index and prevalence of renal impairment in N/A
elderly patients with cardiac disease. Becoming digoxin dose if renal disease develops.
less common in clinical practice as use of DIAGNOSTIC PROCEDURES • Monitor serum digoxin concentration
digoxin has decreased in management of periodically.
ECG
heart failure. • Monitor ECG periodically to assess for
• Conduction disturbances—atrioventricular
arrhythmias or conduction disturbances that
SIGNALMENT (AV) block, arrhythmias, and ST segment
may suggest digoxin toxicity.
• Dog and cat. depression in some patients.
• Monitor bodyweight frequently; alter
• More common in geriatric patients. • Digoxin can cause any arrhythmia.
digoxin dosage accordingly; patients with
SIGNS congestive heart failure often lose weight.
Historical Findings
• Anorexia.
• Vomiting. TREATMENT
• Diarrhea. • Discontinue digoxin until signs of toxicity MISCELLANEOUS
• Lethargy. resolve (24–72 hours); reevaluate need for the
medication; if necessary, resume treatment at SEE ALSO
• Depression.
a dosage based on the serum digoxin concen- • Atrioventricular Block, Complete (Third
Physical Examination Findings tration. Degree).
Heart rate may range from severe bradycardia • Maintain hydration and correct any • Atrioventricular Block, First Degree.
to severe tachycardia. electrolyte disturbance (especially hypoka- • Atrioventricular Block, Second Degree—
lemia) with parenteral fluid administration. Mobitz Type I.
CAUSES & RISK FACTORS • Atrioventricular Block, Second Degree—
• Renal disease—impairs digoxin elimination. • Discontinue drugs that slow digoxin
metabolism or elimination (e.g., quinidine, Mobitz Type II.
• Chronic pulmonary disease—results in
verapamil, amiodarone). • Ventricular Tachycardia.
hypoxia and acid-base disturbances.
• Obesity—if dosage not calculated on lean • Severe arrhythmias (ventricular tachycardia) ABBREVIATIONS
bodyweight. and conduction disturbances—can be life- • AV = atrioventricular.
• Drugs and conditions that alter digoxin threatening; require hospitalization for
treatment and monitoring.
Suggested Reading
metabolism or elimination (e.g., quinidine Teerlink JR, Gersh BJ, Opie LH. Heart
and hypothyroidism). failure. In: Opie LH, Gersh BJ, eds., Drugs
• Rapid IV digitalization. for the Heart, 8th ed. Philadelphia, PA:
• Overdosage or accidental ingestion of Elsevier Saunders, 2013, pp. 169–223.
owner’s medication. MEDICATIONS Author Francis W.K. Smith, Jr.
• Administration of diuretic leading to Consulting Editor Michael Aherne
hypokalemia. DRUG(S) OF CHOICE
• Treat clinically important bradyarrhythmias
with atropine or a temporary transvenous
pacemaker.
• Treat clinically important ventricular
DIAGNOSIS arrhythmias with lidocaine or phenytoin;
phenytoin also reverses high-degree AV block.
DIFFERENTIAL DIAGNOSIS • Digoxin-binding antibodies (e.g., Digibind®)
• Arrhythmias and conduction distur- rapidly drop digoxin concentration in critically
bances—may reflect structural heart disease, ill animals; the use of these products is limited
not digoxin toxicity. in veterinary practice by their exorbitant cost.
• Anorexia—common in animals with heart • Thyroxin supplementation if hypothyroid-
failure. ism confirmed.
Animals with hypokalemia, hypercalcemia,
hypomagnesemia, and renal failure are INTERACTIONS
• Avoid or discontinue drugs that slow
predisposed to toxicity.
digoxin elimination or metabolism (e.g.,
OTHER LABORATORY TESTS quinidine, verapamil, and diltiazem).
• Consider checking thyroid status. • Avoid drugs that could worsen conduction
• Obtain digoxin serum concentration 8–10 disturbances (e.g., beta blockers and calcium
hours after an oral dose—therapeutic range is channel blockers).
0.5–1.5 ng/mL. A recent study in humans • Class 1A antiarrhythmic drugs (e.g., quinidine
found digoxin levels greater than 1 mg/ml and procainamide) may worsen AV block.
were associated with increased mortality; not
Diisocyanate Glues
• Elevated total proteins/prerenal azotemia— PREVENTION/AVOIDANCE
may occur secondary to dehydration from Prevent exposure.
vomiting.
D BASICS EXPECTED COURSE AND PROGNOSIS
IMAGING • With removal of FBO, prognosis is
OVERVIEW Survey radiographs (4–24 hours post excellent.
• Diisocyanate glues include wood glue, exposure)—glue appears as a mottled gas and • Without surgical removal, the FBO is not
construction glue, and some “high-strength soft tissue opacity distending the stomach. expected to resolve on its own.
or extra strength” glues. The appearance can resemble recent food
• Gorilla Glue is one popular brand name. ingestion (see Web Figure 1).
There are non-Gorilla brand glue types that
contain diisocyanate as the active ingredient
and not all types of Gorilla Glue contain MISCELLANEOUS
diisocyanates. Confirm the actual product ASSOCIATED CONDITIONS
with the owner, using the packaging if TREATMENT • Gastritis.
necessary. • Generally, not recommended due to risk
• Dermatitis.
• Typically, the owner finds a chewed bottle of esophageal or GI obstruction. Potential
of glue or glue stuck on the animal. use immediately after a large ingestion. ABBREVIATIONS
• Gastric lavage is rarely of benefit as glue • FBO = foreign body obstruction.
• Diisocyanate glue rapidly expands in the
expands too rapidly. • GDV = gastric dilatation-volvulus.
moist environment of the stomach, causing
• Dilution with water or other fluids should • GI = gastrointestinal.
bloat and foreign body obstruction (FBO).
The glue is not absorbed and does not cause be avoided as excess moisture allows further Suggested Reading
systemic toxicity. Ingestions as small as 2 oz expansion of the glue. Horstman CL, Eubig PA, Cornell KK, et al.
(56 g) can require surgical intervention to • IV fluids as needed for dehydration. Gastric outflow obstruction after ingestion
resolve obstruction. • Wash exposed skin with warm soapy water, of wood glue in a dog. J Am Anim Hosp
• Glue is also adhesive and an irritant to the rub vegetable oil into the hair, or clip hair to Assoc 2003, 39:47–51.
paws, oral cavity, and stomach lining. remove as much glue as possible. Glue can be Peterson KL. Glues and adhesives. In: Hovda
• Inhalation may cause irritation to the left adhered to the skin if nonirritating and LR, Brutlag A, Poppenga R, Peterson K,
lungs. will fall off over time. eds., Blackwell’s Five Minute Veterinary
• Oxygen as needed for signs related to Consult: Small Animal Toxicology, 2nd ed.
SIGNALMENT inhalation.
Dogs and less commonly cats, birds, and Ames, IA: Wiley-Blackwell, 2016, pp.
• Surgical removal of the expanded glue 95–100.
small mammals. Young animals are more foreign body is almost always indicated in
often affected. Author Tyne Hovda
ingestions greater than 2 oz or with lesser Consulting Editor Lynn R. Hovda
SIGNS amounts in smaller animals. Acknowledgment: The author and book
• Occur within 15 minutes to 24 hours after editors acknowledge the prior contribution of
ingestion. Catherine A. Angle.
• Ingestion—consistent with FBO and may
include gagging, retching, vomiting, anorexia,
abdominal distension, abdominal pain;
MEDICATIONS
hematemesis in prolonged or severe cases. DRUG(S) OF CHOICE available online
• Inhalation—coughing, sneezing, increased • Antiemetic—maropitant citrate 1 mg/kg
secretions within 4–8 hours. SC/IV q24h.
• Dermal—irritation, redness, rash. • H2 blocker (for gastric inflammation or
ulceration)—ranitidine 1–2 mg/kg PO/IM/
SC/IV q6–12h; famotidine 0.5–1.1 mg/kg
Pets with access to diisocyanate glue products.
PO q12h; pantoprazole 0.7–1 mg/kg IV over
15 minutes q24h.
• Sucralfate (for a gastric ulcer if present)—
0.5–1 g PO TID on an empty stomach.
DIAGNOSIS CONTRAINDICATIONS
DIFFERENTIAL DIAGNOSIS • Emetics—emesis should not be performed
• History of exposure and clinical signs unless done immediately after a witnessed
generally facilitate diagnosis. ingestion. Expansion of the glue is rapid: late
• Presenting signs are consistent with gastric emesis stresses the stomach wall and could
dilatation-volvulus (GDV), bloat, pancreatitis, damage the esophagus.
inflammatory bowel disease, and other causes • Do not dilute with water as exposure to
of FBO. moisture leads to rapid expansion of the glue.
• Radiographs are highly suggestive of FBO
(see Web Figure 1).
• CBC—generally no significant changes. FOLLOW-UP
• Electrolyte disturbances—consistent with
PATIENT MONITORING
gastrointestinal (GI) obstruction and
Monitor in hospital until eating and drinking
anorexia.
normally. Recheck 10–14 days post surgery.
Discolored Tooth/Teeth
with release into adjacent dentinal tubules; orthophosphate complex in the collagen
discoloration goes from pink to purple matrix of enamel; occurs on multiple teeth;
(pulpitis) to gray (pulpal necrosis) to black results in a yellow-brown discoloration.
BASICS (liquefactive necrosis). Long-term use of tetracyclines in mature D
DEFINITION • Amelogenesis imperfecta—developmental animals can involve secondary dentin
• Normal tooth color varies and depends on alteration in the structure of enamel affecting formation.
the shade, translucency, and thickness of all teeth; chalky appearance with a pinkish • Amalgam (as with extrinsic stains).
enamel. Translucent enamel is bluish-white, hue; problem in the formation of the organic • Iodine/essential oils.
opaque enamel is gray-white. matrix, mineralization of the matrix, or the • In endodontically treated teeth from the
• Extrinsic—from surface accumulation of maturation of the matrix. medicants penetrating the dentinal tubules.
exogenous pigment. • Dentinogenesis imperfecta—developmental • Macrolide antibiotic (reported in humans)—
• Intrinsic—secondary to endogenous factors alteration in dentin formation; enamel results in vacuolar degeneration of the
discoloring the underlying dentin. separates easily from the dentin, resulting in ameloblast and cystic change at maturation
grayish discoloration. and hypocalcification, giving a white
PATHOPHYSIOLOGY
• Infectious agents (systemic)—parvovirus, discolored lesion with horizontal stripes on
Extrinsic Discoloration distemper virus, or any agent that causes a the enamel.
• Bacterial stains—chromogenic bacteria: sustained body temperature rise; affects the • Bacterial “creeping” (leakage)—occurs
green to black-brown to orange color, usually formation of enamel; a distinct line of around the margins of a restoration and
1 mm above the gingival margin on the tooth. resolution is visible on the teeth; affects all usually is blackish in color.
• Plaque related—a black-brown stain; teeth developing at the time of the insult; SYSTEMS AFFECTED
usually secondary to the formation of ferric results in enamel hypoplasia or hypocalcifica- Gastrointestinal—oral cavity.
sulfide from the interaction of bacterial ferric tion where the abnormal enamel can have
sulfide and iron in the saliva. Plaque is usually black edges and the dentin is brownish. GENETICS
white. • Dental fluorosis—affects all teeth; excess • Amelogenesis imperfecta and dentinogenesis
• Foods—charcoal biscuits and similar fluoride consumption affects the maturation imperfecta in humans are inherited conditions
products penetrate the pits and fissures of the of enamel, resulting in pits (enamel hypo- that have many modes of inheritance. The
enamel; food with abundant chlorophyll can plasia) with black edges; the enamel is a mode of inheritance in animals has not been
produce a green discoloration. lusterless, opaque white, with yellow-brown studied.
• Gingival hemorrhage—green or black zones of discoloration. • Congenital hypothyroidism.
staining from the breakdown of hemoglobin • Tooth erosion from constant vomiting • Metabolic diseases.
into green biliverdin. results in enamel pitting and darkened INCIDENCE/PREVALENCE
• Dental restorative materials—amalgam: staining. • Discoloration of the teeth or a tooth is
black-gray discoloration. • Attrition—tooth-to-tooth wear results in extremely common in all animals.
• Medications—products containing iron or crown loss and reparative dentin formation • Extrinsic staining is very common,
iodine give a black discoloration; sulfides, (yellow-brown color). especially bacterial stains; others are less
silver nitrate, or manganese: gray-to-yellow to • Abrasion—tooth wear against another common.
brown-to-black discoloration; copper or surface; chewing on tennis balls or from a • Intrinsic staining is likewise very common,
nickel: green discoloration; cadmium, yellow dermatologic condition. Reparative dentin especially internal and external resorption,
to golden brown discoloration (e.g., 8% (yellow-brown color) forms. followed by localized red blood cell destruc-
stannous fluoride combines with bacterial • Aging—older animals’ dentition is more tion; the other causes are rare.
sulfides, giving a black stain; chlorhexidine yellow and less translucent.
gives a yellowish-brown discoloration). • Malnutrition (generalized, vitamin D GEOGRAPHIC DISTRIBUTION
• Metals—wear from chewing on cages or deficiency, and vitamin A deficiency)—if • Heavy metals from mining operations.
food dishes. severe can result in demarcated opacities on • Fluoridation forms areas of excessive
• From removed orthodontic brackets or the enamel. fluoride in the drinking water.
bands. • Otherwise none.
Internal/External Resorption
• Crown fragments—less translucency due to SIGNALMENT
• Internal—follows pulpal injury (trauma)
dehydration of fragment.
causing vascular changes with increased Species
• Discolored restorations.
oxygen tension and decreased pH, resulting Dogs and cats.
• Tooth wear with dentin exposure—tertiary
in destruction (resorption) of the tooth from Mean Age and Range
dentin, reparative dentin, secondary dentin.
within the pulp from odontoclasts; tooth has The reported age range varies—when the
• A calculus-covered crown ranges in color
pinkish hue. condition affects the developing enamel or
from dark yellow to dark brown.
• External—many factors possible: trauma, dentin it can be first noted after tooth
Intrinsic Discoloration orthodontic treatment, excessive occlusal eruption (6 months of age).
• Hyperbilirubinemia—affects all teeth; forces, periodontal disease (and treatment),
during dentin formation bilirubin accumulates tumors, periapical inflammation, and Predominant Sex
in the dentin from excess red blood cell unknown factors; resorption can start None
breakdown; extent of discoloration depends anywhere along the periodontal ligament and SIGNS
on the length of hyperbilirubinemia (lines of can extend to the pulp and into the crown
resolution occur once the condition has been causing a pinkish discoloration; osteoclasts Historical Findings
resolved); green discoloration. and odontoclasts resorb the tooth structure. Owner reports a variation in color of a tooth
• Localized red blood cell destruction, one or teeth.
Medications and Discoloration
tooth or focal area—usually follows a Physical Examination Findings
• Tetracycline—during enamel formation, it
traumatic injury to the tooth; discoloration • Abnormal coloration of tooth or teeth.
binds to calcium, forming a calcium
from hemoglobin breakdown within the pulp • Pitted enamel with staining.
Discolored Tooth/Teeth (continued)
• Fractured tooth. • Appropriate preoperative diagnostics when

• Rings or lines of discoloration around tooth indicated prior to procedure.
or teeth.
D • Wear on crowns of the dentition or in
PATHOLOGIC FINDINGS MEDICATIONS
See Pathophysiology.
selected areas as in behavioral causes (cage DRUG(S) OF CHOICE
biters—distal aspect of the canines is N/A
affected).
• Erosion of enamel.
TREATMENT
• Extrinsic discoloration—bacterial stains APPROPRIATE HEALTH CARE FOLLOW-UP
from plaque and calculus; foods; gingival • Extrinsic stain removal—mainly cosmetic.
hemorrhage; dental restorative materials, • Intrinsic stain treatment—functional and PREVENTION/AVOIDANCE
medications (chlorhexidine, 8% stannous pain relieving. • See Pathophysiology.
fluoride), metal. • Good oral care at home will help prevent
NURSING CARE the reoccurrence of certain specific stains.
• Intrinsic discoloration—internal (trauma); • Extrinsic stain—remove inciting cause.
external tooth resorption; localized red blood • Intrinsic stain—soft food; remove chew POSSIBLE COMPLICATIONS
cell destruction in the tooth (trauma); toys. See Client Education.
systemic infections; medications (tetracy-
ACTIVITY EXPECTED COURSE AND PROGNOSIS
cline); fluorosis; hyperbilirubinemia;
Curtail or treat specific behavioral abnormali- Vary dependent upon the etiology, but can
amelogenesis imperfecta; dentinogenesis
ties (cage biting). range from mere aesthetics to significant pain.
imperfecta.
DIET
N/A
CLIENT EDUCATION
DIAGNOSIS • To prevent it in future animals or litters if
MISCELLANEOUS
preventable (medication use). ASSOCIATED CONDITIONS
• Intrinsic causes—irregular enamel surfaces are • Enamel hypoplasia/hypocalcification
• Calculus on the teeth.
more likely to accumulate plaque and calculus, • Juvenile purpura.
• Normal tooth aging—increased
translucence. leading to subsequent periodontal disease. AGE-RELATED FACTORS
• Food debris lodged in the spaces between
Abnormally formed teeth or teeth that have All ages affected, depends on the cause.
the teeth (diastema). localized red blood cell destruction are more
prone to fracture or development of tooth ZOONOTIC POTENTIAL
CBC/BIOCHEMISTRY/URINALYSIS abscessation. None.
• Anemia—blood-related disorders. • Some causes are painful (tooth resorption). PREGNANCY/FERTILITY/BREEDING
• Bilirubin—increased with liver diseases. • Tetracycline administration during
OTHER LABORATORY TESTS • Extrinsic stain (cosmetic)—internal and/or pregnancy may result in permanent tooth
• T3/T4—low in congenital hypothyroidism. external bleaching; veneers or crowns. discoloration in offspring.
• Specific metabolic enzyme decrease or Polishing the affected teeth with 3% • See Genetics.
absence—tyrosinemia. hydrogen peroxide in pumice will help SYNONYMS
IMAGING remove external stain. Also good home care • Chlorhexidine staining.
Dental radiography is extremely useful in with plaque control will minimize • Extrinsic staining.
identifying internal or external resorption, redevelopment of some stains (plaque/ • Intrinsic staining.
restorative materials, or bacterial stain from calculus/bacteria stain). • Tetracycline staining.
coronal percolation. • Intrinsic stain (functional and pain
Suggested Reading
relief )—possible endodontic treatment
DIAGNOSTIC PROCEDURES Hale FA. Localized intrinsic staining of teeth
(internal resorption and localized red blood
• If many teeth are affected, one tooth can be due to pulpitis and pulp necrosis in dogs.
cell destruction).
extracted and sent for histologic evaluation J Vet Dent, 2001, 18(1):14–20.
• Restorative procedures such as crowns or
(see below). Lobprise HB, Dodd JR. Wiggs’ Veterinary
veneers to protect both tooth and pulp.
• Transillumination with a strong fiberoptic Dentistry Principles and Practice. Hoboken,
• Extraction of affected teeth may be
light may help distinguish between vital and NJ: Wiley-Blackwell, 2019.
required, especially with external resorption.
necrotic pulp. Author Kristin M. Bannon
Consulting Editor Heidi B. Lobprise
Discospondylitis
Physical Examination Findings • Urine cultures—indicated; positive in about
• Focal or multifocal areas of spinal pain in 30% of patients.
>80% of patients. • Organisms other than Staphylococcus
BASICS • Any disc space may be affected; lumbosacral spp.—may not be the cause. D
DEFINITION space is most commonly involved. • Serologic testing for Brucella canis—
A bacterial, fungal, and rarely algal infection • Paresis or paralysis, especially in chronic, indicated as this presents zoonotic potential.
of the intervertebral end plates, discs, and untreated cases. IMAGING
adjacent vertebral bodies. • Fever in ~30% of patients.
• Spinal radiography—usually reveals lysis of
• Lameness.
PATHOPHYSIOLOGY vertebral end plates adjacent to the affected
• Hematogenous spread of bacterial or fungal CAUSES disc, collapse of the disc space, and varying
organisms—most common cause. • Bacterial—Staphylococcus pseudintermedius degrees of sclerosis of the end plates and
• Seeding secondary to migrating foreign is most common. Others include Streptococcus, ventral spur formation; may not see lesions
body (grass awn) is also reported. Brucella canis, and Escherichia coli, but until 3–4 weeks after infection (therefore
• Neurologic dysfunction—may occur; virtually any bacteria can be causative. normal radiographs do not rule out).
usually the result of spinal cord compression • Fungal—Aspergillus, Paecilomyces, • Myelography—indicated with substantial
caused by proliferation of bone and fibrous Scedosporium apiospermum, and Coccidioides neurologic deficits; determine location and
tissue; less commonly owing to luxation or immitis. degree of spinal cord compression, especially
pathologic fracture of the spine, epidural • Grass awn migration is often associated if considering decompressive surgery; spinal
abscess, or extension of infection to the with mixed infections, especially Actinomyces; cord compression caused by discospondylitis
meninges and spinal cord. tends to affect the L2–L4 disc spaces and typically displays an extradural pattern.
vertebrae. • CT or MRI—more sensitive than radio-
SYSTEMS AFFECTED • Other causes—surgery, bite wounds. graphy; indicated when radiographs are
• Musculoskeletal—infection and
RISK FACTORS normal or inconclusive.
inflammation of the spine.
• Nervous—compression and/or infection of • Urinary tract infection; reproductive tract DIAGNOSTIC PROCEDURES
the spinal cord. infection. • CSF analysis—occasionally indicated to
• Periodontal disease. rule out meningomyelitis; usually normal or
GENETICS • Bacterial endocarditis. reveals mildly high protein.
• No definite predisposition identified.
• Pyoderma. • Bone scintigraphy—occasionally useful for
• An inherited immunodeficiency has been
• Immunodeficiency. detecting early lesions; helps clarify if
detected in a few cases. • Recent steroid administration. radiographic changes are infectious or
INCIDENCE/PREVALENCE • Intact male status. degenerative (spondylosis deformans).
Approximately 0.1–0.8% of dog hospital • Fluoroscopically guided fine-needle
admissions. aspiration of the disc—valuable for obtaining
GEOGRAPHIC DISTRIBUTION tissue for culture when blood and urine
cultures are negative and there is no improve-
• More common in the southeastern United DIAGNOSIS ment with empiric antibiotic therapy.
States.
• Grass awn migration and coccidiomycosis— PATHOLOGIC FINDINGS
• Intervertebral disc protrusion—may cause
more common in certain regions. • Gross—loss of normal disc space; bony
similar clinical signs; differentiated on the
SIGNALMENT proliferation of adjacent vertebrae.
basis of radiography and myelography.
• Microscopic—fibrosing pyogranulomatous
Species • Vertebral fracture or luxation—detected on
destruction of the disc and vertebral bodies.
Dog; rare in cat. radiographs.
• Vertebral neoplasia—usually does not affect
Breed Predilections adjacent vertebral end plates.
Large and giant breeds, especially German • Spondylosis deformans—rarely causes
shepherd and Great Dane. clinical signs; has similar radiographic TREATMENT
Mean Age and Range features, including sclerosis, ventral spur APPROPRIATE HEALTH CARE
• Mean age—4–5 years. formation, and collapse of the disc space; • Outpatient—mild pain managed with
• Range—5 months–12 years. rarely causes lysis of the vertebral end plates. medication.
• Focal meningomyelitis—often identified by
Predominant Sex • Inpatient—severe pain or progressive
cerebrospinal fluid (CSF) analysis. neurologic deficits require intensive care and
Males outnumber females by ~2 : 1.
CBC/BIOCHEMISTRY/URINALYSIS monitoring.
SIGNS
• Hemogram—often normal; may see
Historical Findings
NURSING CARE
leukocytosis. Nonambulatory patients—keep on clean, dry,
• Onset usually relatively acute; however, • Urinalysis—may reveal pyuria and/or
some patients may have mild signs for well-padded surface to prevent decubital
bacteriuria with concurrent urinary tract ulceration.
several months before presenting for infections.
examination. ACTIVITY
OTHER LABORATORY TESTS Restricted
• Pain—difficulty rising, reluctance to jump,
• Aerobic, anaerobic, and fungal blood
and stilted gait are most common signs. CLIENT EDUCATION
cultures identify the causative organism in
• Ataxia or paresis. • Explain that observation of response to
about 35% of cases; obtain if available.
• Weight loss and anorexia. treatment is very important in determining
• Sensitivity testing—indicated if cultures are
• Lameness. the need for further diagnostic or therapeutic
positive.
procedures.
Discospondylitis (continued)
• Instruct the client to immediately contact ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL

the veterinarian if clinical signs progress or • Initial therapy—cephradine (dogs: 20 mg/kg Brucella canis—human infection uncommon
recur or if neurologic deficits develop. PO q8h); amoxicillin trihydrate/clavulanate but may occur.
D potassium (dogs: 13.75–22 mg/kg PO q12h).
SURGICAL CONSIDERATIONS PREGNANCY/FERTILITY/BREEDING
• Curettage of a single affected disc space— • Refractory patients—clindamycin (dogs
N/A
occasionally necessary for patients that are and cats: 10 mg/kg PO q12h), enrofloxacin
(dogs: 10 mg/kg PO q24h; cats: 5 mg/kg PO SYNONYMS
refractory to antibiotic therapy. • Diskitis.
• Goals—remove infected tissue; obtain q24h), orbifloxacin (dogs and cats: 2.5–
7.5 mg/kg PO q24h). • Intervertebral disc infection.
tissue for culture and histologic evaluation. • Intradiskal osteomyelitis.
• Decompression of the spinal cord by
• Vertebral osteomyelitis.
hemilaminectomy or dorsal laminectomy—
indicated for substantial neurologic deficits SEE ALSO
and spinal cord compression evident on MRI FOLLOW-UP Brucellosis
or myelography when there is no improve- ABBREVIATIONS
PATIENT MONITORING
ment with antibiotic therapy; also perform • CSF = cerebrospinal fluid.
• Reevaluate after 5 days of therapy.
curettage of the infected disc space; it may be • NSAID = nonsteroidal anti-inflammatory
• No improvement in pain, fever, or
necessary to perform surgical stabilization if drug.
appetite—reassess therapy; consider a
more than one articular facet is removed from
a disc site.
different antibiotic, percutaneous Suggested Reading
aspiration of the affected disc space, Ameel L, Martlè V, Gielen I, et al.
or surgery. Discospondylitis in the dog: a retrospective
• Improvement—evaluate clinically and study of 18 cases. Vlaams Diergeneeskundig
radiographically every 4 weeks. Tijdschrift 2009, 78(5):347–353.
MEDICATIONS PREVENTION/AVOIDANCE Bagley RS. Diskospondylitis. Fundam Clin
DRUG(S) OF CHOICE Early identification of predisposing causes Neuro 2005, 172–173(283–285):346.
and prompt diagnosis and treatment—help Braund KG, Sharp NJH. Discospondylitis. In:
Antibiotics Vite C, ed., Braund’s Clinical Neurology in
• Selection based on results of blood cultures reduce progression of clinical symptoms and
neurologic deterioration. Small Animals: Localisation, Diagnosis and
and serology or end plate aspirate culture and Treatment. Ithaca, NY: IVIS, 2003. https://
sensitivity. POSSIBLE COMPLICATIONS www.ivis.org/library/braunds-clinical-
• Negative culture and serology—assume • Spinal cord compression owing to neurology-small-animals-localization-
causative organism is Staphylococcus spp.; treat proliferative bony and fibrous tissue. diagnosis-and-treatment/degenerative
with a cephalosporin (e.g., cephalexin 22 mg/kg • Vertebral fracture or luxation. Burkert BA, Kerwin SC, Hosgood GL, et al.
PO q8h) for 8–12 weeks. • Meningitis or meningomyelitis. Signalment and clinical features of
• Acutely progressive signs or substantial • Epidural abscess. diskospondylitis in dogs: 513 cases
neurologic deficits—initially treated with EXPECTED COURSE (1980–2001). J Am Vet Med Assoc 2005,
parenteral antibiotics (e.g., cefazolin; dogs 227(2):268–275.
and cats: 22 mg/kg IV q8h). AND PROGNOSIS
• Recurrence is common if antibiotic therapy Fischer A, Mahaffey MB, Oliver JE.
• Brucellosis—treated with tetracycline (dogs: Fluoroscopically guided percutaneous disk
15 mg/kg PO q8h) and streptomycin (dogs: is stopped prematurely (before 8–12 weeks of
treatment). aspiration in 10 dogs with diskospondylitis.
3.4 mg/kg IM q24h) or enrofloxacin (dogs: J Vet Intern Med 1997, 11:284–287.
10 mg/kg PO q24h). • Some patients require prolonged therapy
(1 year or more). Johnson RG, Prata RG. Intradiskal osteomy-
• One study suggested that antibiosis be elitis: a conservative approach. JAAHA
continued until radiographic signs were • Prognosis—depends on causative organism
and degree of spinal cord damage. 1983, 19:743–750.
resolved (range of 40–80 weeks). The roll of Kerwin SC, Lewis DD, Hribernik TN, et al.
imaging in definitively determining length of • Mild or no neurologic dysfunction
(dogs)—usually respond within 5 days of Diskospondylitis associated with Brucella
treatment has not been proven, however. canis infection in dogs: 14 cases (1989–
starting antibiotic therapy.
Analgesics • Substantial paresis or paralysis (dogs)— 1991). J Am Vet Med Assoc 1992,
• Signs of severe pain—treated with an prognosis guarded; may note gradual 201:1253–1257.
analgesic (e.g., oxymorphone; dogs: 0.05– resolution of neurologic dysfunction after Kornegay JN. Diskospondylitis. In: Kirk RW, ed.,
0.2 mg/kg IV/IM/SC q4–6h). several weeks of therapy; treatment Current Veterinary Therapy IX. Philadelphia,
• Taper dosage after 3–5 days to gauge warranted. PA: Saunders, 1986, pp. 810–814.
effectiveness of antibiotic therapy. • Brucella canis—signs usually resolve with Ruoff CM, Kerwin SC, Taylor AR.
therapy; infection may not be eradicated; Diagnostic imaging of discospondylitis. Vet
CONTRAINDICATIONS
recurrence common. Clin North Am Small Anim Pract 2018,
Glucocorticoids
48:85–94.
PRECAUTIONS Thomas WB. Diskospondylitis and other
Use nonsteroidal anti-inflammatory drugs vertebral infections. Vet Clin North Am
(NSAIDs) and other analgesics cautiously— Small Anim Pract 2000, 30:169–182.
may cause temporary resolution of clinical MISCELLANEOUS Author Mathieu M. Glassman
signs even when infection is progressing; ASSOCIATED CONDITIONS Consulting Editor Mathieu M. Glassman
when used, discontinue after 3–5 days to See Risk Factors.
assess efficacy of antibiotic therapy.
AGE-RELATED FACTORS Client Education Handout
POSSIBLE INTERACTIONS N/A available online
None
Disseminated Intravascular Coagulation

INCIDENCE/PREVALENCE • Suspect DIC any time thrombocytopenia
Associated with severe systemic inflammatory and prolonged clotting tests are seen
disease. together.
BASICS • Patients showing predisposing conditions D
SIGNALMENT
DEFINITION should have laboratory monitoring every
An acquired complex hemostatic defect Species 24–48 hours. A sudden drop in platelet count
arising from a variety of inciting causes that Dogs and cats; diagnosed more in dogs. and a 20–30% prolongation in APTT is
leads to intravascular activation of coagula- Breed Predilections suspicious for non-overt DIC. This is a
tion and consumption of clotting factors. It None critical stage for intervention to prevent
results in widespread formation of micro- progression to overt DIC.
Mean Age and Range • Hepatic insufficiency may mimic DIC.
thrombi with clinical manifestations of
Depends on the primary disease. Decreased production of clotting factors is
thrombosis and/or hemorrhage. Non-overt
disseminated intravascular coagulation (DIC) Predominant Sex common. Decreased clearance of normal
is the early, compensated form of DIC that None fibrin(ogen)olytic by-products may increase
features consumption of coagulation factors SIGNS FDP values. Mild idiopathic thrombocyto
and generation of microthrombi without clear • Vary with the primary disease and with
penia may also be seen. Spontaneous bleeding
clinical signs. Overt (decompensated) DIC DIC-associated organ dysfunction. is uncommon unless DIC is present.
refers to the classic phenotype associated with • Petechiae. CBC/BIOCHEMISTRY/URINALYSIS
hemorrhage, thrombosis, and organ failure. • Bleeding from venipuncture sites, mucosa, • Inflammatory leukogram, often with a
PATHOPHYSIOLOGY or into body cavities. stress component.
• DIC represents a complication of a variety • Bleeding is infrequent in cats, possibly • Mild to moderate thrombocytopenia
of primary conditions. It begins with a leading to underdiagnosis. (40–100 × 103/μL); less reliable in cats.
hypercoagulable state that leads to production • Anemia is possible. Red blood cell (RBC)
CAUSES
or embolization of microthrombi in small • Gastric dilatation-volvulus.
fragmentation is a supportive finding.
vessels. • Biochemical changes reflect affected organs;
• Heart failure.
• The primary conditions act through • Heartworm disease.
acute kidney injury may result in
increased exposure/production of tissue factor • Heat stroke.
isosthenuria, oligo-anuria, or the
(TF) that activates the extrinsic coagulation • Hemolysis, especially immune mediated.
identification of casts in urine sediment.
pathway. • Hemorrhagic gastroenteritis. OTHER LABORATORY TESTS
• TF is normally restricted from intravascular • Infectious diseases, systemic (especially • Prolonged clotting tests (PT, APTT);
exposure. Increased TF exposure occurs endotoxemia). APTT is prolonged first, PT becomes
through widespread endothelial injury and/or • Inflammation, severe—regardless of prolonged with transition to overt DIC.
inflammation. underlying cause. • Hypofibrinogenemia, although
• Inflammation activates endothelial cells, • Liver disease, severe. inflammatory increase may mask
platelets, and monocytes leading to membrane • Malignancies, especially hemangiosarcoma, consumption.
expression of TF. Inflammatory cytokines also mammary carcinoma, and pulmonary • Increased FDPs and D-dimers. D-dimers
induce vesiculation of these membranes, adenocarcinoma in dogs and lymphoma in cats. are very sensitive and specific. DIC is unlikely
releasing large quantities of microparticles • Pancreatitis. if D-dimers are low/negative. Neither test is
into circulation that are enriched with both • Protein-losing nephropathy. specific enough alone to diagnose DIC.
TF and phosphatidylserine (PS) and facilitate • Shock, hypoxia, acidosis. • Decreased AT; may be a positive acute
initiation of coagulation. Some neoplastic • Thrombocytopenia, especially immune- phase reactant in cats, masking consum-
cells constitutively produce membrane TF mediated. ption.
and also release microparticles. • Transfusion incompatibility. • Thromboelastography may provide
• Microparticles provide a suitable membrane • Trauma. evidence of hypocoagulability or fibrinolysis.
surface for amplifying intrinsic and common • Envenomation.
pathway coagulation, potentially leading to DIAGNOSTIC PROCEDURES
uncontrolled production of thrombin that RISK FACTORS Diagnostic procedures should be focused on
overwhelms endogenous coagulation inhibitors. Vary with cause. identifying the inciting cause of inflamma-
Fibrin clots generated by thrombin can cause tion, and may include imaging, tissue biopsy,
vascular occlusion and lead to organ or surgery as dictated by clinical signs.
dysfunction. PATHOLOGIC FINDINGS
• Widespread microthrombus formation DIAGNOSIS • Usually related to the primary disease or
consumes coagulation factors and platelets DIC-affected organs.
while initiating fibrinolysis. By-products of DIFFERENTIAL DIAGNOSIS
• Petechiae common.
• Key differentials—immune-mediated
fibrinolysis (fibrin degradation products
[FDPs]) have anticoagulant properties and thrombocytopenia, anticoagulant toxicity,
inhibit platelet function. Hemorrhage at a coagulation factor deficiency, paraproteinemia.
• Highly variable diagnostic pattern includes
variety of sites can follow.
• Uncontrolled progression leads to
thrombocytopenia, prolonged clotting times TREATMENT
widespread tissue hypoxia, multiorgan (prothrombin time [PT], activated partial APPROPRIATE HEALTH CARE
dysfunction, and death. thromboplastin time [APTT]), decreased • Requires intensive inpatient treatment.
fibrinogen, decreased antithrombin (AT), and • Aggressive treatment of the primary disease
SYSTEMS AFFECTED increased products of fibrinolysis (FDPs,
Multisystemic syndrome. is essential (e.g., antimicrobials for sepsis).
D-dimers).
Disseminated Intravascular Coagulation (continued)
NURSING CARE • Inhibitors of fibrinolysis should not be used. SYNONYMS

• Maintain tissue perfusion and oxygenation • The use of antiplatelet medications in • Consumptive coagulopathy.
using fluids, transfusions, and oxygen therapy. thrombocytopenic patients is not indicated. • Disseminated intravascular coagulopathy.
D • Restore depleted factors by blood/plasma • Corticosteroids impair function of
SEE ALSO
transfusions. Use fresh frozen plasma mononuclear phagocytes and do not have a • Coagulation Factor Deficiency.
(10–20 mL/kg) to correct bleeding due to clear indication for DIC unless important for • Thrombocytopenia.
factor deficiency. therapy of the underlying disease (e.g.,
lymphoma). ABBREVIATIONS
ACTIVITY • APTT = activated partial thromboplastin
Limited by disease severity. PRECAUTIONS time.
• Heparin may cause hemorrhage, and
DIET • AT = antithrombin.
Maintain nutritional support as appropriate therapy should be monitored. • DIC = disseminated intravascular
• Volume overload may occur in cases with
for the clinical condition of the patient. coagulation.
renal or pulmonary compromise. • FDP = fibrin degradation product.
CLIENT EDUCATION
Inform the owner that the condition is POSSIBLE INTERACTIONS • PS = phosphatidylserine.
life-threatening with a guarded to poor None • PT = prothrombin time.
prognosis.
• TF = tissue factor.
Related to primary disease. Plasma or whole Suggested Reading
blood transfusion to restore clotting factors is FOLLOW-UP Dunn ME. Acquired coagulopathies. In:
a presurgical consideration. Surgery may be Ettinger SJ, Feldman EC, eds. Textbook of
PATIENT MONITORING
contraindicated with uncontrolled bleeding. Veterinary Internal Medicine: Diseases of
• Clinical improvement and the arrest of
the Dog and Cat, 7th ed. St. Louis, MO:
bleeding are key positive findings.
Saunders, 2010, pp. 797–801.
• Daily lab testing (e.g., coagulation tests,
O’Brien M. The reciprocal relationship
fibrinogen, platelet counts) is warranted in severe
between inflammation and coagulation.
MEDICATIONS cases to identify positive or negative trends. Less
Top Companion Anim Med 2012,
frequent testing may suffice in milder cases.
DRUG(S) OF CHOICE 27:46–52.
• Coagulation times and fibrinogen often
• There is no specific pharmacologic therapy Ralph AG, Brainard MB. Update on
normalize more rapidly than FDPs and
for DIC per se. disseminated intravascular coagulation:
platelet counts.
• Heparin may be used in patients that have when to consider it, when to expect it,
overt thrombosis or in those at high risk of PREVENTION/AVOIDANCE when to treat it. Top Companion Anim
thrombosis with normal coagulation times. Early detection of non-overt DIC can allow Med 2012, 27:65–72.
Unfractionated heparin is preferred to low therapy before disease progresses to overt DIC. Stokol T. Laboratory diagnosis of dissemi-
molecular weight heparin in human patients POSSIBLE COMPLICATIONS nated intravascular coagulation in dogs and
with DIC. Aside from the primary disease, affected cats: the past, the present, and the future.
• Heparin binds to and potentiates the action organs may have permanent dysfunction or Vet Clin North Am Small Anim Pract 2012,
of AT. Plasma or blood transfusions may be marginal reserve capacity. 42:189–202.
needed to replenish AT for heparin to be an Author John A. Christian
EXPECTED COURSE AND PROGNOSIS Consulting Editor Melinda S. Camus
effective anticoagulant. For overt DIC, mortality rates for dogs range
• Starting doses for unfractionated heparin from 50% to 77%. For cats, rates may be >90%.
are 150–200 U/kg SC q8h. It may also be
given as a CRI starting at 20–30 U/kg/h IV
available online
(i.e., same total daily dosage). Therapy should
be monitored using serial measurements of
APTT or anti-Xa activity. MISCELLANEOUS
CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING
• Heparin therapy should be avoided in Unlike in humans, obstetric complications are
patients with coagulopathy. not a common cause in dogs and cats.
Drowning (Near Drowning)

hemoconcentration and increases in sodium, 10–20 mg/kg IV q24h in the dog, 5 mg/kg
chloride, and urine specific gravity. IV q24h in the cat) for aspiration pneumonia.
• Beta-2 agonists may help animals with
BASICS OTHER LABORATORY TESTS
suspected bronchospasm. • Pentoxifylline D
Arterial blood gas reveals hypoxemia (partial
OVERVIEW pressure of oxygen [PaO2] <80 mmHg), decreased incidence of lung injury in dogs
• Defined as process of experiencing hypoventilation (partial pressure of carbon with experimental freshwater aspiration.
respiratory impairment from submersion or dioxide [PaCO2] >50 mmHg), and acid-base CONTRAINDICATIONS/POSSIBLE
immersion in liquid; near drowning defined as derangements. INTERACTIONS
water submersion followed by survival for at
IMAGING • Corticosteroid therapy not indicated; use
least 24 hours; recent changes in terminology
• Radiographic changes may not be detectable could be detrimental in animals with aspiration
prefer the use of “death, morbidity or no
for 24–48 hours. • Focal or diffuse alveolar pneumonia. • Use of enrofloxacin in young
morbidity following a drowning episode.”
pattern due to aspiration pneumonia or animals may result in cartilage erosion.
• Following submersion, elevations in CO2
levels in the bloodstream stimulate respiration, noncardiogenic pulmonary edema. • Mixed
and subsequent aspiration of water occurs. patterns may be present, ± radiopaque material
• Fresh water aspiration dilutes pulmonary filling the airways (“sand bronchogram”).
surfactant, leading to alveolar collapse ± • Foreign body inhalation may produce FOLLOW-UP
infectious pneumonia; hypertonic seawater segmental atelectasis. • Progression of
pulmonary injury to acute respiratory distress PATIENT MONITORING
aspiration leads to diffusion of interstitial water • Continuous monitoring of heart rate and
into alveoli; large volumes of water are not syndrome (ARDS) is possible and may appear as
bilateral, diffuse, symmetric alveolar infiltrates. rhythm, respiratory rate, mucous membrane
typically aspirated, but any amount results in color and capillary refill time, urine output,
ventilation–perfusion mismatch, hypoxemia, DIAGNOSTIC PROCEDURES arterial blood pressure, rectal temperature, and
and metabolic acidosis. • Submersion time, • Endotracheal or transtracheal wash with neurologic status. • Arterial blood gas, CBC,
temperature of water, and type of water (fresh cytologic evaluation and culture with biochemical profile, coagulation profile, and
vs. salt vs. chemical water) significantly affect sensitivity indicated if animal is stable. • ECG acid-base status checked as needed.
development of organ damage. monitoring. • Cervical radiographs, CT or
MRI of brain, and brainstem auditory evoked PREVENTION/AVOIDANCE
SIGNALMENT Close monitoring of animals (especially
Dogs and cats. Approximately half of animals response (BAER) assessment in select cases.
young and old/debilitated animals) near
involved in immersion accidents are <4 bodies of water. Place barriers around bodies
months of age. of water, life jackets on animals, train owners
SIGNS to perform CPR.
• Noted acutely after exposure to water. TREATMENT
• Initiate mouth-to-muzzle resuscitation POSSIBLE COMPLICATIONS
• Cyanosis, apnea, respiratory distress. Aspiration pneumonia, noncardiogenic
• Coughing ± clear to frothy red sputum. on-site. • Emergency inpatient care is
required. • Airway clearance, if obstructed, is pulmonary edema, ARDS, gastrointestinal
• Vomiting. • Obtunded to comatose. bleeding, diarrhea, vomiting, acute kidney
• Crackles or wheezes auscultated over chest. first priority. • Cardiopulmonary resusci
tation (CPR), if necessary. • Oxygen injury, permanent neurologic derangements,
• Tachycardia or bradycardia, asystole. disseminated intravascular coagulation,
supplementation. • Intubation and mechanical
CAUSES & RISK FACTORS ventilation with positive end-expiratory central diabetes insipidus.
• Greater risk near bodies of water (including pressure may be required in animals with EXPECTED COURSE AND PROGNOSIS
pools, buckets, bathtubs) or ice. • Owner severe hypoxemia, hypercapnia, or imminent Directly related to animal’s status at time of
negligence or inadequate safety precautions respiratory fatigue. • Fluid therapy and admission—animals that present comatose,
vs. purposeful harm. • Animals in or near acid-base/electrolyte management are crucial. severely acidotic (pH <7.0), or requiring
water at time of seizure, head trauma, • Gradually rewarm (over 2–3 hours) cardiopulmonary resuscitation or mechanical
hypoglycemic event, cardiac arrhythmia, or hypothermic animals. • Gravitational ventilation have poor prognosis. Animals that
syncopal episode are at risk of drowning. drainage or abdominal thrusts (Heimlich present conscious have good prognosis if no
maneuver) are not recommended in absence complications ensue; 37.5% mortality rate in
of airway obstruction owing to high risk of 15 dogs and 1 cat with freshwater aspiration.
regurgitation and subsequent aspiration of
DIAGNOSIS stomach contents. • Continuous venovenous
filtration may decrease mortality following
salt water drowning.
• Hypothermia, neck trauma, and meningitis. MISCELLANEOUS
• With drowning secondary to seizure, head ABBREVIATIONS
trauma, hypoglycemic event, cardiac • ARDS = acute respiratory distress syndrome.
arrhythmia, or syncopal episode, history at • BAER = brainstem auditory evoked
time of presentation may be informative. MEDICATIONS response. • CPR = cardiopulmonary
CBC/BIOCHEMISTRY/URINALYSIS DRUG(S) OF CHOICE resuscitation. • PaCO2 = partial pressure of
• Fresh water inhalation/ingestion— • Mannitol 0.5 g/kg IV over 30 min may be carbon dioxide. • PaO2 partial pressure of
hemodilution, hemolysis, and decreases in beneficial in animals with suspected cerebral oxygen.
sodium, chloride, and urine specific gravity. edema. • Broad-spectrum antibiotics (e.g., Author Deborah C. Silverstein
• Hypertonic salt water ingestion/inhalation— ampicillin 22 mg/kg IV q8h; enrofloxacin Consulting Editor Elizabeth Rozanski
Ductal Plate Malformation (Congenital Hepatic Fibrosis)
fibroductal bridging partitions may • Gastrointestinal (GI)—anorexia;

interconnect portal regions; because ECM intermittent vomiting or diarrhea reflects
accrues with aging, transformation to CHF concurrent inflammatory bowel disease (IBD)
D BASICS may occur over time. • von Meyenburg’s or enteric hypertensive vasculopathy (splanchnic
DEFINITION complexes (VMCs)—isolated single microscopic hypertension from presinusoidal PH).
• Ductal plate malformations (DPMs) are DPM composed of clustered proliferative • Nervous—episodic HE if APSS associated
congenital noninflammatory hepatopathies intralobular bile duct profiles embedded in with CHF or if concurrent PSVA.
subject to complicating bacterial cholangitis; expanded ECM; also termed bile duct • Musculoskeletal—stunted growth and poor
recognized most often in juvenile and young hamartomas; usually located adjacent to liver body condition if CHF and APSS or if
adult dogs or cats and reflect malformation of capsule; inconsequential malformation. concurrent PSVA; also may reflect chronic
biliary structures. • DPMs reflect aberrant • Progression of portal tract fibrosis with disease, inappetence, or enteric malassimilation.
development, differentiation, proliferation, or aging can lead to gradual onset of presinusoidal • Urogenital—polyuria and polydipsia (PU/
intussusceptive resorption of embryonic PH, formation of APSS, ascites, and hepatic PD); possible polycystic renal phenotype;
anlage of bile ducts during development of encephalopathy (HE). • Gallbladder (GB) ammonium biurate urolithiasis reflects APSS
ductal plate, embryologic precursor of portal agenesis and severe hypoplasia or agenesis of or rare concurrent PSVA. • Hemic/lymphatic/
tract structures (predominantly bile ducts). entire liver lobes may occur. • Liver lobes may immune—red blood cell (RBC) microcytosis
• Pathomechanisms leading to DPM be variably affected with DPM; unaffected reflects APSS or PSVA; neutrophilic
interfere with tubulogenesis—may affect liver lobes possible. leukocytosis with toxic neutrophils and
kidneys, liver, or pancreatic ductal structures. PATHOPHYSIOLOGY left-shifted leukon reflects sepsis due to
• Four DPM phenotypes defined based on • DPMs not associated with increased liver
suppurative bacterial cholangitis/choledochitis
involved structures and severity of coexistent enzymes or jaundice unless complicated by or infected choledochal cyst.
portal tract fibrosis, severity of fibroductal infection, choleliths, EHBDO, or choledochitis. SIGNALMENT
bridging trabeculae, development of • Different phenotypes acquire different • Dog and cat, no sex predilection. • Juvenile
presinusoidal portal hypertension (PH) disease manifestations. • Choledochal and young adults predominate; dogs: mean
causing splanchnic hypertension, and cysts—not recognized until cystic luminal age 1.5–2.5 years (0.2–12) years. • May
development of acquired portosystemic contents contaminated by bacteria with affect multiple littermates. • Boxer dogs may
shunts (APSS). • Animals with DPM have ensuing infection and cyst expansion, be predisposed. • Persian cats and descendent
propensity for septic suppurative cholangitis, development of choledochitis or EHBDO; breeds with or without polycystic renal disease
choledochitis, cholelithiasis, or extrahepatic until compromised CBD patency patient appear predisposed.
bile duct obstruction (EHBDO). remains anicteric, usually asymptomatic. SIGNS
MAJOR DPM PHENOTYPES • Caroli’s malformation—serendipitously • May be asymptomatic. • Stunted growth,
• Choledochal cyst—diverticulum protruding recognized on abdominal radiography (limy poor body condition if CHF with APSS or
from common bile duct (CBD) or cystic duct; gallbladder, mineralized sacculated concurrent PSVA. • GI signs—inappetence,
propensity for infection similar to appendicitis intrahepatic large bile ducts), or on emesis, diarrhea, enteric hemorrhage;
in humans; may cause systemic sepsis, EHBDO, abdominal US as distended intra- or especially if concurrent IBD. • PU/PD if
and cranial abdominal mass effect; complex extrahepatic bile ducts, mineralized ducts, APSS or rare concurrent PSVA, or polycystic
confusing US appearance. • Caroli’s association with cholelithiasis, or thickened renal disease. • ± Increased liver enzymes.
malformation—irregular duct silhouettes duct walls (infection, choledochitis). • ± Fever, leukocytosis, hyperbilirubinemia—
(sacculation, invagination, or “budding” • Diffuse DPM without extensive bridging due to sepsis evolved from bacterial cholangitis,
protrusions) with occasional periductal fibrosis or presinusoidal PH—not associated choledochitis, or choledochal cyst infection or
satellite ductal elements surrounding large with increased liver enzymes or jaundice, infection-related cholelithiasis. • ± Abdominal
ducts; malformations variably involve hepatic, usually normal total serum bile acid (TSBA) distention—ascites with APSS in CHF; CHF
interlobular, or large intralobular bile ducts; concentrations; diagnosed when infection with PSVA no ascites unless PSVA attenuated.
biliary epithelium may appear normal, increases liver enzyme activity leading to liver • ± Episodic CNS signs due to HE if APSS in
hyperplastic, attenuated, or vacuolated; biopsy. • Diffuse DPM with bridging fibrosis CHF or rare concurrent PSVA. • ± Urolithiasis
intraluminal debris in large ducts; develop (CHF) causes presinusoidal PH—these patients (ammonium urates) if APSS in CHF or rare
choleliths, dystrophic mineralization, septic may present for ascites, increased TSBA concurrent PSVA.
cholangitis. • Small proliferative-like concentrations, ± increased liver enzymes
phenotype—diffuse intralobular bile duct reflecting secondary cholangitis, or for HE; CAUSES & RISK FACTORS
malformation without or with bridging not jaundiced unless infected or have • In humans (and knockout mouse models)
portal-to-portal fibroductular trabeculae: if concurrent EHBDO. DPM reflects gene mutations influencing
fibrosis severe may evolve presinusoidal PH structure or function of primary cilia;
SYSTEMS AFFECTED polycystic kidney disease in Persian cats
and consequent splanchnic hypertension = • Liver—variable size (small, normal, large);
congenital hepatic fibrosis (CHF) phenotype— involves polycystin-1 precursor gene, one
may have GB agenesis or maldevelopment of gene influencing primary ciliary function;
involves small intralobular bile duct malfor entire liver lobe(s); rare concurrent congenital
mation with densely packed proliferative-like ~15% develop hepatic DPM. • Clinical signs
intrahepatic or extrahepatic congenital usually reflect acquired complications.
ductule structures (± luminal apertures) within portosystemic vascular anomaly (shunt,
excessive extracellular matrix (ECM); ECM PSVA); jaundice due to EHBDO from
accrual varies in severity, but appears choledochal cyst, cholelithiasis, rare cholangio-
progressive with aging; histologic features carcinoma, or due to sepsis (Caroli’s
characterized by amalgamation of proliferative malformation, choledochal cyst); increased DIAGNOSIS
bile ductules with numerous stout (muscular) liver enzymes may reflect suppurative
entangling arterials and inconspicuous portal DIFFERENTIAL DIAGNOSIS
cholangitis or unrelated copper associated • Stunted growth, increased TSBA
veins within exuberant ECM that hepatopathy (CuAH) in dogs.
dimensionally expands portal tracts; variable concentrations—PSVA, severe portal vein
(continued) Ductal Plate Malformation (Congenital Hepatic Fibrosis)
atresia, splanchnic portal vein thrombo Additional Imaging predisposed to bacterial cholangitis,
embolism (TE). • Increased liver enzymes ± • Colorectal or splenoportal scintigraphy with choledochitis, and associated cholelithiasis
hyperbilirubinemia—chronic hepatitis, Technetium-99m pertechnetate (see Portosystemic because of blind-ended noncontiguous ductal
CuAH, hepatotoxicity, liver abscess, primary Vascular Anomaly, Congenital)—sensitive structures; in CHF with APSS reduced D
hepatic neoplasia, cholangiohepatitis, noninvasive test confirming macroscopic Kupffer cell surveillance increases risk for
choledochitis, or cholecystitis. • Jaundice— shunting, but cannot differentiate PSVA from infection and systemic sepsis. • In CHF—
acute liver injury, hepatotoxicosis, chronic APSS. • Multisector CT—gold standard remain vigilant for ammonium biurate
hepatitis, CuAH, cholelithiasis, ruptured GB, imaging modality: confirms APSS or PSVA; obstructive uropathy. • If APSS—avoid
EHBDO, hemolysis. • CNS signs— dual-phase angiogram can reveal asymmetric nonsteroidal anti-inflammatories that may
infectious disorders (distemper); toxicities liver development (liver lobe absence or atresia), augment ascites and GI bleeding provoking
(lead); hydrocephalus; epilepsy; metabolic GB atresia, choledochal cyst, sacculated HE; adjust dosage of drugs with high first-pass
disorders (severe hypoglycemia, hypokalemia, interlobular and cystic ducts, cholelithiasis, hepatic extraction. • CuAH diagnosed by
hyperkalemia, hypophosphatemia); thiamine and APSS. liver biopsy should be treated.
deficiency. • Ascites—pure transudate, many DIAGNOSTIC PROCEDURES NURSING CARE
causes (see Hypertension, Portal). • HE— • Fine-needle aspiration cytology—cannot • HE—eliminate causal factors; individualize
APSS, PSVA, portal TE, other causes. diagnose DPM, sometimes identifies diet, supplement water-soluble vitamins, vitamin
CBC/BIOCHEMISTRY/URINALYSIS complicating bacterial infection especially if E, and K depending on prothrombin/activated
• CBC—RBC microcytosis: reflects APSS; bile collected. • Liver biopsy—mandatory for partial thromboplastin time tests or presence of
target cells associated in dogs. definitive diagnosis; open surgical wedge, EHBDO; provide multiple small feedings daily.
• Biochemistry—if APSS with CHF: ± low laparoscopic cup samples; needle core sample • Ascites—see Hypertension, Portal.
albumin, cholesterol, blood urea nitrogen, may be adequate; collect biopsies from several
variable globulin; all DPM phenotypes: ± liver lobes. • Echocardiography—if ascites
increased alkaline phosphatase and alanine present.
aminotransferase activity with cholangitis;
hyperbilirubinemia: if EHBDO due to
PATHOLOGIC FINDINGS MEDICATIONS
• Gross—depends on phenotype.
choledochal cyst or cholelithiasis or if septic. ◦ Choledochal cyst—predominantly occurs in DRUG(S) OF CHOICE
• Urinalysis—ammonium biurate crystalluria cats, variable size (as large as 10 cm) with thick Strategy for DPM is to treat syndrome
if APSS in CHF phenotype. or thin wall; contents acholic or mucinous white complications.
OTHER LABORATORY TESTS bile; may be purulent or bile laden; may envelop HE
• Routine coagulation tests—variable CBD. ◦ Caroli’s malformation—grossly • Lactulose (0.5–1.0 mL/kg PO q8–12h)—
abnormalities (see Coagulopathy of Liver distended hepatic, interlobular, or segmental achieve several soft stools daily; may withdraw
Disease); low protein C and antithrombin bile ducts, thick walls if choledochitis, wall may with optimal diet modification. • Oral
activity may reflect APSS in CHF phenotype. be mineralized, may have pigmented-calcium antibiotics—modify encephalogenic enteric
• TSBA—increased concentrations in carbonate choleliths. ◦ Small-proliferative-type toxin production: first choices metronidazole
anicteric patients reflect APSS or rare DPM—firm fibrotic hepatic parenchyma, fine (7.5 mg/kg PO q12h) or amoxicillin (22 mg/
concurrent PSVA. • Peritoneal fluid nodular to smooth capsular surface, may have kg PO q12h); avoid neomycin (20 mg/kg PO
analysis—pure transudate (protein <2.5 g/ splanchnic APSS if CHF phenotype. ◦ von q8–12h): potential for enteric absorption
dL); modified transudate if chronic: only in Meyenburg complexes—inapparent or tiny pale (esp. if concurrent IBD) causing ototoxicity
CHF phenotype. foci on liver margin. • Possible GB atresia, (deafness) and nephrotoxicity.
IMAGING PSVA, other vascular malformations, liver lobe Ascites
agenesis. • Microscopic—variable severity as • Dietary sodium restriction. • Diuretics—
Radiography described (see Major DPM Phenotypes); furosemide (1–4 mg/kg PO/IM/IV q12–24h):
• Abdominal radiography—variable liver size. stereotypic histologic features of portal venous potassium wasting effect modulated by
• Abdominal effusion—APSS in CHF hypoperfusion are common; direct intersection combination with spironolactone (1–4 mg/kg
phenotype. • Ammonium biurate calculi— of proliferative-like bile ductules and hepatocytes PO q12h, loading dose then maintenance
radiolucent unless radiodense mineral shell. is signature histologic feature of DPM in dose 2–4 mg/kg PO q24h); potassium
• Thoracic radiography—normal. absence of inflammatory infiltrates; islands of sparing; less potent than furosemide.
Abdominal US hepatocytes may be encircled or isolated by • Diuretic-resistant ascites—consider
• Variable liver size—small to large. • GB portal-to-portal fibroductal partitions. therapeutic abdominocentesis (see Hypertension,
may not be discovered if atretic or may be Portal for other medical options). • Antifibrotic—
tiny. • May disclose intra- or extrahepatic not proven effective in humans with DPM;
biliary malformations (sacculated or cystic liver transplant common, unknown in
ductal structures); variable liver texture; TREATMENT veterinary medicine; colchicine not effective.
unremarkable vasculature to portal hypo • Telmisartan—angiotensin receptor blocker
perfusion. • Choledochal cyst—may be APPROPRIATE HEALTH CARE safe for use in dogs and cats; attenuated
difficult to decipher owing to overlying • Inpatient—for septic complications or
progressive ECM accrual in DPM rodent
enteric gas and confusion with CBD and severe HE. • Surgical intervention— model; adverse effects if coadministered with
cystic duct. • Abdominal effusion—if APSS choledochal cyst: best managed by resection spironolactone or angiotensin-converting
in CHF. • APSS—confirm using color-flow but depends on anatomic malformation and enzyme (ACE) inhibitor: leads to serious
Doppler; rule out portal TE and intrahepatic location; may be marsupialized or anastomosed hypotension (collapse, acute renal failure);
arteriovenous malformations as causes of to intestine. • Outpatient—stable patients. initial dose 0.5 mg/kg/day titrated to max of
APSS. • Uroliths—renal pelvis or urinary • Avoid endoparasitism. • Treat infections 1 mg/kg/day.
bladder. promptly—DPM patients (except VMC)
Ductal Plate Malformation (Congenital Hepatic Fibrosis)(continued)

Antioxidant Medications • Biochemistry—initially monitor q2–4 SEE ALSO
Indicated if chronic cholangitis, CuAH, weeks until stabile in animals presenting • Ascites.
chronic increased liver enzymes, or CHF. with sepsis or EHBDO, then q4–6 months • Hepatic Encephalopathy.
D Bleeding Tendencies or if cyclically ill or febrile; monitor for • Hypertension, Portal.
Rare in CHF; may encounter if chronic recurrent septic cholangitis/choledochitis, • Portosystemic Shunting, Acquired.
EHBDO caused by choledochal cyst or development of septic effusion; HE ABBREVIATIONS
cholelithiasis. decompensation. • ACE = angiotensin-converting enzyme.
GI Hemorrhage POSSIBLE COMPLICATIONS • APSS = acquired portosystemic shunts.
Hypertensive enteric vasculopathy may be CHF associated with HE—requires indefinite • CBD = common bile duct.
encountered with CHF because of APSS. nutritional and medical management. If • CHF = congenital hepatic fibrosis.
concurrent PSVA—likely cannot be • CuAH = copper associated hepatopathy.
CONTRAINDICATIONS/POSSIBLE attenuated without causing APSS. • DPM = ductal plate malformation.
INTERACTIONS EXPECTED COURSE AND PROGNOSIS • ECM = extracellular matrix.
• Avoid or reduce dosage of drugs relying on • EHBDO = extrahepatic bile duct occlusion.
• Long-term survival (years) possible.
first-pass hepatic metabolism if APSS; avoid • Guarded prognosis if CHF phenotype with • GB = gallbladder.
drugs reacting with GABA-benzodiazepine APSS. • Short-term or lifelong treatments • GI = gastrointestinal.
receptors if intermittent HE in patients with may be required. • Flare-ups of HE and • HE = hepatic encephalopathy.
APSS-CHF phenotype; avoid drugs inhibiting ascites may require hospitalizations for • IBD = inflammatory bowel disease.
biotransformation and metabolism of other adjustment of nutritional and medical • PH = portal hypertension.
drugs (e.g., cimetidine, chloramphenicol, interventions. • PSVA = portosystemic vascular anomaly.
quinidine, some calcium channel blockers); if • PU/PD = polyuria/polydipsia.
jaundiced avoid drugs undergoing biliary • RBC = red blood cell.
elimination. • Avoid metoclopramide if • TE = thromboembolism.
spironolactone used as diuretic (augments • TSBA = total serum bile acid.
aldosterone). • Avoid combination of MISCELLANEOUS • VMC = von Meyenburg’s complex.
spironolactone with telmisartan or ACE ASSOCIATED CONDITIONS Suggested Reading
inhibitor. • HE. • Ascites. • GI bleeding. • APSS. Brown DL, Van Winkle T, Cecere T, et al.
AGE-RELATED FACTORS Congenital hepatic fibrosis in 5 dogs. Vet
• Prognosis depends on degree of fibrosis and Pathol 2010, 47:102–107.
APSS in CHF; severity of relapsing septic Pillai S, Center SA, McDonough SP, et al.
FOLLOW-UP cholangitis or choledochal cyst infection; Ductal plate malformation in the liver of
intrahepatic infected cholelithiasis; evidence boxer dogs: clinical and histological
PATIENT MONITORING
of hepatic insufficiency and APSS at initial features. Vet Pathol 2016, 53:602–613.
• Instruct owners to monitor body
diagnosis. • Fibrosis progressive with aging in Author Sharon A. Center
temperature, appetite, activity, for jaundice
some patients. Consulting Editor Kate Holan
or other signs of infection or complications.
Dysautonomia (Key-Gaskell Syndrome)

IMAGING autonomic dysfunction that may require
• Megaesophagus ± aspiration pneumonia. constant care.
• Distended bowel loops with no peristalsis.
BASICS • Distended urinary bladder. D
OVERVIEW • Echocardiography may show systolic
• Failure of autonomic function in multiple dysfunction as reduced fractional short-
ening.
MISCELLANEOUS
organs with minimal motor or sensory • Necropsy identification of neuronal loss in
involvement. • Young adult, rural dogs in DIAGNOSTIC PROCEDURES ganglia confirms diagnosis. • Clinical
specific states at greatest risk. • Treatment • If pupils affected, 0.05% pilocarpine drops diagnosis based on autonomic failure in
is symptomatic and prognosis guarded. in one eye will produce miosis within 60 multiple organs without underlying cause or
SIGNALMENT minutes; rules out anticholinergic toxicity. significant motor or sensory involvement and
• Dog and less commonly cat. • No breed or • Atropine (0.03 mg/kg IV) may not produce appropriate response to pharmacologic testing.
sex predilection. • Median age is 18 months expected rise in heart rate; suggests loss of
ABBREVIATIONS
but any age animal may be affected. vagal tone. • Intradermal histamine may
produce no response or wheal but no flare;
SIGNS Suggested Reading
demonstrates loss of sympathetic innervation
• Acute to subacute onset (5–14 days). Berghaus RD, O’Brien DP, Johnson GC,
of arterioles.
• Various combinations of signs may be Thorne JG. Risk factors for development of
present, but both sympathetic and para dysautonomia in dogs. J Am Vet Med Assoc
sympathetic signs in various organs are 2001, 218:1285–1292.
necessary to be confident of diagnosis. Harkin KR, Andrews GA, Nietfeld JC.
• Sensory or motor deficits are minimal. TREATMENT Dysautonomia in dogs: 65 cases (1993–
• IV fluids to prevent dehydration. • High- 2000). J Am Vet Med Assoc 2002,
Presenting Complaints
• Most commonly gastrointestinal (GI) signs
calorie food; feeding tube to ensure adequate 220:633–644.
of vomiting or regurgitation, diarrhea, or nutrition if megaesophagus present; if GI Harkin KR, Bulmer BJ, Biller DS.
occasionally constipation. • Straining to motility absent, parenteral nutrition may be Echocardiographic evaluation of dogs with
urinate and dribbling urine. • Photophobia necessary. • Lubricating eye drops if tear dysautonomia. J Am Vet Med Assoc 2009,
and third-eyelid elevation. • Dyspnea, production insufficient. • Humidification of 235:1431–1436.
coughing, and purulent nasal discharge. air may help with dry mucous membranes. Kidder AC, Johannes C, O’Brien DP, et al.
• Depression, anorexia, and weight loss. • Manual bladder expression. Feline dysautonomia in the Midwestern
Examination Findings
United States: a retrospective study of nine
• Variable combinations of autonomic
cases. J Fel Med Surg 2008, 10:130–136.
dysfunction. • Loss of anal sphincter tone. Longshore RC, O’Brien DP, Johnson GC,
• Dry nose and mucous membranes; lack of MEDICATIONS et al. Dysautonomia in dogs—a retrospective
tear production. • Distended, easily expressed study. J Vet Intern Med 1996,
DRUG(S) OF CHOICE
bladder. • Pupils midrange to maximally 10(3):103–109.
• Antibiotics as needed to treat secondary
dilated with no pupillary light reflex but O’Brien DP, Johnson GC. Dysautonomia
infections. • Prokinetic drug such as
intact vision. • Third-eyelid elevation, ptosis, and autonomic neuropathies. Vet Clin
metoclopramide if GI motility affected.
and enophthalmos. • Lack of gut sounds and North Am Small Anim Pract 2002,
• Bethanechol to stimulate lacrimation and
occasional abdominal pain. • Heart rate and 32:251–265.
urination (start at 0.05 mg/kg q8–12h and
blood pressure typically in low end of normal Author Dennis P. O’Brien
adjust dose based on response); manual
range but do not rise in response to stress. expression of bladder more reliable.
• Secondary aspiration pneumonia or • Ocular pilocarpine to relieve photophobia.
rhinitis. • Cachexia. • Occasionally mild • Pimobendan if poor cardiac contractility.
proprioceptive deficits or weakness.
CAUSES & RISK FACTORS INTERACTIONS
• Cause unknown. • Highest incidence in • Animals with dysautonomia develop
Missouri, Oklahoma, and Kansas as well as denervation supersensitivity to direct acting
Wyoming and northern Colorado, but occasional cholinergic or adrenergic drugs. • Great care
cases reported throughout United States. must be exercised in using such drugs,
• Free-roaming, rural dogs at greatest risk. particularly adrenergic drugs that could
precipitate fatal tachyarrhythmias; best to
start at <10% of low end of dose range when
using direct-acting drugs and escalate dose as
DIAGNOSIS needed to produce desired effect.
• Anticholinergic toxicity. • Other
differential diagnoses depend upon specific
clinical signs: e.g., urinary tract infection for FOLLOW-UP
dysuria, corneal ulcer for photophobia, • Prognosis guarded; most animals die of
dehydration for dry mucous membranes. aspiration pneumonia or euthanasia due to
poor quality of life. • Animals who survive
often have some degree of permanent
Unremarkable
Dyschezia and Hematochezia
Colonic Disease IMAGING
• Neoplasia—adenocarcinoma, lymphoma, • Pelvic radiographs may reveal intrapelvic
other tumors. disease, foreign body, or fracture.
D BASICS • Idiopathic megacolon—cats. • Ultrasonography may demonstrate prostatic
DEFINITION • Inflammation—inflammatory bowel disease or caudal abdominal masses; however,
• Dyschezia—painful or difficult defecation. disease, infectious parasitic agents, colitis a portion of the descending colon cannot be
• Hematochezia—bright red blood in or on secondary to dietary-responsive enteropathy visualized because of the pelvis.
the feces. (see Colitis and Proctitis). DIAGNOSTIC PROCEDURES
• Constipation (see Constipation and
PATHOPHYSIOLOGY Colonoscopy/proctoscopy to evaluate for
Obstipation). inflammatory or neoplastic disease.
Results from inflammatory, infectious, or
neoplastic conditions affecting the colon, Extraintestinal Disease
rectum, or anus. • Fractured pelvis or pelvic limb.
• Prostatic disease.
SYSTEMS AFFECTED • Perineal hernia.
Gastrointestinal • Intrapelvic neoplasia.
TREATMENT
• Depends on the underlying cause.
SIGNALMENT RISK FACTORS • Colonic strictures secondary to neoplasms
• Dog and cat.
• Ingestion of hair, bone, or foreign material can be managed via surgical excision or
• No breed or sex predilection.
may contribute to constipation and subse balloon catheter dilation.
SIGNS quent dyschezia. • Consider laxatives (lactulose) to ease
Historical Findings • Environmental factors such as a dirty litter defecation and discomfort in animals with
• Vocalizing and whimpering during pan or infrequent outside walks may contribute colorectal strictures or masses.
defecation. to constipation and subsequent dyschezia. • Colorectal masses are best removed
• Tenesmus. surgically or via endoscopy (snare and
• Decreased frequency of defecation in cauterization for polyps).
association with severe dyschezia (animal
resists defecating due to pain), resulting in DIAGNOSIS
constipation or obstipation. It is pivotal to recognize that hematochezia in
• Mucoid, bloody diarrhea with a marked animals can be seen with both diffuse colitis MEDICATIONS
increase in frequency and scant fecal volume as well as with focal or discrete colorectal
in patients with colitis. neoplasms. The fundamental differences in DRUG(S) OF CHOICE
• Scooting behavior in association with anal • Antibiotics—if bacterial infection (e.g.,
the clinical presentation between the two
gland infection or impaction. disorders can usually be recognized during the anal sac abscess); amoxicillin/clavulanic acid
• It is pivotal to differentiate hematochezia history and following a thorough physical 15 mg/kg PO q12h for 7–10 days.
secondary to colitis from hematochezia • Anti-inflammatory drugs—sulfasalazine or
examination, including a rectal examination.
secondary to a colorectal mass—the histories are Dogs with colorectal neoplasms do not have prednisone (dogs) and prednisolone (cats) if
profoundly different and a rectal examination diarrhea, and the most important and colitis is present (see Colitis and Proctitis;
should always be performed to further frequent clinical sign is hematochezia in the Colitis, Histiocytic Ulcerative).
differentiate these two disorders (see below). • Cyclosporine (5 mg/kg q12h for 3–4
absence of an increase in defecation frequency
or change in stool consistency. Pencil-thin or months with gradual taper thereafter) for
Physical Examination Findings dogs with perianal fistulae.
• Rectal examination may reveal hard feces ribbon-like stools can be seen when the
• Laxatives—lactulose 1 mL/4.5 kg PO
(constipation or obstipation), diarrhea colorectal neoplasm is advanced, causing a
change in the shape of the stool. A rectal q8–12h to effect; docusate sodium or
(colorectal disease), colorectal masses, docusate calcium: dogs: 50–100 mg PO
anorectal thickening, rectal or colonic examination must be performed on every patient
with a history of hematochezia or dyschezia. q12–24h; cats: 50 mg PO q12–24h.
strictures, anal sac enlargement/pain, • Cisapride—prokinetic indicated for cats
prostatomegaly, or perineal hernias. DIFFERENTIAL DIAGNOSIS with moderate to severe megacolon (and no
• Fistulous tracts around anus occur with • Dysuria, stranguria, or hematuria— evidence of obstruction) in conjunction with
perianal fistulae. abnormal findings on urinalysis, such as lactulose and dietary therapy at a dose of
• Anal occlusion with matted hair and feces pyuria, crystalluria, or bacteriuria. The history 5 mg/cat q12h.
occurs with pseudocoprostasis. and physical examination should differentiate
whether the animal is having difficulty CONTRAINDICATIONS
CAUSES Avoid agents that cause increased fecal bulk
urinating or defecating.
Rectal/Anal Disease • Dystocia—differentiate with history and
(insoluble fiber), unless specifically indicated
• Stricture or spasm. imaging. (colitis).
• Anal sacculitis or abscess.
• Perianal fistulae. CBC/BIOCHEMISTRY/URINALYSIS
• Rectal or anal foreign body. • Usually unremarkable, unless there is a
• Pseudocoprostasis. history of chronic blood loss with secondary
iron deficiency causing a microcytic and FOLLOW-UP
• Rectal prolapse.
hypochromic nonregenerative anemia. • The need for follow-up depends on the
• Trauma—bite wounds, etc.
• Mild neutrophilia (with or without a left underlying cause. Dogs and cats that are
• Neoplasia—adenocarcinoma, lymphoma,
shift) with infection or inflammation. undergoing balloon dilation of colorectal
and anal sac tumors. strictures usually require multiple procedures
• Rectal polyps. OTHER LABORATORY TESTS to manage the stricture properly. Animals
• Mucocutaneous lupus erythematosus. Centrifugation fecal flotation to help rule should always be rechecked at suture removal
out parasitic causes of colitis.
(continued) Dyschezia and Hematochezia

or 10–14 days following surgical resection of • Secondary megacolon may occur if Suggested Reading
colorectal masses. obstipation is severe and long term. Adamovich-Rippe KN, Mayhew PD, Marks
• Animals with hematochezia secondary to SL, et al. Colonoscopic and histologic
colitis should have a marked improvement or features of rectal masses in dogs: 82 cases D
resolution of their clinical signs within 5–7 (1995–2012). J Am Vet Med Assoc 2017,
days following implementation of elimination 250(4):424–430.
dietary therapy.
MISCELLANEOUS
Webb CB. Anal-rectal disease. In: Bonagura
ASSOCIATED CONDITIONS JD, Twedt DC, eds., Current Veterinary
PATIENT MONITORING
N/A Therapy XIV. St. Louis, MO: Elsevier,
Daily monitoring by the owner with periodic
phone calls to the clinician every 2–3 weeks PREGNANCY/FERTILITY/BREEDING 2009, pp. 527–531.
during the beginning of treatment. Caution with corticosteroids, antibiotics. Zoran DL. Rectoanal disease. In: Ettinger SJ,
Feldman EC, eds., Textbook of Veterinary
POSSIBLE COMPLICATIONS SEE ALSO Internal Medicine, 6th ed. St. Louis, MO:
• May see fecal incontinence following • Colitis and Proctitis. Elsevier, 2005, pp. 1408–1420.
surgical resection of anal sacs or colorectal • Constipation and Obstipation. Author Stanley L. Marks
tumors if anal sphincter is compromised. Consulting Editor Mark P. Rondeau
Dysphagia
• Neuromuscular. pharyngeal swallow nor adequacy of
• Respiratory. deglutitive airway protection.
• The importance of the clinician’s carefully
D BASICS GENETICS
observing the dysphagic animal while eating
Breeds that have a hereditary predisposition or
DEFINITION high incidence of dysphagia include golden (kibble and canned food) and drinking in
• Dysphagia refers to difficulty in swallowing retriever (pharyngeal weakness, hospital (or at home via video) is pivotal, and
and is far more commonly seen in dogs than cricopharyngeal muscle dysfunction), cocker such observation helps localize the problem to
cats. and springer spaniels (cricopharyngeal muscle oral cavity, pharynx, or esophagus.
• Dysphagia is divided into three main dysfunction), Bouvier des Flandres and cavalier Oral Dysphagia
categories—oropharyngeal, esophageal, and King Charles spaniel (muscular dystrophy), • Modified eating behavior (e.g., eating with
gastroesophageal causes. and boxer (inflammatory myopathy). In head tilted to one side or having difficulty
• Oropharyngeal causes of dysphagia can be addition, large and giant-breed dogs are prehending the bolus or opening the mouth).
further subcategorized into oral, pharyngeal, predisposed to acquired megaesophagus. • Tongue paralysis or dystrophy, dental
or cricopharyngeal. disease, masticatory muscle myositis,
• Any disorder causing difficulty with INCIDENCE/PREVALENCE
Variable depending on underlying etiology. temporal muscle atrophy, or pain, and food
prehension or mastication can cause packed in buccal folds suggest oral dysphagia.
dysphagia. Megaesophagus one of the most common
• Odynophagia refers to painful swallowing causes of dysphagia in dogs. Pharyngeal Dysphagia
and is most commonly seen in association GEOGRAPHIC DISTRIBUTION • Prehension of food is normal.
with pharyngitis, pharyngeal foreign bodies, None • Repeated attempts at swallowing with food
esophageal foreign bodies, or severe falling out of mouth and excessive gagging
SIGNALMENT suggest pharyngeal dysphagia.
esophagitis.
• Dog and cat. • Saliva-coated food retained in buccal folds,
• Esophageal dysphagia is discussed in
• Congenital disorders that cause dysphagia diminished gag reflex, and nasal discharge
Megaesophagus and in Regurgitation.
(e.g., cricopharyngeal muscle achalasia, cleft may also exist.
PATHOPHYSIOLOGY palate, hiatal hernia) usually diagnosed in
• The oral preparatory phase is voluntary and animals <1 year old. Cricopharyngeal Muscle Dysfunction
begins as food or liquid enters the mouth. • Patients make repeated, nonproductive
• Acquired esophageal dysmotility and
Mastication and lubrication of food are the pharyngeal weakness more common in older efforts to swallow, gag, and cough, then
hallmarks of this phase. Abnormalities of the patients. forcibly regurgitate immediately after
oral preparatory phase usually are associated swallowing.
SIGNS • Gag reflex and prehension are normal.
with dental disease, xerostomia, weakness of
the lips (cranial nerves [CN] V and VII), Historical Findings • Nasal reflux commonly observed when food
tongue (CN XII), and cheeks (CN V and • Drooling (due to pain or inability to swallow hits closed PES.
VII). saliva), gagging, ravenous appetite, repeated or • Coughing commonly observed secondary
• The oral phase of swallowing consists of the exaggerated attempts at swallowing, swallowing to aspiration pneumonia.
muscular events responsible for movement of with head in abnormal position, nasal Esophageal Dysphagia
the bolus from the tongue to the pharynx and discharge (due to nasal reflux of food and • Most common causes include mega
is facilitated by tongue, jaw, and hyoid muscle liquids into nasopharynx), coughing (due to esophagus, esophagitis, esophageal stricture,
movements. aspiration), regurgitation, painful swallowing, esophageal foreign bodies, and esophageal
• The pharyngeal phase begins as the bolus and occasionally anorexia and weight loss. If dysmotility.
reaches the tonsils and is characterized by tongue is not functioning normally, problems • Diagnosis made with survey radiographs of
elevation of the soft palate to prevent the with prehension and mastication may be seen. thorax and neck followed by videofluoroscopic
bolus from entering the nasopharynx, • Ascertain onset and progression. Foreign swallow assessment.
elevation and forward movement of the bodies cause acute dysphagia; pharyngeal
dysphagia may be chronic and insidious in Gastroesophageal Dysphagia
larynx and hyoid, retroflexion of the epiglottis
onset. Most common cause is sliding hiatal hernia in
and closure of the vocal folds to close the
brachycephalic breeds, often associated with
entrance into the larynx, contraction of the Physical Examination Findings gastroesophageal reflux and subsequent
muscles of the pharynx, and relaxation of the • Physical examination must include careful esophagitis.
cricopharyngeus muscle that makes up much examination of oropharynx using sedation or
of the proximal esophageal sphincter (PES) to anesthesia if necessary to help rule out morph- CAUSES
allow passage of the bolus into the esophagus. ologic abnormalities such as dental disease, • Anatomic or mechanical lesions include
Respiration is briefly halted (apneic moment) foreign bodies, cleft palate, glossal abnormalities, pharyngeal inflammation (e.g., abscess,
during the pharyngeal phase. and oropharyngeal tumors. inflammatory polyps, oral eosinophilic
• Abnormalities of the pharyngeal phase of • Evaluation of cranial nerves should be
granuloma), neoplasia, pharyngeal and
swallowing are associated with pharyngeal performed, including assessment of tongue retropharyngeal foreign body, sialocele,
weakness secondary to neuropathies or and jaw tone, and of laryngeal function. temporomandibular joint disorders (e.g.,
myopathies, pharyngeal tumors or foreign • Complete physical and neurologic exam-
luxation, fracture, craniomandibular
bodies, or cricopharyngeus muscle disorders. ination may identify clinical signs supporting osteopathy), mandibular fracture, cleft or
• The esophageal phase is involuntary and generalized neuromuscular disorder, including congenitally short palate, cricopharyngeal
begins with relaxation of the PES and muscle atrophy, stiffness, or decreased or muscle achalasia, lingual frenulum disorder,
movement of the bolus into the esophagus. absent spinal reflexes. pharyngeal trauma.
• Pain as result of dental disease (e.g., tooth
SYSTEMS AFFECTED • Evaluate gag reflex by placing a finger in the
pharynx; however, presence or absence of gag fractures and abscess), mandibular trauma,
reflex does not correlate with efficacy of stomatitis, glossitis, and pharyngeal
• Nervous.
inflammation may disrupt normal prehension,
(continued) Dysphagia
bolus formation, and swallowing. Stomatitis, • Fluoroscopy with barium is useful in • If nutritional requirements cannot be met
glossitis, and pharyngitis may be secondary to evaluating pharyngeal and esophageal motility orally, gastrostomy tube may be necessary.
feline viral rhinotracheitis, feline leukemia as well as proper coordination of upper and
virus (FeLV)/feline immunodeficiency virus lower esophageal sphincters.
CLIENT EDUCATION D
• Variable dependent on underlying cause.
(FIV), pemphigus, systemic lupus • CT and/or MRI for suspected intracranial • Educate the client that not all diseases can
erythematosus (SLE), uremia, and ingestion mass. be cured, but managed.
of caustic agents or foreign bodies. • Esophagram (liquid barium administered • Changes in feeding (see above) may be long
• Neuromuscular disorders that impair orally followed by immediate survey radio- term.
prehension and bolus formation include CN graphs of the thorax) is helpful for diagnosing • Clients should be taught to monitor for signs
deficits (e.g., idiopathic trigeminal neuro radiolucent esophageal foreign bodies and of possible aspiration pneumonia (mucopurulent
pathy CN V, lingual paralysis CN XII) and esophageal strictures, but is insensitive for nasal discharge, increased respiratory rate at rest,
masticatory muscle myositis. diagnosing esophageal functional disorders. coughing, dyspnea, tachypnea).
• Pharyngeal weakness, paresis, or paralysis DIAGNOSTIC PROCEDURES
can be caused by infectious polymyositis (e.g., SURGICAL CONSIDERATIONS
• Endoscopy of nasopharynx—retroflexion of
toxoplasmosis and neosporosis), immune- • Cricopharyngeal myectomy (bilateral
endoscope over soft palate to look for foreign removal) may benefit patients with crico
mediated polymyositis, muscular dystrophy, bodies and evaluate esophagus and lower
polyneuropathies, and myoneural junction pharyngeal muscle dysfunction; correct
esophageal sphincter. diagnosis is essential using videofluoroscopy
disorders (e.g., myasthenia gravis, tick bite • Electromyography of skeletal musculature
paralysis, botulism). before surgery, and to rule out other myopathic
to confirm presence of myopathy. or neuropathic causes of dysphagia.
• Other CNS disorders, especially those • Repetitive nerve stimulation and edroph
involving the brainstem. • Hiatal hernia surgery generally involves
onium chloride (0.1–0.2 mg/kg IV) test for left-sided gastropexy with esophageal hiatal
• Rabies can cause dysphagia by affecting suspected myasthenia gravis.
both brainstem and peripheral nerves. plication and esophagopexy.
• Cerebrospinal fluid analysis in patients with
RISK FACTORS a CNS disorder.
Many causative neuromuscular conditions PATHOLOGIC FINDINGS
have breed predispositions. Variable depending on underlying etiology.
Myopathies can be inflammatory or dystrophic.
MEDICATIONS
DRUG(S) OF CHOICE
Dysphagia is not immediately life-
DIAGNOSIS threatening; direct drug therapy at the
underlying cause.
DIFFERENTIAL DIAGNOSIS TREATMENT
• Differentiate vomiting from regurgitation. PRECAUTIONS
APPROPRIATE HEALTH CARE • Use barium sulfate with caution in patients
• Vomiting is typically associated with • Determine underlying cause to optimize
abdominal contractions; dysphagia is not. with evidence of aspiration.
therapy and outcome. • Use corticosteroids with caution or not at
CBC/BIOCHEMISTRY/URINALYSIS • Most patients can be managed on
all in patients with evidence of, or at risk for,
• Inflammatory conditions often cause a outpatient basis unless there are other aspiration.
leukocytosis, sometimes with a left shift. complicating factors such as aspiration
• High serum creatine kinase activity is pneumonia, dehydration, or weakness.
usually suggestive of a myopathy. NURSING CARE
• May find evidence of renal disease (e.g., • Supportive care may be necessary if patient
azotemia and low urine concentration) in is dehydrated (IV fluids).
FOLLOW-UP
patients with oral and lingual ulcers • Other supportive modalities may be PATIENT MONITORING
secondary to uremia. necessary in case of aspiration pneumonia • Daily for signs of aspiration pneumonia
OTHER LABORATORY TESTS (oxygen, coupage, etc.). (e.g., lethargy, fever, mucopurulent nasal
• Type 2M muscle antibody serology • For patients with generalized weakness due discharge, coughing, dyspnea).
(masticatory muscle myositis). to myopathies, good nursing care is required, • Body condition and hydration status daily;
• Acetylcholine receptor antibody serology such as rotating position, good padding, and if oral nutrition does not meet requirements,
(acquired myasthenia gravis). physical therapy. use gastrostomy tube feeding.
• Antinuclear antibody serology (immune- POSSIBLE COMPLICATIONS
ACTIVITY
mediated diseases). Alterations in activity should be based on Aspiration pneumonia and malnutrition.
• T4, free T4, thyroid-stimulating hormone underlying etiology.
(TSH), anti-thyroglobulin antibodies to rule
out hypothyroidism. DIET
• Resting cortisol and/or adrenocorticotropic • Nutritional support is important for all
hormone (ACTH) stimulation test to rule out dysphagic patients, and consistency of diet MISCELLANEOUS
Addison’s disease. should be altered to optimize swallowing in ASSOCIATED CONDITIONS
affected animals. • Aspiration pneumonia.
IMAGING • Elevating head and neck during feeding and
• Obtain survey radiographs of thorax (3-views) • Megaesophagus.
for 10–15 minutes after feeding may help • Malnutrition.
and neck in all dysphagic animals for which oral patients with esophageal disease. Consider
cause of dysphagia has been ruled out. altering consistency of diet. Dogs with
• Ultrasonography of pharynx may be useful cricopharyngeal muscle dysfunction are able to
in patients with mass lesions and for obtaining handle kibble better than canned food or water.
ultrasound-guided biopsy specimens.
Dysphagia (continued)
AGE-RELATED FACTORS ZOONOTIC POTENTIAL Suggested Reading

• Puppies are more likely to have congenital • Consider rabies in any patient with Kook PH. Gastroesophageal reflux. In:
abnormalities such as cricopharyngeal muscle oropharyngeal dysphagia, especially if Bonagura JD, Twedt DC, eds., Kirk’s
D achalasia, congenital megaesophagus, vascular animal’s rabies vaccination status is unknown Current Veterinary Therapy XV. St Louis,
ring anomalies, and cleft palates. or questionable or it has been exposed to a MO: Elsevier Saunders, 2014, pp. 501–504.
• Puppies with vascular ring anomalies will potentially rabid animal. Marks SL. Oropharyngeal dysphagia. In:
typically present with signs of regurgitation • If a dysphagic animal dies of rapidly Bonagura JD, Twedt DC, eds., Kirk’s
shortly after being weaned onto solid food at progressive neurologic disease, submit the Current Veterinary Therapy XV. St Louis,
6–8 weeks of age. head to a qualified laboratory designated by MO: Elsevier Saunders, 2014, pp. 495–500.
• Puppies with cleft palates usually have milk the local or state health department for rabies Pollard RE, Marks SL, Cheney DM.
or food refluxing from the nasal passage examination. Diagnostic outcome of contrast
during mastication and swallowing. SEE ALSO videofluoroscopic swallowing studies in 216
• Puppies with cricopharyngeal muscle dysphagic dogs. Vet Radiol Ultrasound
• Megaesophagus.
achalasia typically present with repeated • Pneumonia, Bacterial. 2017, 58(4):373–380.
bouts of swallowing, gagging, and retching • Regurgitation. Warnock JJ, Marks SL, Pollard R, et al.
during swallowing with nasal reflux of Surgical management of cricopharyngeal
water or food. ABBREVIATIONS dysphagia in dogs: 14 cases (1989–2001).
• Puppies are more likely to ingest foreign • ACTH = adrenocorticotropic hormone. J Am Vet Med Assoc 2003,
objects that can lodge in the esophagus and • CN = cranial nerve. 223(10):1462–1468.
cause esophagitis and stricture formation. • FeLV = feline leukemia virus. Author Stanley L. Marks
• Older dogs, in particular Labrador • FIV = feline immunodeficiency virus. Consulting Editor Mark P. Rondeau
retrievers, are more likely to have esophageal • GOLPP = geriatric onset laryngeal paralysis
dsymotility secondary to a polyneuropathy polyneuropathy.
(geriatric onset laryngeal paralysis poly • PES = proximal esophageal sphincter. Client Education Handout
neuropathy or GOLPP). • SLE = systemic lupus erythematosus. available online
• TSH = thyroid-stimulating hormone.
Dyspnea and Respiratory Distress

pyothorax/chylothorax. Paradoxical paralysis, myasthenia gravis, elapid snake
respiratory pattern (inward movement of the envenomation, hypokalemia.
abdominal wall during inspiration).
BASICS • Thoracic wall disease—can have paradoxical
Diaphragmatic Disease D
• Trauma—rupture; hernia.
DEFINITION respiratory pattern, visible or palpable trauma • Phrenic nerve disease.
Dyspnea—a subjective term that in human (open pneumothorax, flail chest). • Neoplasia.
medicine means “an uncomfortable sensation • Pulmonary thromboembolism (PTE)— • Fibrosis.
in breathing” or a sensation of air hunger; in may have clinical signs of underlying disease
veterinary medicine, it is used to indicate predisposing to thrombosis, e.g., hyperadreno Abdominal Distention
difficulty breathing or respiratory distress. corticism, immune-mediated hemolytic Organomegaly—hyperplasia; neoplasia,
anemia (IMHA), systemic inflammatory pregnancy; obesity; ascites; gastric dilatation,
PATHOPHYSIOLOGY torsion.
response syndrome (SIRS)/sepsis, protein-
Dyspnea and respiratory distress are believed
losing nephropathy (PLN), protein-losing
to occur when the CNS notes a difference
enteropathy (PLE), neoplasia.
between the afferent feedback from a given
• Other signs will pertain to the underlying
efferent motor drive signal (ventilation
disease, e.g., shock, trauma. DIAGNOSIS
demanded) and what the brain had antici
pated would be the appropriate afferent CAUSES & RISK FACTORS DIFFERENTIAL DIAGNOSIS
response (ventilation achieved). Upper Airway Disease • Inspiratory dyspnea—suggests extrathoracic
SYSTEMS AFFECTED • Nasal obstruction—stenotic nares, upper airway disease.
Respiratory nasopharyngeal polyp or stenosis, infection, • Expiratory dyspnea—suggests intrathoracic
inflammation, neoplasia, trauma, foreign airway disease.
SIGNALMENT • Dyspnea on inspiration and expiration can
body, coagulopathy.
Dogs and cats; age, breed, and sex predis occur with fixed upper airway obstructions
• Pharynx—elongated soft palate, foreign
position vary with inciting cause. and severe intrathoracic disease.
body, neoplasia, granuloma, stenosis.
SIGNS • Larynx—laryngeal paralysis, everted • Congestive heart failure—murmur,
Historical Findings laryngeal saccules, edema, collapse, foreign arrhythmia, tachycardia, poor pulse quality,
• Acute or chronic onset. body, neoplasia, inflammation, trauma, jugular pulses, hypothermia, crackles on
• Often associated with tachypnea, coughing, webbing. auscultation, fluid dripping from nose.
exercise intolerance, lethargy, inappetence. • Trachea—collapse, stenosis, trauma, foreign CBC/BIOCHEMISTRY/URINALYSIS
body, neoplasia, parasites, extraluminal • Anemia—can cause nonrespiratory
Physical Examination Findings compression (lymphadenopathy, enlarged left
• General signs of respiratory distress—
dyspnea.
atrium, heart-base tumors). • Polycythemia—chronic hypoxia.
tachypnea, increased abdominal effort, nasal
Lower Airway Disease • Inflammatory leukogram—pneumonia,
flaring, open-mouth breathing, cyanosis,
orthopnea (neck extension, elbow abduction), Allergic disease, inflammatory, infectious pneumonitis, pyothorax.
(Mycoplasma), parasitic, neoplastic • Eosinophilia—hypersensitivity or parasitic
altered mentation; other signs depend on
underlying cause. (bronchogenic carcinoma). airway disease.
• Thrombocytosis—hyperadrenocorticism
• Nasal disease—stertor, nasal discharge, lack Pulmonary Parenchymal Disease
of airflow through nostrils; dyspnea improves predisposes to PTE.
• Edema—cardiogenic or noncardiogenic.
• Sodium : potassium ratio <27—can be seen
with open-mouth breathing. • Pneumonia—infectious; parasitic;
• Upper airway/laryngeal disease—stridor,
with pleural or abdominal effusions.
aspiration; eosinophilic; interstitial.
• Azotemia—if severe may lead to uremic
panting, cough, hyperthermia, dysphonia, • Neoplasia (primary or metastatic).
respiratory effort and noise on inspiration, pneumonitis.
• Inflammatory— acute respiratory distress
• Proteinuria—can predispose to PTE.
fixed obstruction such as a mass or foreign syndrome (ARDS); uremic pneumonitis;
• Multiple organ dysfunction—ARDS.
body in a large airway: dyspnea on inspiration smoke inhalation.
• Hypoproteinemia—may suggest protein-
and expiration. • Hemorrhage—trauma; coagulopathy.
• Tracheal collapse—honking cough, tracheal
losing disease that can predispose to PTE or
• PTE—IMHA; PLN, PLE; heartworm
sensitivity, respiratory effort and noise: pleural effusion.
disease; hyperadrenocorticism; neoplasia.
inspiratory effort if cervical tracheal collapse, • Others—lung lobe torsion, atelectasis. OTHER LABORATORY TESTS
expiratory effort if intrathoracic tracheal • Pleural fluid analysis.
Pleural Space Disease
collapse. • Fecal examination for parasites if
• Pneumothorax—traumatic; iatrogenic;
• Lower airway disease—cough, expiratory indicated
secondary to pulmonary parenchymal disease;
wheezes on auscultation, abdominal effort. • Serum antigen or antibody titers—
ruptured bulla; migrating foreign body;
• Pulmonary parenchymal disease—may have heartworm, toxoplasmosis, distemper, feline
primary spontaneous (no underlying cause).
crackles, harsh or moist lung sounds on leukemia virus (FeLV), feline immuno
• Pleural effusion—transudates, exudates;
auscultation. deficiency virus (FIV).
hemothorax; chylothorax.
• Pneumonia—fever, may have tracheal • Increased urine protein : creatinine ratio
• Soft tissue—neoplasia; diaphragmatic hernia.
sensitivity. with PLN could indicate loss of antithrombin
• Fibrosing pleuritis.
• Cardiogenic pulmonary edema—heart and hypercoagulability resulting in PTE.
murmur, arrhythmia, hypothermia, pale Thoracic Wall Disease • PaO2—partial pressure of oxygen dissolved
mucous membranes, prolonged capillary • Open pneumothorax—trauma. in arterial blood; normoxemia: PaO2
refill time. • Flail segment—trauma. 80–120 mmHg (room air, sea level);
• Pleural space disease—diminished breath • Neoplasia. hypoxemia: PaO2 <80 mmHg; FIO2—
sounds: ventrally—fluid; dorsally—air; • Paralysis due to cervical spinal disease, fraction of inspired oxygen ranges from 0.21
unilaterally—space-occupying lesions or botulism, polyradiculoneuritis, tick bite (room air) to 1.0; PaO2/FIO2 ratio—measure
Dyspnea and Respiratory Distress (continued)
of lung efficiency during oxygen therapy; • Pulmonary vascular angiography—gold • Abdominal distention—drain ascites as
PaO2/FIO2 ≥400—normal lung efficiency; standard for diagnosis of PTE. needed; relieve gastric distention.
300–400—mild insufficiency; 200–300— • Ventilation perfusion scintigraphy—
D moderate insufficiency; <200—severe abnormal perfusion scan is considered
NURSING CARE
• Oxygen therapy via cage, nasal cannula,
insufficiency. Reduction in lung efficiency supportive of PTE. Elizabethan collar covered in plastic wrap,
can be due to venous admixture, hypo DIAGNOSTIC PROCEDURES mask, or flow-by. Humidify oxygen source if
ventilation, low inspired oxygen. • Pulse oximetry—SpO2; peripheral capillary giving oxygen therapy for more than a few
• PaCO2 or PvCO2—partial pressure of hemoglobin oxygen saturation. The relation hours.
CO2 dissolved in arterial or venous blood; ship between PaO2 and SpO2 is defined by • Maintain in sternal recumbency and turn
measure of ventilation; normal 30 mmHg the oxygen hemoglobin dissociation curve: hips every 3–4 hours if patient cannot tolerate
<PCO2 <40 mmHg. PCO2 > 45 mmHg = PaO2 of 60 mmHg = SpO2 of 90%; PaO2 of lateral recumbency.
hypercapnia = hypoventilation = decreased 80 mmHg = SpO2 of 95%; PaO2 of • Monitor temperature regularly, as excess
alveolar minute ventilation (MV). >100 mmHg = SpO2 of 100%. Below 95%, work of breathing results in hyperthermia,
• Coagulation testing—if suspect hemothorax small changes in SpO2 signify large changes in which augments respiratory distress.
and/or pulmonary hemorrhage. PaO2. SpO2 measurements in animals on high
• Plasma NT-proBNP and cardiac troponin-I DIET
inspired oxygen lack sensitivity. Weight-reducing diet if obesity is a
(cTNI) concentrations may aid in different • Thoracentesis—fluid analysis and culture.
iation of cardiac and noncardiac causes of contributing cause.
• Laryngoscopy/nasopharyngoscopy/
dyspnea. tracheoscopy—evaluate upper airway; SURGICAL CONSIDERATIONS
IMAGING laryngeal paralysis, tracheal collapse, foreign • Anesthesia must be carefully tailored to the
• Cervical and thoracic radiography—upper bodies, masses. patient. Securing an airway is essential and
airway disease: soft palate elongation, large • Bronchoscopy—evaluate upper and lower rapid intravenous induction is important.
airway narrowing, lymphadenopathy, airways; perform bronchoalveolar lavage for The ability to positive-pressure ventilate
intraluminal abnormalities. Lower airway cytology and culture. Requires anesthesia, patients is often required.
disease: bronchial thickening, middle lung perform only when stabilized. • Animals with upper airway obstruction
lobe consolidation (cats), atelectasis, hyper are fragile and can rapidly decompensate.
inflation, and diaphragmatic flattening Have multiple-sized endotracheal tubes
(primarily cats). Pneumonia: alveolar available.
infiltrates; aspiration pneumonia usually • Dyspnea associated with a laryngeal mass can
cranioventral distribution or middle lobe
TREATMENT respond to debulking surgery, but edema and
affected. Cardiogenic pulmonary edema: APPROPRIATE HEALTH CARE hemorrhage can lead to worsened obstruction.
enlarged cardiac silhouette, pulmonary venous • Inpatient care until the cause is identified Warn owners of increased likelihood of
distention, enlarged left atrium with perihilar and treated or determined not to be life- aspiration pneumonia complications in
pulmonary infiltrates in dogs; infiltrates can threatening; therapy dependent on underlying animals with laryngeal disease.
be of any distribution in cats. Noncardiogenic cause. • Avoid positive-pressure ventilation in
pulmonary edema: usually caudodorsal • Always administer oxygen and keep patient patients with a closed pneumothorax. Must
distribution. ARDS: diffuse, symmetric in sternal recumbency until ability to monitor oxygenation status of anesthetized
alveolar infiltrates. Pulmonary vascular oxygenate is determined. patients with pulse oximetry and when
abnormalities: PTE, heartworm disease. • May require intubation and positive-pressure possible arterial blood gases.
Pleural space disease: pneumothorax, pleural ventilation in patients with severe respiratory
effusion, mass lesions, diaphragmatic hernias. distress refractory to oxygen therapy.
Thoracic wall disease: rib fractures, neoplasia. • Upper airway disease—use sedation to reduce
• Thoracic ultrasonography—evaluation of respiratory effort. Check body temperature and MEDICATIONS
distribution of pleural effusion, pneumothorax actively cool patients as needed.
(absence of “glide sign”), and parenchymal • Lower airway disease—bronchodilators; DRUG(S) OF CHOICE
disease (presence of “comet tail” artifact). systemic corticosteroids may be required to Varies with underlying cause (see Appropriate
Pulmonary mass identification: guide stabilize cats with acute bronchoconstriction. Health Care).
fine-needle aspiration; mediastinal evaluation. • Pulmonary parenchymal disease—
• Echocardiography—evaluate cardiac antibiotics if pneumonia; treat coagulation
function and chamber size if cardiogenic disorders; cardiogenic edema requires
pulmonary edema or pleural effusion furosemide ± vasodilators. Noncardiogenic FOLLOW-UP
suspected; elevated pulmonary artery pressure, edema requires oxygen therapy, may require
right ventricular overload with ventricular positive-pressure ventilation. PATIENT MONITORING
septal flattening can support diagnosis of • Pleural space disease—thoracocentesis for • Patients receiving oxygen therapy can be
PTE; visualize heart-based masses. air and fluid. Place a chest tube if repeated monitored by assessing the degree of
• Abdominal radiography or ultrasound— thoracocentesis is necessary to keep patient respiratory effort. As the animal stabilizes,
evaluation of abdominal distention. stable. perform a room air trial and reevaluate the
• Fluoroscopy—evaluate tracheal and • Thoracic wall disease—surgery as indicated, level of respiratory difficulty. Arterial and
bronchial collapse; evaluate diaphragmatic particularly if open chest wound is present; venous blood gases can be a useful assessment.
function. flail chest may require surgery if medical • Pulse oximetry is an effective and
• CT—airway, pulmonary parenchymal, and management fails or there is a severe noninvasive tool for monitoring patients on
pleural space disease can be evaluated; can displacement of fractures. Thoracic wall room air.
detect lesions not clearly defined on radio- paralysis/muscle fatigue: positive-pressure • Repeat radiographs are often indicated in
graphs. ventilation if severely hypercapnic. assessing pulmonary parenchymal disease and
pleural space disease.
(continued) Dyspnea and Respiratory Distress

• FIO2 = fraction of inspired oxygen. Mellema MS. The neurophysiology of dyspnea.
• FIV = feline immunodeficiency virus. J Vet Emerg Crit Care 2008, 18:561–571.
• IMHA = immune-mediated hemolytic Rozanski E. Respiratory distress. In: Drobatz
MISCELLANEOUS anemia. KJ, Hopper K, Rozanski EA, et al. Textbook D
SEE ALSO • MV = minute ventilation. of Small Animal Emergency Medicine.
• Acute Respiratory Distress Syndrome. • PaCO2 = partial pressure of carbon Hoboken, NJ: Wiley, 2018, pp. 18–21.
• Asthma, Bronchitis—Cats. dioxide. Smith KF, Quinn RL, Rahilly LJ. Biomarkers
• Brachycephalic Airway Syndrome. • PaO2 = partial pressure of oxygen. for differentiation of causes of respiratory
• Congestive Heart Failure, Left-Sided. • PLE = protein-losing enteropathy. distress in dogs and cats: Part 1 – Cardiac
• Congestive Heart Failure, Right-Sided. • PLN = protein-losing nephropathy. disease and pulmonary hypertension. J Vet
• Laryngeal Diseases. • PTE = pulmonary thromboembolism. Emerg Crit Care 2015, 25(3):311–329.
• Panting and Tachypnea. • SIRS = systemic inflammatory response Author Yu Ueda
• Pneumonia, Aspiration. syndrome. Consulting Editor Elizabeth Rozanski
• Pneumothorax. • SpO2 = oxygen saturation. Acknowledgement The author and book
• Pulmonary Edema, Noncardiogenic. Suggested Reading editors acknowledge the prior contribution of
Herndon WE, Rishniw M, Schrope D, et al. Kate Hopper.
ABBREVIATIONS
• ARDS = acute respiratory distress Assessment of plasma cardiac troponin I
syndrome. concentration as a means to differentiate
• cTNI = cardiac troponin-I. cardiac and noncardiac causes of dyspnea in
available online
• FeLV = feline leukemia virus. cats. JAVMA 2008, 233:1261–1264.
Dystocia
Cats • Uterine rupture.
Brachycephalic (Persian, Himalayan) or • Uterine neoplasia, cysts, or adhesions.
dolichocephalic (Devon Rex) breeds.
D BASICS RISK FACTORS
SIGNS • Age.
DEFINITION • Brachycephalic and toy breeds.
Difficult birth. Historical Findings
• Persian, Himalayan, and Devon Rex breeds.
• More than 30 min of persistent, strong,
PATHOPHYSIOLOGY • Obesity.
abdominal contractions without fetal delivery.
• Dystocia may occur due to maternal or fetal • Abrupt changes in peripartum
• More than 4h from onset of stage 2 to
factors and may occur during any stage of labor. environment.
delivery of first fetus (bitch).
• May be caused by abnormal fetal present • Previous history of dystocia.
• More than 2h between delivery of fetuses
ation, posture, or position. (bitch).
• Normal stages of labor: • Failure to commence stage 1 labor within
Stage 1 24h of rectal temperature drop below 37.2 °C
• Onset of uterine contractions and relax- (99 °F) or within 36h of serum progesterone DIAGNOSIS
ation of cervix; ends with rupture of first concentration <2 ng/mL (bitch). DIFFERENTIAL DIAGNOSIS
chorioallantoic sac—averages 6–12h (up to • Female cries, displays signs of pain, and
Uterine inertia—hypocalcemia versus
36h in primiparous bitch). constantly licks vulvar area when contracting. hypoglycemia.
• Bitch—may be restless, nervous, shiver, • Prolonged gestation—more than 72 days
pant, pace, and nest. from day of first mating (bitch); more than Physical Examination
• Queen—tend to vocalize initially; purr and 59 days from first day of cytologic diestrus • Complete physical examination—careful
socialize as Stage 1 progresses. (bitch); more than 66 days from luteinizing abdominal palpation to confirm presence of
hormone (LH) peak (bitch); more than 68 fetuses.
Stage 2 • Digital vaginal examination—fetus or fetal
days from last day of mating (queen).
• Delivery of fetuses. membranes in vaginal canal, assess maternal
• Bitch—obvious abdominal contractions; Physical Examination Findings
pelvic canal, Ferguson’s reflex.
beginning of stage 2 to delivery of first • Presence of greenish-black discharge
• Bitch unresponsive to oxytocin or lacking
offspring usually <4h; average time to (uteroverdin) preceding birth of first fetus by Ferguson’s reflex—uterine inertia more likely
delivery of subsequent fetus 20–60 min (may more than 2h or increasing amounts before than obstructive dystocia unless obstructed
be as long as 2–3h). delivery of first fetus. for several hours.
• Queen—average length of parturition 16h, • Bloody discharge prior to delivery of first fetus.
with range of 4–42h (up to 3 days in some • Diminished or absent Ferguson’s reflex CBC/BIOCHEMISTRY/URINALYSIS
cases); important to consider this variability (stimulation or pressure to dorsal vaginal wall Minimum database—packed cell volume
when intervening. to elicit abdominal straining: “feathering”) (PCV), total protein, serum glucose, urea
• Number of fetuses present may significantly indicates uterine inertia. nitrogen, and calcium (ionized preferable to total
affect length of stages 2 and 3. concentration corrected for albumin) concentra
CAUSES tions. Pregnant females have mild anemia.
Stage 3 Fetal
• Delivery of fetal membranes. OTHER LABORATORY TESTS
• Oversize; fetal monsters, fetal anasarca, fetal
• May alternate between stage 2 and 3 with Serum progesterone concentration.
hydrocephalus, prolonged gestation due to
multiple fetuses. inability of singleton fetus to initiate labor. IMAGING
INCIDENCE/PREVALENCE • Abnormal presentation, position, or posture • Radiography—determine pelvic
• Dog—incidence unknown due to breed of fetus in birth canal. conformation, number and position of fetuses,
variability and breeder intervention. • Fetal death. evidence of fetal obstruction, oversize, or death.
• Cat—3.3–5.8% of parturitions; mixed- • Fetal death—collapse of fetal skeletons,
Maternal
breed cats 0.4%, higher in pedigree cats, to abnormal association of fetal bones to axial
• Inadequate uterine contractions (primary or
18.2% in Devon Rex. skeleton, presence of air/gas surrounding
secondary uterine inertia)—myometrial fetus, fetal balling.
SIGNALMENT defect, hypocalcemia electrolyte imbalance, • Ultrasonography—recommended for
psychogenic disturbance, exhaustion. monitoring fetal viability, heart rate (fetal
Breed Predilections
• Ineffective abdominal press—pain, fear,
Dogs heart rate <180 bpm indicates fetal stress,
debility (exhaustion), diaphragmatic hernia, age. >260 bpm indicates need for close
• Higher incidence with miniature and small • Placentitis, metritis, endometritis.
breeds (small litter size, concurrent large fetal monitoring), placental separation, and
• Pregnancy toxemia, gestational diabetes.
size); may occur in large breeds with large or character of fetal fluids (presence of
• Abnormal pelvic canal—previous pelvic injury,
singleton litters. meconium or blood in amniotic fluid).
abnormal conformation, pelvic immaturity.
• Brachycephalic breeds—broad head and • Congenitally small pelvis—Welsh corgis,
narrow pelvis. brachycephalic breeds.
• Large fetal head : maternal pelvis ratio— • Inguinal hernia.
Sealyham terrier, Scottish terrier. • Abnormality of vaginal vault—stricture, TREATMENT
• Uterine inertia—Scottish terrier, dachshund, septae, vaginal hyperplasia, hypoplastic
border terrier, Aberdeen terrier, Labrador APPROPRIATE HEALTH CARE
vagina, intra- or extraluminal cysts, neoplasia. • Inpatient—until delivery of all fetuses and
retriever. • Abnormal vulvar opening—stricture,
• Other breeds with increased incidence of dam is stable.
fibrosis from trauma, neoplasia. • Treat hypoglycemia and hypocalcemia.
dystocia—chihuahua, dachshund, Pekingese, • Insufficient cervical dilation.
Yorkshire terrier, miniature poodle, • Uterine inertia—medical treatment if no
• Lack of adequate lubrication. evidence of fetal stress.
Pomeranian. • Uterine torsion.
(continued) Dystocia
• Ecbolic agents contraindicated with with supplemental propofol or alfaxalone
possible obstructive dystocia—may accelerate for intubation, if needed.
placental separation and fetal death or cause ◦ Maintenance may include inhalant
uterine rupture. anesthetics or propofol IV CRI. FOLLOW-UP D
• WhelpWise® tocodynamometer monitors ◦ Use of a midline lidocaine line block PREVENTION/AVOIDANCE
fetal heart rates and uterine contraction (1–2 mg/kg SC) can decrease inhalant • Schedule elective C-section for bitches with
patterns; useful for bitches with large litters or anesthetic requirement. abnormal pelvic canal, anatomic
history of uterine inertia to determine need • Epidural—0.5% bupivacaine (0.2 mg/kg) abnormalities, predisposition to dystocia,
for intervention. and preservative-free morphine (0.1 mg/kg) previous history of uterine inertia.
Manual Delivery or 2% lidocaine (2–4 mg/kg). • Scheduling surgery—extremely important
• Postoperative analgesia may be provided that D1 diestrus, LH peak, or ovulation is
Fetus lodged in vaginal vault:
• Lubricate liberally.
with opioids, although they are excreted in identified during breeding to ensure
• Digital manipulation—least amount of
the milk to varying degrees. acceptable fetal survivability. If ovulation
damage to fetus and dam. Apply traction in • Reversal agents—repeated dosing may be timing is not available, ultrasonographic
postero-ventral direction. necessary until neonate has processed all gestational aging and maturation assessment
• Instrument delivery not recommended due
anesthetic drugs: is necessary.
to inadequate space—may mutilate fetus or ◦ Opioids used during anesthesia can be
lacerate dam. reversed in neonate with naloxone (0.04 mg/
• If dystocia is identified promptly and
• Never apply traction to distal extremities or
kg IV/IM/SC/sublingual/intranasal).
intervention is successful—good to fair for
tail of a live fetus. ◦ Benzodiazepines used during anesthesia can
survival of dam; fair for fetuses.
• Failure to deliver fetus located in vaginal
be reversed in neonate with flumazenil (0.01
• If dystocia unrecognized or untreated for
canal within 30 min—Cesarean section mg/kg IV/IM/SC/sublingual/intranasal).
24–48h—poor to guarded for life of dam;
(C-section) indicated. fetal survival unlikely.
• Indications for C-section—uterine inertia
unresponsive to oxytocin or uterine inertia MEDICATIONS
with more than four fetuses remaining in DRUG(S) OF CHOICE MISCELLANEOUS
utero (maximizes fetal survivability), pelvic or • Hypoglycemia—treat prior to hypo-
vaginal obstruction, inability to correct fetal PREGNANCY/FERTILITY/BREEDING
calcemia:
malposition, fetal oversize, fetal stress, in Dystocia may or may not impact future
◦ Bolus 0.5 g/kg IV (diluted 1 : 3).
utero fetal death. fertility, but may recur depending on cause.
◦ Add 5% dextrose to balanced electrolyte
• Elective C-section—breeds prone to Resolution of dystocia by C-section does not
solution and infuse IV at 60–80 mL/kg/day.
dystocia, bitches with a history of dystocia, preclude natural whelping for future
• Hypocalcemia:
bitches with singleton or large litter size, deliveries.
◦ Bitch—10% calcium gluconate 0.2 mL/
performed to maximize fetal survivability. kg IV over 10 min; monitor for SEE ALSO
General Comments bradycardia. Repeat q4–6h as needed. • Breeding, Timing.
• Provide fluid therapy with balanced electrolyte ◦ May also be given SC at a dose of 0.5 • Uterine Inertia.
solution before, during, and after surgery. mL/4.5 kg diluted 1:1 with sterile saline. • Vaginal Malformations and Acquired Lesions.
• Gravid uterus can compress great vessels and If using 23% solution, dilute at least 1:3 ABBREVIATIONS
place pressure on diaphragm, compromising prior to administration. • C-section = Cesarean section.
venous return and tidal volume. ◦ Queen—10% calcium gluconate • LH = luteinizing hormone.
• Preoxygenation of patient before anesthesia 0.5–1.0 mL/cat IV over 10 min—use with • PCV = packed cell volume.
is indicated. caution; risk of uterine rupture increased
due to strong uterine contractions following Suggested Reading
• Anesthetic protocol for C-section:
calcium. Johnston SD, Root Kustritz MV, Olson PNS.
◦ Premedication can include glycopyrrolate
• Oxytocin—once calcium and glucose Canine parturition; Feline parturition. In:
(bitches, queens: 0.01 mg/kg IV/IM) if fetal
deficits are treated: microdose at 0.5–3.0 IU Canine and Feline Theriogenology.
heart rates are normal; or atropine (bitches,
IM/SC depending on size of bitch and Philadelphia, PA: Saunders, 2001,
queens: 0.04 mg/kg IM) if fetal bradycardia
response to treatment. May repeat q30 min as pp. 105–128, 431–437.
present.
long as delivery progresses. Consider Author Cheryl Lopate
◦ Alpha-2 agonist agents (xylazine,
C-section if more than three doses of Consulting Editor Erin E. Runcan
dexmedetomidine) are contraindicated.
◦ Rapidly acting induction agents include oxytocin per fetus are required or more than
propofol or alfaxalone; ketamine may cause four fetuses remain.
dose-dependent neonatal respiratory and CONTRAINDICATIONS available online
neurologic depression; severely depressed or Oxytocin—contraindicated with obstructive
exhausted patients may be induced with dystocia, fetal stress, longstanding in utero
combination of opioid and benzodiazepine fetal death, uterine rupture, uterine torsion.
Dysuria, Pollakiuria, and Stranguria

• Neoplasia—see above; local invasion by • Rule out colorectal disease for stranguria.
malignant neoplasms of adjacent structures. • Rule out cyclophosphamide cystitis—
• Trauma. history.
D BASICS • Anatomic anomalies—e.g., congenital or • Rule out iatrogenic disorders—history of
DEFINITION acquired strictures, urethrorectal fistulas, catheterization, reverse flushing, contrast
• Dysuria—difficult or painful urination. pseudohermaphrodites. radiography, urohydropropulsion, urethro
• Pollakiuria—voiding small quantities of • Urethral sphincter hypertonicity—e.g., cystoscopy, or surgery/complications from
urine with increased frequency. upper motor neuron spinal cord lesions, reflex interventional devices.
• Stranguria—straining to urinate. dyssynergia, urethral spasm/urethritis. CBC/BIOCHEMISTRY/URINALYSIS
• Proliferative urethritis—secondary to
PATHOPHYSIOLOGY • Results of bloodwork often normal.
chronic UTI. Lower urinary tract disease complicated by
The urinary bladder and urethra normally
serve as a reservoir for urine. Inflammatory Prostate Gland urethral obstruction may be associated
and noninflammatory disorders of the lower • Prostatitis, prostatic, or paraprostatic cyst or with azotemia, hyperphosphatemia,
urinary tract including the urethral orifice prostatic abscess. acidosis, and hyperkalemia. Patients with
may decrease bladder compliance and storage • Neoplasia—adenocarcinoma, transitional concurrent pyelonephritis may have
capacity by damaging structural components cell carcinoma. impaired urine-concentrating capacity,
of the bladder wall or by stimulating sensory RISK FACTORS leukocytosis, azotemia, and thrombo
nerve endings located in the bladder or • Diseases, diagnostic procedures, or treat-
cytopenia if ureteral obstruction occurs
urethra. Sensations of bladder fullness, ments that alter normal host urinary tract concurrently. Patients with acute
urgency, and pain stimulate premature defenses and predispose to infection, prostatitis or prostatic abscesses may have
micturition and reduce functional bladder predispose to formation of uroliths, or leukocytosis, discospondylitis, and/or heart
capacity. Dysuria and pollakiuria are caused damage urothelium or other tissues of lower murmur. Dehydrated patients may have
by lesions of the urinary bladder and/or urinary tract. elevated total plasma protein.
urethra and provide unequivocal evidence of • Disorders of urinary bladder are best
• Mural or extramural diseases that compress
lower urinary tract disease; these clinical signs bladder or urethral lumen. evaluated with urine specimen collected by
do not exclude concurrent involvement of the • Diseases that encourage repeated urination
cystocentesis. Urethral disorders best
upper urinary tract or disorders of other body despite full void such as juvenile vaginitis may evaluated with mid-catch voided urine sample
systems. Stranguria may be caused by bladder, present as stranguria. or by comparison of results of analysis of
intraluminal, and extraluminal urethral voided and cystocentesis samples. (Caution:
disease. cystocentesis may induce hematuria.)
• Pyuria, hematuria, and proteinuria indicate
SYSTEMS AFFECTED
urinary tract inflammation, but are
Renal/urologic/pelvic structures—bladder, DIAGNOSIS nonspecific findings that may result from
urethra, prostate gland, colon, others.
DIFFERENTIAL DIAGNOSIS infectious and noninfectious causes of lower
SIGNALMENT urinary tract disease.
Dog and cat. Differentiating from Other Abnormal • Identification of bacteria, fungi, or parasite
Patterns of Micturition ova in urine sediment suggests, but does not
CAUSES
• Polyuria—increased frequency and volume prove, that UTI causing or complicating
Urinary Bladder of urine >2 mL/kg/h and urine specific lower urinary tract disease. Consider
• Urinary tract infection (UTI)—bacterial, gravity <1.025. contamination of urine during collection and
fungal, mycoplasmal, parasitic, or viral. • Rule out urethral obstruction—anuria, storage when interpreting urinalyses.
• Cystolithiasis. overdistended urinary bladder, signs of • Identification of neoplastic cells in urine
• Neoplasia—e.g., transitional cell carcinoma. postrenal uremia. sediment indicates urinary tract neoplasia.
• Trauma. • Urinary incontinence—involuntary Use caution in establishing diagnosis of
• Anatomic abnormalities—e.g., ureterocele/ urination, urine dribbling, enuresis, neoplasia based on urine sediment exam
urethrocele, ectopic ureter, persistent uterus incomplete bladder emptying. ination. Urinary tract inflammation or
masculinus, perineal hernias containing the • Behavioral causes. extremes in urine pH or osmolality can cause
urinary bladder, and spay granulomas. epithelial cell atypia that is difficult to
Differentiate Causes of Dysuria,
• Detrusor atony—e.g., chronic partial differentiate from neoplasia. Follow up with
obstruction, neurologic damage, and dysaut- Pollakiuria, Stranguria
• Rule out UTI—hematuria; malodorous or
traumatic catheterization, cystoscopic
onomia. biopsies, or urine BRAF assay.
• Chemicals/drugs—e.g., cyclophosphamide. cloudy urine; small, painful, thickened bladder
• Crystalluria occurs in normal patients,
• Iatrogenic—e.g., catheterization, palpation, (also evaluate for mineralization or gas in wall).
• Rule out urolithiasis—hematuria; palpable
patients with urolithiasis, or patients with lower
reverse flushing, overdistension of the bladder urinary tract disease unassociated with uroliths.
during contrast radiography, urohydro uroliths in urethra or bladder.
• Rule out neoplasia—hematuria; palpable
Interpret significance of crystalluria cautiously.
propulsion, urethrocystoscopy, and surgery/ • Hematuria, proteinuria, and variable
interventional hardware (e.g., ureteral stent, masses in urethra or bladder.
• Rule out neurogenic disorders—flaccid
crystalluria occur in cats with nonobstructive
subcutaneous ureteral bypass, stent, hydraulic idiopathic cystitis. Significant pyuria is rare.
occluder). bladder wall; residual urine in bladder
• Idiopathic—e.g., feline idiopathic cystitis. lumen after micturition; other neurologic OTHER LABORATORY TESTS
deficits to hind legs, tail, perineum, and • Quantitative urine culture—most definitive
Urethra anal sphincter. means of identifying and characterizing
• UTI—see above. • Rule out prostatic diseases—urethral bacterial UTI. If not affordable then rapid
• Urethrolithiasis—see above. discharge, prostatomegaly, pyrexia, depression, culture can still be performed for species
• Urethral plugs—e.g., matrix and tenesmus, caudal abdominal pain, stiff gait. identification at limited cost.
matrix-crystalline.
(continued) Dysuria, Pollakiuria, and Stranguria

• Cytologic evaluation of urine sediment, urinary tract disease may benefit from POSSIBLE COMPLICATIONS
prostatic fluid, urethral or vaginal discharges, symptomatic therapy with propantheline or • Dysuria and pollakiuria may be associated
or biopsy specimens obtained by catheter or oxybutynin that may reduce the force and with formation of macroscopic vesicourachal
needle aspiration—may help in evaluating frequency of uncontrolled detrusor diverticula. D
patients with localized urinary tract disease; contractions. • Refer to specific chapters describing diseases
may establish definitive diagnosis of urinary • Propantheline—dogs: 0.2 mg/kg PO listed under Causes.
tract neoplasia, but cannot rule it out. q6–8h; cats: 0.25–0.5 mg/kg PO q12–24h.
IMAGING Oxybutynin—dogs: 0.2 mg/kg PO q8–12h;
Survey abdominal radiography, urinary tract cats: 0.5–1.25 mg/cat PO q8–12h.
• Stranguria due to physiologic causes may be
ultrasonography, cystoscopy, and fluoroscopic
treated with prazosin in female dogs or cats,
MISCELLANEOUS
urography are important means of identifying
or in male dogs or cats with tamsulosin. If ASSOCIATED CONDITIONS
and localizing causes of dysuria, pollakiuria,
secondary to inflammation, meloxicam or • Hematuria, pyuria, and proteinuria.
and stranguria.
carprofen can be utilized (caution with • Disorders predisposing to UTI.
DIAGNOSTIC PROCEDURES elevated liver values and azotemia), although • Disorders predisposing to formation of
• Use cystoscopy in patients with persistent short-term catheterization may also be uroliths.
lesions of lower urinary tract for which no warranted. • Macroscopic vesicourachal diverticula.
definitive diagnosis has been established by • Patients with transitional cell carcinoma of SYNONYMS
other, less invasive means. the urinary bladder or urethra may be treated • Feline urological syndrome.
• Use light microscopic evaluation of tissue with piroxicam (0.3 mg/kg PO q24h), which • Lower urinary tract disease.
biopsy specimens from patients with persistent reduces the severity of clinical signs, improves
lesions of urinary tract. Tissue specimens may quality of life, and in some cases induces SEE ALSO
be obtained by traumatic catheterization, tumor remission. Chemotherapeutic and • Feline Idiopathic Lower Urinary Tract
cystoscopy and biopsy, or surgery. radiation oncology treatment options are also Disease.
available, as is urethral stenting. • Lower Urinary Tract Infection, Bacterial.
• Lower Urinary Tract Infection, Fungal.
CONTRAINDICATIONS • Urinary Retention, Functional.
• Glucocorticoids or other • Urinary Tract Obstruction.
TREATMENT immunosuppressive agents in patients • Urolithiasis, Calcium Oxalate.
• Patients with nonobstructive lower urinary suspected of having urinary or genital tract • Urolithiasis, Calcium Phosphate.
tract diseases typically managed as outpatients; infection. • Urolithiasis, Cystine.
diagnostic evaluation may require brief • Potentially nephrotoxic drugs (e.g., • Urolithiasis, Pseudo (Dried Blood, Ossified
hospitalization. gentamicin) in patients that are febrile, Material).
• Dysuria, pollakiuria, and stranguria dehydrated, or azotemic or that are suspected • Urolithiasis, Struvite—Cats.
associated with systemic signs of illness (e.g., of having pyelonephritis, septicemia, or • Urolithiasis, Struvite—Dogs.
pyrexia, depression, anorexia, vomiting, and preexisting renal disease. • Urolithiasis, Urate.
dehydration) or laboratory findings of • Urolithiasis, Xanthine.
PRECAUTIONS
azotemia or leukocytosis warrant aggressive • Vesicourachal Diverticula.
N/A
diagnostic evaluation and initiation of
supportive and symptomatic treatment. POSSIBLE INTERACTIONS ABBREVIATIONS
• Treatment depends on underlying cause N/A • UTI = urinary tract infection.
and specific sites involved. Author Ewan D.S. Wolff
ALTERNATIVE DRUG(S)
• Clinical signs of dysuria, pollakiuria often Consulting Editor J.D. Foster
N/A
resolve rapidly following specific treatment of Acknowledgment The author and book
underlying cause(s). If not related to infection, editors acknowledge the prior contributions
stranguria may be more challenging to resolve. of John M. Kruger and Carl A. Osborne
FOLLOW-UP
PATIENT MONITORING
MEDICATIONS Monitor response to treatment by status of
clinical signs, serial physical examination,
DRUG(S) OF CHOICE laboratory testing, and imaging evaluations
• Patients with urge incontinence, severe or appropriate for each specific case.
persistent signs, or untreatable lower
Ear Mites
• Diet and activity—no alteration necessary.
• Very contagious—all animals in contact
with the affected animal must be treated.
BASICS • Thoroughly clean and treat the environ- MISCELLANEOUS
OVERVIEW ment. ZOONOTIC POTENTIAL
E Otodectes cynotis mites infest primarily the Transient papular dermatitis in human
external ear canal and cause variable degrees beings.
of otic discharge and pruritus. Suggested Reading
SIGNALMENT MEDICATIONS Helton Rhodes KA, Werner A. Blackwell’s
• Common in young dogs and cats, although DRUG(S) OF CHOICE Five-Minute Veterinary Consult Clinical
it may occur at any age. • Ears should be thoroughly cleaned with a Companion: Small Animal Dermatology,
• No breed or sex predilection. commercial ear cleaner. 3rd ed. Hoboken, NJ: Wiley-Blackwell,
SIGNS • Otic parasiticides should be used for 2018.
• Pruritus is usually present, but can be minimal. 7–10 days to eradicate mites and eggs; Thomas RC. Treatment of ectoparasites. In:
• Pruritus primarily located around the ears, effective topical commercial products Bonagura JD, Twedt DC, eds. Current
head, and neck; occasionally generalized. contain pyrethrins, thiabendazole, Veterinary Therapy XV. St. Louis, MO:
• Thick, red-brown, or black otic exudate ivermectin, and milbemycin; treat during Elsevier Saunders, 2014, pp. 428–432.
(“coffee grounds” appearance)—usually seen alternative weeks for two to three treatment Author Karen A. Kuhl
in the outer ear. cycles recommended to prevent reinfesta- Consulting Editor Alexander H. Werner
• Otic exudate and pruritus demonstrate tion from eggs. Resnick
individual variability. • Selamectin—per label instructions or
• Crusting and scales may occur on the neck, repeated at 2 weeks.
rump, and tail (dogs). • Imidacloprid/moxidectin (Advantage
• Excoriations on the convex surface of the Multi/Advocate)—per label instructions.
pinnae often occur, owing to the intense • Ivermectin—200–300 μg/kg PO (three
pruritus. treatments) or SC (two treatments) at 14-day
CAUSES & RISK FACTORS intervals; non-FDA-approved usage.
• Isoxazolines—per label instructions;
Otodectes cynotis.
non-FDA-approved usage.
• Flea treatments should be applied to animal
for elimination of ectopic mites.
• Mites may persist in the environment;
DIAGNOSIS environmental treatment may be helpful.
DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS/POSSIBLE
• Pediculosis. INTERACTIONS
• Pelodera dermatitis. • Ivermectin and moxidectin—sensitivity in
• Sarcoptic mange. ABCB-1 mutant dogs; do not use orally or by
• Notoedric mange. injection in collies, shelties, their crosses, or
• Chiggers. other herding breeds; use only if absolutely
• Otitis externa secondary to allergy/ necessary in animals <6 months of age; an
hypersensitivity. increasing number of toxic reactions have
• Flea bite hypersensitivity. been reported in kittens.
CBC/BIOCHEMISTRY/URINALYSIS • Ivermectin and milbemycin—cause elevated
Normal levels of monoamine neurotransmitter
metabolites, which could result in adverse
drug interactions with amitraz and benzo-
N/A
diazepines.
DIAGNOSTIC PROCEDURES • Isoxazolines—use with caution in pets with
• Ear swabs placed in mineral oil—usually previous history of seizures.
effective means of identification.
• Skin scrapings—may identify mites if signs
are generalized.
• Mites may be visualized in external ear canal.
• Diagnosis may be made by response to
FOLLOW-UP
• Ear swab and physical examination should
treatment.
be done 1 month after therapy commences.
• Prognosis is good.
• If signs persist after treatment, an addi-
tional, underlying cause may be present.
TREATMENT • Repeat infestation indicates an uncontrolled
• Outpatient. source of mites.
Eclampsia
• Toxicosis—distinguished by signalment and 7.2% hypertonic saline 1–3 mL/kg IV over
history. 15–20 min.
• Epilepsy or other neurologic disorder— • Long-term therapy—calcium carbonate or
BASICS differentiated by signalment; calcium calcium gluconate 10–30 mg/kg PO q8h
OVERVIEW concentration diagnostic. until lactation ends (calcium carbonate
• Postparturient hypocalcemia. 500 mg tablets supply 200 mg calcium).
E
• Usually develops 1–4 weeks postpartum; • Magnesium supplementation may be
• Total serum calcium <9 mg/dL in bitches;
may occur at term, prepartum, or during late <8 mg/dL in queens. helpful in hypomagnesemic bitches.
lactation. • Start puppies/kittens on solid food at 3–4
• Although ionized calcium (<2.4–3.2 mg/dL)
• Hypocalcemia alters cell membrane is the form important for normal neuro weeks of age.
potentials, causing spontaneous discharge of muscular function, measurement of total CONTRAINDICATIONS/POSSIBLE
nerve fibers and tonic–clonic contraction of serum calcium is usually sufficient for INTERACTIONS
skeletal muscles. diagnosis. Corticosteroids—avoid; cause decreased
• Life-threatening tetany and convulsions, • Hypoglycemia—may be concurrent. intestinal absorption and increased renal
leading to hyperthermia. • Hypomagnesemia has been reported in excretion of calcium.
• Cerebral edema possible. 44% of affected bitches; may promote tetany.
SIGNALMENT • Serum potassium elevated in 56% of cases,
• Dog—postpartum bitch; most common in due to metabolic acidosis or respiratory
toy breeds; higher incidence with first litter. alkalosis.
• Most common prior to day 40 postpartum;
FOLLOW-UP
occasionally occurs prepartum. N/A PATIENT MONITORING
• Breeds at increased risk—chihuahua, • Serum calcium concentration—monitor
miniature pinscher, shih tzu, miniature IMAGING until stabilized in the normal range.
poodle, Xoloitzcuintli, Pomeranian. N/A • Avoid calcium supplementation during
• Cat—rare. DIAGNOSTIC PROCEDURES gestation.
ECG may show prolonged QT interval, • Diet—maternal: ensure calcium : phosphorus
SIGNS
bradycardia, tachycardia, or ventricular ratio of 1.1 : 1 or 1.2 : 1; avoid high-phytate
Historical Findings premature complexes. foods (e.g., soybeans); puppies: supplement
• Poor mothering. feeding for large litters.
• Restlessness, nervousness.
• Panting, whining.
• Cerebral edema.
• Vomiting, diarrhea.
• Ataxia, stiff gait, limb pain. TREATMENT • Death.
• Emergency inpatient. • Hand-raising of puppies.
• Facial pruritis.
• Muscle tremors, tetany, convulsions. • Hyperthermia—cool by wetting haircoat EXPECTED COURSE AND PROGNOSIS
• Recumbency, extensor rigidity—usually and exposing to breeze from fan. • Probably will recur with subsequent litters;
seen 8–12 hours after onset of signs. • Puppies—remove from dam onto a foster calcium supplementation can be started after
dam or hand-raise; if not possible or parturition for bitches with history of
Physical Examination Findings undesirable due to behavioral need for
• Hyperthermia.
eclampsia in prior litters.
contact with dam, remove pups from dam for • Prognosis—good with immediate treatment;
• Rapid respiratory rate. 24 hours, or until serum calcium is stabilized,
• Dilated pupils, sluggish pupillary light
poor with delayed treatment.
and provide supplemental calcium for
responses. remainder of lactation; continue to monitor
• Muscle tremors, muscular rigidity, serum calcium level.
convulsions.
CAUSES & RISK FACTORS MISCELLANEOUS
• Calcium supplementation during gestation, Suggested Reading
including dairy products. Davidson AP. Reproductive causes of
• Inappropriate Ca : P ratio in gestational
MEDICATIONS
hypocalcemia. Topics Compan Anim Med
diet. DRUG(S) OF CHOICE 2012, 27:165–166.
• Low bodyweight : litter size ratio. • Calcium gluconate—10% solution Drobatz KJ, Casey KK. Eclampsia in dogs:
• Poor prenatal nutrition. 0.22–0.44 mL/kg IV given slowly to effect 31 cases (1995–1998). J Am Vet Med Assoc
• First litter. over 5 min; monitor heart rate or ECG 2000, 217(2):216–219.
• Large litter size. during administration; corresponds to dosage Gonzalez, K. Periparturient diseases in the
of 50–150 mg/kg. dam. Vet Clin North Am Small Anim Pract
• Correct hypoglycemia—50% dextrose: 2018, 48(4):663–681.
0.5 g/kg diluted 1 : 3 with saline IV; can Author Joni L. Freshman
supplement maintenance IV fluids to 2.5% Consulting Editor Erin E. Runcan
DIAGNOSIS or 5% dextrose for longer-term treatment.
DIFFERENTIAL DIAGNOSIS • Diazepam—0.5 mg/kg IV; for unresponsive
• Hypoglycemia—may be concurrent; hypo- seizures.
glycemia alone does not cause muscular • Cerebral edema—if present, can treat with
rigidity. mannitol: 0.25–0.5 g/kg IV over 20 min, or
Ectopic Ureter
• CT (91% sensitivity).
• Urinary tract ultrasonography (60–91%
sensitivity) can provide accurate diagnosis and
BASICS anatomic information of the upper urinary FOLLOW-UP
OVERVIEW tract. Color-flow Doppler ultrasonography EXPECTED COURSE AND PROGNOSIS
E • Congenital ureteral orifice(s) is inapprop can provide location of ureteral jets, but does • Warn owners that incontinence may
riately positioned caudal to the bladder not guarantee the absence of a multifene continue in some patients after surgery. Many
trigone (i.e., trigone, urethra, vagina, strated ureter. patients become continent with the addition
vestibule, uterus, or prostate), resulting in • Excretory urography (50–75% sensitivity) of medications, collagen bulking, and/or
incontinence. with positive contrast cystogram or a placement of a hydraulic occlude.
• A common cause of urinary incontinence in pneumocystogram. • Dogs—continence with surgery (25–50%)
juvenile female dogs. Also seen in adult dogs. • Retrograde urethrography (47% or laser ablation (40–55%) alone, which
• Dogs—>95% tunnel intramurally, sensitivity). improves to 60% with medications, 65%
traversing the urethra in the submucosa. DIAGNOSTIC PROCEDURES with bulking agent injection, and ~80–90%
• Male dogs—commonly associated with Cystoscopy—definitive diagnosis and with placement of a hydraulic occlude.
severe hydronephrosis and hydroureter due to characterization of EU, short urethra
ureteral opening stenosis. syndrome, location of ectopic orifice in the
• Commonly associated with multiple anomalies genitourinary tract. Also allows for simultane
of the urinary tract—including concurrent ous treatment.
urethral sphincter mechanism incompetence
MISCELLANEOUS
(USMI), hydroureter, hydronephrosis, short ASSOCIATED CONDITIONS
urethra/intrapelvic bladder. • Hydronephrosis.
• Hydroureter.
SIGNALMENT TREATMENT • Ureterocele.
• Dog and cat. • Cystoscopic-guided laser ablation (CLA)— • Pelvic bladder.
• Juvenile incontinent dogs. performed for intramural EU only. Opens • Persistent paramesonephric remnant.
• Infrequently reported in cats and male ureteral tract in a minimally invasive manner; • Vaginal septum.
dogs; 20 : 1 ratio of female : male dogs. addresses concurrent vaginal defects, which • Renal dysplasia.
• Dog breeds may be predisposed—retrievers, may lead to considerable deviation of the • Renal agenesis.
Siberian huskies, Newfoundlands, poodles, urethra. Patients treated with CLA typically • USMI.
terriers. discharged the same day. • Short urethra/intrapelvic bladder.
SIGNS • Surgical—treatment of choice for extra
SEE ALSO
• Constant or intermittent incontinence since mural EU: neoureterostomy, reimplantation,
• Incontinence, Urinary.
birth. or rarely ureteronephrectomy; complication
• Pelvic Bladder.
• Normal voiding in some. rates range between 14% and 25% including
• Chronic urinary tract infection(s) (UTIs). ureteral strictures, leakage, and infection. ABBREVIATIONS
• May be asymptomatic (male dogs) and can • CLA = cystoscopic-guided laser ablation.
have moderate to severe hydroureter/hydro- • EU = ectopic ureter.
nephrosis. • USMI = urethral sphincter mechanism
incompetence.
MEDICATIONS • UTI = urinary tract infection.
DRUG(S) OF CHOICE Author Ewan D.S. Wolff
• Use if incontinence persists after surgery. Consulting Editor J.D. Foster
DIAGNOSIS • Phenylpropanolamine (1–1.5 mg/kg PO Acknowledgment The author and book
DIFFERENTIAL DIAGNOSIS q8h) will improve continence after surgery/ editors acknowledge the prior contribution
• USMI. laser therapy in 10–20% of dogs, improving of Allyson C. Berent.
• Inappropriate urination—urge incontinence, continence levels to 50–60%.
“overactive bladder,” behavioral (conscious • Testosterone propionate (2.2 mg/kg IM
urination). q2–3 days) or methyltestosterone (0.5 mg/kg/
• UTI—pollakiuria and urge incontinence. day) is administered to male dogs. For longer
• Vaginal pooling. action, testosterone cypionate (2.2 mg/kg IM
• Congenital hydroureter/hydronephrosis— q30 days) can be used; this approach is not
male dogs with ectopic ureter(s) (EUs) often advised in immature or intact males.
continent. • Estriol (2 mg once daily per dog for 14
• Short urethra/intrapelvic bladder syndrome. days, followed by the lowest effective daily
CBC/BIOCHEMISTRY/URINALYSIS dose tapered every 7 days).
Labwork is typically normal, except when Other
patients have concurrent anomalies (e.g., Treatment for persistent incontinence after
renal dysplasia, pyelonephritis). surgery/laser ablation—transurethral
OTHER LABORATORY TESTS submucosal bulking agent injections: can
Urine bacterial culture and sensitivity—via improve continence to ~60–65%; placement
cystocentesis. of an artificial urethral sphincter (called a
hydraulic occluder) can improve continence
IMAGING to ~80–90%.
• Cystoscopy (96% sensitivity).
Ectropion
• Loss of orbital or periorbital mass—may • Nonsurgically treated patient—monitor for
occur in patients with masticatory myositis. signs of infectious conjunctivitis, exposure
• Facial nerve paralysis—associated with lack keratopathy, corneal ulceration, and facial
BASICS of muscle tone of orbicularis oculi muscles. dermatitis.
OVERVIEW CBC/BIOCHEMISTRY/URINALYSIS E
• Eversion or rolling out of the eyelid margin, N/A
resulting in exposure of the palpebral
conjunctiva. OTHER LABORATORY TESTS
• Possible masticatory myositis—test for MISCELLANEOUS
• Can be conformational/congenital
(primary) or acquired (secondary). auto-antibodies against type 2M muscle fibers. ASSOCIATED CONDITIONS
• Exposure and poor tear retention/ • Palpebral nerve paralysis or tragic facial • Hypothyroidism.
distribution may predispose patient to expression—consider testing for hypo- • Masticatory myositis, extraocular myositis.
irritation, recurrent infections, and sight- thyroidism.
AGE-RELATED FACTORS
threatening corneal disease. IMAGING Old animals more likely to have ectropion
SIGNALMENT N/A secondary to loss of facial muscle tone.
• Dogs, seldom cats. DIAGNOSTIC PROCEDURES SEE ALSO
• Breeds with higher than average prevalence— • Palpebral nerve paralysis—full neurologic • Hypothyroidism.
sporting breeds (e.g., spaniels, hounds, and evaluation; potential for hypothyroidism. • Myopathy – Masticatory and Extraocular
retrievers); giant breeds (e.g., Saint Bernard, • Secondary conjunctivitis—flush fornix and Myositis.
mastiff ); any breed with loose facial skin examine for follicles.
(especially bloodhounds). • Fluorescein or rose Bengal staining of
Suggested Reading
• Primary—genetic predisposition in listed
Stades FC, van der Woerdt A. Diseases and
cornea and conjunctiva—to identify corneal
breeds; may occur in dogs <1 year old. surgery of the canine eyelid. In: Gelatt KN,
ulcerations; may reveal severity of exposure
• Acquired—noted in other breeds; occurs
Gilger BC, Kern TJ, eds., Veterinary
problem.
late in life secondary to age-related loss of Ophthalmology, 5th ed. Ames, IA:
facial muscle tone and skin laxity. Wiley-Blackwell, 2013, pp. 853–864.
• Intermittent—caused by fatigue; may be
Author Sarah L. Czerwinski
observed after strenuous exercise or when Consulting Editor Kathern E. Myrna
drowsy. TREATMENT Acknowledgment The author and book
• Supportive care (topical lubricant, rinsing editor acknowledge the prior contribution
SIGNS eyes with eyewash after being outside to of J. Phillip Pickett.
• Eversion of the lower eyelid with lack of remove debris) and good ocular and facial
contact of the lower lid to the globe and hygiene—sufficient for most mild disease.
exposure of the palpebral conjunctiva and • Surgical treatment—eyelid shortening or
third eyelid. radical facelift; necessary for severely affected
◦ Often excessively long palpebral fissure patients that have chronic ocular irritation.
(macroblepharon). • Intermittent, fatigue-induced condition—
◦ Conjunctivitis and history of mucoid to do not treat surgically.
mucopurulent discharge caused by chronic
exposure to air and debris. Debris generally
located between lid and globe in inferior
conjunctival cul-de-sac.
◦ Tear staining of periocular skin caused by MEDICATIONS
poor tear drainage. DRUG(S) OF CHOICE
• History of bacterial conjunctivitis. • Topical broad-spectrum ophthalmic
CAUSES & RISK FACTORS antibiotics—bacterial conjunctivitis or
• Primary disease—most common due to corneal ulceration. Neomycin/polymyxin B/
breed-associated facial conformation and bacitracin (or based on culture and
alterations in eyelid support. sensitivity) q6–8h.
• Acquired disease—from marked weight loss • Lubricant ointments (e.g., Puralube®)—
or muscle mass loss about the head and reduce conjunctival and corneal desiccation
orbits, tragic facial expression in hypothyroid secondary to exposure.
dogs, and cicatricial ectropion from scarring • Hypothyroid and masticatory myositis-
of the eyelids secondary to injury or from induced conditions—may respond well to
surgical overcorrection of entropion. appropriate medical treatment of underlying
disease.
INTERACTIONS
DIAGNOSIS N/A
• Usually clinically obvious.
• Look for any underlying disorder in
nonpredisposed breeds and dogs with late-age FOLLOW-UP
onset. • May become more severe as patient ages.
Ehrlichiosis and Anaplasmosis
platelets; persistent or cyclic thrombo- mediated thrombocytopenia—no fever or
cytopenia. lymphadenopathy; rule out VBD. • Systemic
SYSTEMS AFFECTED lupus erythematosus—positive antinuclear
BASICS antibody (ANA) test. • Multiple myeloma—
• Multisystemic disease. • Vasculature—
DEFINITION monoclonal gammopathy, bony lesions.
E Caused by Ehrlichia and Anaplasma—tick-
bleeding tendencies (thrombocytopenia and
• Chronic lymphocytic leukemia—bone
vascular inflammation). • Hemic/lymphatic/
borne rickettsial disease. immune—bone marrow, spleen, lymph marrow cytology; PCR for antigen receptor
nodes. • Nervous (meningitis, cerebral rearrangements (PARR; E. canis infrequently
Dogs
hemorrhage). • Ophthalmic (anterior PARR negative). • Brucellosis.
• Obligate intracellular pathogens in three
genera: Ehrlichia, Anaplasma, and uveitis). • Joint (neutrophilic arthritis). CBC/BIOCHEMISTRY/URINALYSIS
Neorickettsia. • Ehrlichia—predominant PREVALENCE/GEOGRAPHIC Acute
species: E. canis: canine monocytic • Thrombocytopenia, anemia, leukopenia
DISTRIBUTION
ehrlichiosis (CME); E. ewingii: granulocytic (lymphopenia, neutropenia, and eosino
• E. canis—year round, worldwide; higher
ehrlichiosis; E. chaffeensis: primarily human penia), or leukocytosis (granular
prevalence in warm climates. • E. ewingii—
pathogen, may cause canine disease. lymphocytosis, monocytosis). • Morulae—
warmer months; seroprevalence eastern
• Anaplasma—A. phagocytophilum: intracytoplasmic inclusions in leukocytes,
and midwest United States.
granulocytic anaplasmosis; A. platys: rare. • Hyperglobulinemia—progressive
• A. phagocytophilum—warmer months;
thrombocytic anaplasmosis. • Neorickettsia— increase 1–3 weeks postinfection. • Hypoalbu-
eastern, upper midwest, and Pacific coast
infect mononuclear cells (monocytes and minemia. • Mild increases in liver enzyme
United States.
macrophages): N. risticii: Potomac horse activities, azotemia, hyperbilirubinemia.
fever; rarely infects dogs; acquired by SIGNALMENT • Proteinuria.
ingesting infected vectors; serum from Species
infected dogs does not cross-react with Chronic
Dogs and cats (infrequent). • Pancytopenia—anemia, thrombocytopenia,
Ehrlichia; N. helminthoeca: salmon poisoning,
primarily northwestern United States. Breed Predilections neutropenia, but monocytosis and lympho
Chronic CME—German shepherd dogs, cytosis possible. • Hyperglobulinemia—
Cats Belgian Malinois. magnitude correlates with duration of
Feline ehrlichiosis (rare)—serologic, PCR, infection; usually polyclonal gammopathy,
and cytologic evidence for Ehrlichia (E. canis, Mean Age and Range
• Average age 5.2 years. • Range 2 months–14
occasionally monoclonal. • Hypoalbuminemia.
E. canis-like, E. chaffeensis, E. ewingii) and
Anaplasma (A. phagocytophilum); clinical signs years. OTHER LABORATORY TESTS
may include fever, lethargy, joint pain, SIGNS Serologic Testing
anemia, hyperglobulinemia, and thrombo • Antibodies present ~3 weeks postinfection.
General Comments
cytopenia; may also be asymptomatic. • Immunofluorescent antibody test (IFAT)—
Vary in severity and duration, dependent on
PATHOPHYSIOLOGY host, coinfections, and strain variations. sensitive; cross-reactivity between Ehrlichia
• Anaplasma and Ehrlichia transmitted via species; use same laboratory to compare acute
Historical Findings and convalescent titers; fourfold increase
tick bite; transmission time between 3h
• Fever, lethargy, anorexia, weight loss. paired in convalescent titer indicates active
(E. canis) and 18h; can occur via blood
• Spontaneous bleeding—sneezing, epistaxis, infection; detection at one time-point may
transfusion. • E. canis—Rhipicephalus
petechia, ecchymosis. • Ocular discharge/ represent past exposure or active infection.
sanguineus tick vector; infects mononuclear
pain. • Lameness. • Ataxia, head tilt • Rapid point-of-care (POC) screening
cells; 1–3-week incubation period; three
stages of canine disease: ◦ Acute (2–4 Physical Examination Findings test—sensitivity and specificity vary
weeks)—spread to spleen, liver, lymph nodes; Acute depending on test; overtly healthy dogs with
causes endothelial cell and perivascular • Bleeding diathesis. • Fever. • Generalized
positive POC tests should have CBC,
inflammation, thrombocytopenia (possible lymphadenopathy. • Organomegaly (spleen, Biochemistry, UA, PCR or paired IFAT to
antiplatelet antibodies), mild anemia; liver). • Ocular discharge. • Lameness. • Ticks. identify evidence of infection before
infections may be subclinical. ◦ Subclinical treatment; animals can remain seropositive by
Chronic E. canis POC for years, even after infection cleared.
(months–years)—organism persists; hyper-
• Pale mucous membranes (anemia).
globulinemia; mild thrombocytopenia; dogs PCR Testing
• Ulcerative stomatitis. • Hind limb or
may eliminate infection, others remain • Detects pathogen DNA; sensitive indicator
scrotal edema. • Uveitis, hyphema, retinal
persistently infected or develop chronic of active or recent infection. • Whole blood
hemorrhages. • Ataxia, vestibular dysfunction,
disease. ◦ Chronic—myelosuppression; or tissue (spleen, lymph node, liver, bone
cervical pain.
pancytopenia. • E. ewingii—Amblyomma marrow); identifies species; detect as early as
americanum tick vector; infects granulocytes; RISK FACTORS 7 days postinfection. • Negative PCR result
dogs can be persistently infected and Coinfection with other vector-borne diseases cannot rule out VBD infections; false
asymptomatic; acute clinical signs include (VBDs). negative can occur due to low organism load;
fever, neutrophilic polyarthritis, neutrophilia, genetic variations can prevent PCR detection.
reactive lymphocytes, and proteinuria; • Combining serology and PCR optimal for
bleeding disorders uncommon. accurate diagnosis.
• A. phagocytophilum—Ixodes spp. tick DIAGNOSIS Additional Tests
vector; infects granulocytes; infections can
DIFFERENTIAL DIAGNOSIS • Coombs’ positive anemia; indicates
be asymptomatic and self-limiting; acute
• Rocky Mountain spotted fever (Rickettsia concurrent immune-mediated erythrocyte
clinical signs include fever, lameness, thrombo-
rickettsii)—seasonal (Mar–Oct); diagnose destruction; may be positive in dogs with
cytopenia, and lymphopenia. • A. platys—
with serology; same treatment. • Immune- babesiosis, other VBD. • Test for VBD
tick vector likely R. sanguineus; infects
(continued) Ehrlichiosis and Anaplasmosis

coinfections. • Culture and sensitivity • Prednisolone or prednisone, use with EXPECTED COURSE AND PROGNOSIS
testing (blood, urine) indicated in febrile antibiotics; anti-inflammatory (0.5–1 mg/kg • Acute—excellent prognosis with
patients. PO q12–24h for 3–5 days) for polyarthritis; appropriate treatment; most immuno
DIAGNOSTIC PROCEDURES immunosuppressive (1–2 mg/kg PO q12h for competent dogs recover, enter subclinical
5 days; rarely exceed 60 mg/dog/day) when phase, or clear infection; treatment accelerates
Bone Marrow Aspirate immune-mediated disease suspected. • For recovery, may prevent chronic phase.
E
• Acute—hypercellularity of megakaryocytic CME, prophylactic antibiotics if neutrophils • Chronic—may take 4 weeks for clinical
and myeloid series. • Chronic—erythroid <1000 cells/μl for >1 week. response, 6 months for cytopenia rebound;
hypoplasia with increased M : E ratio, prognosis poor and expensive medical
plasmacytosis. • Increased number of mast CONTRAINDICATIONS
• Glucocorticoids in myelosuppressive CME. management with hypoplastic marrow.
cells. • Ehrlichia and Anaplasma antibodies do not
• Glucocorticoids in animals with diabetes
PATHOLOGIC FINDINGS mellitus, gastrointestinal ulceration, protect against reinfection.
• Acute—serosal and mucosal petechiae; concurrent or recent nonsteroidal anti-
lymphadenopathy, splenomegaly, inflammatory drug (NSAID) use.
hepatomegaly, and red bone marrow;
perivascular infiltrates of macrophages and PRECAUTIONS
• Prolonged immunosuppressive cortico MISCELLANEOUS
lymphocytes (lung); periportal infiltrates of
lymphocytes and macrophages (liver); steroid use may interfere with elimination of ASSOCIATED CONDITIONS
lymphoid hyperplasia (spleen). • Chronic— E. canis. • Doxycycline in dogs with liver • Babesia. • Bartonella. • Hemotropic
pale marrow, subcutaneous edema; disease or abnormal liver enzyme values. Mycoplasma. • Leishmania.
histologically, perivascular plasma cell ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL
infiltrates in organs; multifocal nonsuppurative • Minocycline—10 mg/kg PO q12h for 3–4 E. canis, E. ewingii, E. chaffeensis,
meningoencephalitis with lymphoplasmacytic weeks. • Rifampicin: 10 mg/kg PO q24h for A. phagocytophilum, and A. platys can infect
infiltrate. 3 weeks (do not exceed 10 mg/kg/day in humans via tick bite; R. sanguineus prefers
dogs); less effective. dogs, will bite humans in living conditions
with high vector population; A. americanum
bites humans; Ixodes bite humans and
TREATMENT transmit Borrelia burgdorferi, Babesia microti,
FOLLOW-UP likely E. muris.
• Inpatient—medical stabilization for acute PATIENT MONITORING SYNONYMS
signs. • Outpatient—stable patients; frequent • CBC, blood smear examination—2, 4, 8 • Canine hemorrhagic fever. • Canine
monitoring for therapeutic response. weeks after starting antibiotics; recurrence rickettsiosis. • Canine typhus. • Tracker dog
of clinical signs post treatment suggests disease. • Tropical canine pancytopenia.
NURSING CARE
• Balanced electrolyte solution IV. • Blood or
treatment failure, reinfection, or concurrent ABBREVIATIONS
platelet-rich plasma transfusion for severe infection with pathogen partially sensitive • ANA = antinuclear antibody. • CME =
anemia or thrombocytopenia. to therapy (Babesia, Bartonella). • IFAT—9 canine monocytic ehrlichiosis. • IFAT =
months post treatment; most dogs become indirect fluorescent antibody test. • NSAID =
CLIENT EDUCATION seronegative; extended seropositivity nonsteroidal anti-inflammatory drug.
• Acute—prognosis excellent with appropriate may indicate reinfection or ineffective • PARR = PCR for antigen receptor
therapy. • Chronic—prognosis guarded; treatment. • PCR—1–2 months post rearrangements. • POC = point of care.
cytopenia resolution may take >6 months; treatment for evidence of pathogen • VBD = vector-borne disease.
prognosis poor if hypoplastic bone marrow. clearance; if PCR positive, repeat anti
• Progression to chronic prevented by early Suggested Reading
biotics for 4–6 weeks, ensure use of Mylonakis ME, Harrus S, Breitschwerdt EB.
effective treatment; serological tests may stay acaricides; if persistently negative, change
positive (IFAT ≤1 year and POC for years); An update on the treatment of canine
drug. • POC assay—not used to monitor monocytic ehrlichiosis (Ehrlichia canis). Vet
reinfection can occur if animals reexposed. treatment response.
• Breed risks for chronic CME. J 2019, 246:45–53.
PREVENTION/AVOIDANCE Author Barbara Qurollo
• Control tick infestation—acaricides: topical Consulting Editor Amie Koenig
(spot treatments and collars)—imidacloprid/ Acknowledgment The author and book
flumethrin, fipronil, permethrin, deltamethrin, editors acknowledge the prior contribution of
MEDICATIONS and amitraz (do not use permethrin, delta Stephen C. Barr.
DRUG(S) OF CHOICE methrin, or amitraz on cats); systemic—
• Doxycycline—5 mg/kg PO q12h or isoxazolines. • Manually remove ticks; use
10 mg/kg PO q24h for 3–4 weeks; clinical gloves; ensure removal of mouth parts. Client Education Handout
available online
response usually in 1–2 days; slower response
in chronic ehrlichiosis or neurologic disease.
Elbow Dysplasia
SIGNALMENT • Panosteitis.
• Avulsion or calcification of flexor muscles.
Species
• Synovial sarcoma.
BASICS Dog
Breed Predilections CBC/BIOCHEMISTRY/URINALYSIS
E DEFINITION N/A
A group of developmental abnormalities that Large and giant breeds—Labrador retrievers;
lead to malformation, degeneration, and Rottweilers; golden retrievers; German IMAGING
secondary osteoarthritis of the elbow joint. shepherds; Bernese mountain dogs; chow Radiography
chows; bearded collies; Newfoundlands. • Image both elbows—high incidence of
PATHOPHYSIOLOGY
• Four abnormalities—un-united anconeal Mean Age and Range bilateral disease.
process (UAP), osteochondritis dissecans • Age at onset of clinical signs—typically • UAP, OCD, FMCP, and incongruity—
(OCD), fragmented medial coronoid process 4–10 months. elbow DJD recognized by osteophytes on
(FMCP), and incongruity; alone or in • Age at diagnosis—generally 4–18 months. cranial margin of radial head (37%),
combination; may be seen in one or both • Onset of symptoms related to degenerative anconeal process (70%), and epicondyles
elbows; bilateral disease common (50% of cases). joint disease (DJD)—any age. (medial and lateral), and medial coronoid
• Terminology— medial compartment disease Predominant Sex process; sclerosis of ulna caudal to coronoid
(MCompD) involves any pathology within • FMCP—males predisposed.
process and trochlear notch; stairstep
the medial compartment, while medial • UAP, OCD, incongruity—none established.
between joint surface of radius and lateral
coronoid process disease (MCD) is used to coronoid.
SIGNS • UAP—best diagnosed from mediolateral
describe all pathologies of the medial coronoid
process such as fissuring, fragmenting, General Comments hyperflexed view; may see lack of bony union.
sclerosis, microfracture, and cartilage damage. • Lameness—if no distinct abnormalities noted Comparison to contralateral elbow may be
• FMCP and incongruity are the most on physical examination or radiographs, early helpful, although high incidence of bilateral
common documented MCompD pathologies. intervention may demand advanced imaging. disease should be kept in mind.
• UAP—delayed closure of growth plate • Any resistance at all in flexion in immature • OCD—best diagnosed from craniocaudal
between anconeal process and proximal ulnar dog should raise suspicion of elbow dysplasia. and craniocaudal-lateromedial oblique views;
metaphysis (olecranon) by 5 months of age; • Not all patients are symptomatic when young. reveals radiolucent defect or flattening of
may be result of abnormal mechanical stress • Intermittent episodes of elbow lameness medial aspect of humeral condyle.
on anconeal process. due to advanced DJD changes in mature • FMCP—may not be visualized in some
• OCD—affects medial aspect of humeral patient—common. cases; diagnosis then presumptive based on
condyle; disturbance in endochondral DJD and lack of UAP or OCD lesions;
Historical Findings commonly see trochlear sclerosis and/or early
ossification causes retention of articular Intermittent or persistent thoracic limb
cartilage and subsequent mechanical stress osteophyte formation on proximal caudal
lameness—exacerbated by exercise; progressed surface of anconeal process with FMCP.
leads to cartilage flap lesion. from stiffness seen only after rest.
• FMCP—chondral or osteochondral Other
fragmentation or fissure of medial coronoid Physical Examination Findings CT, MRI, and linear tomography—can
process of ulna; possibly manifestation of • Pain—elicited on elbow hyperflexion or provide more definitive evidence for fissures
osteochondrosis of coronoid process; extension; elicited when holding elbow and and nondisplaced fragments. CT is necessary
coronoid does not have separate ossification carpus at 90° while pronating and supinating in many cases of MCD as survey radiographs
center; may be result of abnormal mechanical carpus and applying pressure to medial have low sensitivity.
stress on medial coronoid process considered compartment.
• Affected limb—tendency to be held in DIAGNOSTIC PROCEDURES
to be due to incongruity.
abduction and supination. • Joint tap and analysis of synovial fluid—
• Incongruity—asynchronous growth
• Joint effusion and capsular distension— confirm involvement of joint.
between radius and ulna may lead to
especially noted between lateral epicondyle • Synovial fluid—should be straw colored
abnormal loading, wearing, and erosion of
and olecranon. with normal to decreased viscosity; cytology
cartilage in humeroulnar compartment.
• Crepitus—may be palpated with advanced reveals <5,000 nucleated cells/μL (>90% are
Malformation of trochlear notch of ulna;
DJD. mononuclear cells); normal results do not
elliptical trochlear notch with decreased arc of
• Diminished range of motion. necessarily rule out the diagnosis.
curvature is too small to articulate with
• Arthroscopy—may help diagnose UAP,
humeral trochlea—resulting in major points CAUSES MCD, OCD, and incongruity.
of contact at anconeal process, coronoid • Genetic.
process, and medial humeral condyle. • Developmental. PATHOLOGIC FINDINGS
• Nutritional. • UAP—fibrous union between anconeal
SYSTEMS AFFECTED
process and proximal ulnar metaphysis;
Musculoskeletal RISK FACTORS fibrous tissue invasion and degeneration of
GENETICS • Rapid growth and weight gain. anconeal process; DJD.
High heritability • High-calorie diet. • OCD—chondral flap on medial humeral
INCIDENCE/PREVALENCE condyle; sclerosis of underlying subchondral
• Most common cause for elbow pain and bone with fibrous tissue invasion; erosive
lameness. lesion on apposing coronoid cartilage; DJD.
• One of the most common causes for DIAGNOSIS • FMCP—chondral or osteochondral
thoracic lameness in large-breed dogs. fragmentation of cranial tip or lateral margin
of medial coronoid; erosive lesion on cartilage
GEOGRAPHIC DISTRIBUTION • Trauma.
of apposing medial aspect of humeral
N/A • Septic arthritis.
condyle; DJD.
(continued) Elbow Dysplasia

• Incongruity—a step greater than 2 mm incongruity, degree of DJD, patient’s age, and
noted between medial border of radial head surgical expertise.
and lateral border of medial coronoid process. • Arthroscopic diagnosis and treatment—excel-
• MCompD—erosive lesions involving part lent option for FMCP, OCD, and incongruity; MISCELLANEOUS
or all of medial coronoid process and benefits: superior visualization, minimally ASSOCIATED CONDITIONS
apposing articular cartilage of medial aspect invasive, superior to arthrotomy in outcome. N/A
E
of humeral condyle; DJD; linear striations in
AGE-RELATED FACTORS
articular cartilage.
N/A
ZOONOTIC POTENTIAL
MEDICATIONS N/A
DRUG(S) OF CHOICE
TREATMENT • None that promotes healing of osteochon-
N/A
APPROPRIATE HEALTH CARE dral or chondral fragments.
Surgery—controversial but recommended for • Nonsteroidal anti-inflammatory drugs SYNONYMS
most patients. (NSAIDs)—minimize pain, decrease Elbow osteochondrosis.
NURSING CARE inflammation, symptomatically treat SEE ALSO
• Cold packing elbow joint—perform
associated DJD. Osteochondrosis
immediately post surgery to help decrease • Deracoxib (3–4 mg/kg PO q24h, chewable).
• Carprofen (2.2 mg/kg PO q12h or q24h). ABBREVIATIONS
swelling and control pain; perform at least • DJD = degenerative joint disease.
20 minutes q8h for 3–5 days. • Meloxicam (load 0.2 mg/kg PO, then 0.1
mg/kg PO q24h—liquid). • FMCP = fragmented medial coronoid
• Passive range-of-motion exercises—benefi- process.
cial until patient can bear weight on limb(s), • Tepoxalin (load 20 mg/kg, then 10 mg/kg
PO q24h). • MCD = medial coronoid process disease.
then progress into static and dynamic • MCompD = medial compartment disease.
therapeutic exercises. CONTRAINDICATIONS • NSAID = nonsteroidal anti-inflammatory
• If osteoarthritis is present, then multimodal Avoid corticosteroids—potential side effects; drugs.
management is necessary as for arthritic articular cartilage damage associated with • OCD = osteochondritis dissecans.
management of any joint. long-term use. • UAP = un-united anconeal process.
ACTIVITY PRECAUTIONS INTERNET RESOURCES
• Restricted for all patients postoperatively. NSAIDs—gastrointestinal irritation may https://www.ofa.org/diseases/elbow-dysplasia
• Consideration for avoidance of high preclude use in some patients.
concussive activities for life. Suggested Reading
POSSIBLE INTERACTIONS Cook CR, Cook JL. Diagnostic imaging of
DIET N/A canine elbow dysplasia: a review. Vet Surg
• Weight control—important for decreasing 2009, 38(2):144–153.
ALTERNATIVE DRUG(S)
load and stress on affected joint(s). Chondroprotective drugs (e.g., polysulfated Fitzpatrick N, Yeadon R. Working algorithm
• Restricted weight gain and growth in for treatment decision making for develop-
glycosaminoglycans, glucosamine, and
young dogs—may decrease incidence and chondroitin sulfate)—may help limit cartilage mental disease of the medial compartment
severity. damage and degeneration; may help alleviate of the elbow in dogs. Vet Surg 2009,
CLIENT EDUCATION pain and inflammation. 38(2):285–300.
• Discuss heritability of disease. Sallander MH, Hedhammar A, Trogen ME.
• Discuss likelihood of DJD progression Diet, exercise, and weight as risk factors in
regardless of intervention. hip dysplasia and elbow arthrosis in
• Discuss influence of excessive intake of Labrador retrievers. J Nutr 2006, 136(7
nutrients that promote rapid growth.
FOLLOW-UP Suppl):2050S–2052S.
PATIENT MONITORING Samoy Y, Van Ryssen B, Gielen I, et al.
SURGICAL CONSIDERATIONS Review of the literature: elbow incongruity
• Post surgery—limit activity for minimum
• Severity of DJD and advanced age of
of 12 weeks; encourage early, active, in the dog. Vet Comp Orthop Traumatol
patient—negatively influence outcome. 2006, 19(1):1–8.
controlled movement of affected joint(s);
Generally DJD progresses faster without Author David Dycus
consider formal rehabilitation therapy.
treatment. Consulting Editor Mathieu M. Glassman
• Yearly to twice-yearly examinations—
• UAP—four options: removal, lag screw
recommended to evaluate progression of DJD. Acknowledgment The author and book
fixation, dynamic proximal ulnar osteotomy, editors acknowledge the prior contribution of
and lag screw fixation plus dynamic proximal PREVENTION/AVOIDANCE
Walter C. Renberg.
osteotomy; base decision on degree of DJD, • Discourage breeding of affected animals.
patient’s age, and surgical expertise. • Do not repeat dam–sire breeding that
• OCD and FMCP—medial approach to resulted in affected offspring. Client Education Handout
elbow (diagnostic differentiation not POSSIBLE COMPLICATIONS available online
necessary); removal of loose fragment(s). N/A
• Incongruity—controversial; four options:
no surgery, subtotal coronoidectomy, EXPECTED COURSE AND PROGNOSIS
dynamic proximal ulnar osteotomy, intra- • Progression of DJD—expected.
articular osteotomy; base decision on type of • Prognosis—fair to good for all forms.
Electric Cord Injury

pneumonia—history, physical examination, required. • Oral and cutaneous burns—treated
thoracic radiographs. symptomatically.
BASICS CBC/BIOCHEMISTRY/URINALYSIS
May help rule out other systemic causes of
E OVERVIEW noncardiogenic pulmonary edema.
• Electric cord injury is an uncommon event FOLLOW-UP
that occurs when an animal bites an electric OTHER LABORATORY TESTS
cord. • Other causes of electrocution are Arterial blood gas analysis may be useful to PATIENT MONITORING
uncommon in dogs and cats but can occur. document hypoxemia; this may be difficult to • Patient should be monitored until stable.
• Household electrical currents are alternat- perform in unstable patients. • Physical examination. • Monitor oral
ing (50–60 Hz), 110–120 or 220–240 volts IMAGING lesion; may prevent patient from eating.
depending on geographic location, and are • Thoracic radiographs may help distinguish • ECG. • Central venous pressure. • Blood
dangerous. • Injury can be caused due to between cardiogenic and noncardiogenic pressure. • Arterial blood gas. • Thoracic
thermal injury or due to disruption of normal causes of pulmonary edema. • Radiographic radiographs.
electrophysiologic activity of excitable tissue. pattern is usually a generalized, mixed alveolar PREVENTION/AVOIDANCE
• Pulmonary edema can be a sequela to bronchial pattern; edema is often most • Damaged electric cords should be discarded.
electrocution and the pathophysiology is notable in caudal dorsal lung fields. • Avoid animal exposure to electric cords.
thought to be neurogenic and centrally • Pulmonary venous congestion is absent • Follow child safety rules for a safe home.
mediated, leading to pulmonary hyperten- with noncardiogenic pulmonary edema.
sion. • Cataract formation is reported POSSIBLE COMPLICATIONS
• Echocardiography may help identify or rule
• Infected burn wounds can occur but are
following electrocution. out underlying cardiac disease.
uncommon. • Oronasal fistula due to severe
SIGNALMENT DIAGNOSTIC PROCEDURES burns.
• Most commonly dogs; also cats. • Most • ECG—may help distinguish cardiogenic
commonly young animals; in published EXPECTED COURSE AND PROGNOSIS
disease from noncardiogenic disease; however,
• Prognosis based on response to therapy.
report age ranged from 5 months to 1.5 years. dysrhythmias may be seen with electrocution
• No breed or sex predilections. • No genetic • Pulmonary edema can develop as soon as
and other causes of noncardiogenic pulmo-
basis. 1 hour and as late as 36 hours after incident.
nary edema.
• Pulmonary edema associated with electro-
SIGNS PATHOLOGIC FINDINGS cution is associated with high mortality
• Burns associated with gingiva, tongue, • Pink, frothy fluid in airways. • Fluid-filled, (38.5%). • If patient survives first 24 hours,
palate. • Singed hair or whiskers. • Most congested lungs. • Subendocardial and prognosis improves. • Resolution of pulmonary
common clinical signs are related to acute subepicardial petechiae. • Circumscribed, edema may take 3–5 days. • Most oral lesions
dyspnea. • Coughing. • Tachypnea. pale gray or tan oral lesions. resolve. • Inappetence related to oral lesions
• Orthopnea. • Increased respiratory effort. resolves.
• Cyanosis. • Crackles during pulmonary
auscultation. • Tachycardia. • Muscle
tremors. • Tonic–clonic activity. • Collapse.
TREATMENT
CAUSES & RISK FACTORS • If patient is close to live wire, turn off MISCELLANEOUS
• Chewing electric cord. • Young animals. electricity and/or remove patient to safe area.
• Establish patent airway if patient is
Cataracts have been reported in one dog 18
unconscious. • Oxygen supplementation.
months after electrocution.
• Mechanical ventilation may be required.
DIAGNOSIS • Establish venous access. Suggested Reading
Brightman AH, Brogdon JD, Helper LC,
DIFFERENTIAL DIAGNOSIS Everds N. Electrical cataracts in the canine:
• Left-sided congestive heart failure due to a case report. J Am Anim Hosp Assoc 1984,
congenital or acquired heart disease; the 20:895–898.
presence of cardiac murmur or dysrhythmia MEDICATIONS Drobatz KJ, Saunders HM, Pugh CR,
may help differentiate; however, dysrhythmias DRUG(S) OF CHOICE Hendricks JC. Noncardiogenic pulmonary
may be seen with electric cord injury. • If in shock—treat with intravenous crystalloids edema in dogs and cats: 26 cases (1987–
• Vitamin K antagonist, rodenticide (90 mL/kg/h in dog, 45–60 mL/kg/h in cat) or 1995). J Am Vet Med Assoc 1995,
intoxication history (pulmonary hemorrhage). colloids (20 mL/kg in dogs, 5–10 mL/kg in 206:1732–1736.
• Thoracic trauma (pulmonary contusions)— cats). • If pulmonary edema is present— Kolata RJ, Burrows CF. The clinical features
history, thoracic radiographs. • Other causes furosemide 2–4 mg/kg IV; this is controversial of injury by chewing electrical cords in dogs
of noncardiogenic pulmonary edema. as this is a form of noncardiogenic pulmonary and cats. J Am Anim Hosp Assoc 1981,
• Pleural space disease—muffled lung sounds edema. • Anxiolytic therapy if dyspneic— 17:219–222.
during auscultation, thoracic radiographs. butorphanol 0.1–0.2 mg/kg IV. Author Steven L. Marks
• Thermal or chemical injuries—history, • Corticosteroids have been employed, but are Consulting Editor Michael Aherne
physical examination, thoracic radiographs. controversial and of unknown value. • Inotropic
• Exposure to fire and smoke inhalation— support if required. • Antiarrhythmic therapy if
history, physical examination. • Atypical
Enamel Hypoplasia/Hypocalcification
• Fluoride treatment can be used to decrease
sensitivity and enhance enamel strength.
BASICS DIAGNOSIS
OVERVIEW DIFFERENTIAL DIAGNOSIS E
• Enamel hypoplasia is the inadequate • Enamel staining—discolored but smooth MEDICATIONS
deposition of normal enamel matrix, affecting surface (tetracycline).
one or several teeth. • Carious lesions—cavities with decay. DRUG(S) OF CHOICE
• The crowns can have areas of normal • Amelogenesis imperfecta—genetic and/or N/A
enamel next to hypoplastic or missing developmental formation and maturation
enamel. abnormalities other than hypomineralization.
• Apparent defect in enamel surfaces, often • Tooth resorption—similar to that found in
pitted and discolored; focal or generalized, cats, also found in dogs. FOLLOW-UP
due to disruption of normal enamel CBC/BIOCHEMISTRY/URINALYSIS
formation. PATIENT MONITORING
• Usually normal. Inform the owner that further degeneration
• Most cases are primarily aesthetic; some • Appropriate preanesthetic diagnostic when of remaining enamel may occur, necessitating
have extensive structural damage, even root indicated.
involvement. The dentin is rarely exposed additional therapy in the future, or that
with hypoplasia. OTHER LABORATORY TESTS affected teeth may become nonvital over
• Enamel hypoplasia is less common than N/A time, requiring root canal therapy or
hypocalcification. extraction.
IMAGING
• Enamel hypocalcification refers to • Intraoral radiographs are necessary to PREVENTION/AVOIDANCE
inadequate mineralization (calcification) of determine the structure and viability of roots. • Regular professional dental cleaning and a
enamel, affecting several or all teeth. The • Cases reported of abnormal root formation, routine homecare program (brushing); may
crowns are covered by poorly formed, rough no root formation, or separated crown and include weekly application of stannous
enamel that may easily be worn or flaked root. fluoride at home (minimize ingestion because
away and have light brown discoloration. of toxicity).
There can be areas of normal enamel next to DIAGNOSTIC PROCEDURES
• Avoid chewing on hard objects.
areas of abnormal enamel. None
• Systemic influences during enamel
formation (e.g., distemper, fever) over an
extended time may cause generalized changes;
local or focal influences (e.g., trauma, even TREATMENT MISCELLANEOUS
from deciduous tooth extraction) over a short • Treatment depends upon extent of lesions INTERNET RESOURCES
time may cause specific patterns or bands. and equipment and materials available. https://avdc.org/avdc-nomenclature
• Teeth may be more sensitive with exposed • Goal is to provide the smoothest surface Suggested Reading
dentin, and occasionally fractures of severely possible. Bittegeko SB, Arnbjerg J, Nkya R, Tevik A.
compromised teeth occur; usually they • Enamel hypoplasia typically does not require Multiple dental developmental abnormalities
remain fully functional. treatment as the enamel is normal, just following canine distemper infection. J Am
SIGNALMENT decreased in thickness. Enamel hypocalcification Anim Hosp Assoc 1995, 31(1):42–45.
• Dogs and less commonly cats. typically benefits from treatment. Lobprise HB, Dodd JR. Wiggs’ Veterinary
• Often apparent at time of tooth eruption Optimal Treatment Dentistry Principles and Practice. Hoboken,
(after 6 months of age) or shortly thereafter • Gently remove diseased enamel (enamel NJ: Wiley-Blackwell, 2019.
(with signs of wear). scrub) with white stone burs or finishing Author Kristin M. Bannon
SIGNS disks on high-speed handpiece (adequate Consulting Editor Heidi B. Lobprise
water coolant).
Historical Findings • Take care not to damage the tooth—excess
Discolored teeth. enamel/dentin removal; hyperthermic damage
Physical Examination Findings to pulp.
• Irregular, pitted, or flaky enamel surface • Focal defects may be amenable to
with discoloration of diseased enamel and composite restoration; many restorative
potential exposure and staining of underlying materials (bonding agents, composites)
dentin (light brown). require use of light-curing units and
• Early or rapid accumulation of plaque and appropriate skill levels.
calculus on roughened tooth surface; possible • Bonding agent recommended to seal
gingivitis and/or accelerated periodontal disease. exposed dentinal tubules and protect surfaces.
• Teeth may fracture easily. • Extraction is recommended if the root is
• Animals may show cold sensitivity significantly malformed; extraction or root canal
(avoiding outdoor water or refrigerated food). therapy if tooth is radiographically nonvital.
CAUSES & RISK FACTORS Alternative Treatment
• Insult during enamel formation. • Soft, diseased enamel can sometimes be
• Canine distemper virus, fever, trauma (e.g., removed with ultrasonic scalers or hand
accidents, fractured deciduous tooth, excessive instruments, but avoid excessive removal and
force during deciduous tooth extraction). hyperthermia.
Encephalitis
Physical Examination Findings anomaly—primarily young animals.
• Immune mediated—none. • Infectious— • Trauma—usually reported in history.
fever, lethargy, diffuse pain, ocular lesions, • Metabolic encephalopathy—usually
BASICS coughing, diarrhea. symmetric deficits, CBC/biochemistry
DEFINITION abnormalities common. • Toxic—usually
E Inflammation of the brain with or without
Neurologic Examination Findings
acute. • Neoplasia—signs may be similar;
• Rostral fossa—seizures, blindness, abnormal
concurrent inflammation of the meninges mentation, absent menace and nasal septum usually in older patients. • Degenerative—
and spinal cord. stimulation responses, delayed postural usually slow, progressive signs.
PATHOPHYSIOLOGY reactions. • Caudal fossa—lethargy, cranial CBC/BIOCHEMISTRY/URINALYSIS
• Immune-mediated mechanism, usually of nerve deficits, ataxia (proprioceptive, vestibular, • Immune mediated—usually normal.
unknown triggering factor. • Infection of and/or cerebellar), paresis. • Progression (e.g., • Infectious—CBC: leukocytosis if systemic
the brain. anisocoria, pinpoint pupils, decreasing level of signs; distemper: lymphopenia; FIP:
consciousness, poor physiologic nystagmus)— lymphopenia, anemia; rickettsial disease:
SYSTEMS AFFECTED
suggests increased intracranial pressure with anemia, thrombocytopenia; fungal/parasitic:
• Nervous. • Multisystemic signs—usually
potential brain herniation. occasionally eosinophilia; biochemistry: FIP:
seen if infectious cause.
CAUSES hyperglobulinemia; distemper: hyper/
INCIDENCE/PREVALENCE hypoglobulinemia; rickettsial disease:
Unknown Dogs hyperglobulinemia; some fungal diseases:
• Idiopathic—MUO, GME, NME, NLE, hypoalbuminemia, hyperglobulinemia,
• Immune-mediated—worldwide.
EME, pyogranulomatous meningoencephalo- hypercalcemia; urinalysis: fungus rarely seen.
• Infectious—varies depending on infectious myelitis, greyhound nonsuppurative menin-
goencephalitis, idiopathic tremor syndrome. OTHER LABORATORY TESTS
agent distribution. • Serology—in serum or cerebrospinal fluid
• Postvaccinal—distemper, rabies. • Viral—
SIGNALMENT distemper, rabies, pseudorabies, herpesvirus, (CSF); available for fungal, protozoal, rickettsial,
parvovirus, coronarivus, parainfluenza, West and viral diseases; may not differentiate exposed/
Species
Nile virus, eastern, western and Venezuelan vaccinated animals from active disease;
Dog and cat.
equine encephalomyelitis virus, Bunyaviridae, antibodies appear 2–3 weeks after infection;
Breed Predilections immunoglobulin (Ig) M higher predictive
Flaviviridae. • Rickettsial—Ehrlichia canis,
Immune Mediated Neorickettsia helminthoeca, Anaplasma phagocyt- positive value than IgG for Toxoplasma,
• Meningoencephalitis of unknown origin ophilum, Rocky mountain spotted fever. preferred test for Neospora, low sensitivity/
(MUO) can happen in any breed. • Bacterial—aerobic, anaerobic, mycoplasma, specificity for FIP. • Histology—postmortem;
• Granulomatous meningoencephalitis mycobacterium. • Fungal—Blastomyces, lacks specificity; may reveal specific inclusion
(GME)—toy poodle and terrier. • Necrotizing Histoplasma, Cryptococcus, Coccidioidomyces, bodies for viral infections (e.g., distemper,
meningoencephalitis (NME)—pug and Aspergillus, Phaeohyphomyces. • Protozoal— rabies). • Immunohistochemistry—
chihuahua. • Necrotizing leukoencephalitis Toxoplasma, Neospora. • Algal—Prototheca. postmortem; usually high sensitivity and
(NLE)—Yorkshire terrier and French bulldog. • Parasitic—sarcocystis, encephalitozoon, larva specificity; best test to confirm FIP. • PCR—
• Eosinophilic meningoencephalitis (EME)— migrans (Dirofilaria, Toxocara, Ancylostoma, available for viral, fungal, rickettsial, protozoal
golden retriever and Rottweiler. • Idiopathic Cuterebra, Baylisascaris, Cysticercus), diseases in blood and CSF; highly sensitive for
tremor syndrome—West Highland white trypanosoma. distemper; low sensitivity but high specificity for
terrier, Maltese. • Greyhound nonsuppurative FIP. • Culture—bacterial culture of CSF
meningoencephalitis—greyhound. Cats commonly unrewarding despite bacterial
• Viral—FIP, rabies, feline immunodeficiency infection; fungal and viral culture unrewarding
Infectious virus (FIV), pseudorabies, paramyxovirus,
• Pyogranulomatous meningoencephalomy- and potential zoonoses. • Urine galactomannan
Borna disease virus, West Nile virus, assay (ELISA)—high sensitivity and specificity
elitis—pointer dogs. • Aspergillosis—German Bunyaviridae. • Bacterial—aerobic, anaerobic,
shepherd. • Protothecosis—boxer, collie. for Blastomyces, Aspergillus, and Histoplasma.
mycoplasma, mycobacterium. • Fungal— • Blood/urine cultures—low sensitivity and
• Cryptococcosis—American cocker spaniel. Cryptococcus, Blastomyces, Histoplasma, specificity; may help discriminate agent in
Feline Infectious Peritonitis (FIP) Coccidioidomyces. • Protozoal—Toxoplasma. bacterial encephalitis and help in antibiotics
Burmese • Algal—Prototheca. • Parasitic—larva migrans choice. • Rabies—no premortem diagnostic test.
Mean Age and Range (Dirofilaria, Toxocara, Ancylostoma, Cuterebra,
Baylisascaris, Cysticercus). • Idiopathic— IMAGING
Immune Mediated lymphohistiocytic meningoencephalomyelitis. • Thoracic radiographs—may reveal fungal/
• Peak 3–7 years old; can happen at any age toxoplasma infection or concurrent bacterial
in dogs older than 4 months old. • GME— RISK FACTORS pneumonia. • Spine radiographs—may reveal
peak 4–8 years old. • NME and NLE—mean • Immunosuppressive drugs and FIV or concurrent fungal/bacterial discospondylitis.
2.5 years old (6 months–7 years). • Cats— feline leukemia virus (FeLV) infection— • Brain MRI—shows focal/multifocal lesions.
mean 9 years old. infectious encephalitides. • FIP: recent stress, • Brain CT—may show focal/multifocal brain
multicat environment. • Tick-infected lesions; less sensitive and specific than MRI
Infectious areas—tick-borne rickettsial and viral
Two peaks: <2 years and >8 years. DIAGNOSTIC PROCEDURES
infections. • Travel history—geographically
Predominant Sex localized infectious agents. • CSF cytology—used to confirm inflamm
MUO—females slightly predisposed. ation; may be normal if meninges not
affected. ◦ Immune mediated—increased
SIGNS protein and cellular content (lymphocytes
Historical Findings and/or macrophages), increased eosinophils in
• Immune mediated—acute to chronic onset DIAGNOSIS EME; predominantly neutrophilic in some
and progression (days to months). DIFFERENTIAL DIAGNOSIS cases. ◦ Viral—predominantly lymphocytic.
• Infectious—acute onset with rapid • Cerebrovascular accident—should not ◦ Bacterial—predominantly degenerated
progression (days). progress after 24 hours. • Congenital neutrophils. ◦ Fungal—mixed inflammation.
(continued) Encephalitis
• Infectious agent rarely seen (except <8 months of age—enrofloxacin contra prognosis. • Idiopathic tremor syndrome—
Cryptococcus). indicated. • Cats - ocular toxicity with excellent prognosis with complete resolution.
PATHOLOGIC FINDINGS enrofloxacin > 5mg/kg/day.
Findings depend on specific type of immune- POSSIBLE INTERACTIONS
mediated inflammation (e.g., granulomatous, Prior corticosteroid treatment may alter MRI E
necrotic) and infectious agent. and CSF results and decrease chance of MISCELLANEOUS
diagnosis.
ZOONOTIC POTENTIAL
ALTERNATIVE DRUG(S) • Rabies—consider in endemic areas if patient
• Some patients may have better response if is outdoor animal that has rapidly progressive
TREATMENT treated with prednisone plus another encephalitis. • Humans may be infected by
immunosuppressive drug compared to the same vector tick that affected the patient.
prednisone alone; no increased benefits of • Exudates and diagnostic samples from
Inpatient medical management—may require
using 3 or more drugs; second immuno animals with mycosis can be contagious.
initial intensive care management if elevated
suppressive drug progressively tapered once
intracranial pressure. SYNONYMS
prednisone dose is 0.5 mg/kg/day. • Cytosine
• Meningoencephalitis of unknown etiology
NURSING CARE arabinoside—first administration IV CRI
• Increased intracranial pressure—hypertonic
(MUE). • Idiopathic tremor syndrome—
100 mg/m2/24h for 24–48h, then 100 mg/m2
saline, mannitol, dexamethasone. • Anti- white shaker syndrome.
IV CRI over 8–24h every 3 weeks for 6
seizure treatment—diazepam, phenobarbital, months; time between administration SEE ALSO
levetiracetam in boluses or CRI. • Analgesic progressively lengthened thereafter; SC • Seizures (Convulsions, Status
medication—necessary if painful from injection protocol exists but likely less Epilepticus)—Cats.
associated meningitis: opioids, gabapentin. efficient. • Azathioprine—2 mg/kg PO • Seizures (Convulsions, Status
• Nursing care for nonambulatory patients— q24h. • Cyclosporine—5–10 mg/kg PO Epilepticus)—Dogs.
bedding, switching sides, physiotherapy. q12h. • Mycophenolate—10–20 mg/kg PO • Stupor and Coma.
ACTIVITY q12h. • Leflunomide—2–4 mg/kg PO q24h. • Vestibular Disease, Geriatric—Dogs.
As tolerated. • Radiation therapy—reported. • Vestibular Disease, Idiopathic—Cats.
DIET ABBREVIATIONS
No oral intake if unable to swallow, e.g., • CSF = cerebrospinal fluid. • EME =
depressed, dysphagia, vomiting. eosinophilic meningoencephalitis. • FeLV =
FOLLOW-UP feline leukemia virus. • FIP = feline infectious
CLIENT EDUCATION peritonitis. • FIV = feline immunodeficiency
Relapse possible with both immune-mediated PATIENT MONITORING virus. • GME = granulomatous meningo
and infectious encephalitis. • Frequent neurologic evaluations in first encephalitis. • Ig = immunoglobulin. • MUE
48–72 hours to monitor progress. • Recheck = meningoencephalitis of unknown etiology.
SURGICAL CONSIDERATIONS CBC/biochemistry every month initially and
Brain biopsy—may be needed in specific cases. • MUO = meningoencephalitis of unknown
then every 3–6 months while on immuno origin. • NLE = necrotizing leukoencephalitis.
suppressive therapy. • Relapse as medication is • NME = necrotizing meningoencephalitis.
withdrawn—chance of relapse increased if
abnormal recheck MRI and CSF before Suggested Reading
MEDICATIONS stopping treatment. • Stop treatment for Bentley RT, Taylor AR, Thomovsky SA.
fungal diseases when antigen titers negative. Fungal infections of the central nervous
DRUG(S) OF CHOICE system in small animals. Vet Clin North Am
• Apply specific therapy once diagnosis is PREVENTION/AVOIDANCE Small Anim Pract 2018, 48:63–83.
reached or highly suspected. • Immune • Avoid outdoor roaming and use effective Coates JR, Jeffery ND. Perspectives on
mediated—prednisone/prednisolone 2 mg/kg/ tick control in endemic areas. • No definitive meningoencephalomyelitis of unknown
day until most of recovery achieved (usually association between immune-mediated origin. Vet Clin North Am Small Anim
1–2 weeks), then tapered progressively each encephalitis and vaccination. Pract 2014, 44:1157–1185.
month over 6 months; initially, dexamethasone POSSIBLE COMPLICATIONS Cornelis I, Van Ham L, Gielen I, et al.
0.25 mg/kg q24h can be given IV. • Viral—no • General anesthesia and CSF collection— Clinical presentation, diagnostic findings,
specific: treat symptomatically. • Bacterial— contraindicated in unstable patients with prognostic factors, treatment and outcome
broad-spectrum IV antibiotics initially (e.g., increased intracranial pressure. in dogs with meningoencephalomyelitis of
fluoroquinolones + amoxicillin/clavulanate); • Immunosuppressive drugs—predispose to unknown origin: a review. Vet J 2019,
continue PO depending on sensitivity or with infections. • Long-term corticosteroid 244:37–44.
broad-spectrum if agent unknown. • Fungal— therapy—signs of iatrogenic hyperadreno Sykes JE, Greene CE. Infectious Diseases of
itraconazole (Aspergillus), fluconazole (may be corticism and related side effects. • Increased the Dog and Cat, 4th ed. St. Louis, MO:
preferred if intra-axial), amphotericin B, intracranial pressure—poor prognosis factor, Elsevier Health Sciences, 2011.
voriconazole. • Protozoal—clindamycin, increased chance of death early in course of Author Thomas Parmentier
trimethoprim/sulfamides. • Rickettsial— disease. Acknowledgment The author and book
doxycycline. • Parasitic—ivermectin, editors acknowledge the prior contribution of
albendazole. EXPECTED COURSE AND PROGNOSIS
• Resolution progressive—2–8 weeks.
Allen Franklin Sisson.
CONTRAINDICATIONS • Rickettsial, bacterial, protozoal—fair
• Prednisone not to be used more than a few chance of survival if treated early. • Fungal,
days if infectious. • Puppies <6 months of Client Education Handout
algal, viral—almost always fatal. • Immune
age—doxycycline contraindicated. • Puppies available online
mediated—necrotic encephalitis has worse
Encephalitis Secondary to Parasitic Migration

vessels. Nonspecific and often inconclusive,
but could lead to surgical exploration and
removal of migrating parasite.
BASICS MISCELLANEOUS
PATHOLOGIC FINDINGS
E OVERVIEW • The parasite or its tracts may or may not be SEE ALSO
• Aberrant parasitic migration into the CNS. identified. • Encephalitis.
• Parasites usually affect another organ system • Infarction, vascular rupture, and hemor- • Feline Ischemic Encephalopathy.
of the same host (e.g., Dirofilaria immitis, rhage or vascular emboli may cause local to • Heartworm Disease—Cats.
Taenia, Ancylostoma caninum, Angiostrongylus, extensive necrosis and malacia; there may be • Heartworm Disease—Dogs.
or Toxocara canis) or a different host species granulomatous proliferation or/and obstruc- ABBREVIATIONS
(e.g., raccoon roundworm, Baylisascaris tive hydrocephalus. • CSF = cerebrospinal fluid.
procyonis; skunk roundworm, B. columnaris; • Dirofilaria immitis—intravascular or • NSAID = nonsteroidal anti-inflammatory
Coenurus spp.; or Cysticercus cellulosae). extravascular. drug.
• Access to CNS—hematogenously (dirofila- • Worms produce focal inflammation.
riasis) or through adjacent tissues, including • Cuterebriasis is the suspected cause of feline
Suggested Reading
the middle ear, skull foramina, cribriform Braund KG. Neurovascular disorders. In: Vite
ischemic encephalopathy.
plate through nasal cavities, or open CH, ed., Clinical Neurology in Small
fontanelles (cuterebraiasis). Animals—Localization, Diagnosis and
Treatment. Ithaca, NY: IVIS, 2003. https://
SIGNALMENT www.ivis.org/library/braunds-clinical-
• Dirofilariasis—adult animals only. TREATMENT neurology-small-animals-localization-
• Other parasites—young dogs and cats with • Surgical removal of intracranial cuterebra. diagnosis-and-treatment/neurovascular
access to outdoors: rare and sporadic occurrence. • Parasiticides (see below) could potentiate Dewey CW. Verminous encephalitis. In:
SIGNS illness. Dewey CW, ed., A Practical Guide to
• Vary with the portion of CNS affected. • Supportive and nursing care. Canine and Feline Neurology, 2nd ed.
• Likely asymmetric. Ames, IA: Wiley-Blackwell, 2008,
• May suggest a focal mass lesion or a pp. 184–185.
multifocal disease process. Glass EN, Cornetta AM, deLahunta A, et al.
• Cuterebriasis—seasonal (July–October) Clinical and clinicopathologic features in 11
acute or peracute onset of behavior changes,
MEDICATIONS cats with Cuterebra Larvae myiasis of the
seizures, visual deficits, etc.; previous history DRUG(S) OF CHOICE central nervous system. J Vet Intern Med
of respiratory disease is common. • Dirofilariasis and neural angiostrongylosis— 1998, 12:365–368.
• Rat parasite, Angiostrongylus cantonensis anthelmintic treatment may cause worsening James FMK, Poma R. Neurological manifes-
(Australia)—lumbosacral syndrome (hind of signs and sometimes death. tations of feline cuterebriasis. Can Vet J
limbs, tail, and bladder paralysis/paresis) in • Mild neural angiostrongylosis—puppies 2010, 51:213–215.
puppies that may ascend to thoracic limbs may recover with supportive care and Vite CH. Inflammatory diseases of the central
and cranial nerves. corticosteroid therapy. nervous system. In: Vite CH, ed., Clinical
• A single dose of ivermectin (400 mg/kg SC) Neurology in Small Animals—Localization,
may kill cuterebra larvae in cats with Diagnosis and Treatment. Ithaca, NY: IVIS,
Housing in a cage previously occupied by
suspected cuterebriasis; pretreatment with 2005.
wildlife (raccoons, skunks).
diphenhydramine (4 mg/kg) and intravenous Williams KJ, Summers BA, de Lahunta A.
dexamethasone (0.1 mg/kg) may mitigate Cerebrospinal cuterebriasis in cats and its
allergic/anaphylactic reactions to dead or association with feline ischemic encepha-
dying larvae. lopathy. Vet Pathol 1998, 35:330–343.
DIAGNOSIS • Treat inflammation and secondary Author Christine F. Berthelin-Baker
DIFFERENTIAL DIAGNOSIS infections—corticosteroids/nonsteroidal
• Rule out other causes of focal encephalopathy—
anti-inflammatory drugs (NSAIDs),
infectious diseases (viral, bacterial, protozoan, antibiotics.
or fungal); granulomatous
meningoencephalomyelitis; brain tumor.
• Diagnosis often made on necropsy.
CBC/BIOCHEMISTRY/URINALYSIS FOLLOW-UP
Normal unless the parasite also affects PATIENT MONITORING
non-neural tissues. As necessary.
OTHER LABORATORY TESTS PREVENTION/AVOIDANCE
Cerebrospinal fluid (CSF)—may show • Keep pets indoors or/and segregated from
eosinophilic, neutrophilic, or mononuclear wildlife.
pleocytosis (also found in protozoal, fungal, • Use preventive anthelmintics and
and prototheca encephalitides); may be dirofilaricides.
normal (strictly parenchymal lesions).
IMAGING Acute or insidious onset, then usually
CT or MRI—brain; focal lesion and/or progressive.
cerebral infarction from occlusion of cerebral
Endocarditis, Infective
SIGNS with sepsis (septic triad). • Renal azotemia—
General Comments secondary to renal emboli, pyelonephritis, and/
• Gram-negative bacteremia results in peracute
or hypovolemia-induced renal failure.
BASICS • Proteinuria caused by septic emboli,
or acute signs; Gram-positive bacteremia results
DEFINITION immune-mediated glomerulonephritis, or renal
The invasion of the cardiac endocardium,
in subacute or chronic clinical signs. • Systemic
infarction; hematuria, pyuria, and granular
E
signs secondary to infarction, infection
usually the valves, by infectious agents. (inflammation), toxemia, or immune-mediated casts associated with pyelonephritis.
Usually Gram-positive bacteria, especially damage; usually override cardiac signs. OTHER LABORATORY TESTS
staphylococci or streptococci. Occasionally • Blood culture—three samples taken at least 1
Rickettsia or Bartonella in dogs. Rarely fungi Historical Findings
• Infectious disease involving skin, oral,
hour apart over 24 hours; at least two should
in dogs. Culture-negative cases may be due to yield the same microbe; both aerobic and
Bartonella or fungi (e.g., Aspergillus). Less gastrointestinal (GI), or genital tracts (e.g.,
prostatitis). • Predisposing factors— anaerobic cultures recommended; antibiotic
likely due to Brucella, Coxiella, removal systems available for diagnosis of
Corynebacterium, and Chlamydia. immunosuppressive drug therapy, SAS, recent
surgery, infected wound, abscess, pyoderma, or patients given antibiotics. • PCR with bacterial
PATHOPHYSIOLOGY recent implantation of cardiovascular device 16s primers, in combination with blood
• Bacteremia from various portals of entry; (i.e., pacemaker, Amplatz® canine ductal culture, increases likelihood of identification of
bacteria invade and colonize the heart occluder). • Presenting complaints include bacteremia. • Culture-negative bacteremia
valves—usually the aortic, occasionally the lethargy, paresis, fever, anorexia, GI disturbance, often due to prior antibiotic administration or
mitral, and rarely the tricuspid and pulmonic and lameness; in cats, cardiac decompensation fastidious microbes, especially Bartonella.
valves. • Endocardial ulceration exposes • Catheter tips—culture. • Urine culture (not
and/or locomotor abnormalities are common
collagen causing platelet aggregation, presenting complaints. a substitute for blood culture)—easy; often
activation of the coagulation cascade, and positive; does not necessarily incriminate the
formation of vegetations. • Vegetations on Physical Examination Findings urinary tract as the source of infection. • Tests
heart valves are composed of an inner layer of • Usually diverse and misleading—the “great for prostate, kidney, and bone infection may be
platelets, fibrin, red blood cells, and bacteria; imitator.” • Pyrexia and general malaise. warranted. • Positive antinuclear antibody,
a middle layer of bacteria; and an outer layer • Dyspnea due to CHF. • Arrhythmias lupus erythematosus, rheumatoid factor, and
of fibrin. • Valvular insufficiency develops in (ventricular, supraventricular, or heart block). Coombs’ test results occasionally found—
virtually all patients; aortic insufficiency • Single or shifting leg lameness. • Systolic nonspecific; tend to confound the diagnosis.
almost invariably leads to intractable heart murmur. • “To-and-fro” murmur— • Bartonella alpha-Proteobacteria growth
left-sided congestive heart failure (CHF) associated with aortic valve vegetation causing medium (BAPGM) and PCR—for Bartonella.
within weeks to several months. • CHF is less systolic turbulence and diastolic regurgitation.
• Diastolic murmur with hyperdynamic
IMAGING
frequent and latent when only the mitral
valve is affected. • Vegetative lesions may femoral pulses are a strong indication of Radiography
dislodge causing infarction or metastatic advanced aortic endocarditis. Left cardiomegaly; rarely, calcification of one
infection to any organ; organs commonly CAUSES or more heart valves.
infected include the spleen, kidneys, brain, • Bacterial infection associated with oral Echocardiography
and skeletal muscles. cavity, bone, prostate, skin, and other sites. Best test—vegetative aortic endocarditis easily
SYSTEMS AFFECTED • Invasive diagnostic or surgical procedures discerned; mitral valve infection may be
• Cardiovascular—valvular insufficiency; causing bacteremia. difficult to differentiate from degenerative
arrhythmias, myocarditis. • Nervous—para/ RISK FACTORS valve disease; hyperechoic with chronicity.
tetraparesis; cranial nerve deficits; abnormal • SAS. • Immunosuppression from long- DIAGNOSTIC PROCEDURES
mentation. • Hemic/lymphatic/immune— term or high-dose corticosteroids, neoplasia, Arthrocentesis
hypercoagulation; disseminated intravascular or cytotoxic drug administration. Joint taps for cytology and culture—cytology
coagulation. • Musculoskeletal—septic or
usually does not differentiate septic from
immune-mediated polyarthropathy; hyper-
immune-mediated arthritis; either, though
trophic osteopathy; discospondylitis. • Renal/
usually not septic, can exist with infective
urologic—renal infarction; immune-mediated
glomerulonephritis; urinary tract infections. DIAGNOSIS endocarditis; usually nondegenerate neutro-
phils regardless of cause.
• Respiratory—pulmonary edema and/or DIFFERENTIAL DIAGNOSIS
emboli. • Bacteremia of any cause. • Polysystemic, ECG
immune-mediated disorders. • Left-sided CHF • May be normal; occasionally reflects left
SIGNALMENT
caused by dilated cardiomyopathy or SAS. cardiomegaly; often detects ventricular
Species tachyarrhythmias; occasionally heart block of
Dog; rarely cat. CBC/BIOCHEMISTRY/URINALYSIS
variable severity or supraventricular
• Inflammatory leukogram (i.e., neutrophilia,
Breed Predilections tachyarrhythmias. • Heart block suggests
left shift, and monocytosis)—patients with
• Medium to large breeds. • Breeds aortic valve involvement with infection or
chronic, relatively inactive, or walled-off
predisposed to subaortic stenosis (SAS). infarction of the adjacent septum.
infection may have normal or nearly normal
Mean Age and Range leukogram; those with chronic infection may PATHOLOGIC FINDINGS
Most affected dogs are 4–8 years of age; have mature neutrophilia with monocytosis. • Cardiomegaly, almost always left sided
infection can occur at any age. • Nonregenerative anemia. when present. • Vegetations and thrombi on
• Thrombocytopenia—variable severity. one or more valves. • Infection, hemorrhage,
Predominant Sex • Low-normal or low albumin, low-normal or and infarction of adjacent myocardium.
Most studies report male predominance— low glucose, and high serum alkaline phosphatase/ • Renal infarcts usually present. • Primary or
may be as great as 2 : 1. bilirubin activity are inconsistently associated secondary sites of infection, especially
Endocarditis, Infective (continued)
kidneys and spleen. • Pulmonary hemorr fluoroquinolones. • Gram-negative PREVENTION/AVOIDANCE

hage or edema. bacteria—often sensitive to third-generation • Indwelling catheters—restrict to
cephalosporins, fluoroquinolones, and appropriate indications; aseptic placement;
aminoglycosides. • Bartonella—only replace within 3–5 days. • Administer
aminoglycosides appear bactericidal; can try antibiotics to dogs with moderate to severe
E doxycycline, fluoroquinolone, rifampin, or SAS during dentistry or “dirty” procedures.
TREATMENT azithromycin. • First-generation • Avoid careless use of corticosteroids.
Early index of suspicion with aggressive, rapid
cephalosporins—reasonable choice for POSSIBLE COMPLICATIONS
diagnostic testing, followed by appropriate
stable patients until culture results are • CHF. • Renal failure. • Septic embolization
treatment are imperative for cure. Cure is a
obtained. • Treat life-threatening sepsis of many tissues and organs. • Persistent or
reasonable expectation when mitral valve
immediately with drug combinations; latent immune-mediated polyarthropathy.
(alone) endocarditis is identified early in its
pending culture results, one of three
course and treatment is aggressive. EXPECTED COURSE AND PROGNOSIS
regimens is recommended: ◦ Penicillin,
NURSING CARE ampicillin, ticarcillin, or a first-generation • Best prognosis associated with short history
• Aggressive fluid therapy—overt or cephalosporin is combined with an of bacteremia, rapid diagnosis, and aggressive
impending CHF limits fluid volumes that can aminoglycoside; aminoglycosides are not treatment; given that diagnosis is often
be administered; this problem is virtually good choices for animals with overt or delayed in cats, prognosis is often grave.
insurmountable in patients with concomitant impending CHF or those with renal • Mortality relatively higher in animals
renal failure. • Imminent CHF—provide no azotemia; gentamicin (2 mg/kg q8h) is recently given corticosteroids. • Grave
more than maintenance volumes of fluid; recommended for only 5–10 days because prognosis for patients with aortic valve
alternate 5% dextrose in water (D5W) with of renal toxicity; a fluoroquinolone may be endocarditis. • Patients with mitral valve
lactated Ringer’s solution (LRS; or 2.5% substituted for an aminoglycoside. endocarditis can be saved with appropriate
dextrose in half-strength LRS); potassium ◦ Clindamycin (2–10 mg/kg IV q8h) plus treatment. • Latent CHF can occur with
supplementation usually required. enrofloxacin (10 mg/kg q24h given diluted advanced, late diagnosis, or inadequate
1 : 1 in sterile water and injected slowly treatment for mitral valve endocarditis.
CLIENT EDUCATION
Guarded prognosis if only mitral valve over 15–20 min). ◦ Advanced-generation
involved. Grave prognosis if aortic valve is cephalosporins or ticarcillin–clavulanic acid
involved. (Timentin®)—high dosages, but only
normal dosages if patient has renal failure. MISCELLANEOUS
Treatment of CHF ASSOCIATED CONDITIONS
• Pimobendan, angiotensin-converting Congenital heart defects (usually SAS) in
MEDICATIONS enzyme inhibitor, spironolactone, and some animals.
furosemide (± amlodipine) indicated for
DRUG(S) OF CHOICE patients with overt or impending CHF. SYNONYMS
Treatment variable—depends on severity of • Oxygen, high-dose furosemide—2–8 mg/ • Bacterial endocarditis. • Vegetative
sepsis and presence or absence of CHF. kg IV (± nitroglycerin and/or hydralazine endocarditis.
Antibiotics 1–2 mg/kg q12h) for patients with acute, SEE ALSO
• Backbone of treatment but usually do not severe pulmonary edema. • Bartonellosis. • Congestive Heart Failure,
eradicate infection before irreversible aortic CONTRAINDICATIONS Left-Sided. • Discospondylitis. • Prostatitis
valve damage occurs; more than minimal • Avoid antibiotics that cannot penetrate and Prostatic Abscess. • Sepsis and Bacteremia.
damage to the aortic valve is life-threatening fibrin (e.g., sulfonamides). • Corticosteroids. ABBREVIATIONS
because aortic insufficiency tends to be a • BAPGM = Bartonella alpha-Proteobacteria
lethal complication. • High-dose IV ALTERNATIVE DRUG(S)
• Anticoagulant therapy—controversial in the growth medium. • CHF = congestive heart
administration of bactericidal antibiotics is failure. • D5W = 5% dextrose in water.
imperative and recommended for as long as prevention of embolization; heparin not
recommended in human medicine as it • GI = gastrointestinal. • LRS = lactated
feasible (at least 1 week), followed by SC Ringer’s solution. • SAS = subaortic stenosis.
administration for 1 or more weeks. • Oral increases risk of hemorrhage. • Aspirin
administration—recommended only after at (5–7 mg/kg PO q24h) and/or dalteparin Suggested Reading
least 4 weeks of injectable therapy and at (100 U/kg SC q8h) and/or clopidogrel Calvert C, Thomason J. Cardiovascular
least 1 week after hematologic and clinical (2–4 mg/kg PO q24h)—may reduce bacterial infections. In: Greene CE, ed., Infectious
signs of infection and inflammation have dissemination and embolization. Diseases of the Dog and Cat. St. Louis,
disappeared; long-term (>4 months) MO: Saunders Elsevier, 2012: 912–936.
treatment may be required to eradicate the Palerme JS, Jones AE, Ward JL, et al.
infection from vegetations. • Selection Infective endocarditis in 13 Cats. J Vet
determined by both urgency of septic FOLLOW-UP Cardiol 2016, 18:213–225.
complications and results of bacterial Author Justin D. Thomason
PATIENT MONITORING Consulting Editor Michael Aherne
culture; coagulase-positive staphylococci
• Emergence of antibiotic resistance— Acknowledgment The author and book
and streptococci are most often incrim
relapsing fever and inflammatory leukogram; editors acknowledge the prior contribution of
inated, so choices can be logically made
imperative to adjust treatment based on Clay A. Calvert
before culture results are obtained.
culture results. • Frequent examination and
• Coagulase-positive staphylococci—usually
CBC after discharge. • Repeat blood cultures
resistant to penicillin, hetacillin, amoxicillin,
1 week after antibiotics are discontinued or if Client Education Handout
and ampicillin. • Streptococci—often
fever recurs. available online
resistant to aminoglycosides and
Endomyocardial Diseases—Cats
• Dyspnea and increased lung sounds or • Hyperechoic endomyocardium reported—
crackles. incidence seems to vary and is subjective; in
• Paresis or paralysis with weak or absent one report it was as high as 86%.
BASICS femoral pulses. Endocardial Fibroelastosis
OVERVIEW • Arrhythmias possible.
• Endomyocarditis—acute cardiopulmonary
• Limited data available. E
CAUSES & RISK FACTORS • Reduced left ventricular function and
disease that typically develops following a • Cause unknown for all three diseases. enlarged left atrium.
stressful event; characterized by interstitial • Risk factors for endomyocarditis include
pneumonia and endomyocardial inflamma- EMBs
stressful incidents such as anesthesia Many findings can overlap with restrictive
tion; pneumonia is usually severe and (commonly associated with neutering or
commonly causes death; one report recorded cardiomyopathy. A network of false tendons
declawing), vaccination, relocation, or can sometimes be imaged with 2D echo-
the incidence of endomyocarditis at postmor- bathing.
tem to be equivalent to that of hypertrophic cardiography.
• Endocardial fibroelastosis may be familial
cardiomyopathy. in Burmese and Siamese cats. DIAGNOSTIC PROCEDURES
• Endocardial fibroelastosis—congenital • Appearance of EMBs in a young cat would ECG Findings
heart disease in which severe fibrous endo- suggest a congenital malformation. • Endomyocarditis—sinus tachycardia
cardial thickening leads to heart failure
common; ventricular premature complexes,
secondary to diastolic and systolic failure.
atrial premature complexes, bundle branch
• Excessive moderator bands (EMBs)—a rare
block, and complete atrioventricular (AV)
and unique pathologic disease; moderator
DIAGNOSIS block reported.
bands are normal muscular bands in the right
• Endocardial fibroelastosis—evidence for
ventricle, but they can sometimes occur in the DIFFERENTIAL DIAGNOSIS left-sided enlargement; sinus rhythm typically
left ventricle.
Other Causes of Cardiac Disease present, but various arrhythmias possible.
SIGNALMENT • Hypertrophic cardiomyopathy. • EMBs—various electrocardiographic
• Cats. • Unclassified cardiomyopathy. findings have been reported: AV block, sinus
• Endomyocarditis—predominantly males • Restrictive cardiomyopathy. bradycardia, right bundle branch block, and
(62%) age 1–4 years. • Dilated cardiomyopathy. left axis deviation.
• Endocardial fibroelastosis—early development • Congenital heart malformations. PATHOLOGIC FINDINGS
of biventricular or left heart failure, usually
Other Causes of Dyspnea Endomyocarditis
prior to 6 months of age.
• Other forms of cardiac disease as above. • Interstitial pneumonia.
• EMBs—can be seen in any age of cat.
• Primary respiratory disease. • Left heart enlargement and opacity of the
SIGNS • Pleural space disease. left ventricular endomyocardium with foci of
Historical Findings • Mediastinal disorders, infection, trauma, hemorrhage; fibroplasia of the endocardium
Endomyocarditis neoplasia. is striking.
• Hemoglobin disorders, anemia, methemo- • Varying degrees of endomyocardial
• Dyspnea following a stressful event in a
young, healthy cat. globinemia, causes of central cyanosis. inflammation with infiltrates of neutrophils,
• Respiratory signs usually occur 5–21 days Other Causes of Collapse, Weakness, or lymphocytes, plasma cells, histiocytes, and
after the stressor. Syncope macrophages seen histologically.
• In one report, 73% of cases presented • Arrhythmias. Endocardial Fibroelastosis
between August and September. • Neurologic or musculoskeletal disease. • Left ventricular and atrial dilation with
Endocardial Fibroelastosis and EMBs • Metabolic disease or electrolyte disorders. severe diffuse white opaque thickening of the
• Lethargy, weakness, collapse, syncope. • Other forms of paresis or paralysis. endocardium.
• Poor appetite and weight loss. • Arterial thromboembolism secondary to • Diffuse hypocellular, fibroelastic thickening
• Dyspnea. any form of cardiac disease or neoplasia. of the endomyocardium; prominent endo-
• Tachypnea. • Neurologic or musculoskeletal disease. myocardial edema with dilation of lymphatics.
• Cyanosis. • Neoplasia.
EMBs
• Abdominal distention. CBC/BIOCHEMISTRY/URINALYSIS Changes typically include an irregular left
• Paresis or paralysis; signs of thromboem- Not diagnostic. ventricular endocardial contour with a rounded
bolic disease. apex and numerous irregular left ventricular
Physical Examination Findings N/A false tendons; heart weight can be greater than
Endomyocarditis normal; the moderator bands are composed of
IMAGING central Purkinje fibers and collagen.
• Severe dyspnea.
• Occasional crackles. Thoracic Radiographic Findings for All
• May have murmur or gallop; murmur may Three Diseases
vary in intensity. • Cardiomegaly.
• May have evidence of thromboembolic disease. • Interstitial or alveolar infiltrates or pleural TREATMENT
• Typically no significant abnormalities prior effusion if congestion has developed.
Endomyocarditis
to the stressful event. Echocardiographic Findings • No single therapy protocol to date.
Endocardial Fibroelastosis and EMBs Endomyocarditis • Small percentage of cats have survived;
• Gallop. • Normal to mildly large left atrium. these cats do not require long-term
• Systolic murmur, possible mitral • Left ventricular wall thickness can be therapy.
regurgitation. normal to mildly thick (0.6–0.7 cm).
Endomyocardial Diseases—Cats (continued)
• Supportive care with oxygen and possibly may be wise before starting antiarrhythmic SEE ALSO
ventilation. therapy. • Aortic Thromboembolism.
• Intractable edema—nitroprusside 1–5 μg/ • Congestive Heart Failure, Left-Sided.
Endocardial Fibroelastosis and EMBs
• Oxygen therapy via cage delivery is least
kg/min may be helpful. • Congestive Heart Failure, Right-Sided.
• Myocarditis.
E stressful. Chronic CHF
• Thoracocentesis if pleural effusion. • Treat as other CHF, with furosemide and ABBREVIATIONS
angiotensin-converting enzyme inhibitors • AV = atrioventricular.
(e.g., enalapril, benazepril). • CHF = congestive heart failure.
• Digoxin can be added for SV arrhythmia • EMB = excessive moderator band.
control when patient is stable and eating. • SV= supraventricular.
MEDICATIONS
CONTRAINDICATIONS Suggested Reading
DRUG(S) OF CHOICE
N/A Bossbaly MB, Stalis I, Knight D, Van Winkle
Endomyocarditis T. Feline endomyocarditis: a clinical/
Steroids, furosemide, and vasodilators have pathological study of 44 cases. Proceedings
been tried, but efficacy is unknown. of the 12th ACVIM Forum, 1994, p. 975.
Liu S, Tilley LP. Excessive moderator bands in
Endocardial Fibroelastosis and EMBs FOLLOW-UP the left ventricle of 21 cats. JAVMA 1982,
with Acute Congestive Heart Failure EXPECTED COURSE AND P 180:1215–1219.
(CHF) ROGNOSIS Stalis IH, Bossbaly MJ, Van Winkle TJ.
• Parenteral administration of furosemide • Endomyocarditis—poor, although some Feline endomyocarditis and left ventricular
0.5–1 mg/kg IV/IM q1–6h. animals survive; animals that survive endocardial fibrosis. Vet Pathol 1995,
• Dermal application of 2% nitroglycerin respiratory phase may progress to left 32(2):122–126.
ointment one-eighth to one-fourth inch ventricular endocardial fibrosis. Wray JD, Gajanayake I, Smith SH.
q4–6h has been suggested but is of unknown • Endocardial fibroelastosis and EMBs— Congestive heart failure associated with a
efficacy. medical treatment of CHF may prolong life, large transverse left ventricular moderator
• Arrhythmias may resolve with stabilization. but recovery is unlikely. band in a cat. J Feline Med Surg 2007,
If there is rapid atrial fibrillation (heart rate 9:56–60.
>200), a calcium channel blocker or beta Author Carl D. Sammarco
blocker can be considered to control the Consulting Editors Michael Aherne
ventricular response. If there is dilated
cardiomyopathy, digoxin may be a better MISCELLANEOUS
choice for controlling the atrial fibrillation ASSOCIATED CONDITIONS
rate. For other supraventricular (SV) • Aortic thromboembolism.
arrhythmias and ventricular arrhythmias, • Relationship possible between endomyocar-
waiting for a response to heart failure therapy ditis and left ventricular endocardial fibrosis.
Entropion
caused by chronic blepharospasm (spastic • Medial canthoplasty should be considered if
entropion); also in older cats due to entropion results in pigmentary keratitis,
enophthalmos from retrobulbar fat loss. chronic epiphora, or corneal scarring.
BASICS
Mature Dogs and Cats
OVERVIEW • Chronic entropion—requires eyelid E
• Inversion or rolling in of eyelid margin, margin–everting surgery; ranges from simple
resulting in frictional irritation of cornea and/ DIAGNOSIS Hotz-Celsus procedure to more radical lateral
or conjunctiva from contact with outer canthoplasty procedures; often combined
surface of eyelid. DIFFERENTIAL DIAGNOSIS
with lid-shortening procedures.
• May result in keratitis, corneal ulceration, • Underlying causes of spastic entropion
• No history of previous entropion and
or corneal perforation. (eyelid hair anomalies, foreign bodies,
clinical signs of acute condition—identify
• Can be conformational/congenital infectious keratitis/conjunctivitis) should be
cause of spastic condition and correct; may
(primary) or acquired (secondary). ruled out and corrected, if possible, before an
attempt temporary eversion sutures before
• Severe corneal disease may threaten vision. attempt at surgical correction is made.
permanent skin resection.
• Puppies—common for first-time breeders of
SIGNALMENT chow chows and Chinese Shar-Peis to mistakenly
• Common in dogs—seen in chow chow, think that eyelids have not opened at 4–5 weeks
Chinese Shar-Pei, Norwegian elkhound, of age, when puppies actually have severe
sporting breeds (e.g., spaniel, retriever), blepharospasm and spastic entropion. MEDICATIONS
brachycephalic breeds, toy breeds, and giant
breeds; age—puppies as early as 2–6 weeks CBC/BIOCHEMISTRY/URINALYSIS DRUG(S) OF CHOICE
old; usually identified in dogs <1 year old. N/A • Topical ophthalmic ointment—triple
• Cats—usually in brachycephalic breeds, in OTHER LABORATORY TESTS antibiotic (in dogs only, q6–12h) or antibiotic
young cats due to chronic ocular surface disease, N/A based on culture and sensitivity testing; may
and older animals due to retrobulbar fat loss. be used if cornea is ulcerated, postoperatively,
IMAGING or as presurgical lubricant.
SIGNS N/A • Topical petrolatum-based artificial tear
• Mild, medial—chronic epiphora and ointments (e.g., Puralube® q8–12h) may be
medial pigmentary keratitis (toy dogs and DIAGNOSTIC PROCEDURES
• Observe patient with minimal restraint to used temporarily in mild cases without
brachycephalic dogs and cats). corneal ulceration.
• Mild, lateral—chronic mucoid to mucopurulent
assess degree of entropion without distortion
ocular discharge (giant-breed dogs). from tension on eyelids or periocular area. CONTRAINDICATIONS/POSSIBLE
• Apply a topical anesthetic to reduce spastic INTERACTIONS
• Upper lid, lower lid, or lateral canthal—
severe blepharospasm, purulent discharge, component to differentiate spastic versus N/A
pigmentary or ulcerative keratitis, potential physiologic entropion.
cornea rupture (chow chow, shar-pei,
bloodhound, sporting breeds).
• Cats—often have associated keratoconjunc-
FOLLOW-UP
tivitis, corneal ulceration, or corneal TREATMENT Temporary eversion suture technique—entro-
sequestrum (brown-black corneal opacity).
Puppies pion may revert when sutures are removed or
CAUSES & RISK FACTORS • Do not initially perform skin resection spontaneously pull through the skin; repeat as
• Genetic predisposition—based on facial surgery. necessary until patient is mature enough to
conformation and eyelid support. • If cornea ulcerated—topical antibiotic (e.g., undergo more permanent repair. Consider
• Brachycephalic breeds (dogs and cats)— neomycin/polymyxin B/bacitracin) ointment hyaluronic acid filler injection as alternative.
excessive tension on ligamentous structures of q6–8h.
medial canthus plus nasal folds and facial • If mildly entropic and cornea not ulcerated,
conformation results in rolling inward of lubricate with artificial tear ointment q8–12h.
medial aspects of upper and lower eyelids at • If moderate to severe entropion with or
the medial canthus. without corneal ulceration, temporarily evert
MISCELLANEOUS
• Giant breeds and breeds with excessive eyelid eyelid margins with sutures to break the Suggested Reading
length (macroblepharon), heavy/loose facial irritation–spasm cycle; if successful, Stades FC, van der Woerdt A. Diseases and
skin, or excessive facial folds—laxity of lateral permanent procedure is unnecessary; may surgery of the canine eyelid. In: Gelatt KN,
canthus allows entropion of upper and lower need to be repeated every 2–4 weeks until Gilger BC, Kern TJ, eds., Veterinary
eyelids and lateral canthus. adult facial conformation is achieved. Ophthalmology, 5th ed. Ames, IA:
• Spastic entropion—from ocular irritation • Semi-permanent eyelid eversion with Wiley-Blackwell, 2013, pp. 843–864.
(e.g., distichia, ectopic cilia, trichiasis, foreign hyaluronic acid filler injection—lasts up to Williams DL, Kim JY. Feline entropion: a case
body, irritant conjunctivitis); leads to excessive several months, often until adult facial series of 50 affected animals (2003–2008).
blepharospasm. conformation is achieved. Vet Ophthalmol 2009, 12(4):221–226.
• Non-predisposed breeds—may be primary • Permanent skin resection technique— Author Sarah L. Czerwinski
irritant causing secondary spastic entropion. postponed until patient’s facial conformation Consulting Editor Kathern E. Myrna
• Loss of orbital fat or periorbital musculature matures (usually 1.5–2 years). Acknowledgment The author and book
may lead to enophthalmos and entropion. editors acknowledge the prior contribution of
Medial Entropion
• Secondary cicatricial entropion—from J. Phillip Pickett.
• Temporary eversion of medial canthus with
scarring due to eyelid wounds or eyelid surgery.
sutures may aid in determining contribution
• Cats—chronic infectious conjunctivitis or
of medial entropion to epiphora.
keratitis: may lead to functional entropion
Eosinophilia
BASICS DIAGNOSIS MEDICATIONS

OVERVIEW DIFFERENTIAL DIAGNOSIS Dependent on cause.
E • Eosinophilia refers to an increased number • HES represents an idiopathic response that
of circulating eosinophils. may be due to an occult immunologic stimulus.
• Reference intervals may be difficult to • Eosinophilic leukemia is a myeloproliferative
accurately determine, as numbers do not tend disease that often has immature forms in
to have normal (Gaussian) distribution. circulation and in the bone marrow. FOLLOW-UP
Absolute counts >1.5 x 103/μl often indicate • Differentiation between HES and Dependent on cause.
clinically significant eosinophilia. eosinophilic leukemia can be extremely
• Diseases associated with eosinophilia are difficult and is somewhat controversial.
highly variable. However, they often CBC/BIOCHEMISTRY/URINALYSIS
involve those causing release of cytokines
including IL-5, IL-2, IL-3, and/or GM-CSF.
• Caution should be taken in interpreting MISCELLANEOUS
the results of some in-house hematology
• Prevalence varies; 4.8% of cats and 10% of SEE ALSO
analyzers, as they only show good correlation
dogs have been identified with eosinophilia in Hypereosinophilic Syndrome (HES).
with gold standard instruments. A blood
large retrospective studies. smear should always be evaluated as part of ABBREVIATIONS
SIGNALMENT the CBC. • ACTH = adrenocorticotropic hormone.
• Breed and sex predilections are directly • Eosinophils tend to be larger and • HES = hypereosinophilic syndrome.
correlated to the characteristics of specific hypolobulated compared to neutrophils. Suggested Reading
diseases. • Feline eosinophils have small, rod-shaped Center SA, Randolph JR, Erb HN, Reiter S.
• Rottweilers and German shepherd dogs show granules. Eosinophilia in the cat: a retrospective study
the highest overall prevalence of eosinophilia. • Sight hounds and sporadic other individuals of 312 cases. J Am Anim Hosp Assoc 1990,
SIGNS have “gray eosinophils,” which have poorly 26(4):349–358.
• Clinical signs directly associated with
staining granules and occasionally empty Lillieöök I, Gunnardsson L, Zakrisson G,
eosinophilia per se are lacking. vacuoles in their cytoplasm. Tvedten H. Diseases associated with
• Eosinophils are grouped into one large pronounced eosinophilia: a study of 105
• Specific clinical signs are dependent on the
disease causing the eosinophilia. category; bands, metamyelocytes, etc. are dogs in Sweden. J Small Anim Pract 2000,
typically not divided out, as they are with 41(6):248–253.
CAUSES & RISK FACTORS neutrophils. Lillieöök I, Tvedten H. Investigation of
• Diseases associated with eosinophilia are
OTHER LABORATORY TESTS hypereosinophilia and potential treatments.
widely variable and can be categorized in
Additional testing (e.g., adrenocorticotropic Vet Clin North Am Small Anim Pract 2003,
many ways.
hormone (ACTH) stimulation test, fecal 33(6):1359–1378.
• Infectious diseases typically involve tissues
flotation, cytology, etc.) are dependent on the Author Craig A. Thompson
rather than peripheral blood, and are more
differential diagnosis/disease in question. Consulting Editor Melinda S. Camus
likely to be parasitic than bacterial.
• Tissues involved are frequently those that IMAGING
contain abundant mast cells, such as skin, Diagnostic imaging utilized (e.g., radio-
lungs, and intestine, and often involve graphs, ultrasound, CT, etc.) is dependent on
hypersensitivity. the differential diagnosis/disease in question.
• Metabolic—hypoadrenocortisim.
• Neoplastic—mast cell tumor; eosinophilic
Diagnostic procedures utilized (e.g.,
leukemia; lymphoma (both T-cell and B-cell); transtracheal wash, endoscopy, serologic
thymoma; mammary carcinoma; oral testing, biopsy, etc.) are dependent on the
fibrosarcoma; transitional cell carcinoma. differential diagnosis/disease in question.
• Immune mediated—hypereosinophilic
syndrome (HES); idiopathic HES in PATHOLOGIC FINDINGS
Rottweilers; feline asthma; eosinophilic • No specific lesions are ascribed solely to
bronchopneumopathy; feline gastro eosinophilia other than peripheral blood
intestinal eosinophilic sclerosing findings.
fibroplasia; flea bite allergy; eosinophilic • Lesions are dependent on the disease(s) present.
granuloma complex.
• Infectious—Angiostrongylus vasorum;
heartworm disease (Dirofilaria immitis);
Ehrlichia spp. infections; Anaplasma spp.
infections; histoplasmosis; sarcocytosis; TREATMENT
Aelurostrongylus spp.; larval migration of • No specific treatment is described
various parasites. exclusively for eosinophilia.
• Toxic methimazole therapy. • The treatment employed is dependent on
the cause of the eosinophilia.
Eosinophilic Granuloma Complex

eosinophilic plaque: no sex predilection. deficiency virus (FIV). • Unresponsive
• EGD—males (72% of cases). lesions—pemphigus foliaceus,
SIGNS dermatophytosis and deep fungal infection,
BASICS demodicosis, pyoderma, and neoplasia
DEFINITION General Comments—Cats (metastatic adenocarcinoma, squamous cell
• Cats—also called feline eosinophilic skin • Distinguishing among the syndromes carcinoma, and lymphoma). • EGD—
E
disease; term used for three distinct syndromes: depends on clinical signs. • Lesions of more neoplasia, infectious and noninfectious
eosinophilic plaque, eosinophilic granuloma, than one syndrome may occur simultaneously granuloma.
and indolent ulcer; grouped primarily or may change over time.
according to their clinical similarities, their Historical Findings—Cats CBC—mild to moderate eosinophilia.
frequent concurrent (and recurrent) develop • Lesions may develop spontaneously and
ment, and their positive response to acutely. • Eosinophilic granuloma—variable OTHER LABORATORY TESTS
corticosteroids; reaction pattern and not a final but typically nonpruritic. • Eosinophilic FeLV and FIV.
diagnosis unless idiopathic. • Dogs— plaque—severe pruritus. • Indolent ulcer— DIAGNOSTIC PROCEDURES
eosinophilic granuloma in dogs (EGD) rare; pain and pruritus rare. • Seasonal incidence • Impression smears (cytology) from lesions—
specific differences from cats listed separately. possible (related to insects and allergy). large numbers of eosinophils (indolent ulcer
PATHOPHYSIOLOGY • Waxing and waning of clinical signs may be more neutrophilic). • Comprehensive
• Eosinophil—major infiltrative cell for common in all syndromes. flea and insect control—assist in excluding flea
eosinophilic granuloma and eosinophilic Physical Examination Findings or mosquito bite hypersensitivity. • Food
plaque, but not typically with indolent ulcer; • Eosinophilic plaque—single or multiple,
elimination trial and provocation—appropriate
most often associated with allergic or parasitic alopecic, erythematous, eroded/ulcerated in all cases. • Atopy—intradermal skin testing
conditions but has a more general role in well-demarcated and flat-topped ± white (preferred) or serum allergy testing followed by
inflammatory reactions. • Eosinophilic necrotic foci; most commonly seen on the immunotherapy. • Biopsy.
granuloma complex (EGC)—most often in abdomen and medial thighs, but may also see in PATHOLOGIC FINDINGS
cats with hypersensitivities to inhaled allergens, mucocutaneous junctions and other areas of the • Histopathologic diagnosis—mainly to rule
food, or insects, but can also be idiopathic with skin; frequently moist or glistening; may appear out other differentials. • Eosinophilic
possible genetic causes. • EGD—may have oval or linear due to pattern of licking. granuloma—nodular to diffuse granulo
both a genetic predisposition and a hyper • Eosinophilic granuloma—caudal thigh (linear matous dermatitis with flame figures,
sensitivity cause (especially in non-genetically granuloma)—distinctly linear orientation on the eosinophils, multinucleated histiocytic giant
susceptible breeds). caudal thigh; chin (“pouting cats”)—lip margin cells; mucinosis of epidermis/hair follicle
SYSTEMS AFFECTED and chin swelling; paw pads—footpad swelling, outer root sheath, mural eosinophilic
Skin/exocrine. pain, and lameness; oral cavity—ulceration folliculitis/furunculosis, eosinophilic
common (especially on the tongue, palate): cats panniculitis possible. • Eosinophilic
GENETICS with oral lesions may be dysphagic, have plaque—superficial to deep perivascular
• Related individuals with disease halitosis, and may drool; can be located dermatitis with eosinophilia to interstitial to
development in a colony of specific anywhere on the body; spontaneous regression— diffuse eosinophilia; mucinosis of epidermis/
pathogen-free cats indicate that genetic especially in young cats with the inheritable hair follicle outer root sheath, diffuse
predisposition (possible inheritable form. • Indolent ulcer—classically concave and spongiosis of outer root sheath, eosinophilic
dysfunction of eosinophilic regulation) may indurated ulcerations with a granular, orange- microvesicles/microabscesses possible.
be significant component for development. yellow color, confined to the upper lips near • Indolent ulcer—variable; may be predomin-
• Genetically predisposed development of philtrum or upper canine teeth. • Peripheral antly neutrophilic or eosinophilic. • EGD—
hypersensitivity. lymphadenopathy possible for EGC lesions. foci of palisading granulomas and flame
GEOGRAPHIC DISTRIBUTION • EGD—ulcerated plaques and nodules; green/ figures; infiltrate with eosinophils mixed with
Seasonal incidence in some geographic orange color; most often affects the tongue and macrophages.
locations—insect or environmental allergen palatine arches; uncommon cutaneous lesions on
exposure. the abdomen, cheek, digits, prepuce, and flanks.
• Cavalier King Charles spaniels—lesions on the
SIGNALMENT
soft palate or near the tonsils.
Species TREATMENT
• Cats—eosinophilic granuloma, eosinophilic CAUSES APPROPRIATE HEALTH CARE
plaque, indolent ulcer. • Dogs—eosinophilic • Hypersensitivity—flea or insect (mosquito • Most patients treated as outpatients unless
granuloma. bite), food hypersensitivity, and atopy; a severe oral disease prevents adequate fluid
heritable dysfunction has been proposed. intake. • Identify and eliminate offending
Breed Predilections • Idiopathic. • EGD—unknown; genetics in
• Cats—none. • Dogs—EGD: Siberian allergen(s) before providing medical inter-
susceptible breeds; a hypersensitivity reaction vention. • Atopy—immunotherapy:
husky (76% of cases), cavalier King Charles often suspected (insect bite) in non-geneti
spaniel. successful in a majority of cases; preferable to
cally susceptible breeds. long-term corticosteroid administration.
Mean Age and Range
• Eosinophilic granuloma and plaque—younger NURSING CARE
cats. • Spontaneously regressing eosinophilic Discourage patient from damaging lesions by
granuloma—<1 year. • Indolent ulcer—any age. excessive grooming.
• EGD— usually <3 years of age (80%).
DIAGNOSIS
DIET
DIFFERENTIAL DIAGNOSIS No restrictions unless a food allergy is
Predominant Sex
• Herpes virus dermatitis. • Feline suspected. Elimination diet for suspected
• Cats (eosinophilic granuloma, indolent
leukemia virus (FeLV) or feline immuno food allergy.
ulcer)—predilection for females reported;
Eosinophilic Granuloma Complex (continued)
CLIENT EDUCATION SYNONYMS

• Inform clients about the possible allergic or • Eosinophilic granuloma—feline collagenolytic
heritable causes. • Discuss the waxing and granuloma; feline linear granuloma. • Indolent
waning nature of these diseases. FOLLOW-UP ulcer—eosinophilic ulcer; rodent ulcer; feline
PATIENT MONITORING upper lip ulcerative dermatitis.
E SURGICAL CONSIDERATIONS
• Corticosteroids—baseline and frequent
EGD—individual lesions may be excised/ SEE ALSO
removed by carbon dioxide laser if being hemograms, serum chemistry profiles, and
urinalyses with culture; excessive or too- • Atopic Dermatitis.
mechanically traumatized and medically • Food Reactions, Dermatologic.
unresponsive. frequent use of corticosteroids increases risk
for development of diabetes mellitus and
ABBREVIATIONS
acquired skin fragility. • Cyclosporine—
• DMSO = dimethyl sulfoxide.
baseline and frequent hemograms, serum
• EGC = eosinophilic granuloma complex.
chemistry profiles, and urinalyses with
• EGD = eosinophilic granulomas in dogs.
culture; measurement of plasma cyclosporine
MEDICATIONS levels as needed to establish dosage within
DRUG(S) OF CHOICE therapeutic levels (especially cats); avoid raw
• Cases may improve with antibiotics— meat and keep cats indoors. • Selective Suggested Reading
amoxicillin trihydrate–clavulanate 10–20 mg/ immunosuppressant drugs—frequent Buckley L, Nuttall, T. Feline eosinophilic
kg q12h; cefovecin 8 mg/kg every 14 days; or hemograms (biweekly at first, then monthly granuloma complex(ities): some clinical
clindamycin 11–22 mg/kg q24h. • Oral or bimonthly as therapy continues) to clarification. J Feline Med Surg 2012,
corticosteroids—ongoing treatment necessary monitor for bone marrow suppression; 14:471–481.
unless the primary cause is controlled; routine serum chemistry profiles and King S, Favrot C, Messinger L, et al. A
prednisolone 2–4 mg/kg q24h, then as urinalyses with culture (monthly at first, then randomized double-blinded placebo-
required to control lesions; steroid tachy every 3 months) to monitor for complications controlled study to evaluate an effective
phylaxis may occur and may be specific to the (renal disease, diabetes mellitus, and urinary ciclosporin dose for the treatment of feline
drug administered; may be useful to change tract infection). hypersensitivity dermatitis. Vet Derm 2012,
the form; other drugs: methylprednisolone 23:440–e84.
EXPECTED COURSE AND PROGNOSIS Knight EC, Shipstone MA. Canine eosino
2–3 mg/kg q24h, dexamethasone 0.1–
• Lesions should resolve permanently if a philic granuloma of the digits treated with
0.2 mg/kg q24–72h, and triamcinolone
primary cause can be identified and prednisolone and chlorambucil. Vet Derm
0.2–0.3 mg/kg q24–72h; higher induction
controlled. • Most lesions wax and wane, 2016, 27:446–e119.
dosages may be required but should be
with or without therapy; an unpredictable Miller WH, Griffin CE, Campbell KL. Muller
tapered as quickly as possible. • Cyclosporine
schedule of recurrence should be anticipated. & Kirk’s Small Animal Dermatology, 7th ed.
modified, 7 mg/kg q24–48h. • Topical—
• Drug dosages should be tapered to the St. Louis, MO: Elsevier Mosby, 2013.
fluocinolone/dimethyl sulfoxide (DMSO;
lowest possible level (or discontinued, if Rosenkrantz WS. Feline eosinophilic
Synotic® lotion) to individual lesions; not
possible) once the lesions have resolved. granuloma complex. In: Griffin CE,
practical and/or may cause systemic effects in
• Lesions in cats with the inheritable disease Kwochka KW, MacDonald JM, eds.,
patients with large numbers of lesions.
may resolve spontaneously after several years. Current Veterinary Dermatology: The
Alternate Therapies • EGD—lesions may be recalcitrant to Science and Art of Therapy. St. Louis, MO:
• Chlorambucil 0.1–0.2 mg/kg q24–72h. medical intervention. Mosby, 1993, p. 319.
• α-interferon 300–1000 IU/day; limited
Author Heather D. Edginton
success. • Megestrol acetate—significant side
effects (e.g., diabetes, mammary cancer,
Resnick
pyometra); use not recommended except in
Acknowledgment The author acknowledges
severe, recalcitrant cases. MISCELLANEOUS the prior contribution of Alexander H.
EGD PREGNANCY/FERTILITY/BREEDING Werner Resnick.
• Oral prednisolone 0.5–2.2 mg/kg/day Systemic glucocorticoids and immuno
initially; then taper gradually. • Some may suppressive drugs should not be used during
undergo spontaneous remission. pregnancy. Client Education Handout
available online
Epididymitis/Orchitis
IMAGING
• Ultrasonographic evaluation of testes and
epididymides—inflamed testes have patchy
BASICS hypoechoic areas; inflamed epididymides FOLLOW-UP
have irregular contours and hypoechoic or • Prognosis for fertility—guarded to poor,
OVERVIEW E
• Epididymitis—inflammation of an hyperechoic areas; obtain measurements for especially with bilateral orchitis. • Testicular
epididymis; a prominent clinical sign of future comparisons. • Ultrasonographic degeneration of remaining contralateral testis
brucellosis. • Orchitis—inflammation of evaluation of prostate to identify underlying may occur due to elevated intrascrotal
testis; may be concurrent with epididymitis causes (i.e., prostatitis). temperature (inflammation), even following
(orchiepididymitis). • May be acute or unilateral castration. • Trauma or inflammation
DIAGNOSTIC PROCEDURES can cause obstruction of efferent tubules or
chronic. • Bacterial culture of semen (differentiate epididymal duct, leading to spermatocele or
SIGNALMENT results from normal flora). • Semen cytologic sperm granuloma. • Semen—evaluate
• Often unilateral. • Infrequent in dogs; rare evaluation—leukocytes; bacteria; spermatozoa characteristics 3 months after treatment for
in cats. • No genetic basis or breed predilec with morphologic abnormalities; head-to- orchitis is completed (dogs).
tions. • Mean age 3.7 years; range: 11 head agglutination (B. canis). • Prostate fluid
months–10 years. cytologic examination and bacterial culture;
sample collected aseptically by performing
SIGNS
prostatic massage (per rectum) after urethral
• Swollen testis. • Pain (if acute). • Pyrexia.
catheter placed where tip can be palpated (per MISCELLANEOUS
• Infertility. • Anorexia. • Listlessness.
rectum), followed with 5 mL saline infusion SEE ALSO
• Reluctance to walk. • Reluctance to breed.
and aspiration. • Open wounds—bacterial • Brucellosis
• Scrotal wound or abscess. • Scrotal
culture. • Fine-needle aspirate—sample • Torsion of thr Spermatic Cord
dermatitis (from licking behavior).
enlarged testes/epididymides for cytology and
CAUSES & RISK FACTORS culture; leukocytes vary from numerous ABBREVIATIONS
• Infectious—Brucella canis (brucellosis), neutrophils (suppurative) to minimal • AGID = agar gel immunodiffusion.
canine distemper virus, Rickettsia rickettsii inflammatory cells (granulomatous). • ME-RSAT = modified rapid slide
(Rocky Mountain spotted fever). • Urethritis, agglutination test.
prostatitis, cystitis. • Blunt abdominal or • RSAT = rapid slide agglutination test.
scrotal trauma, including scrotal bite or • TAT = tube agglutination test.
puncture wounds. • Auto-immune response Suggested Reading
to spermatozoa antigens—secondary to TREATMENT Hollett RB. Canine brucellosis: outbreaks and
trauma or inflammation. • Lymphoplasmacytic • Castration—if fertility is not a priority; compliance. Theriogenology 2006,
auto-immune orchitis with, or without, before castration, culture appropriate 66(3):575–587.
thyroiditis. specimen; administer antibiotics perioperat Johnston SD, Root Kustritz MV, Olson PNS.
ively to avoid scirrhous cord. • Unilateral Disorders of the canine testes and epididy
castration—for unilateral orchitis when mides. In: Johnston SD, Kustritz MVR,
patient’s fertility must be maintained; Olson PN, eds., Canine and Feline
administer appropriate perioperative Theriogenology. Philadelphia, OA:
DIAGNOSIS antibiotics. Saunders, 2001, pp. 313–317.
DIFFERENTIAL DIAGNOSIS Kauffman LK, Petersen CA. Canine brucellosis:
• Inguinoscrotal hernia. • Scrotal dermatitis. old foe and reemerging scourge. Vet Clin North
• Torsion of the spermatic cord. • Hydrocele. Am Small Anim Pract 2019, 49(4):763–779.
• Sperm granuloma. • Testicular neoplasia. Author Candace C. Lyman
• Prostatitis. • Cystitis. MEDICATIONS Consulting Editor Erin E. Runcan
CBC/BIOCHEMISTRY/URINALYSIS DRUG(S) OF CHOICE Acknowledgment The author and book
• Leukocytosis—may be found with acute or • If B. canis is diagnosed, removal of affected editors acknowledge the prior contribution of
infectious orchitis. • Pyuria, hematuria, testicle(s) is strongly recommended due to Carlos R.F. Pinto.
proteinuria—may be found if epididymitis/ zoonotic potential. • If infection present,
orchitis is secondary to prostatitis or cystitis. antibiotic choice should be based on culture
OTHER LABORATORY TESTS and sensitivity if available; broad-spectrum
• Serology—tests identifying B. canis
antibiotics (e.g., ampicillin sulbactam
antibodies or antigens may take up to 12 22–30 mg/kg IV q8h) may be administered
weeks to become detectable: perform until cultures are available. • If attempting to
immediate testing in any dog with scrotal treat B. canis, combined antibiotic regimes
enlargement (see Brucellosis). • Rapid slide generally more successful; treatments may fail
agglutination test (RSAT)—screening test; to completely clear infection. • Reported
sensitive but not specific. • Due to occurrence success with doxycycline (10 mg/kg PO
of false positives with RSAT, retest all q12h), gentamicin (5 mg/kg SC q24h for 7
positives for B. canis with a more specific test days and repeated every 3 weeks), rifampin
method: modified rapid slide agglutination (5 mg/kg PO q24h), or enrofloxacin (5 mg/
test (ME-RSAT), agar gel immunodiffusion kg PO q12h) for 1–3 months.
test (AGID), tube agglutination test (TAT), CONTRAINDICATIONS/POSSIBLE
PCR, or bacterial culture of whole blood or INTERACTIONS
lymph node aspirate. N/A
Epilepsy, Genetic (Idiopathic)—Dogs

or asleep; often at night or early morning; PATHOLOGIC FINDINGS
frequency tends to increase if left untreated; • No primary lesion. • Secondary neuronal
affected animal falls on its side, becomes stiff, loss and gliosis from prolonged seizures.
BASICS chomps its jaw, salivates profusely, urinates,
DEFINITION defecates, vocalizes, and paddles with all limbs
E Syndrome that is only epilepsy, with no in varying combinations; short duration
demonstrable underlying brain lesion or other (30–90 seconds). • Postictal behavior—
confusion, disorientation; aimless, compulsive,
TREATMENT
neurologic signs or symptoms; age-related;
assumed genetic. The term “idiopathic” blind, pacing; frequent polydipsia and APPROPRIATE HEALTH CARE
replaced by “genetic” according to the polyphagia; recovery immediate or may take • Outpatient—recurrence of isolated seizures.
International League Against Epilepsy (ILAE) up to 24 hours. • Dogs with established • Inpatient—for cluster seizures (>1 seizure
classification (see Appendix IX). epilepsy might have clustered generalized q24h) or status epilepticus.
seizures at intervals of 1–4 weeks. • No NURSING CARE
PATHOPHYSIOLOGY
asymmetry should be observed during seizure, Inpatients with seizure disorders require
• Exact mechanism unknown. • Likely
e.g., twitching more pronounced on one side, constant monitoring.
different mechanisms between breeds.
limb contractions on one side, compulsive
SYSTEMS AFFECTED circling just prior to or after the seizure. DIET
Nervous • Stimulus-induced seizures—seizures only • Dogs on chronic phenobarbital (PB) and
upon specific stimulus (sound, event). potassium bromide (KBr) treatment often
GENETICS become overweight; weight-reducing program
Genetic basis suspected in Australian shepherd, Physical Examination Findings as necessary. • KBr treatment—insure steady
beagle, Belgian shepherd (Groenendael and • Patients often have recovered at time of levels of salt in diet; increase in salt causes
Tervuren), Bernese mountain dog, border presentation. • Patients may have postictal increase in bromide excretion preferentially
collie, dachshund, English springer spaniel, behavior. over chloride, with subsequent decreased
Finnish spitz, German shepherd, golden serum KBr levels; alternatively, decreased salt
CAUSES
retriever, keeshond, Irish wolfhound, Italian content increases KBr serum level. • Trial
Genetic in some breeds; of unknown cause in
spinone, Labrador retriever, Shetland with high-fat, low-carbohydrate diet—no
others.
sheepdog, standard poodle, vizsla. improvement in seizure control.
RISK FACTORS
INCIDENCE/PREVALENCE CLIENT EDUCATION
Known epilepsy in the family line.
0.5–2.3% of all dogs. • Severe cluster seizures and status epilepticus
GEOGRAPHIC DISTRIBUTION are life-threatening emergencies requiring
Widespread immediate medical attention. • Keep seizure
calendar noting date, time, length, and
SIGNALMENT DIAGNOSIS severity of seizures to assess response to
Species DIFFERENTIAL DIAGNOSIS treatment. • Once treatment instituted,
Dog • Seizure pattern (breed, age at onset, type and medication is lifelong in most cases. • Abrupt
Breed Predilections frequency of seizures)—most important factor drug withdrawal may cause seizures.
Beagles; all shepherds (German, Australian, toward diagnosis. • Acute onset of cluster
Belgian); Bernese mountain dogs; boxers; seizures or status epilepticus—rule out toxicity
cocker spaniels; border collies; dachshunds; or structural brain disease. • >2 seizures within
golden retrievers; Irish setters; Labrador the first week of onset—consider diagnosis
other than genetic epilepsy. • Seizures at <6
MEDICATIONS
retrievers; poodles (all sizes); Saint Bernards;
Shetland sheepdogs; Siberian huskies; months or >5 years of age—consider metabolic DRUG(S) OF CHOICE
springer spaniels; Welsh corgis; wirehaired fox or intracranial structural disease; rule out • Initiate treatment at second generalized
terriers. Can occur in any breed. hypoglycemia in older dogs. • Focal seizures or seizure if dog <2 years; when interictal period
presence of neurologic deficits—rule out gradually shortens in others. • Antiepileptic
Mean Age and Range intracranial structural disease. treatment—decreases frequency, severity, and
• Mean age 10 months–3 years. • Range 6 length of seizures; perfect control rarely
months–5 years. CBC/BIOCHEMISTRY/URINALYSIS
achieved. • Tolerance and refractoriness to
• Usually normal. • Perform before initiating
Predominant Sex treatment may develop.
drug therapy as baseline data.
Male predisposition in Bernese mountain dog. Phenobarbital
SIGNS • Most efficacious antiepileptic drug (AED)
Bile acids to rule out hepatic encephalopathy
in the dog. • Traditional first-line drug; initial
General Comments unnecessary in dogs with seizures without
dosage 3–5 mg/kg PO q12h; steady state
• Seizures may be generalized (convulsive) accompanying episodic abnormal behavior.
reached at 12–15 days, but levels decrease
from onset, or have a short aura (focal onset) IMAGING significantly in first 6 months owing to
with rapid secondary generalization. • An MRI—if seizure pattern does not fit genetic activation of lysosomal enzymes. • Optimal
aura (animal appears frightened, dazed, seeks (idiopathic) epilepsy, neurologic deficits are therapeutic serum levels—100–120 μmol/L or
attention, or hides, etc.) frequently precedes present, or intracranial structural disease is 23–28 μg/mL. • Oral loading dose (if
the generalized seizure. • Focal seizures suspected. needed)—6–10 mg/kg PO q12h for 2–3 days
reported in the border collie, Finnish spitz,
DIAGNOSTIC PROCEDURES to reach therapeutic range rapidly.
English springer spaniel, Labrador retriever,
viszla, Belgian shepherd, standard poodle. • Cerebrospinal fluid (CSF)—for suspected Zonisamide
structural intracranial diseases. First-line drug when seizure frequency allows
Historical Findings • Electroencephalography—may see interictal (<1/week); 5 mg/kg PO q12h; 10 mg/kg PO
• First seizure—between 6 months and 5 spikes, polyspikes, and spike slow wave q12h as add-on to PB; half-life 15 hours;
years. • Seizures—often when patient is resting complexes.
(continued) Epilepsy, Genetic (Idiopathic)—Dogs

steady state 4 days; therapeutic range in • Phenytoin, valproic acid, carbamazepine, renal tubular acidosis and one case of acute
human 10–45 μg/mL. and ethosuximide—unsuitable pharmaco idiosyncratic hepatic necrosis reported.
Levetiracetam kinetics in dogs. • Others—acupuncture, • Levetiracetam—transient sedation.
First-line drug when seizures have focal onset; vagal nerve stimulation, transcranial magnetic EXPECTED COURSE AND PROGNOSIS
motor stimulation. • CBD-infused oil 2.5
<1 seizure/week; 20–70 mg/kg (smaller
mg/kg (1.1 mg/lb) q12h.
• Treatment for life. • Some dogs are well E
breeds require higher dosage) PO q8h; must controlled with same drug and dosage for
be given q8h to reach adequate levels; no years; others remain poorly controlled despite
hepatic metabolism; safe; steady state 3 days; polypharmacy. • Patient may develop status
therapeutic range in human 10–40 μg/mL. epilepticus and die. • Early treatment does
Potassium Bromide FOLLOW-UP not decrease occurrence of status epilepticus.
• Normal expected lifespan, but survival time
• Traditional first-line drug; initial dosage PATIENT MONITORING
30 mg/kg PO q24h or divided q12h; half-life shorter if episodes of status epilepticus.
• Serum drug levels—preferentially at trough,
24–46 days; steady state 3–4 months; varies • Treatment with 2 AEDs not linked to poor
at same time for each sampling; use same
with salt concentration in diet; bioavailability prognosis. • Increased risk of premature
laboratory. • Phenobarbital—measure PB
differs between dogs. • Optimal therapeutic death. • Marked breed differences in
level 4 weeks after initiating therapy; adjust
serum levels—20–25 mmol/L or 1.6–2 mg/ incidence and mortality rates. • Prognosis
dose as needed; then repeat level every 2
mL; if sole antiepileptic drug, 25–32 mmol/L depends on combined veterinary expertise,
weeks until optimal levels reached; with
or 2–2.25 mg/mL can be safely used. • Add therapeutic success, and owner’s motivation.
chronic use perform CBC, biochemistry, and
on to PB if seizures uncontrolled with PB level every 6–12 months; tabulate
optimal PB level—beneficial and synergistic albumin, liver enzymes, and serum drug levels
effect. • Loading dose—may cause vomiting, to monitor trend; drug essentially hepatotoxic;
diarrhea, profound longstanding sedation; if most dogs eventually develop hepatotoxicity MISCELLANEOUS
needed, double daily PO doses for 2 weeks. if serum levels >140 μmol/L (>33 μg/mL) for ASSOCIATED CONDITIONS
• Renal insufficiency decreases bromide long time (>6–8 months); if hepatotoxicity Idiopathic epilepsy can be a reason for
elimination; half initial dosage. suspected, perform bile acids. • KBr—serum euthyroid sick syndrome in dogs.
Diazepam (At-Home Use) level (along with PB level) 4–6 weeks after
initiating (should be 8–12 mmol/L or AGE-RELATED FACTORS
• To abort ongoing seizures—dogs with cluster
0.5–1 mg/mL) and at 3–4 months; if diet If onset <2 years of age, epilepsy more likely
seizures or status epilepticus. • Insert 0.5–1 mg/kg
change required, consider diet salt content; to be difficult to control; condition may
injectable drug in rectum (or intranasal) via 1
monitor level accordingly; monitor KBr level become intractable.
inch teat cannula as soon as a seizure occurs;
repeat 20 and 40 minutes later for a total of 3 closely if renal insufficiency (isosthenuria or PREGNANCY/FERTILITY/BREEDING
insertions within 40 minutes; can be safely azotemia). • Zonisamide—measure level at 1 • Avoid breeding affected animals. • Reported
repeated once more in 24h period. • Given week; monitor electrolytes and acid-base association between estrus and onset of
early in course of ongoing seizures, helps abort status to check for renal tubular acidosis. seizures in intact bitches with presumptive
subsequent seizures. • Intransal midazolam can • Levetiracetam—measure level at 4 days. “idiopathic” epilepsy; two hormonally based
also be used 0.5 mg/kg. Can be repeated once PREVENTION/AVOIDANCE patterns recognized: during heat; and during
after 20 minutes. • Abrupt discontinuation of medication may a specific time point at the end of diestrus.
CONTRAINDICATIONS precipitate seizures. • Avoid salty treats in SEE ALSO
Aminophylline, theophylline. dogs treated with KBr. • Seizures (Convulsions, Status Epilepticus)—
POSSIBLE COMPLICATIONS Cats. • Seizures (Convulsions, Status
PRECAUTIONS
• Recurrent episodes of cluster seizures and epilepticus)—Dogs.
α-adrenergic agonists (e.g., phenylpropanola-
mine)—CNS excitation. status epilepticus. • PB and KBr—polyuria, ABBREVIATIONS
polydipsia, polyphagia, weight gain. • AED = antiepileptic drug.
POSSIBLE INTERACTIONS • Phenobarbital-induced corticosteroid • ALT = alanine aminotransferase. • C-AP =
• Cimetidine and chloramphenicol—interfere alkaline phosphatase (C-AP) elevation occurs corticosteroid alkaline phosphatase. • CSF =
with PB metabolism; may cause toxic PB levels. frequently; may be early sign of hepatotoxicity, cerebrospinal fluid. • ILAE = International
• PB lowers serum levels of zonisamide and but of less concern if alanine aminotransferase League Against Epilepsy. • KBr = potassium
levetiracetam. • PB may lower T4 and cause (ALT) is within reference range. • PB-induced bromide. • PB = phenobarbital. • TSH =
upward trend in thyroid-stimulating hormore hepatotoxicity—after chronic treatment at thyroid-stimulating hormone.
(TSH) without signs of hypothyroidism. • PB high serum levels (>140 μmol/L or >33 μg/
does not interfere with low-dose mL); often insidious in onset; only biochemical INTERNET RESOURCES
dexamethasone suppression tests regardless of abnormality may be decreased albumin. http://www.canine-epilepsy.net
dose and treatment. • Zonisamide decreases • Higher incidence of pancreatitis in patients Suggested Reading
total T4. • Whenever animals on lifetime treated with PB and/or KBr; once pancreatitis Muñana KR. Management of refractory epilepsy.
medication, refer to manufacturer’s drug profile develops, recurrence is frequent. Top Companion Anim Med 2013, 28:67–71.
or to pharmacist for interaction information. • Phenobarbital—rare bone marrow suppression Podell M. Antiepileptic drug therapy and
ALTERNATIVE DRUG(S) with severe neutropenia (± sepsis) early in monitoring. Top Companion Anim Med
• With polypharmacy, initiate add-on course of treatment; discontinue drug. 2013, 28:59–66.
gradually to avoid sedation. • Gabapentin • Paradoxical hyperexcitability; discontinue Author Joane M. Parent.
10–20 mg/kg PO q8h; low efficacy as drug; risk factor for superficial necrolytic
add-on; newer analog pregabalin may be dermatitis. • KBr—when levels are >22 mmol/L
more efficacious, 2–4 mg/kg q8h PO. or >1.8 mg/mL, owners may complain of Client Education Handout
• Clorazepate 0.5–1 mg/kg PO q8h. patient’s unsteadiness while managing stairs. available online
• Felbamate 30–70 mg/kg q12h–8h. • Zonisamide—mild sedation, decreased
• Topiramate 2–10 mg/kg PO q12h. appetite, gastrointestinal signs. • One case of
Epiphora
Obstruction of the Nasolacrimal IMAGING
Drainage System • Skull radiographs—may show a nasal,
sinus, or maxillary bone lesion.
BASICS Congenital • Dacryocystorhinography—radiopaque
• Imperforate nasolacrimal puncta—Bedlington
DEFINITION contrast material to help localize obstruction.
E Abnormal overflow of the aqueous portion of
terriers, cocker spaniels, bulldogs, poodles. • MRI or CT—may help localize obstruction
• Ectopic nasolacrimal openings—extra
the precorneal tear film. (usually with contrast media) and characterize
openings along the side of the face ventral to associated lesions.
PATHOPHYSIOLOGY the medial canthus.
Caused by one of three common problems: • Nasolacrimal atresia—lack of distal DIAGNOSTIC PROCEDURES
overproduction of the aqueous portion of tears openings into the nose. • Bacterial culture and sensitivity testing and
(usually in response to ocular irritation); poor • Punctal displacement. cytologic examination of purulent material from
eyelid function secondary to eyelid malforma- • Lack of ventral canaliculus, nasolacrimal the puncta (e.g., dacryocystitis); performed
tion, breed conformation, or deformity; or sac, or nasolacrimal duct. before instilling any substance into the eye.
blockage of the nasolacrimal drainage system. • Jones test—topical fluorescein dye
Acquired application to the eye; most physiologic test
SYSTEMS AFFECTED • Rhinitis or sinusitis—causes swelling
for nasolacrimal function; should be
Eye and periocular skin. adjacent to the nasolacrimal duct. performed first (after culture); dye flows
SIGNALMENT • Trauma—resulting in fractures of the
through the nasolacrimal system and reaches
Dogs and (less frequently) cats. See Causes. lacrimal or maxillary bones or laceration of the external nares in approximately 10
the nasolacrimal duct. seconds (or longer) in normal dogs, 15
SIGNS • Foreign bodies—grass awns, seeds, sand,
N/A seconds to 1 minute in cats.
parasites. • Nasolacrimal irrigation—see below.
CAUSES • Neoplasia—of third eyelid, conjunctiva,
• Rhinoscopy—with or without biopsy or
medial eyelids, nasal cavity, maxillary bone, or bacterial culture; may be indicated if previous
Overproduction of Tears Secondary periocular sinuses causing invasion or
to Ocular Irritants tests suggest a nasal or sinus lesion.
compression of the nasolacrimal system. • Exploratory surgery—may be the only way
Congenital • Dacryocystitis—inflammation of canaliculi,
to obtain a definitive diagnosis.
• Distichiasis or trichiasis—common in lacrimal sac, or nasolacrimal ducts. • Temporary tacking out of the lower medial
young Shetland sheepdogs, shih tzus, Lhasa RISK FACTORS eyelid with suture—may help determine
apsos, cocker spaniels, miniature poodles. • Breeds prone to congenital eyelid abnormalities whether repair of medial lower entropion or
• Entropion—Chinese Shar-Peis, chow (see Causes). repositioning of the eyelid would reduce
chows, Labrador retrievers. • Active outdoor dogs—at risk for foreign epiphora secondary to eyelid conformational
• Eyelid agenesis—domestic shorthair cats. bodies. abnormalities.
Acquired Nasolacrimal Irrigation
• Corneal or conjunctival foreign bodies— • Confirms obstruction.
usually young, large-breed, active, outdoor • May dislodge foreign material.
dogs.
• Eyelid neoplasms—old dogs (all breeds).
DIAGNOSIS • A nasolacrimal cannula or 22- or 24-gauge
IV catheter without stylet is inserted into the
• Blepharitis—infectious or immune DIFFERENTIAL DIAGNOSIS upper nasolacrimal punctum.
mediated. • Other ocular discharges (e.g., mucous or
• Eyewash in a 6 ml syringe is attached and
• Conjunctivitis—infectious or immune purulent)—epiphora is a watery, serous irrigated through the cannula or catheter—if
mediated. discharge. fluid does not exit the lower nasolacrimal
• Ulcerative keratitis (traumatic or viral). • Primary ocular abnormalities—usually the
punctum, the obstruction is in the upper or
• Anterior uveitis. eye is red when the epiphora is caused by lower canaliculi, the nasolacrimal sac, or the
• Glaucoma. overproduction and quiet when secondary to lower punctum (imperforate).
impaired outflow. • Lower punctum is manually obstructed—if
Eyelid Abnormalities or Poor Eyelid
• Irritative causes and some congenital causes
Function flushed fluid does not exit the external nares,
of obstruction—thorough ocular examination. the obstruction is in the nasolacrimal duct or
• Abnormal eyelid function does not direct • Acute onset, unilateral condition with
tears toward the medial canthus and naso- at its distal opening (atresia or blockage from
ocular pain (blepharospasm)—usually a nasal sinus lesion).
lacrimal puncta. indicates a foreign body or corneal injury.
• Tears never reach the nasolacrimal puncta • Chronic, bilateral condition—usually
and subsequently spill over the eyelid margin. indicates a congenital problem.
Congenital • Facial pain, swelling, nasal discharge, or
• Macropalpebral fissures—brachycephalic sneezing—may indicate nasal or sinus infection; TREATMENT
breeds. may indicate obstruction from neoplasm. • Remove cause of ocular irritation—removal
• Ectropion—Great Danes; bloodhounds; • With mucous or purulent discharge at of a conjunctival or corneal foreign body,
spaniels. the medial canthus—may indicate treatment of the primary ocular disease (e.g.,
• Entropion—brachycephalic dogs: medial dacryocystitis. conjunctivitis, ulcerative keratitis, and
lower eyelid; Labrador retrievers: lateral lower CBC/BIOCHEMISTRY/URINALYSIS uveitis), cryosurgery or electroepilation for
eyelid. N/A distichiasis, entropion correction, medial or
lateral canthoplasty (for medial trichiasis and
Acquired OTHER LABORATORY TESTS macropalpebral fissures), correction of
• Post-traumatic eyelid scarring. N/A cicatricial eyelid abnormalities.
• Facial nerve paralysis.
(continued) Epiphora
• Treat primary obstruction (e.g., third eyelid PRECAUTIONS or closure of the dacryocystorhinotomy or
mass, nasal or sinus mass, and infection)— N/A conjunctivorhinostomy openings into the
successful management may allow normal POSSIBLE INTERACTIONS nasal cavity.
nasolacrimal flow to resume. N/A
• In patients predisposed to nasolacrimal
obstruction, recurrence is common.
E
• Inform client that early detection and
intervention provide better long-term prognosis. MISCELLANEOUS
SURGICAL CONSIDERATIONS FOLLOW-UP ASSOCIATED CONDITIONS
• Chronic conjunctivitis.
Imperforate Puncta PATIENT MONITORING
• Recurrent eye “infections.”
• Surgical opening of the puncta is indicated. Dacryocystitis • Moist dermatitis (hot spots) ventral to the
• If one of the puncta is patent (usually the • Reevaluate every 7 days until the condition medial canthus.
upper punctum), flushing eyewash through is resolved. • Nasal discharge.
the upper opening will cause “tenting” of the • Continue treatment for at least 7 days after
conjunctiva at the site of the lower punctum. resolution of clinical signs. AGE-RELATED FACTORS
Place patient under topical or general • If problem persists more than 7–10 days
N/A
anesthesia. Grasp conjunctiva overlying the with treatment or recurs soon after ZOONOTIC POTENTIAL
lower canaliculi with forceps and cut with cessation of treatment—indicates a foreign N/A
scissors to leave a patent punctum. body or nidus of persistent infection; PREGNANCY/FERTILITY/BREEDING
• Puncta closed by conjunctival scarring requires further diagnostics (e.g., N/A
(symblepharon) caused by severe conjunctivi- dacryocystorhinography).
tis (e.g., herpesvirus conjunctivitis in cats)— • Nasolacrimal catheter; commonly required SEE ALSO
use same procedure. for persistent dacryocystitis, maintains • Conjunctivitis—Cats.
• Recurrent disease—may be necessary to patency of the duct and prevents stricturing. • Conjunctivitis—Dogs.
suture Silastic® tubing in place to prevent • Procedure—pass 2-0 nylon via the upper • Eyelash Disorders (Trichiasis/Distichiasis/
stricture formation. punctum and thread it through the nasolacri- Ectopic Cilia).
mal duct to exit the external nares; pass • Keratitis—Ulcerative.
Obstructed or Obliterated Distal
Silastic or polyethylene (PE90) tubing • Third Eyelid Protrusion.
Nasolacrimal Duct
retrograde over the suture; suture the upper Suggested Reading
• Dacryocystorhinotomy, conjunctivorhinos-
and lower portions of the tubing to the face. Binder DR, Herring IP. Evaluation of
tomy, conjunctival maxiallary sinusostomy, Most dogs tolerate the tubing well; however,
conjunctival buccostomy—create an opening to nasolacrimal fluorescein transit time in
an Elizabethan collar may be needed to ophthalmically normal dogs and
drain the tears into the nasal cavity or oral cavity. prevent self-trauma. Continue topical
• See Suggested Reading for surgical nonbracycephalic cats. Am J Vet Res 2010,
antibiotics as before. Leave in place 2–4 71:570–574.
technique. weeks. Giuliano EA. Diseases and surgery of the
Dacryocystorhinotomy/ canine nasolacrimal system. In: Gelatt KN,
Conjunctivorhinostomy Gilger BC, Kern T, eds., Veterinary
• Tubing—reevaluate every 7 days to ensure
Ophthalmology, 5th ed. Ames, IA:
MEDICATIONS it remains intact; may need to resuture if it Wiley-Blackwell, 2013, pp. 912–944.
DRUG(S) OF CHOICE becomes loosened or dislodged. Miller PE. Lacrimal system. In: Maggs DJ,
• Topical broad-spectrum antibiotic ophthalmic • After tubing has been removed—reevaluate
Miller PE, Ofri R, Slatter’s Fundamentals of
solutions—while awaiting results of bacterial in 14 days; for this and future examinations, Veterinary Ophthalmology, 6th ed. St.
culture; q4–6h; may try neomycin, gramicidin, place fluorescein on the eye and check naso- Louis, MO: Elsevier, 2018, pp. 186–-203.
polymyxin B triple ophthalmic antibiotic lacrimal patency by examining the external Author Silvia G. Pryor
solution, or ophthalmic ciprofloxacin solution. nares for fluorescein; may evaluate further by Consulting Editor Kathern E. Myrna
• Dacryocystitis—based on bacterial culture cannulating and flushing with eyewash. Acknowledgment The author and book
and sensitivity test results; continue antibiotic • Dacryocystorhinography contrast study—
therapy for at least 21 days. repeated 3–4 months after surgery to evaluate Brian C. Gilger.
CONTRAINDICATIONS size of nasal opening; repeated for recurrence

• Topical corticosteroids or antibiotic–corti- or with no nasolacrimal fluorescein drainage.
costeroid combinations—avoid unless a POSSIBLE COMPLICATIONS available online
definitive diagnosis has been made. Recurrence—most common complication;
• Topical corticosteroids—never use if the caused by recurrence of ocular irritation
cornea retains fluorescein stain (corneal ulcer (e.g., corneal ulceration, distichiasis,
present). entropion), recurrence of dacryocystitis,
Episcleritis
• Secondary—may see abnormalities • Azathioprine—may induce potentially fatal
consistent with systemic disease. myelosuppression, hepatotoxicosis.
• Niacin—do not substitute for niacinamide.
BASICS OTHER LABORATORY TESTS
Serologic testing—may help diagnose fungal
E OVERVIEW infection.
• Focal or diffuse infiltration of episclera and/
or scleral stroma by inflammatory cells and IMAGING
fibroblasts. • Abdominal ultrasound, thoracic and FOLLOW-UP
• Primary—affects only the eye; probably abdominal radiographs—may help rule out PATIENT MONITORING
immune mediated; appears either as a fungal infection or disseminated neoplasia. • Primary—monitor for nodule regression or
perilimbal episcleral/scleral nodule (nodular • Ocular ultrasound—may reveal other reduction in episcleral thickening or reddening
episcleritis) or as a diffuse thickening of the abnormalities if ocular media opacities every 2–3 weeks for 6–9 weeks and then as
episclera (diffuse episcleritis); nodular form may prevent thorough ocular examination. needed; prognosis usually good; may require
affect cornea and third eyelid with nodules. DIAGNOSTIC PROCEDURES therapy for months to rest of life.
• Secondary—usually diffuse; from spillover • Incisional biopsy and histopathologic • Secondary—follow-up, prognosis, and
of inflammatory cells into the episclera from examination of affected tissue. complications depend on primary disease.
other ocular disorders (e.g., endophthalmitis • Nodular—varying numbers of histiocytes, • Azathioprine—repeat CBC, platelet count,
and panophthalmitis); may affect virtually lymphocytes, plasma cells, and fibroblasts. and measurement of liver enzymes every 1–2
any other organ system. • If uveitis prominent—see Anterior weeks for first 8 weeks, then periodically.
SIGNALMENT Uveitis—Dogs. POSSIBLE COMPLICATIONS
• Dog. • Vision loss.
• Young to middle-aged collie, Shetland • Chronic ocular pain.
sheepdog. • Uveitis.
• Secondary glaucoma.
SIGNS TREATMENT
• Nodular—typically appears as a smooth, • Verify the diagnosis histologically or
painless, localized, raised, pink-tan, firm cytologically before treatment.
episcleral/scleral mass. • Primary nodular—benign course; observa-
• Diffuse—less common; appears as a diffuse tion alone may be appropriate with mild MISCELLANEOUS
reddening and thickening of the entire disease.
• Outpatient treatment if ocular pain, diffuse SYNONYMS
episclera/sclera; accompanied by variable
scleral involvement, eyelid function is • Collie granuloma.
amounts of ocular pain.
disrupted, cornea is affected, or vision is • Fibrous histiocytoma.
• Secondary—uveitis often pronounced.
threatened. • Limbal granuloma.
• Conjunctiva—usually moves freely over the
• Necrogranulomatous sclerouveitis.
surface of the lesion.
• Nodular fasciitis.
• Nodules—tend to be slowly progressive,
• Nodular granulomatous episcleritis.
bilateral, and prone to recurrence.
• Proliferative keratoconjunctivitis.
CAUSES & RISK FACTORS MEDICATIONS Suggested Reading
• Nodular and diffuse primary—idiopathic;
DRUG(S) OF CHOICE Maggs DJ. Diseases of the cornea and sclera.
believed to be immune mediated.
• Progress down the list only if the previous In: Maggs DJ, Miller PE, Ofri R, Slatter’s
• Secondary—may result from deep fungal or
modality was ineffective. Fundamentals of Veterinary
bacterial ocular infection, lymphoma,
• Topical 1% prednisolone acetate q4h for Ophthalmology, 6th ed. St. Louis, MO:
systemic histiocytosis in Bernese mountain
1 week, then q6h for 2 weeks, then Elsevier 2018, pp. 213–253.
dogs, chronic glaucoma, and ocular trauma.
tapered. Rothstein E, Scott DW, Riis RC. Tetracycline
• Systemic prednisolone 1–2 mg/kg/day PO; and niacinamide for the treatment of sterile
taper with improvement. pyogranuloma/granuloma syndrome in a dog.
• Systemic azathioprine 1–2 mg/kg/day PO for J Am Anim Hosp Assoc 1997, 33:540–543.
DIAGNOSIS 3–7 days; then tapered to as low as possible. Author Paul E. Miller
• Cryosurgery or attempted excision. Consulting Editor Kathern E. Myrna
• Alternative to listed drugs or surgery—may
• Other causes of a red eye—differentiated by
try a combination of tetracycline and niacina-
complete ophthalmic examination.
mide (q8h PO); 250 mg each for dogs <10 kg;
• Other mass-like lesions—differentiated by
500 mg each for dogs >10 kg; may not observe
biopsy or cytologic examination.
good clinical response for at least 8 weeks; side
• Neoplasia—lymphoma, squamous cell
effects uncommon and primarily the result of
carcinoma, extension of intraocular mass,
gastrointestinal upset by niacinamide.
other tumors.
• Granuloma—deep fungal infection, CONTRAINDICATIONS/POSSIBLE
retained foreign body. INTERACTIONS
• Granulation tissue—trauma, healing corneal • Avoid systemic immunosuppressive drugs
ulcer, globe perforation with uveal prolapse. with fungal infections.
CBC/BIOCHEMISTRY/URINALYSIS • Systemically administered prednisolone—
• Usually normal if lesion is confined to eye may precipitate pancreatitis, iatrogenic
or adnexa. hyperadrenocorticism.
Epistaxis
• Bone marrow disease—neoplasia; aplastic
anemia; infectious (fungal, rickettsial, or viral).
• Paraneoplastic disorder.
BASICS • Disseminated intravascular coagulation DIAGNOSIS
DEFINITION (DIC). DIFFERENTIAL DIAGNOSIS
Bleeding from the nose. See Causes.
E
Thrombopathia
PATHOPHYSIOLOGY • Congenital—von Willebrand disease; CBC/BIOCHEMISTRY/URINALYSIS
Results from one of three abnormalities— thrombasthenia; thrombopathia. • Anemia—if enough hemorrhage has
coagulopathy; local disease or space- • Acquired—nonsteroidal anti-inflammatory occurred.
occupying lesion; vascular or systemic disease. drugs (NSAIDs); clopidogrel; hyperglobulinemia • Thrombocytopenia—possible.
(Ehrlichia, multiple myeloma); uremia; DIC. • Neutrophilia—infection; neoplasia.
SYSTEMS AFFECTED
Coagulation Factor Defects • Pancytopenia—if bone marrow disease.
• Respiratory—hemorrhage; sneezing
• Congenital—hemophilia A (factor VIIIc • Hypoproteinemia—if enough hemorrhage
• Gastrointestinal (GI)—melena.
• Hemic/lymphatic/immune—anemia. deficiency) and hemophilia B (factor IX has occurred.
deficiency). • High blood urea nitrogen (BUN) with
GENETICS normal creatinine—possible, owing to blood
• Acquired—anticoagulant rodenticide
Varies depending on underlying cause. ingestion.
(warfarin) intoxication, hepatobiliary
INCIDENCE/PREVALENCE disease, DIC. • Hyperglobulinemia—possible with
Varies depending on underlying cause. ehrlichiosis, multiple myeloma.
Local Lesion • Azotemia—with renal failure-induced
SIGNALMENT • Foreign body. hypertension.
Species • Trauma. • High alanine transaminase (ALT), aspartate
Dog and cat. • Infection—fungal (Aspergillus, Cryptococcus, aminotransferase (AST), and total bilirubin—
Rhinosporidium); viral or bacterial. Usually with coagulopathy from severe hepatic disease.
Age, Breed, and Sex Predilections blood-tinged mucopurulent exudate rather • Urinalysis—usually normal; possible to see
Vary depending on underlying cause. than frank hemorrhage. hematuria (if coagulopathy), isosthenuria (if
SIGNS • Neoplasia—adenocarcinoma; carcinoma; renal failure–induced hypertension), and
chondrosarcoma; squamous cell carcinoma; proteinuria (if glomerulotubular disease and
Historical Findings
fibrosarcoma; lymphoma; transmissible hypertension).
• Nasal hemorrhage—unilateral or bilateral
venereal tumor.
possible. OTHER LABORATORY TESTS
• Dental disease—oronasal fistula, tooth root
• Sneezing and/or stertorous respiration. • Coagulation profile—prolonged times with
abscess.
• Melena. coagulation factor defects; normal with
• Lymphoplasmacytic rhinitis.
• With coagulopathy—hematochezia, thrombocytopenia and thrombopathia.
melena, hematuria, or hemorrhage from other Vascular or Systemic Disease • Platelet function testing (e.g., buccal
areas of the body. • Hypertension—renal disease; hyperthyroid mucosal bleeding time, von Willebrand factor
• With hypertension—possibly blindness, ism; hyperadrenocorticism; pheochromocy- analysis)—may be abnormal with platelet
intraocular hemorrhage, neurologic signs, toma; idiopathic disease. dysfunction (platelet count and coagulation
cardiac or renal signs. • Hyperviscosity—hyperglobulinemia profile may be normal).
(multiple myeloma, Ehrlichia); polycythemia. • Ehrlichia, Anaplasma, Rocky Mountain
• Vasculitis—immune-mediated and rickettsial spotted fever, or Babesia testing—may be
• Nasal hemorrhage.
diseases. positive in thrombocytopenia or thrombo
• Melena—from swallowing blood or
concurrent upper GI hemorrhage. RISK FACTORS pathia-induced epistaxis.
• Nasal stridor—may be present with • Aspergillus serology—may help establish a
Coagulopathy
neoplasia, foreign body, or advanced diagnosis of fungal rhinitis; false-negative results
• Immune-mediated disease—young to middle-
inflammatory disease. are common, so results must be interpreted in
aged, small-to medium-sized female dogs.
• With coagulopathy—possibly petechiae, light of other clinical and diagnostic findings.
• Infectious disease—dogs living in or traveling
ecchymosis, hematomas, intracavitary bleeds, • Thyroid hormone assay—elevated in cats
to endemic areas; tick exposure.
hematochezia, melena, and hematuria. with epistaxis due to hyperthyroid-induced
• Thrombasthenia—otter hounds.
• With coagulopathy or hypertension— hypertension.
• Thrombopathia—basset hounds, spitz.
possibly retinal or intraocular hemorrhages or • von Willebrand disease—Doberman IMAGING
retinal detachment; with hypertension— pinschers, Airedales, German shepherds, • Thoracic radiograph—screen for metastasis.
possibly heart murmur or arrhythmia. Scottish terriers, Chesapeake Bay retrievers, and • Nasal series—under anesthesia, including
CAUSES many other breeds; cats. open-mouth ventrodorsal and skyline sinus
• Hemophilia A—German shepherds and views when space-occupying or local lesion is
Coagulopathy suspected; osteolysis with neoplasia and
many other breeds; cats.
Thrombocytopenia • Hemophilia B—Cairn terriers, coonhounds, fungal sinusitis; foreign bodies usually not
• Immune-mediated disease—idiopathic Saint Bernards, and other breeds; cats. seen; dental disease may be identified.
disease; drug reaction; modified live virus • CT or MRI—more sensitive than
Space-Occupying Lesions
(MLV) vaccine reaction. radiographs.
• Aspergillosis—German shepherds,
• Infectious disease—ehrlichiosis;
Rottweilers, mesocephalic and dolichocephalic DIAGNOSTIC PROCEDURES
anaplasmosis; Rocky Mountain spotted fever, • Blood pressure evaluation—indicated when
breeds.
babesiosis, feline leukemia virus (FeLV) or coagulopathies and space-occupying lesions
• Neoplasia—dolichocephalic breeds.
feline immunodeficiency virus (FIV)-related have been ruled out and particularly when
illness. azotemia or proteinuria is noted.
Epistaxis (continued)
• Rhinoscopy, nasal lavage, nasal biopsy (blind • Infectious disease—rickettsial disease • Beta blockers—propranolol (0.5–1 mg/kg
or guided via rhinoscopy or CT)—indicated (doxycycline 5 mg/kg PO q12h for 3–6 q8h); atenolol (0.25–1.0 mg/kg q12–24h).
for space-occupying disease; aimed at removing weeks); Babesia (imidocarb 6.6 mg/kg SC 2 • Diuretics—hydrochlorothiazide (2–4 mg/
foreign bodies and evaluating and sampling doses 2 weeks apart, diminazene aceturate kg q12h); furosemide (0.5–2 mg/kg q8–12h).
nasal tissue for causal diagnosis (e.g., evaluate 5 mg/kg IM once, or 10 days of atovaquone • Phenoxybenzamine (0.2–1.5 mg/kg q12h)
E nasal tissue samples for neoplasia, inflamm 13.3 mg/kg PO q8h with azithromycin for pheochromocytoma.
ation, and infection via cytology and/or 10 mg/kg PO q24h). CONTRAINDICATIONS
histopathology and bacterial/fungal culture • Bone marrow neoplasia—see • Avoid drugs that may predispose patient to
and sensitivity testing). Myeloproliferative Disorders. hemorrhage—NSAIDs; heparin; clopidogrel;
• Bone marrow aspiration biopsy—indicated if • Thrombopathia and thrombasthenia—no phenothiazine tranquilizers.
pancytopenia identified. treatment unless lymphoproliferative disease. • Topical antifungals—do not use in patients
• von Willebrand disease—plasma or with disruption of the cribriform plate.
cryoprecipitate for acute bleeding; 1-desamino-
8-d-arginine vasopressin (DDAVP) 1 μg/kg PRECAUTIONS
SC/IV diluted in 20 mL 0.9% NaCl given over • Chemotherapeutic drugs (immune-
TREATMENT 10 min may help control or prevent mediated thrombocytopenia therapy, e.g.,
APPROPRIATE HEALTH CARE hemorrhage prior to invasive procedures; azathioprine)—monitor neutrophil counts
• Coagulopathy—usually inpatient intranasal formulation (less expensive) may be and liver enzymes weekly until a pattern has
management. used after passing through a bacteriostatic filter. been established that shows that the patient is
• Space-occupying lesion or vascular or systemic • Hemophilia A—plasma or cryoprecipitate for tolerating the drug.
disease—outpatient or inpatient management, acute bleeding; no long-term treatment. • Enalapril and/or diuretics—closely monitor
depending on disease and its severity. • Hemophilia B—plasma for acute bleeding; patients with renal failure; avoid severe salt
• Nasal tumors—radiotherapy; various no long-term treatment. restriction when using angiotensin-converting
response rates. • Anticoagulant rodenticide intoxication— enzyme (ACE) inhibitors.
plasma for acute bleeding; vitamin K at 5 mg/ • Avoid topical clotrimazole preparations
NURSING CARE
kg loading dose followed by 1.25 mg/kg q12h with propylene glycol, as life-threatening
Provide basic supportive care if needed
for 1 week (if warfarin formulation) to 4 weeks mucosal irritation, ulceration, and naso
(fluids, nutrition).
(longer-acting formulation). pharyngeal swelling can occur.
ACTIVITY • Hyperglobulinemia—plasmapheresis.
Minimize activity or stimuli that precipitate • Polycythemia—phlebotomy; hydroxyurea.
hemorrhage episodes. • Liver disease and DIC—treat and support
CLIENT EDUCATION underlying cause; plasma may be beneficial. FOLLOW-UP
• Inform client about the disease process. Space-Occupying Lesion
• Teach client how to recognize a serious PATIENT MONITORING
• Secondary bacterial infection—antibiotics • Platelet count with thrombocytopenia.
hemorrhage (e.g., weakness, collapse, pallor, based on culture and sensitivity testing.
and blood loss >30 mL/kg bodyweight). • Coagulation profile with coagulation factor
• Fungal infection—for aspergillosis, topical defects.
SURGICAL CONSIDERATIONS treatment of nasal cavity and frontal sinuses • Blood pressure with hypertension.
• Surgery indicated if a foreign body is unable with 1% clotrimazole in polyethylene glycol • Clinical signs.
to be removed by rhinoscopy or blind attempt. (see Precautions) or 1–5% enilconazole (see
• Fungal rhinitis (e.g., Aspergillus and Aspergillosis, Nasal for protocol); for PREVENTION/AVOIDANCE
Rhinosporidium) require debulking (also see cryptococcosis—oral and injectable anti • Restrict access to areas that might contain
Medications). fungal agents (see Cryptococcosis); for anticoagulant rodenticides.
rhinosporidiosis—surgery followed by • Practice dental preventative care.
dapsone (1 mg/kg PO q8h for 2 weeks, then POSSIBLE COMPLICATIONS
1 mg/kg PO q12h for 4 months). Anemia and collapse (rare).
MEDICATIONS Vascular or Systemic Disease EXPECTED COURSE AND PROGNOSIS
• Hyperviscosity—treat underlying disease Varies depending on underlying cause.
DRUG(S) OF CHOICE (e.g., ehrlichiosis, multiple myeloma, or
General polycythemia); plasmapheresis.
• Whole blood, packed red blood cell (RBC), • Vasculitis— doxycycline for rickettsial
or hemoglobin solution transfusion—can be disease (5 mg/kg q12h for 3–6 weeks);
needed with severe anemia. prednisone for immune-mediated disease MISCELLANEOUS
• Acepromazine (0.05–0.1 mg/kg SC/IV if (1.1 mg/kg q12h; taper over 4–6 months). PREGNANCY/FERTILITY/BREEDING
normothermic and no platelet disorder present) Hypertension Avoid teratogenic drugs (e.g., itraconazole).
to lower blood pressure and promote clotting; • Treat underlying disease—renal disease, ABBREVIATIONS
may help control serious hemorrhage. hyperthyroidism, hyperadrenocorticism. • ACE = angiotensin-converting enzyme.
• Discontinue all NSAIDs. • Reduce weight if overconditioned. • ALT = alanine transaminase.
Coagulopathy • Restrict sodium. • AST = aspartate aminotransferase.
• Immune-mediated thrombocytopenia— • Calcium channel blockers—amlodipine • BUN = blood urea nitrogen.
prednisone (1.1 mg/kg q12h; taper over 4–6 (dogs: 0.1 mg/kg PO q12–24h; cats: • DDAVP = 1-desamino-8-d-arginine
months); other drugs can be used in addition 0.625–1.25 mg/cat PO q12–24h); treatment vasopressin.
to prednisone for refractive cases (see of choice. • DIC = disseminated intravascular coagulation.
Thrombocytopenia, Primary Immune • ACE inhibitors—benazepril (0.5 mg/kg • FeLV = feline leukemia virus.
Mediated). q24h); enalapril (0.25–0.5 mg/kg q12–24h). • FIV = feline immunodeficiency virus.
(continued) Epistaxis
• GI = gastrointestinal. and platelet disorders. In: Ettinger SJ, Internal Medicine, 7th ed. St. Louis, MO:
• MLV = modified live virus. Feldman EC, eds., Textbook of Veterinary Saunders Elsevier, 2010, pp. 1030–1040.
• NSAID = nonsteroidal anti-inflammatory Internal Medicine, 7th ed. St. Louis, MO: Author Meghan Vaught
drug. Saunders Elsevier, 2010, pp. 772–783. Consulting Editor Elizabeth Rozanski
• RBC = red blood cell. Dunn ME. Acquired coagulopathies. In: Acknowledgment The author and book
Ettinger SJ, Feldman EC, eds., Textbook of editors acknowledge the prior contribution of
E
Suggested Reading
Bissett SA, Drobatz KJ, McKnight A, Degernes Veterinary Internal Medicine, 7th ed. Mitchell A. Crystal.
LA. Prevalence, clinical features, and causes of St. Louis, MO: Saunders Elsevier, 2010,
epistaxis in dogs: 176 cases (1996–2001). J pp. 797–801.
Am Vet Med Assoc 2007, 231:1843–1850. Venker-van Haagen AJ, Herrtage ME. Diseases Client Education Handout
Brooks MB, Catalfamo JL. Immune-mediated of the nose and nasal sinuses. In: Ettinger SJ, available online
thrombocytopenia, von Willebrand disease, Feldman EC, eds., Textbook of Veterinary
Erythrocytosis
• Greyhounds have higher PCV values endocrine disorders, neoplasms that produce
(reference interval is 50–65%). EPO or an EPO-like substance independent
Mean Age and Range of hypoxia, history of EPO administration.
BASICS • Polycythemia vera—diagnosed by
Primary absolute polycythemia vera—cats
DEFINITION elimination of other causes.
E An increase in packed cell volume (PCV),
6–7 years; dogs 7 years or older.
Predominant Sex CBC/BIOCHEMISTRY/URINALYSIS
hemoglobin concentration, or red blood cell • Increased PCV or hematocrit.
(RBC) count above the reference interval due Male cats, female dogs.
• Physiologic leukocytosis (neutrophilia and
to a relative or absolute increase in the SIGNS lymphocytosis) may occur with splenic
number of circulating RBCs. contraction.
Historical Findings
PATHOPHYSIOLOGY • Relative—excitement or dehydration. OTHER LABORATORY TESTS
• Circulating RBC numbers are affected by • Absolute—lethargy, seizures, altered • Serial monitoring of PCV—diagnosis of
changes in plasma volume, rate of RBC mentation, anorexia, epistaxis, mucous polycythemia vera requires an unexplained
destruction or loss, splenic contraction, membrane hyperemia. high PCV documented on multiple occasions
erythropoietin (EPO) secretion, and bone (several weeks) with no underlying cause.
marrow production. • Arterial blood gas analysis may demonstrate
• Relative—dehydration and clinical evidence
• Erythropoiesis is also affected by hormones a low PaO2 in cases of secondary appropriate
of fluid loss.
from the adrenal cortex, thyroid gland, ovary, absolute erythrocytosis; pulse oximetry may
• Absolute—lethargy, low exercise tolerance,
testis, and anterior pituitary gland; normal also be used to assess oxygen saturation
behavioral change, brick red or cyanotic
PCV is maintained by an endocrine loop. (SpO2).
mucous membranes, sneezing, epistaxis, large
• Erythrocytosis is either relative or absolute. • EPO measurement—not currently
size and tortuosity of retinal and sublingual
• Relative—develops when hemoconcentra- recommended due to lack of veterinary-
vessels, cardiopulmonary impairment.
tion or splenic contraction produces an specific assays and extensive overlap in EPO
• Primary absolute—variable degrees of
increase in circulating RBCs. concentration between normal and affected
splenomegaly, hepatomegaly, thrombosis, and
• Absolute—increase in circulating RBC animals.
hemorrhage; seizures.
mass due to an increase in bone marrow • Thyroid testing (cats).
• Secondary appropriate absolute—clinical
production; either primary or secondary to an
signs of hypoxemia caused by chronic IMAGING
increase in the production of EPO.
pulmonary disease, cardiac disease with Radiography and abdominal ultrasonography
• Primary absolute (polycythemia vera)—
right-to-left shunting, or hemoglobinopathy. to detect cardiopulmonary disease and
myeloproliferative disorder characterized by
• Secondary absolute (inappropriate EPO neoplasia.
neoplastic proliferation of all marrow cell
secretion)—signs associated with neoplasia,
precursors independent of EPO. DIAGNOSTIC PROCEDURES
space-occupying renal lesion, or endocrine
• Secondary absolute—caused by physiologi- • Biopsy of any masses.
disorder.
cally appropriate release of EPO due to • Bone marrow aspirate.
chronic hypoxemia, excessive production of CAUSES
• Relative—hemoconcentration/dehydration PATHOLOGIC FINDINGS
EPO or an EPO-like substance in an animal
or splenic contraction due to excitement. Polycythemia vera—gross findings: general-
with normal partial pressure of oxygen
• Primary absolute—rare myeloproliferative ized vascular congestion, arterial thrombosis,
(PaO2), or by excessive exogenous administra-
disorder. splenomegaly, diffusely red bone marrow with
tion of EPO or darbepoetin.
• Secondary appropriate absolute—chronic reduced fat; microscopic findings: hyperplas-
SYSTEMS AFFECTED tic bone marrow with normal or reduced
pulmonary disease, cardiac disease or anomaly
Cardiovascular, respiratory, nervous, renal/ myeloid/erythroid ratio and reduced iron
with right-to-left shunting, high altitude,
urologic—blood hyperviscosity causes poor content.
methemoglobinemia, and impairment of
perfusion and oxygen delivery to tissues.
renal blood supply.
GENETICS • Secondary absolute caused by inappropriate
Mutations of the JAK2 gene have been EPO secretion (rare)—neoplasia (e.g., T-cell
associated with polycythemia vera in humans. lymphoma, nasal fibrosarcoma, renal
carcinoma, pheochromocytoma, cecal TREATMENT
Relative erythrocytosis due to hemoconcen- leiomyosarcoma), hyperadrenocorticism, APPROPRIATE HEALTH CARE
tration or splenic contraction is the most hyperthyroidism, hyperandrogenism. • Relative—rehydration with IV fluids
common cause of erythrocytosis. • Secondary absolute caused by inappropriate appropriate for primary cause; assessment of
EPO or darbepoetin administration in renal function, gastrointestinal system,
GEOGRAPHIC DISTRIBUTION animals undergoing therapy for anemia. acid-base status, and electrolyte balance; if
• Reference intervals for PCV, hemoglobin, not hemoconcentrated, allow patient to calm
and RBC count vary with geographic location down.
and breed. • Absolute—phlebotomy recommended
• Animals living at high altitudes have higher (20 mL/kg over 1 to several days) to reduce
PCV than those at sea level. DIAGNOSIS RBC mass to PCV of 55%; blood volume
SIGNALMENT DIFFERENTIAL DIAGNOSIS should be replaced concurrently with isotonic
• Moderately high PCV and total plasma fluids.
Species
protein with concurrent dehydration—sug- • Secondary inappropriate absolute—
Dog and cat.
gest relative polycythemia. phlebotomy combined with identification
Breed Predilections • Secondary absolute—caused by diseases and removal of EPO source.
• Excitable breeds and cats are prone to that produce chronic hypoxemia or by • Secondary appropriate absolute—
splenic contraction. space-occupying lesions of the kidney, phlebotomy and hydroxyurea. The high PCV
(continued) Erythrocytosis
is an appropriate compensatory response; thrombocytopenia, anemia, and neutropenia, • Primary absolute erythrocytosis (polycythemia
thus, phlebotomy may be dangerous; if alopecia, changes in skin pigmentation, and vera)—prognosis is guarded, although cats
indicated, remove blood at a lower volume sloughing of toenails. have had survival times up to 5 years.
(5 mL/kg). A higher PCV (60–65%) may be • Methemoglobinemia and hemolytic
necessary to sustain life until the cause of anemia reported in cats treated with hydro-
hypoxemia can be corrected. xyurea.
E
• Polycythemia vera—phlebotomy (20 mL/
ALTERNATIVE DRUG(S)
kg) and hydroxyurea; frequency of bleeding Polycythemia vera—chlorambucil (dogs and MISCELLANEOUS
and dosage adjusted to maintain a PCV of cats: 0.2 mg/kg PO q24h) or busulfan
55% in dogs and 45% in cats. PREGNANCY/FERTILITY/BREEDING
(dogs: 2–4 mg/m2 PO q24h). Hydroxyurea may arrest or inhibit
NURSING CARE spermatogenesis.
Oxygen therapy may be indicated for patients
with cyanosis, hypoxemia, cardiopulmonary SYNONYMS
disease, or weakness following phlebotomy. Polycythemia—although use of this term
FOLLOW-UP should be avoided, due to its similarity with
ACTIVITY polycythemia vera.
Excessive exercise should be avoided. PATIENT MONITORING
• PCV, total protein, urine output, and SEE ALSO
DIET • Hyperviscosity Syndrome.
Normal diet, free-choice water. bodyweight daily in severely dehydrated
animals. • Polycythemia Vera.
CLIENT EDUCATION • Patients treated for polycythemia vera by ABBREVIATIONS
• Patients need to be observed at home for chemotherapy—monitor weekly for changes • EPO = erythropoietin.
changes in activity, difficulty breathing, or in PCV, leukocytes, and platelets during • PaO2 = partial pressure of oxygen.
bleeding. initial treatment; then monthly for adjust- • PCV = packed cell volume.
• Patients treated with EPO for anemia must ment of chemotherapy and periodic • RBC = red blood cell.
have PCV rechecked and dose adjusted at phlebotomy. • SpO2 = oxygen saturation.
regular intervals. • Periodic assessment of bone marrow iron
stores or serum iron levels is indicated to
Suggested Reading
SURGICAL CONSIDERATIONS Cook SM, Lothrop CD. Serum erythropoietin
If surgery is necessary, preoperative detect iron deficiency.
concentrations measured by radioimmunoassay
phlebotomy and close monitoring of POSSIBLE COMPLICATIONS in normal, polycythemic, and anemic dogs
oxygenation and vital parameters may be • Hyperviscosity in patients with absolute and cats. J Vet Intern Med 1994, 8:18–25.
necessary. Postoperatively, monitor for polycythemia, especially polycythemia vera, Darcy H, Simpson K, Gajanayake I, et al.
bleeding or thrombosis. may lead to thrombosis, infarction, or Feline primary erythrocytosis: a multicenter
hemorrhage. case series of 18 cats. J Fel Med Surg 2018,
• Chemotherapy may cause bone marrow 1:1–7.
suppression. Randolph JF, Peterson ME, Stokol T. 2010.
• Patients undergoing repeated phlebotomies Erythrocytosis and polycythemia. In:
MEDICATIONS
can develop iron deficiency, hypoproteinemia, Weiss DJ, Wardrop KJ, eds., Schalm’s
DRUG(S) OF CHOICE and peripheral edema. Veterinary Hematology, 6th ed. Ames, IA:
• Polycythemia vera—hydroxyurea (dogs: Wiley-Blackwell, 2010, pp. 162–166.
40–50 mg/kg PO divided twice daily; cats: EXPECTED COURSE
Author Bridget C. Garner
30 mg/kg PO q24h). AND PROGNOSIS
• Erythrocytosis secondary to hypoxemia— • Relative erythrocytosis—fair to good
hydroxyurea (40–50 mg/kg PO q48h). prognosis depending on primary cause.
• Secondary absolute appropriate
CONTRAINDICATIONS Alan H. Rebar.
erythrocytosis—clinical course and prognosis
Phlebotomy may be contraindicated in are determined by the severity of the lesion
hypoxemic patients. causing hypoxemia. Client Education Handout
PRECAUTIONS • Secondary inappropriate absolute available online
• Rapid removal of blood can cause erythrocytosis—if the tissue source of
hypotension and cardiovascular collapse. excessive EPO secretion can be identified
• Adverse effects of hydroxyurea include and removed or corrected, prognosis is good
bone marrow hypoplasia with to fair depending on cause.
Esophageal Diverticula
CBC/BIOCHEMISTRY/URINALYSIS • Maintain positive nutritional balance
Usually within normal limits. throughout disease process.
BASICS OTHER LABORATORY TESTS POSSIBLE COMPLICATIONS
N/A Patients with diverticula and impaction are
E OVERVIEW predisposed to perforation, fistula, stricture,
• Pouch-like sacculations of the esophageal IMAGING
• Thoracic radiography—may show air or
and postoperative incisional dehiscence.
wall that accumulate fluids and ingesta.
• Diverticula may be congenital or acquired soft tissue opacity cranial to the diaphragm or EXPECTED COURSE
and are rare. cranial to the thoracic inlet. AND PROGNOSIS
• Pulsion diverticula occur secondary to • Contrast esophagram—shows contrast • Prognosis is guarded in patients with large
increased intraluminal pressure. Seen with accumulation within the diverticulum. diverticula and overt clinical signs.
esophageal obstructive disorders such as • Videofluoroscopy—useful to evaluate for • Motility disturbances may persist
foreign body or mass lesions. disturbances in esophageal motility. post-surgery.
• Traction diverticula occur secondary to DIAGNOSTIC PROCEDURES
periesophageal inflammation where fibrosis Esophagoscopy confirms ingesta/debris
contracts and pulls out the wall of the within outpouchings of the esophagus.
esophagus into a pouch.
• Localized inflammation around (esophagitis) MISCELLANEOUS
and lining the diverticulum may be present.
INTERNET RESOURCES
• Potential complications include ingesta TREATMENT https://www.vin.com/vin/default.aspx
impaction, mechanical obstruction (large • If the diverticulum is small and not causing
diverticulum), and/or esophageal hypomotility. Suggested Reading
significant clinical signs, treat conservatively with
• Organ systems affected include gastrointes- Marks SL. Diseases of the pharynx and
elevated feedings of a soft, bland diet followed by
tinal (regurgitation), musculoskeletal (weight esophagus. In: Ettinger SJ, Feldman EC,
copious liquids or a semi-liquid diet.
loss), and respiratory (aspiration pneumonia). eds., Textbook of Veterinary Internal
• If the diverticulum is large or is associated
Medicine, 8th ed. Philadelphia, PA:
SIGNALMENT with significant clinical signs, surgical
Saunders, 2017.
• Rare; more common in dog than cat. resection is recommended.
Sherding RG, Johnson SE. Esophagoscopy.
• Congenital or acquired (no genetic basis • Client education should include the
In: Tams TR, Rawlings CA, eds., Small
proven). importance of dietary management and the
Animal Endoscopy, 3rd ed. Philadelphia,
• No important breed or sex predisposition. potential for aspiration pneumonia.
PA: Mosby, 2011, pp. 41–95.
• Fluid therapy, antibiotics, and aggressive
SIGNS Author Albert E. Jergens
• Postprandial regurgitation, dysphagia,
nursing, if concurrent aspiration pneumonia
Consulting Editor Mark P. Rondeau
anorexia, coughing. is present; alternative enteral nutrition via
• Weight loss, respiratory distress.
gastrostomy tube may be necessary in patients
with aspiration pneumonia.
CAUSES & RISK FACTORS • Treat for esophagitis if present.
Pulsion Diverticulum
• Embryonic developmental disorders of the
esophageal wall.
• Esophageal foreign body, mass or focal MEDICATIONS
motility disturbances (uncommon).
DRUG(S) OF CHOICE
Traction Diverticulum • Drug therapy for esophagitis, if present.
Inflammatory processes associated with the • Proton pump inhibitors, such as omeprazole or
trachea, lungs, hilar lymph nodes, or pantoprazole, are potent and effective anti-secre-
pericardium; resultant fibrous connective tory agents (omeprazole: 0.7–1.5 mg/kg PO
tissue adheres to the esophageal wall. q12h; pantoprazole: 0.7–1.5 mg/kg IV once
daily) for treatment of severe esophagitis.
• Use broad-spectrum antibiotics if patient
has concurrent aspiration pneumonia; if
DIAGNOSIS recurrent or severe pneumonia is present, base
antibiotic selection on culture and sensitivity
DIFFERENTIAL DIAGNOSIS of samples obtained by transtracheal wash or
• Esophageal redundancy—barium contrast bronchoalveolar lavage.
accumulation in the region of the thoracic inlet
can occur normally in young dogs (especially CONTRAINDICATIONS/POSSIBLE
brachycephalic breeds and Chinese Shar-Pei). INTERACTIONS
• Periesophageal mass—esophagram or N/A
esophagoscopy should differentiate the
presence of a mass causing luminal
narrowing.
• Esophagitis. FOLLOW-UP
• Esophageal foreign body.
PATIENT MONITORING
• Hiatal hernia.
• Evaluate for evidence of infection or
• Gastroesophageal intussusception.
aspiration pneumonia.
Esophageal Foreign Bodies

• Foreign bodies which cannot be removed
through the mouth may be pushed aborally
into the stomach.
BASICS DIAGNOSIS
NURSING CARE
DEFINITION DIFFERENTIAL DIAGNOSIS • If the procedure to remove the foreign body E
Ingestion of foreign material or foodstuffs • Esophagitis. is atraumatic and the esophagus has sustained
too large to pass through the esophagus, • Esophageal stricture. minimal damage, no special aftercare is
causing partial or complete luminal • Esophageal neoplasia. needed.
obstruction. • Megaesophagus. • Severe mucosal trauma may require placing
• Other esophageal disorders. a gastrostomy tube for enteral nutritional
PATHOPHYSIOLOGY
Esophageal foreign bodies cause mechanical CBC/BIOCHEMISTRY/URINALYSIS support during esophageal healing. Fluid
obstruction, mucosal inflammation with • Usually unremarkable. therapy may also be required to maintain
edema, and possibly ischemic necrosis and • Occasionally, electrolyte abnormalities, an normal hydration status during periods of
esophageal perforation. inflammatory leukogram, and/or hemocon- prolonged esophageal rest.
SYSTEMS AFFECTED centration, depending upon the severity of ACTIVITY
signs and degree of dehydration. The patient may resume normal activity after
• Respiratory—if aspiration pneumonia. OTHER LABORATORY TESTS a foreign body has been routinely removed.
GENETICS N/A DIET
N/A IMAGING • No change needed other than, perhaps,
altering the food to a more liquid consistency.
INCIDENCE/PREVALENCE Thoracic Radiography
• Feeding should be withheld 12–24 hours
Unknown • Most esophageal foreign bodies are
following foreign body removal.
GEOGRAPHIC DISTRIBUTION radiodense and are readily visualized. These
objects most commonly lodge at points of CLIENT EDUCATION
N/A
minimal esophageal distension, including the Discuss the possibility of complications and
SIGNALMENT thoracic inlet, base of the heart, and repeat offenders.
Species esophageal hiatus. SURGICAL CONSIDERATIONS
Due to the indiscriminate eating habits of • Esophageal distension with air may be • Surgery is indicated when endoscopy fails
many dogs, they have a higher incidence visualized cranial to the foreign body. to retrieve the foreign body; when endoscopy
than cats. Retained air in the esophagus is not always enables advancement of the object into the
associated with esophageal foreign bodies. gastric lumen but it is too large to pass
Breed Predilections • A contrast esophagram or videofluoroscopy
More common in small-breed dogs; terrier through the gastrointestinal tract; or when a
is required to identify radiolucent objects. If large esophageal perforation or area of
breeds often overrepresented. perforation is suspected, use an aqueous necrosis requires resection.
Mean Age and Range organic iodide contrast agent for imaging • The short-term prognosis for esophageal
More common in young to middle-aged studies. surgery is dogs and cats is favorable (~90%).
animals. • Air and/or fluid in the mediastinum or • It is often less traumatic to advance a bone
Predominant Sex pleural space suggests esophageal perforation; foreign body into the stomach than to attempt
N/A depending on severity, this can be an retrieval transorally via endoscopy. Gastrostomy,
indication for surgery versus esophagoscopy. if required, may then be performed.
SIGNS • Pulmonary infiltrates suggest aspiration • Most bone foreign bodies can be safely
General Comments pneumonia. left to dissolve in the stomach without need
The pet may have been observed ingesting a DIAGNOSTIC PROCEDURES for surgical removal. Nondigestible foreign
foreign body. Esophagoscopy allows removal of most (80%) objects (wood, metal, plastic) passed into
Historical Findings foreign bodies using retrieval forceps. It also the stomach may need to be removed
Most common include retching, gagging, allows for visual inspection of the mucosa for surgically.
lethargy, anorexia, ptyalism, regurgitation, trauma after foreign body removal. Use of an
restlessness, dysphagia, odynophagia, and endoscope with an accessory channel
persistent gulping. diameter of >2.8 mm will allow use of the
largest types of retrieval forceps.
Physical Examination Findings MEDICATIONS
• Ptyalism. PATHOLOGIC FINDINGS
DRUG(S) OF CHOICE
• Can be unremarkable. N/A
If there is significant mucosal injury (i.e.,
• Occasional discomfort when palpating the esophagitis), recommendations include:
neck or cranial abdomen. • Sucralfate slurry (0.5–1 g/dog PO q8h) for
CAUSES mucosal cytoprotection and healing.
Occurs most often with an object whose size, TREATMENT • Proton pump inhibitor (omeprazole or
shape, or texture does not allow free move- pantoprazole at 1 mg/kg q12h) for robust
ment through the esophagus, causing it to suppression of gastric acid secretions that may
• Emergencies—treat as inpatient and perform
become lodged before it can pass. contribute to reflux esophagitis.
endoscopy as soon as possible after diagnosis.
• Broad-spectrum antibiotics (amoxicillin or
RISK FACTORS • If endoscopic retrieval of the foreign body
Clavamox®) are only administered to animals
• Indiscriminate eating habits. succeeds and esophageal damage is minimal,
with mucosal perforation.
• Access to foreign materials. the patient may be discharged the same day.
Esophageal Foreign Bodies (continued)
• Metoclopramide (0.2–0.5 mg/kg IV/SC/ • Esophageal stricture—most common ZOONOTIC POTENTIAL

PO q8h) or cisapride (0.5 mg/kg q8–12h clinical sign is regurgitation with evidence of None
PO) to stimulate gastric motility and odynophagia in many animals; esophagram or PREGNANCY/FERTILITY/BREEDING
minimize reflux esophagitis. videofluoroscopy and/or esophagoscopy may N/A
• Gastrostomy tube placement for enteral be indicated to confirm a stricture.
E nutrition in animals with severe mucosal trauma. SEE ALSO
PREVENTION/AVOIDANCE • Esophageal Diverticula.
CONTRAINDICATIONS Carefully monitor the environment and what • Esophageal Stricture.
N/A is fed to the pet. • Regurgitation.
PRECAUTIONS POSSIBLE COMPLICATIONS INTERNET RESOURCES
• Approximately 25% of patients with
N/A https://www.vin.com
foreign bodies develop complications.
POSSIBLE INTERACTIONS • Complications most frequently encountered Suggested Reading
N/A include esophageal perforation, esophageal Deroy C, Corcuff JB, Billen F, et al. Removal
strictures, esophageal fistulas, and severe of oesophageal foreign bodies: comparison
ALTERNATIVE DRUG(S) esophagitis. Focal, transient esophageal between oesophagoscopy and oesophagotomy
N/A motility disturbances can occur secondary to in 39 dogs. J Small Anim Pract 2015,
esophageal trauma. 56:613–617.
• Pneumomediastinum, pneumothorax, Pratt CL, Reineke EL, Drobatz KJ. Sewing
pneumonia, pleuritis, mediastinitis, and needle foreign body ingestion in dogs and
FOLLOW-UP bronchoesophageal fistulas can all occur cats: 65 cases (2000–2012). J Am Vet Med
secondary to perforation. Assoc 2014, 245(3):302–308.
PATIENT MONITORING Sutton JS, Culp WTN, Scotti K, et al.
• Examine the esophagus closely via endo- EXPECTED COURSE AND Perioperative morbidity and outcome of
scopy for mucosal damage after foreign body PROGNOSIS esophageal surgery in dogs and cats: 72
removal. • Most patients do well and recover cases (1993-2013). J Am Vet Med Assoc
• Mild erythema/erosions are not uncommon uneventfully. 2016, 249(7):787–793.
and tend to heal uneventfully. • With complications, the prognosis is guarded. Tams TR. Endoscopic removal of gastrointesti-
• If an esophageal laceration/perforation is nal foreign bodies. In: Tams TR, Rawlings
detected—gastrostomy tube feedings allow CA, eds., Small Animal Endoscopy, 3rd ed.
esophageal rest and healing. Philadelphia, PA: Mosby, 2011, pp. 247–295.
• Advise post-procedural survey thoracic Author Albert E. Jergens
radiographs to assess for pneumomediastinum/ MISCELLANEOUS
Consulting Editor Mark P. Rondeau
pneumothorax. ASSOCIATED CONDITIONS
• Monitor at least 2–3 weeks for evidence of None
stricture formation. AGE-RELATED FACTORS Client Education Handout
available online
N/A
Esophageal Stricture
CAUSES PATHOLOGIC FINDINGS
• Reflux during anesthesia is the most • If an esophageal mass is present, biopsy with
common cause of benign esophageal stricture, histopathology is warranted; otherwise, benign
BASICS accounting for about 65% of cases; decreased strictures are not typically biopsied. • Strictures
DEFINITION LES tone during anesthesia may promote can be focal, multifocal, or coalescing.
A fixed narrowing of the esophagus resulting gastroesophageal reflux, resulting in
E
in partial or complete obstruction. subsequent acid injury to the esophageal
mucosa. • Esophageal foreign bodies (if >270°
PATHOPHYSIOLOGY
mucosal damage occurs). • Esophagitis from
• Benign strictures occur when there is
certain tablets and capsules; commonly
TREATMENT
circumferential erosion and ulceration of the APPROPRIATE HEALTH CARE
incriminated drugs are doxycycline,
esophageal mucosa; regardless of the initiating • Outpatient medical management is only
clindamycin, alendronate, and aspirin.
event, once esophagitis develops there is a successful for mild strictures; most strictures
• Gastroesophageal reflux. • Prolonged
decrease in the lower esophageal sphincter require intervention. • If there are complications
vomiting of gastric contents. • Swallowing of
(LES) tone; this results in more acid reflux (esophageal perforation, aspiration pneumonia),
caustic substances. • Esophageal neoplasia
and subsequent worsening of esophagitis; then inpatient care is required.
(squamous cell carcinoma and lymphoma
once severe esophagitis is present, damage can
most common). • Spirocerca lupi granuloma. NURSING CARE
extend to the lamina propria and muscularis
• Iatrogenic trauma during endoscopy. IV fluids may be necessary if the animal is
layers of the esophagus; this incites fibroblas-
• Vascular ring anomaly as an extraluminal dehydrated.
tic proliferation and contraction, leading to
cause for focal esophageal narrowing.
stricture formation. • Malignant strictures ACTIVITY
occur rarely in dogs and cats, and result from RISK FACTORS • Exercise restriction is not necessary after
direct tumor invasion. • General anesthesia, especially with drugs dilation. • If pneumonia is present, the degree
that decrease LES tone, when the patient is in of hypoxia will determine appropriate activity
SYSTEMS AFFECTED
Trendelenburg position, and in large-breed, level.
• Gastrointestinal—a single site of stricture is
deep-chested dogs positioned in sternal
most common, although multiple strictures DIET
recumbency. • Oral medications given with a
can occur anywhere through the esophagus. • Recommend feeding a fat-restricted diet to
dry swallow. • Foreign body ingestion.
• Respiratory—regurgitation is common with enhance gastric emptying. • Canned food can
strictures, increasing risk for aspiration be fed in small frequent amounts following
pneumonia. dilation. • If a balloon esophagostomy (BE)
GENETICS tube is placed, supplemental nutrition can be
N/A DIAGNOSIS provided as needed through the tube; for
DIFFERENTIAL DIAGNOSIS refractory cases, placement of a percutaneous
INCIDENCE/PREVALENCE endoscopic gastrostomy tube could be
• Megaesophagus. • Esophageal foreign body.
Infrequent considered.
• Esophageal neoplasia. • Extrinsic esophageal
GEOGRAPHIC DISTRIBUTION compression (mass, abscess). • Gastroesophageal CLIENT EDUCATION
Spirocerca lupi granuloma occurs in the reflux. • Vomiting (any cause). • Oropha • Owners should be aware that dilation
southern United States, parts of Europe, ryngeal dysphagia. • Vascular ring anomaly. procedures are not always successful, and that
South Africa, and Israel. CBC/BIOCHEMISTRY/URINALYSIS multiple attempts are required in many
SIGNALMENT Usually unremarkable. patients; it is important that medical
management for esophagitis be diligently
Species OTHER LABORATORY TESTS employed following dilation procedures to
Dog and cat. Usually unremarkable. reduce the risk of restricture. • Placement of a
Breed Predilections IMAGING BE tube could be discussed if multiple
None • Thoracic radiographs—usually unremarkable dilation procedures are not feasible or desired,
unless aspiration pneumonia develops. or in the case of severe stricture.
Mean Age and Range
• Videofluoroscopic barium swallow should SURGICAL CONSIDERATIONS
Any. Puppies and kittens with extraluminal
identify most strictures; if videofluoroscopy is • First-line treatment of benign esophageal
compression of the esophagus from a vascular
not available, barium swallow of liquid, paste, strictures is mechanical dilatation of the
ring anomaly typically become symptomatic
or food followed immediately by radiography stricture; techniques have evolved from rigid
at weaning.
is performed; peristalsis proximal to the bougienage, to flexible bougies, to balloon
Predominant Sex stricture site can be abnormal with concurrent dilation; the theoretical advantage of balloon
None esophagitis; may demonstrate more than one dilatation is that the forces applied to the
SIGNS stricture. stricture are a radial stretch, whereas some of
Historical Findings DIAGNOSTIC PROCEDURES the forces applied with bougienage are
• Odynophagia, dysphagia, increased • Endoscopy—diagnostic test of choice. longitudinal, resulting in possibly greater
salivation, regurgitation, anorexia, and weight • A focal narrowing (single or multiple) is potential for esophageal perforation.
loss; signs tend to be progressive as the easily identified; there is an abrupt decrease in • Esophageal dilatation balloons are made of
stricture progressively narrows. • If regurgita- luminal diameter at the stricture site. special plastic that makes the balloon
tion leads to aspiration pneumonia, cough • Usually the mucosa is normal (smooth and extremely rigid when maximally inflated at
and dyspnea can develop. pink), but can appear hyperemic and high pressures; balloons are positioned within
ulcerated if esophagitis is present. the stricture under direct endoscopic
Physical Examination Findings visualization; the balloon is slowly inflated
May have poor body condition secondary to with saline using a commercially available
malnutrition.
Esophageal Stricture (continued)
inflation device until it reaches the manufac- (0.5–0.75 mg/kg PO q8h) to increase LES EXPECTED COURSE AND PROGNOSIS
turer’s rated pressure for that balloon; to tone and enhance gastric emptying, and • With standard balloon dilation, reported
ensure adequate dilation of the stricture has omeprazole (1 mg/kg PO q12h) to decrease successful outcomes defined as ability to
occurred, inflation of the balloon with gastric acidity. swallow at least semi-solid food range from
ioxhexol and fluoroscopic monitoring during 71.4% to 88.0%, with 12–23.1% able to eat
E inflation is recommended; inadequate stricture
CONTRAINDICATIONS
a normal diet. • With BE tube placement, the
Caustic substances and emetic medications.
effacement is commonly seen if this procedure majority (66.7%; 8/12) of patients were able
is only performed with endoscopy. PRECAUTIONS to eat a normal diet with no dysphagia. • The
• Initial balloon diameter is ideally selected • Esophageal perforation can occur with prognosis for esophageal neoplasia is poor,
following measured diameters of normal overzealous balloon dilation of the stricture, but these cases tolerate esophageal stents well.
esophagus obtained via a contrast study therefore incremental increase in balloon
during the procedure; if fluoroscopy is not diameter is recommended. • Ineffective
available, a balloon diameter 50–100% larger balloon dilation can occur with incomplete
than the estimated stricture diameter can be tearing of the stricture; monitoring with
selected; it is important to avoid assuming size videofluoroscopy could be considered to MISCELLANEOUS
based on weight of the animal as this can monitor for this. • Using a balloon over a ASSOCIATED CONDITIONS
result in under- or overestimation; the guidewire is the safest way to perform this • Aspiration pneumonia. • Esophagitis.
sequence of subsequent larger dilations is then procedure; perforation is most common when
AGE-RELATED FACTORS
determined by the degree of mucosal tearing, a guidewire is not used through the lumen of
None.
ideally visualized fluoroscopically; the final the balloon and the balloon tip is advanced
dilation diameter is usually chosen by the accidentally into the esophageal wall—use ZOONOTIC POTENTIAL
degree of mucosal tearing and the size of the caution. None.
normal esophagus for the patient. • BE tube POSSIBLE INTERACTIONS PREGNANCY/FERTILITY/BREEDING
placement is a newer treatment option; this Sucralfate may inhibit the absorption of other N/A
device allows for balloon dilation twice daily drugs. SYNONYMS
for 4–6 weeks at home to prevent stricture
ALTERNATIVE DRUG(S) • Esophageal narrowing. • Esophageal
recurrence; the small number of reported
• Metoclopramide can be used to increase blockage or obstruction.
patients have had improved short- and
long-term outcomes compared to other LES tone. • Histamine H2-receptor blockers SEE ALSO
treatments; the BE tube is placed similarly to a can be used to decrease gastric acid. • Dysphagia.
standard esophagostomy tube after balloon • Esophageal Foreign Bodies.
dilation is performed; placement of the balloon • Esophagitis.
is confirmed with fluoroscopy to ensure the • Regurgitation.
balloon spans the length of the stricture and FOLLOW-UP ABBREVIATIONS
does not interfere with the upper or lower • BE = balloon esophagostomy.
PATIENT MONITORING
esophageal sphincter. • For persistent • LES = lower esophageal sphincter.
Patients are monitored for signs of recurrent
strictures, despite multiple balloon dilations, a
stricture, including regurgitation and Suggested Reading
salvage procedure with placement of a self-
gagging. Lam N, Weisse C, Berent A, et al. Esophageal
expanding or bioabsorbable stent can be
employed; it is important that the stent be PREVENTION/AVOIDANCE stenting for treatment of refractory benign
secured with sutures to prevent migration; • Preanesthetic administration of cisapride esophageal strictures in dogs. J Vet Intern
esophageal stenting has been associated with decreases the number of reflux events in Med 2013, 27(5):1064–1070.
adverse effects including ptyalism, regurgita- anesthetized dogs. • Preanesthetic administra- Leib MS, Dinnel H, Ward DL, et al.
tion, megaesophagus requiring removal, and tion of omeprazole will minimize the likeli- Endoscopic balloon dilation of benign
incision infection/drainage; given the hood of acid reflux. • Medications with esophageal strictures in dogs and cats. J Vet
unpredictability for which patients will ulcerogenic potential should be given with at Intern Med 2001, 15:547–552.
tolerate stent placement, this procedure least 6 mL of water or food. Tan DK, Weisse CW, Berent AB, Lamb KE.
should be considered only for highly Prospective evaluation of an indwelling
POSSIBLE COMPLICATIONS esophageal balloon dilation feeding tube for
refractory cases that fail BE tube placement. • Complications of balloon dilatation
• Surgical management (resection and treatment of benign esophageal strictures in
include perforation, severe mucosal tearing cats and dogs. J Vet Intern Med 2018,
anastomosis) is typically only performed as a and esophagitis, and stricture recurrence;
last resort. 32:693–700.
with BE tube placement additional Authors Melissa L. Milligan and Allyson
complications include infection at the tube Berent
site and migration of the tube beyond the Consulting Editor Mark P. Rondeau
stricture; this is typically well tolerated. Acknowledgment The author and book
MEDICATIONS • Complications with stent placement editors acknowledge the prior contribution of
include hyperplastic tissue ingrowth or Keith Richter
DRUG(S) OF CHOICE overgrowth, dysphagia, gagging, perceived
• Following dilation, give sucralfate suspen- discomfort, and stricture recurrence.
sion (0.5–1 g/patient PO q6h) to reduce • Aspiration pneumonia secondary to Client Education Handout
esophagitis and pain. • Medications for regurgitation. available online
esophagitis are used, including cisapride
Esophagitis
• Weight loss. • Megaesophagus—survey radiography
• Coughing and/or nasal discharge with revealing diffuse dilation of esophageal
aspiration pneumonia, reflux laryngitis, body.
BASICS pharyngitis, and/or rhinitis. • Esophageal diverticula—detected by survey
DEFINITION or contrast radiography or esophagoscopy.
Inflammation of the esophagus typically
• Vascular ring anomaly—usually revealed by
E
• Often normal.
affecting the esophageal body and lower • Oral and pharyngeal inflammation and/or
leftward deviation of trachea at heart base on
esophageal sphincter (LES). ulceration with ingestion of caustic substances survey thoracic radiographs, or barium
or oropharyngeal reflux of gastric acid. contrast radiography as focal dilation of
PATHOPHYSIOLOGY
• Fever and pain with ulcerative esophagitis
proximal esophageal body.
• Disruption of esophageal defense mecha-
or aspiration pneumonia. • Esophageal neoplasia—mass effect with
nisms can result in esophageal inflammation,
• Halitosis, ptyalism, possibly pain on
possible esophageal dilation diagnosed with
most commonly due to the effects of gastric
palpation of neck. survey or contrast radiography, thoracic CT,
acid from gastroesophageal reflux (GER) or
• Cachexia and weight loss, with chronicity.
or esophagoscopy.
vomiting.
• Esophagitis can result in impaired • Nasal discharge and congestion with reflux CBC/BIOCHEMISTRY/URINALYSIS
esophageal motility and LES incompetence, rhinitis. Usually unremarkable; patients with
which may result in further GER perpetuat- • Cough, increased bronchovesicular sound, ulcerative esophagitis or aspiration pneumo-
ing esophageal damage. pulmonary crackles, and dyspnea with nia may have leukocytosis and neutrophilia.
aspiration pneumonia. IMAGING
SYSTEMS AFFECTED
• Gastrointestinal (GI)—esophagus and in CAUSES • Survey thoracic radiography—often
the vomiting patient primary or secondary GI • Most commonly GER secondary to general unremarkable, but may reveal mild esophageal
disease. anesthesia (Web Figure 1), hiatal hernia (Web dilation or fluid accumulation in distal
• Respiratory—regurgitation and GER may Figure 2), persistent or chronic vomiting, and GI esophagus; aspiration pneumonia may be
lead to aspiration pneumonia, reflux disease resulting in delayed gastric emptying. evident; dilation of esophagus cranial to a
laryngitis, pharyngitis and/or rhinitis; • Gastroesophageal reflux disease (GERD) stricture; esophageal foreign body, HH, or
respiratory signs may be covert presentation secondary to primary LES abnormality is esophageal mass may be detected.
for GER. poorly understood in veterinary patients. • Barium contrast esophagram (static images
• Esophageal retention of tablets or capsules and/or fluoroscopic)—may reveal esophageal
(doxycycline, clindamycin, nonsteroidal dilation with retention of barium, strictures,
Unknown—relatively common; probably
anti-inflammatory drugs [NSAIDs], foreign bodies, or masses; fluoroscopic studies
underestimated, as most cases are not
alendronate). allow for evaluation of swallowing, esophageal
definitively diagnosed.
• Esophageal foreign body (Web Figure 3). motility, strictures that may not be apparent on a
GEOGRAPHIC DISTRIBUTION • Infectious agents—Pythium spp., Spirocerca static esophagram, sliding HH (Web Figure 2),
Worldwide, except when caused by Pythium lupi, Candida infection secondary to immune and GER (the latter two conditions may require
spp. (US Gulf Coast) and Spirocerca lupi suppression. abdominal compressions to demonstrate).
(southern states). • Uncommonly esophageal tumors, radiation • Thoracic CT can be helpful for esophageal
SIGNALMENT injury, megaesophagus, vascular ring masses, foreign bodies, and HHs.
anomalies, gastrinoma, eosinophilic esophagi- DIAGNOSTIC PROCEDURES
Species tis and esophageal tubes.
Dog and cat. • Endoscopy and biopsy—most reliable
• Idiopathic. means of diagnosis (Web Figures 1 and 3).
Breed Predilections Mild cases of esophagitis may appear normal.
RISK FACTORS
Reflux esophagitis in brachycephalic breeds Visual findings of mucosal hyperemia and
• General anesthesia.
due to negative intrathoracic pressure upon edema are common and in more severe cases
• HH.
inspiration increasing the tendency for GER ulceration. With GER, changes usually most
• GI or metabolic/endocrine disease resulting
and hiatal hernia (HH). apparent in distal third of esophagus. Gastro-
in vomiting or gastric hyperacidity.
Mean Age and Range • Preanesthetic fasting for prolonged periods duodenoscopy may also be performed to
• Any age. (≥24h) increases risk for GER and gastric evaluate for GI causes of vomiting that caused
• Young animals with congenital esophageal hyperacidity. esophagitis.
HH and older animals that are anesthetized • Histopathology provides most definitive
are at greater risk of developing reflux evidence of esophagitis, although endoscopy
esophagitis. and biopsies usually reserved for cases
unresponsive to therapy. Diagnostic quality
Predominant Sex
None
DIAGNOSIS esophageal biopsies difficult to obtain
DIFFERENTIAL DIAGNOSIS endoscopically due to tough stratified
SIGNS squamous epithelium.
• Esophageal foreign body—usually detected
Historical Findings • Endotracheal or transtracheal aspiration
by survey radiography or esophagoscopy.
• Regurgitation. • Esophageal stricture—revealed by barium
and/or bronchoalveolar lavage for cytology,
• Ptyalism. contrast radiography or esophagoscopy. and culture and sensitivity testing, may be
• Dysphagia (difficulty swallowing, gagging, • Oropharyngeal dysphagia—diagnosed with
considered in patients with aspiration
retching). videofluoroscopic swallow study. pneumonia.
• Odynophagia (pain when swallowing, • HH—may be diagnosed by thoracic PATHOLOGIC FINDINGS
repeated swallowing efforts, and extension of radiographs or esophagoscopy; contrast Mucosal squamous hyperplasia or dysplasia
head and neck during swallowing). esophagram with fluoroscopy may be with erosions and ulcers; lymphocytic
• Hyporexia or anorexia. required to document (Web Figure 2). plasmacytic and neutrophilic inflammation.
Esophagitis (continued)
suppressors. PPIs provide superior gastric acid lidocaine solution (2.0 mg/kg PO q4–6h) for
suppression compared to H2RAs. local analgesia; tramadol 2–4 mg/kg PO
• PPIs should be administered at dose of q8–12h.
TREATMENT 1 mg/kg PO or IV q12h. Most common PPIs • Anti-inflammatory dosage of corticosteroids
APPROPRIATE HEALTH CARE prescribed are omeprazole and pantoprazole. (e.g., prednisone 0.5–1 mg/kg PO per day or
E • Mildly affected animals can be managed as Other choices include lansoprazole and divided q12h) may decrease fibrosis and
outpatients; those with more severe esophagi- esomeprazole. esophageal stricture formation in severe cases;
tis (persistent regurgitation, dehydration) and • Fractionated enteric-coated omeprazole controversial and efficacy not been supported
complications (aspiration pneumonia) require tablets remain effective despite disruption of by literature. Avoid when evidence of aspiration
hospitalization. the enteric coating. Tablets need to be cleanly pneumonia.
• Successful treatment of esophagitis involves split and cannot be crushed.
addressing underlying risk factors and • In humans widespread media attention has CONTRAINDICATIONS
predisposing conditions when possible; gastric concerned potential adverse effects of PPIs. None
acid suppression to reduce esophageal mucosal Current evidence is inadequate to establish PRECAUTIONS
injury; increasing LES pressure and promot- cause and effect for most associations. Caution None
ing gastric emptying to reduce GER; and should be exercised when prescribing PPIs as
protecting esophageal mucosa from further they are among the most overprescribed drugs
Sucralfate may interfere with GI absorption
injury. in humans and veterinary medicine.
of other drugs and it is best to separate dosing
• Famotidine is most effective and commonly
NURSING CARE by 2 hours from other drugs; may not be
recommended H2RA given at dose of
• Upright or elevated feeding will be of clinically important.
0.5–1.0 mg/kg PO/SC/IV q12h. Has
benefit with regurgitation associated with ALTERNATIVE DRUG(S)
diminished effect over time with repeated
abnormal esophageal motility secondary to • Narcotic analgesics including buprenor-
administration. Is appropriate for short-term
esophagitis. phine, methadone, and fentanyl may be
gastric acid suppression, but long-term
• Coupage and nebulization are provided for necessary in severe cases of painful esophagitis.
administration not advised.
patients with aspiration pneumonia. • Ranitidine 2.0 mg/kg PO q12h, nizatidine
• When prescribing a PPI, overlap with an
• IV fluids to maintain hydration in severe cases. 2.5–5.0 mg/kg PO q24h, and erythromycin
H2RA during initial dosing is unnecessary.
• Oxygen therapy may be necessary in 0.5–1.0 mg/kg PO/IV have GI prokinetic
• When discontinuing a PPI after >3–4
patients with aspiration pneumonia. effects and may be alternate or additive
weeks of therapy, PPI should be gradually
DIET tapered by 50% increments over 2–3 weeks to drugs.
• Fat-restricted diets recommended to avoid rebound gastric hyperacidity.
minimize gastric acid production. • Dosing for metabolic disease (renal failure
• With severe esophagitis oral food and water and liver failure) not established; lower dose
may need to be withheld until regurgitation or longer dose interval may be appropriate for
resolved; gastrostomy tube feedings may be these conditions. FOLLOW-UP
required.
GI Prokinetics PATIENT MONITORING
CLIENT EDUCATION • Second most common class of drugs used • For patients with mild esophagitis,
• Advise upright or elevated feeding when to treat GER and esophagitis. Increase LES monitoring of clinical signs is sufficient.
there is esophageal dysmotility. pressure and promote gastric emptying, • Consider follow-up endoscopy in patients
• Discuss potential complications, including therefore reducing GER. with ulcerative esophagitis and those at risk
aspiration pneumonia, esophageal stricture, • Most effective is cisapride at 0.5–1.0 mg/kg for esophageal stricture.
esophageal perforation, and/or esophageal PO q8h. Readily available from compounding PREVENTION/AVOIDANCE
motility abnormalities. pharmacies. • Consider two doses of omeprazole 1 mg/kg
SURGICAL CONSIDERATIONS • Metoclopramide is GI prokinetic with
PO or famotidine 1 mg/kg PO given 12–24h
• Percutaneous endoscopic gastrostomy or antiemetic effects in dogs dosed at 0.2– and 1–4h prior to anesthesia to reduce gastric
surgical gastrostomy tube placement in severe 1.0 mg/kg PO/SC q8h or 1.0–3.0 mg/kg/ acidity.
cases. day as CRI. • Prokinetic drug (cisapride 1 mg/kg PO;
• Surgical correction for HH when medical Mucosal Protectants metoclopramide 0.2–1.0 mg/kg PO/SC) with
management not effective. • Sucralfate 0.25–1.0 g PO q6–8h is given as acid suppressor may also help reduce GER
• Esophageal surgery may be necessary for suspension mixed into slurry with water and during anesthesia and surgery.
large perforations, difficult esophageal foreign administered on empty stomach. Forms • Maropitant useful to prevent vomiting and
bodies, or esophageal neoplasia, but should be insoluble complex that binds to inflamed regurgitation associated with opioid premedi-
avoided if possible. tissue, creating protective barrier and cations and anesthesia.
preventing further damage caused by pepsin, • If GER is cause of esophagitis, owners
acid, and bile. Additionally increases mucosal should avoid late-night feedings that tend to
defense and repair mechanisms through diminish LES pressure during sleep.
stimulation of bicarbonate and prostaglandin • Proper patient preanesthesia fasting decreases
MEDICATIONS E production and binding of epidermal risk of GER. Withholding water for 4–8h
DRUG(S) OF CHOICE growth factor, at neutral pH. Reported to and food for 8–12h prior to anesthesia is
relieve symptoms in humans. recommended.
Acid Suppression
• Antibiotics indicated with aspiration • Follow oral administration of capsules and
• Most important therapy for treatment of
pneumonia, severe esophageal ulceration, and tablets with 5–10 mL bolus of water
GERD and associated esophagitis. H2-receptor esophageal perforation. (especially for doxycycline) amd a meal, or
antagonists (H2RAs) and proton pump • Analgesics, especially in severe cases— give with a treat such as a pill pocket to hasten
inhibitors (PPIs) are two main classes of acid
(continued) Esophagitis
transit time of pills to stomach. Coating pills • NSAID = nonsteroidal anti-inflammatory
with butter or applying Nutri-Cal® to the nose drug.
to stimulate licking after administration of • PPI = proton pump inhibitor.
tablets may also be effective. MISCELLANEOUS
Suggested Reading
ZOONOTIC POTENTIAL Garcia RS, Belafsky PC, DellaMaggiore A, E
None et al. Prevalence of gastroesophageal reflux
• Esophageal stricture formation.
• Aspiration pneumonia. PREGNANCY/FERTILITY/BREEDING in cats during anesthesia and effect of
• Chronic reflux esophagitis. H2RAs, PPIs, and glucocorticoids should all omeprazole on gastric pH. J Vet Intern Med
• Permanent esophageal dysmotility. be used with caution during pregnancy. 2017, 31(3):734–742.
• Chronic cough due to laryngopharyngeal Golly E, Odunayo A, Daves M, et al. The
SYNONYMS
aspiration or tracheal microaspiration. frequency of oral famotidine administration
Esophageal inflammation.
• Esophageal perforation (rare). influences its effect on gastric pH in cats over
• Barrett’s esophagus (rare complication of SEE ALSO time. J Vet Intern Med 2019, 33(2);544–550.
chronic reflux esophagitis reported in cats). • Dysphagia. Marks SL, Kook PH, Papich MG, et al.
• Esophageal Diverticula. ACVIM consensus statement: Support for
EXPECTED COURSE AND PROGNOSIS • Esophageal Foreign Bodies. rational administration of gastrointestinal
• Best results when treated with gastric acid • Esophageal Stricture. protectants in dogs and cats. J Vet Intern
suppressant, GI prokinetic, and possibly • Gastroesophageal Reflux. Med 2018, 32:1823–1840.
mucosal protectant. • Hiatal Hernia. Tolbert K, Odunayo A, Howell RS, et al.
• Mild esophagitis—good to excellent • Megaesophagus. Efficacy of intravenous administration of
prognosis. • Regurgitation. combined acid suppressants in healthy dogs.
• Severe or ulcerative esophagitis—greater J Vet Intern Med 2015, 29:556–560.
potential for complications, which warrants ABBREVIATIONS
• GER = gastroesophageal reflux. Author Steve Hill
guarded prognosis. Consulting Editor Mark P. Rondeau
• Complete recovery can be expected • GERD = gastroesophageal reflux disease.
especially when treated before serious • GI = gastrointestinal.
complications develop. • H2RA = H2 receptor antagonist.
• HH = hiatal hernia.
available online
• LES = lower esophageal sphincter.
Essential Oils Toxicosis

• Indirect ingestion—essential oils used on • Anticholinergics if bradycardic, as long as
human skin, animal licks skin. normotensive.
• Direct dermal or oral use as owners try natural • Bronchodilators with respiratory distress.
BASICS remedies (e.g., flea control) on their animals. • Anti-emetics.
OVERVIEW • Hepatoprotectants with elevated LEs.
E • Essential oils—volatile, organic constituents CONTRAINDICATIONS/POSSIBLE
extracted from plants; contribute to fragrance/
INTERACTIONS
taste. Often used as natural remedies by
owners for their own medical issues. Essential
DIAGNOSIS Do not induce vomiting. Do not give AC to
DIFFERENTIAL DIAGNOSIS a patient with CNS signs.
oil insecticides (low %) manufactured for use
on animals. • Aspirin toxicity—wintergreen and sweet Precautions
• Known toxicants to cats—d-Limonene birch oil contain methyl salicylate; anemia/GI Use hepatically metabolized medications with
(citrus oil), pine oil, ylang ylang oil, pepper- hemorrhage may develop. caution in the presence of LE elevation.
mint oil, cinnamon oil. • Hepatotoxins xylitol, acetaminophen,
• Known toxicants to cats and dogs—winter- cycads (sago palm), others.
green oil, sweet birch oil, eucalyptus oil, clove • Toxins or conditions that affect CNS—
oil, tea tree (aka melaleuca) oil. ethylene glycol, hypoglycemia, hypotension,
• Known toxicants to dogs—pennyroyal oil. drug overdoses. FOLLOW-UP
CBC/BIOCHEMISTRY/URINALYSIS PATIENT MONITORING
Systems Affected
• Most often no specific diagnostic features.
Recheck LEs 48–72 hours post discharge,
• Cardiovascular—bradycardia, peripheral
• CBC and chemistry—possible increase in LEs.
then as needed based on values and clinical
vasodilation.
signs.
• Endocrine/metabolic—hypothermia. IMAGING
• Gastrointestinal (GI)—hypersalivation, • Thoracic radiographs with respiratory PREVENTION/AVOIDANCE
vomiting. irritation/distress. • Do not apply essential oils directly to
• Hepatobiliary—elevated liver enzymes • Abdominal radiographs if abdominal pain.
animals.
(LEs), hepatic failure. • Use essential oil products manufactured for
• Nervous—ataxia, tremors, CNS depression. PATHOLOGIC FINDINGS use on animals with caution.
• Respiratory—respiratory irritation/distress. Limited data—lesions of severe hepatic • Avoid using essential oil diffusers.
• Skin—irritation, possible ulceration. necrosis with pennyroyal oil.
SIGNALMENT • Aspiration pneumonia—if neurologic
Cats are more sensitive than dogs. Cats lack patient with concurrent GI signs.
glucuronyl transferase; cannot metabolize/ • Pennyroyal oil—disseminated intravascular
eliminate toxins via hepatic glucuronidation. TREATMENT coagulation, chronic hepatic insufficiency.
SIGNS Appropriate Health Care EXPECTED COURSE AND PROGNOSIS
• Signs vary based on type/concentration of Fresh air, emergency examination, bathing, • Prognosis—good if treated early and
oil. Higher the concentration the greater the inpatient care until signs resolve. aggressively. May take several days for
risk. Only 7–8 drops of 100% oil may be complete resolution.
Nursing Care • More guarded prognosis with use of 100%
needed to cause toxicosis.
• Intravenous crystalloids. oil (i.e., tea tree oil, pennyroyal oil), especially
• Onset—1–8 hours post exposure.
• Prevent aspiration of vomitus. if treatment is delayed or inadequate.
• Animal may smell of oil (hair coat, skin,
• Oxygen therapy. Fatalities can occur.
breath) or feel greasy.
• Monitor BP, heart rate, thermoregulation.
• Nausea, hypersalivation, vomiting,
abdominal pain. Diet
• Hypothermia. Do not feed patients that are vomiting,
• Ataxia, tremors, CNS depression. having CNS signs, or are in respiratory
• Coughing, wheezing, panting, tachypnea, distress. MISCELLANEOUS
and dyspnea. ABBREVIATIONS
• Bradycardia, hypotension. • AC = activated charcoal.
• Elevated LEs (cats, sometimes dogs—pen- • GI = gastrointestinal.
nyroyal oil). • LEs = liver enzymes.
MEDICATIONS Suggested Reading
• Passive oil diffusers—animals inhale odor, DRUG(S) OF CHOICE Hovda L, Brutlag A, Poppenga R, et al.
develop mild to severe respiratory irritation/ • No specific antidote. Essential oils/liquid potpourri; Tea tree oil/
distress. • Bathe with warm water and liquid hand melaleuca oil. In: Hovda LR, Brutlag AG,
• Active diffusers—release micro-droplets of dishwashing detergent. Poppenga RH, Peterson KL, eds., Five-
oil. Respiratory difficulties, but droplets can • Activated charcoal (AC) with a cathartic × 1 Minute Veterinary Consult Clinical
land on animal’s coat causing direct absorp- in large or concentrated oral ingestions. Companion: Small Animal Toxicology, 2nd
tion or ingestion via grooming. Repeat AC only q8h × 2 doses if tea tree oil ed. Ames, IA: Wiley-Blackwell, 2016, pp.
• History of preexisting respiratory issues (enterohepatic recirculation). 585–591, 592–597.
(e.g., asthmatic cats) places animals at greater • Fluid boluses or vasopressors as needed for Author Kia J. Benson
risk. hypotension. Consulting Editor Lynn R. Hovda
Ethanol Toxicosis
BASICS DIAGNOSIS MEDICATIONS

OVERVIEW DIFFERENTIAL DIAGNOSIS DRUG(S) OF CHOICE E
• Ethanol (CH3CH2OH)—short-chain • Other alcohols—methanol, isopropanol, • Dextrose—0.5–1.5 ml/kg 50% dextrose
alcohol; highly miscible with water; less butanol. diluted 1 : 4 in 0.9% NaCl as a bolus for
volatile than comparable hydrocarbons (e.g., • Human drugs of abuse—marijuana, immediate correction of severe hypoglycemia;
ethane); solvent for medications; component barbiturates, benzodiazepines. 2.5–5% dextrose supplementation in fluids
of alcoholic beverages; metabolized to • Early stages of ethylene glycol (antifreeze) for hypoglycemia.
acetaldehyde. toxicosis. • Fomepizole (4-methylpyrazole)—not
• Used intravenously to treat ethylene glycol • Early stages of xylitol toxicosis. specifically cleared for use in ethanol
poisoning. • Halogenated or aliphatic hydrocarbon intoxication
• Denatured forms may contain other toxic solvents. • Sodium bicarbonate (if needed)—mEq of
fractions (e.g., acetone, benzene, camphor, • Hypoglycemia inducing metabolic and bicarbonate required = 0.5 × bodyweight in
castor oil, phthalates, kerosene, sulfuric acid, neurologic disorders. kg × (desired total CO2 mEq/L − measured
terpinols); may complicate effects. • Pesticides—amitraz, macrolide CO2 mEq/L); give half the total calculated
• Ethanol concentration—expressed as proof antiparasiticides. dose slowly over 3–4 hours IV; recheck
(twice the % concentration). blood gases and clinical status of the
• Acute oral lowest toxic dosage—5–8 mL/kg CBC/BIOCHEMISTRY/URINALYSIS animal.
as pure alcohol; consider % alcohol in specific • PCV and total solids.
• Monitor for hypoglycemia; blood glucose CONTRAINDICATIONS/POSSIBLE
product consumed.
• Other alcohols—toxicity of methanol is <60 mg/dL considered serious. INTERACTIONS
similar to that of ethanol; the LD50 of 70% • Metabolic acidosis likely from ethanol-induced Avoid other CNS depressants.
isopropanol is 2 mL/kg. lactic acidemia.
• Cell membrane damage; impaired sodium OTHER LABORATORY TESTS
and potassium nerve conduction. • Blood ethanol levels routinely available at
• May inhibit glutamate receptors in brain reference labs—clinical signs in puppies at FOLLOW-UP
with reduction of cyclic guanosine monophos- >0.6 mg/mL and in adults at >1–4 mg/mL. • Monitor for metabolic acidosis—blood pH,
phate (GMP). • Blood methanol and isopropanol levels blood gases, urine pH, anion gap.
SIGNALMENT available at some reference labs. • Recovery from clinical signs—usually
• Most common in dogs. • Blood gases and increased anion gap— within 8–12 hours.
• No breed or sex predilections. evaluate potential acidosis.
• Young, curious animals more susceptible.
SIGNS N/A
• CNS—develop within 15–30 minutes after
ingestion on an empty stomach or 1–2 hours MISCELLANEOUS
on a full stomach; ataxia, reduced reflexes, ABBREVIATIONS
behavioral changes, excitement, depression. • GMP = guanosine monophosphate.
• Cardiovascular—cardiac arrest. TREATMENT Suggested Reading
• Gastrointestinal—flatulence (bread dough). • Activated charcoal—not effective. Dorman DC. Alcohols (ethanol, methanol,
• Respiratory—respiratory depression, • Emesis or gastric lavage—only in very isopropanol). In: Hovda LR, Brutlag AG,
narcosis. recent exposures (less than 15 minutes) due Poppenga RH, Peterson KL, eds., Blackwell’s
• Urologic—polyuria, incontinence. to rapid absorption and rapid onset of clinical Five-Minute Veterinary Consult: Small
• Hypothermia. signs. Animal Toxicology, 2nd ed. Ames, IA:
CAUSES & RISK FACTORS • Respiratory depression—provide artificial Wiley-Blackwell, 2016, pp. 71–77.
• Alcoholic beverages, either accidental or ventilation. Kammerer M, Sachot E, Blanchot D. Ethanol
intentional, are most common source. • IV isotonic crystalloid fluids—correct toxicosis from ingestion of rotten apples by
• Exposure to deicers, sanitizers, mouthwash, dehydration. a dog. Vet Hum Toxicol 2001,
dyes, inks, some fuels, paint, varnishes, • Acidosis—sodium bicarbonate if pH <7.0, 43(6):349–350.
perfume, pharmaceuticals. BE <15 mmHg, HCO3 <11 mmHg. Means C. Bread dough toxicosis in dogs. J
• Exposure to rising bread doughs containing • Cardiac arrest—cardiac therapy (see Vet Emerg Crit Care 2003, 13(1):39–41.
active yeast. Cardiopulmonary Arrest). Author Tabatha J. Regehr
• Fermented products—rotten apples, • Hemodialysis—may aid in elimination of Consulting Editor Lynn R. Hovda
garbage. ethanol after life-threatening exposure. Acknowledgment The author and book
• Dermal exposure—alcohol-containing • Yohimbine may be effective for CNS editors acknowledge the prior contribution of
products. depression. Gary D. Osweiler
Ethylene Glycol Toxicosis

• Dogs—with increasing depression, patient of renal dysfunction. • Calcium oxalate
drinks less but polyuria continues, resulting crystalluria—consistent finding; as early as 3
in dehydration; CNS signs abate transiently hours post ingestion in cats and 6 hours in
BASICS after approximately 12 hours, but recur later. dogs; monohydrate form more common.
DEFINITION • Cats—usually remain markedly depressed; • Urine—pH consistently decreases;
E Results primarily from ingesting substances do not exhibit polydipsia. • Oliguria (dogs: inconsistent findings—hematuria; proteinuria;
containing ethylene glycol (EG; e.g., 36–72 hours; cats: 12–24 hours) and anuria glucosuria; may note granular and cellular
antifreeze). Rarely from other products. (72–96 hours post ingestion)—often develop casts, white blood cells (WBCs), red blood
if untreated. • May note severe hypothermia. cells (RBCs), and renal epithelial cells.
PATHOPHYSIOLOGY
• Severe lethargy or coma. • Seizures.
• EG—rapidly absorbed from the gastrointestinal OTHER LABORATORY TESTS
• Anorexia. • Vomiting. • Oral ulcers.
tract; food in the stomach delays absorption.
• Salivation. • Kidneys—often swollen and Blood Gases
• Toxicity—initially causes CNS depression,
painful, particularly in cats. • Metabolites cause severe metabolic
ataxia, gastrointestinal irritation, and polyuria or
polydipsia; rapidly metabolized in the liver by CAUSES acidosis. • Total CO2, plasma bicarbonate
alcohol dehydrogenase to glycoaldehyde, Ingestion of EG, the principal component concentration, and blood pH—low by 3
glycolic acid, glyoxalic acid, and oxalic acid; (95%) of most antifreeze solutions. hours post ingestion; markedly low by 12
leads to severe metabolic acidosis and renal hours. • Partial pressure of CO2 (PCO2)
RISK FACTORS decreases, owing to partial respiratory
epithelial damage. • Minimum lethal dosage— Access to EG—widespread availability;
cats: 1.4 mL/kg; dogs: 6.6 mL/kg. compensation. • Anion gap—increased by
somewhat pleasant taste; small minimum 3 hours post ingestion; peaks at 6 hours
SYSTEMS AFFECTED lethal dose; lack of public awareness of toxicity. post ingestion; remains increased for
• Gastrointestinal—irritated mucosa. approximately 48 hours (EG metabolites
• Nervous—inebriation from EG and are unmeasured anions. Glycolate, a
glycoaldehyde owing to inhibition of metabolite of EG, can result in a false
respiration, glucose metabolism, and serotonin DIAGNOSIS increase in plasma lactate, which could lead
metabolism, and alteration of amine concen- to the assumption that acidosis is due to
trations. • Renal/urologic—initially, osmotic DIFFERENTIAL DIAGNOSIS increased lactate, rather than EG toxicosis.
diuresis; later, metabolites, especially calcium • Acute (30 minutes–12 hours post
ingestion)—ethanol, methanol, and Other
oxalate monohydrate crystals, are directly
marijuana toxicosis; ketoacidotic diabetes • Serum osmolality and osmole gap—high by
cytotoxic to renal tubular epithelium, resulting
in renal failure; mechanism of toxicity is now mellitus; pancreatitis; gastroenteritis. • Renal 1 hour post ingestion, in parallel with serum
thought to involve attachment of oxalate to stage—acute renal failure by nephrotoxins, EG concentrations; dose related; usually
cell plasma membrane, activation of enzyme e.g., aminoglycoside antibiotics, amphotericin remain high for approximately 18 hours post
activity, and production of free radicals and B, cancer chemotherapeutic drugs, ibuprofen, ingestion; EG toxicosis most common
lipid peroxidation, leading to cell necrosis. oxalate-containing plants such as philodendrons, cause of high osmolal gap. • EG serum
plants of the lily family (cats), cyclosporin, concentration— peaks 1–6 hours post
INCIDENCE/PREVALENCE grape and raisin toxicosis (causes hypercalcemia, ingestion; usually not detectable in serum or
• Common in small animals. • Highest unlike EG toxicosis), and heavy metals; urine by 72 hours. • Commercial kits—PRN
fatality rate of all poisons; fatality rates higher leptospirosis, tubulointerstitial nephritis; Pharmacal REACT EG measures concentra-
for cats than dogs. • Incidence similar in cats glomerular and vascular disease; renal tions at >50 mg/dL; estimate by multiplying
and dogs. ischemia (hypoperfusion). osmole gap by 6.2. ◦ Test does not detect
GEOGRAPHIC DISTRIBUTION metabolites, so must be used within the first
CBC/BIOCHEMISTRY/URINALYSIS few hours post ingestion. ◦ Results available
Higher incidence in colder areas where • Packed cell volume (PCV) and total
antifreeze is more commonly used. in 6 minutes but should not be read over 10
protein—often high owing to dehydration. minutes. ◦ Labeled for dogs and cats; some
SIGNALMENT • Stress leukogram— common. • High blood cats may have toxicosis at levels below 50 mg/
Species
urea nitrogen (BUN) and creatinine—dog: dL. ◦ False-positive test results can be seen
Dogs, cats, and many other species, including 36–48 hours post ingestion; cat: 12 hours with propylene glycol, glycerol, mannitol, and
birds. post ingestion. • Hyperphosphatemia may sorbitol. Ethanol may combine with
occur transiently 3–6 hours post ingestion, propylene glycol or glycerol to give a false
Mean Age and Range owing to phosphate rust inhibitors in
• Any age susceptible (3 months–13 years).
positive. • Wood’s lamp examination of
antifreeze; hyperphosphatemia is also seen urine, face, paws, or vomitus may detect
• Mean: 3 years. with azotemia owing to decreased glomerular fluorescein that is sometimes added to
SIGNS filtration. • Hyperkalemia if oliguric or anuric. antifreeze to detect radiator leaks. This
• Hypocalcemia—occurs in approximately method is nonspecific and may be unreliable;
General Comments half of patients, owing to chelation of calcium
• Dose dependent. • Almost always acute. fluorescein has a half-life of approximately
by oxalic acid; clinical signs infrequently 4 hours.
• Caused by unmetabolized EG and its toxic observed because of acidosis.
metabolites (frequently fatal). • Hyperglycemia—occurs in approximately IMAGING
Physical Examination Findings half of patients, owing to inhibition of Ultrasonography—renal cortices may be
• Early—from 30 minutes to 12 hours post glucose metabolism by aldehydes, increased hyperechoic as a result of crystals.
ingestion in dogs: nausea and vomiting; mild epinephrine and endogenous corticosteroids,
to severe depression; ataxia and knuckling; and uremia. • Isosthenuria—by 3 hours post
• Kidney biopsy—with anuria; confirm
muscle fasciculations; nystagmus; head ingestion, owing to osmotic diuresis and
diagnosis. • Cytologic examination of kidney
tremors; decreased withdrawal reflexes and serum hyperosmolality-induced polydipsia;
imprints—often diagnostic; numerous
righting ability; polyuria and polydipsia. continues in later stages of toxicosis because
calcium oxalate crystals.
(continued) Ethylene Glycol Toxicosis

PATHOLOGIC FINDINGS Cats <5 hours post ingestion—prognosis excellent
• Kidneys often swollen. • Fomepizole—cats must be given a higher dose with fomepizole treatment. • Dogs treated up
• Postmortem examination of kidney reveals of fomepizole than dogs; 125 mg/kg IV initially, to 8 hours post ingestion—most recover.
the presence of calcium oxalate crystals in the then 31.25 mg/kg at 12, 24, and 36 hours. • Dogs treated up to 36 hours post ingestion—
tubules. • Ethanol—use if fomepizole not available; may be of benefit to prevent metabolism of any
20% at 5mL/kg diluted in fluids and given in remaining EG. • Cats treated within 3 hours
E
an IV drip over 6 hours for 5 treatments; then post ingestion—prognosis good. • If a large
over 8 hours for 4 more treatments. quantity of EG is ingested, prognosis is poor,
unless treated within 4 hours of ingestion.
TREATMENT CONTRAINDICATIONS
• Patients with azotemia and oliguric renal
Avoid drugs that cause CNS depression,
APPROPRIATE HEALTH CARE including ethanol. failure—prognosis poor; almost all of the EG
• Cats—usually inpatient. will have been metabolized.
• Dogs—usually outpatient if <5 hours post PRECAUTIONS
ingestion and treated with fomepizole; • Competitive substrates (alcohols, such as
inpatient if >5 hours for IV fluids to correct ethanol) contribute to CNS depression;
dehydration, increase tissue perfusion, and monitor respiration. • Cats may become
promote diuresis. hypothermic; require heat. • Other pyra- MISCELLANEOUS
zoles—may be toxic to the marrow and liver; AGE-RELATED FACTORS
NURSING CARE do not substitute for fomepizole.
• Goals—prevent absorption; increase
Patients <6 months of age with oliguric renal
excretion; prevent metabolism. • Induction POSSIBLE INTERACTIONS failure sometimes fully recover.
of vomiting and gastric lavage with activated • Fomepizole—contributes slightly to CNS SYNONYMS
charcoal not recommended unless can be depression in cats; none in dogs. • Ethanol— Antifreeze poisoning.
performed in first 30 minutes following contributes to CNS depression; further
increases serum osmolality. SEE ALSO
ingestion due to rapid absorption of EG. • IV Hyperosmolarity
fluids—correct dehydration, increase tissue ALTERNATIVE DRUG(S)
perfusion, and promote diuresis; accompa- • Ethanol, propylene glycol, and
ABBREVIATIONS
nied by bicarbonate given slowly IV to correct • ADH = alcohol dehydrogenase. • BUN =
1,3-butanediol—have higher affinity for
metabolic acidosis. • Monitor serial plasma ADH than does EG; effectively inhibit EG blood urea nitrogen. • EG = ethylene glycol.
bicarbonate concentrations—0.5 × body • PCO2 = partial pressure of carbon dioxide.
metabolism; may cause CNS depression
weight (kg) × (24 – plasma bicarbonate) = • PCV = packed cell volume. • RBC = red
and increase serum osmolality; constant
sodium bicarbonate needed (mEq). serum ethanol concentrations of 100 mg/ blood cell. • WBC = white blood cell.
• Monitor urine pH in response to therapy. dL will inhibit most EG metabolism. Suggested Reading
• Azotemia and oliguric renal failure • Ethanol treatment requires hospitaliza- Connally HE, Thrall MA, Forney SD, et al.
(dogs)—most of the EG has been metabo- tion, constant IV infusion (ethanol and Safety and efficacy of 4-methylpyrazole as
lized; little benefit from inhibition of alcohol fluids); continuous monitoring for treatment for suspected or confirmed
dehydrogenase (ADH); correct fluid, electrolyte, respiratory and acid-base status. ethylene glycol intoxication in dogs: 107
and acid-base disorders; establish diuresis; cases (1983–1995). J Am Vet Med Assoc
diuretics (particularly mannitol) may help; 1996, 209:1880–1883.
hemodialysis or peritoneal dialysis may be Connally HE, Thrall MA, Hamar DW. Safety
useful; may need extended treatment (several and efficacy of high-dose fomepizole
weeks) before renal function reestablished. FOLLOW-UP compared with ethanol as therapy for
SURGICAL CONSIDERATIONS PATIENT MONITORING ethylene glycol intoxication in cats. J Vet
Kidney transplantation—successfully employed BUN, creatinine, acid-base status, and urine Emerg Crit Care 2010, 20(2):191–206.
in cats with EG-induced renal failure. output—monitored daily. Tart KM, Powell LL. 4-Methylpyrazole as a
treatment in naturally occurring ethylene
PREVENTION/AVOIDANCE glycol intoxication in cats. J Vet Emerg Crit
• Increasing client awareness of toxicity— Care 2011, 21(3):268–272.
helps prevent exposure; earlier treatment of Authors Mary Anna Thrall, Gregory F. Grauer,
MEDICATIONS patients. • Use of antifreeze products (e.g., Heather E. Connally, and Sharon M. Dial
DRUG(S) OF CHOICE Sierra®, Prestone LowTox®) that contain Consulting Editor Lynn R. Hovda
propylene glycol, which is much less toxic. Acknowledgment The author and book
Dogs
POSSIBLE COMPLICATIONS editors acknowledge the prior contribution of
Fomepizole (4-methyl pyrazole, available
• Without azotemia—usually no complica- Gary D. Osweiler.
from Kacey Diagnostics)—effective and
nontoxic liver ADH inhibitor; much more tions. • Urine concentrating ability—may be
expensive than ethanol but less intensive care impaired with azotemia; may recover. Client Education Handout
required; 5% (50 mg/mL) at 20 mg/kg IV EXPECTED COURSE AND PROGNOSIS available online
initially; then 15 mg/kg IV at 12 and 24 • Untreated—oliguric renal failure (dogs:
hours; then 5 mg/kg IV at 36 hours. 36–72 hours; cats: 12–24 hours); anuria by
72–96 hours post ingestion. • Dogs treated
Excessive Vocalization and Waking at Night—Dogs and Cats
SIGNS IMAGING
Historical Findings To rule out medical/neurologic if indicated.
BASICS • Vocalization at times or in intensity that DIAGNOSTIC PROCEDURES
disturbs owners or neighbors. • Behavioral diagnosis based on history;
DEFINITION
E • Vocalization that is uncontrollable,
• Sleeping pattern altered—does not fall observation of pet, owner, and their interactions;
asleep at bedtime, awakens during the night, video if available.
excessive, at inappropriate times of day or or sleeps more during the day. • Intraocular pressure.
night, or that disrupts owners, neighbors, or • Signs reported vary with how disruptive • Brainstem auditory evoked response
other animals. they are to the family, neighbors, and the pet’s (BAER) if indicated to rule out auditory
• In night-time waking, the pet wakes during quality of life. decline.
the night, does not fall asleep at bedtime, or • Pets with CDS may pace, wander aimlessly, • Endoscopy and biopsy if gastrointestinal
awakens early, leading to disruption of have decreased interest in social interactions, cause suspected.
owner’s sleep. be less responsive to stimuli and increasingly PATHOLOGIC FINDINGS
PATHOPHYSIOLOGY anxious. N/A
• Additional signs related to medical causes.
• Varies with cause.
• Barking may be normal canine communication Physical Examination Findings
(social, threat, warning, care-soliciting) but Signs associated with underlying medical
unacceptable to owners. issues.
• Owner responses may reinforce or increase
TREATMENT
CAUSES
anxiety (punishment). APPROPRIATE HEALTH CARE
• Vocalization and night waking—medical:
• Cats are crepuscular, so early morning If any medical issues.
gastrointestinal, metabolic (renal, hepatic),
waking may be normal. urogenital, CNS disorders, CDS, hypertension, NURSING CARE
• May be due to medical conditions that hyperadrenocorticism or hypothyroidism (dog), If any medical issues.
cause anxiety, discomfort, irritability, or hyperthyroidism (cat), pain, sensory decline.
altered sleep–wake cycles. ACTIVITY
• Vocalization: Insure behavioral needs (e.g., social inter-
• Hearing decline may be associated with ◦ Anxiety or conflict.
increased vocalization. actions, exercise, elimination, routine, and
◦ Normal for individual or breed. mental stimulation) are adequately met
• Cognitive dysfunction syndrome (CDS) ◦ Alarm barking—response to novel
can lead to sleep disturbances, anxiety, and each day.
stimuli.
excessive vocalization. ◦ Territorial—warning or guarding. DIET
• Night waking may be due to a change in ◦ Owner inadvertently reinforces. • Feed from toys to encourage normal
schedule, environment, or activity, especially ◦ Also reinforced each time stimulus retreats. hunting and scavenging behaviors.
in senior pets that are more sensitive to ◦ Distress vocalization, e.g., howl or whine • Timed feeders and multiple small meals.
change. may be related to separation from social CLIENT EDUCATION
SYSTEMS AFFECTED group. Individualize for the pet, home, and
• Behavioral. ◦ Growl—associated with agonistic displays.
problem.
• Diseases of other systems may cause or ◦ Stereotypic behaviors—dog.
◦ Mating/sexual—cat. Behavior Modification
contribute to signs.
• Night waking: • Identify and minimize or avoid exposure to
GENETICS ◦ Normal crepuscular rhythm—cat. inciting stimuli.
N/A ◦ Changes in routine and/or environment— • Provide a quiet and calm environment for
insufficient enrichment/scheduling. security, rest, and sleep.
INCIDENCE/PREVALENCE • Structure all interactions (i.e., calm sit or
◦ Owner inadvertently reinforces.
Unknown down and quiet behavior for all rewards).
◦ Hyperactivity/hyperkinesis—dog.
SIGNALMENT ◦ Mating/sexual—cat. • Reward-based training to teach calm/settle
on cue (“Sit,” “Down,” “Mat”).
Species RISK FACTORS • Response substitution—use settle commands
Dog and cat. • Increasing age.
to train alternative acceptable behavior.
• Changes in schedule or environment.
Breed Predilections • Head halter may provide more immediate
• Asian breeds of cats may be prone to excess control to quiet and calm.
vocalization. • Eliminate any owner reinforcement.
• Working and hunting breeds may be more • Owner anxiety, verbal reprimands, and
prone to barking. DIAGNOSIS punishment may increase anxiety and
potentiate barking.
Mean Age and Range DIFFERENTIAL DIAGNOSIS
• Desensitize and countercondition—
• Puppies may not be able to sleep Sleep disorders.
expose the pet to the inciting stimulus at a
through the night without waking to CBC/BIOCHEMISTRY/URINALYSIS low level (under the response threshold) and
eliminate. To determine if underlying medical cause. pair a favored reward (e.g., food treat) with
• Senior pets may be more prone to
OTHER LABORATORY TESTS each exposure to change the emotional
vocalization and night waking due to
• T4 and blood pressure—senior cats. response. Gradually progress to more
underlying medical conditions.
• Rule out hypothyroidism and hyperadreno- intense stimulus.
Predominant Sex corticism in dogs. • Interrupting vocalization by directing into
Intact females during estrus and mating. an alternative behavior may help to achieve
(continued) Excessive Vocalization and Waking at Night—Dogs and Cats
quiet, which can then be reinforced; however, • Monitor for undesirable behavioral effects.
aversive techniques may increase anxiety. • Avoid anticholinergic drugs in pets with
Environmental Modification CDS.
MISCELLANEOUS
Modify environment to avoid or minimize POSSIBLE INTERACTIONS
exposure to stimuli that incite vocalization Do not use SSRIs and TCAs together with ASSOCIATED CONDITIONS E
or wake the pet, e.g., covered crate, quiet monoamine oxide (MAO) inhibitors such CDS
room, thunder cap, classical music, white as selegiline and amitraz, and use cautiously AGE-RELATED FACTORS
noise or fan. or avoid with buspirone and tramadol. Increased anxiety and night waking more
SURGICAL CONSIDERATIONS ALTERNATIVE DRUG(S) common in senior pets.
N/A • Concurrent sedation with acepromazine ZOONOTIC POTENTIAL
0.5–2.2 mg/kg might be considered, but it is None, but sleep disruption and anxiety in
not anxiolytic and may increase noise pets can contribute to sleep disruption and
sensitivity and vocalization. anxiety in owners.
• For a less sedating anxiolytic consider
MEDICATIONS buspirone at 0.5–1 mg/kg (dogs: q8–12h;
DRUG(S) OF CHOICE N/A
cats: q12h).
• Short term or as needed for situations of • Analgesics for pain control. SYNONYMS
anxiety or for inducing sleep. Sleep disturbances.
• Benzodiazepines—dog: clonazepam
SEE ALSO
0.05–0.25 mg/kg, diazepam 0.5–2.2 mg/kg; • Cognitive Dysfunction Syndrome.
cat: oxazepam 0.2–0.5 mg/kg, alprazolam
0.125–0.25 mg/cat, clonazepam 0.02– FOLLOW-UP • Compulsive Disorders—Cats.
• Compulsive Disorders—Dogs.
0.2 mg/kg. PATIENT MONITORING • Separation Anxiety Syndrome.
• Trazodone—dog: 5–10 mg/kg; cat: Modify the program based on response to
25–50 mg/cat. therapy. ABBREVIATIONS
• Gabapentin—dog: 20–30 mg/kg; cat: • BAER = brainstem auditory evoked
PREVENTION/AVOIDANCE response.
50–100 mg/cat. • Train calm and settle on cue (sit, down, go
• Melatonin—dog and cat: 3–6 mg • CDS = cognitive dysfunction syndrome.
to mat). • MAO = monoamine oxide.
(1.5–12 mg). • Predictable interactions, e.g., insure calm sit
• For ongoing therapy for chronic anxiety or • SAMe = S-adenosyl-L-methionine-tosylate
or down and quiet before any reward given. disulfate.
compulsive disorders—clomipramine • Reward desirable, do not punish undesir-
(tricyclic antidepressant [TCA]): dog: • SSRI = selective serotonin reuptake
able behavior. inhibitor.
1–3 mg/kg PO q12h, cat: 0.5–1 mg/kg PO • Socialize and habituate pet when young to a
q24h; fluoxetine or paroxetine (selective • TCA = tricyclic antidepressant.
wide range of people, pets, stimuli, and
serotonin reuptake inhibitors [SSRIs]): dog: environments. Suggested Reading
1–2 mg/kg PO q24h, cat: 0.5–1.5 mg/kg PO • Provide enrichment to meet needs Landsberg GM, DePorter T, Araujo JA.
q24h. including food puzzles and multiple small Management of anxiety, sleeplessness and
• Natural products that might be used meals for cats. cognitive dysfunction in the senior pet. Vet
adjunctively for anxiety—Adaptil®, Feliway®, Clin North Am Small Anim Pract 2011,
l-theanine, alpha-casozepine, Harmonease®, POSSIBLE COMPLICATIONS 41(3):565–590.
S-adenosyl-L-methionine-tosylate disulfate • Night-time waking can lead to fatigue,
Horwitz DF (ed.). Blackwell’s Five-Minute
(SAMe), or aromatherapy (lavender). increased irritability, and possibly aggression. Veterinary Consult Clinical Companion:
• For CDS—selegiline and cognitive • Both night waking and vocalization can be
Canine and Feline Behavior, 2nd ed.
supplements (see Cognitive Dysfunction particularly distressing to the pet owner’s Hoboken: NJ: Wiley, 2018, pp. 885–894.
Syndrome). health and wellbeing and greatly weaken the Authors Sagi Denenberg and Gary M.
bond. Landsberg
CONTRAINDICATIONS
Review contraindications and side effects for EXPECTED COURSE AND PROGNOSIS Consulting Editor Gary M. Landsberg
each drug used. • Variable—based on diagnosis, environment,
pet, and owner expectations.
PRECAUTIONS • Most can be improved over time, but might
• Caution with drugs that might sedate in not be eliminated.
elderly pets.
Exercise-Induced Weakness/Collapse in Labrador Retrievers
CAUSES dogs with EIC and they collapse with mild

• Genetic disorder—inherited as an exercise of short duration.
autosomal recessive trait. • Centronuclear myopathy—inherited
BASICS • Symptomatic dogs are homozygous for a muscle disorder in Labrador retrievers that
DEFINITION mutation in the dynamin 1 gene. Dynamin 1 causes generalized muscle atrophy, constant
E Inherited nervous system disorder causing (DNM1) is a protein important in neuro- weakness that worsens with exercise, and
weakness and collapse during intensive transmission in the brain and spinal cord absent patellar reflexes at rest. Diagnosis of
exercise in otherwise normal Labrador during high-level neuronal activity. There is this disorder is by muscle biopsy or DNA
retrievers and a few other breeds. evidence that the DNM1 mutation associated testing (http://labradorcnm.vet-alfort.fr/
with EIC has its most profound effect on pages/site/Overview_history.html).
SIGNALMENT DNM1 function when body temperature is • Cardiac arrhythmia—as a cause of exercise
• Labrador retrievers—approximately 6% of elevated, as normally occurs with exercise. intolerance can be ruled out by cardiac
all pet, show, and field Labrador retrievers are auscultation, palpation of femoral pulses, and
affected. RISK FACTORS
• Genetically affected dogs are at risk for
performing an ECG at rest and during
• Also occurs in Chesapeake Bay retrievers, collapse. Holter monitor or an ECG event
curly-coated retrievers, and Boykin spaniels, collapse when participating in high-intensity
exercise with concurrent excitement or stress. recorder may be required to rule out
and rarely in Old English sheepdogs, German intermittent cardiac arrhythmia.
• Trigger activities most likely to induce collapse
wirehaired pointers, Bouvier des Flandres, • Pulmonary hypertension—can cause exercise
Pembroke Welsh corgis, and cocker spaniels. include repetitive fun or training retrieves, upland
bird hunting, intense play with other dogs, and intolerance and syncopal episodes as exercise
• No sex or color predilection. and excitement increase systolic pressure in an
running alongside an all-terrain vehicle.
SIGNS • Increased ambient temperature and
already overloaded right ventricle and pulmo-
humidity increase the risk of collapse in nary arteries, resulting in reflex bradycardia,
General Comments vasodilation, and hypotension.
• No systemic signs.
affected dogs.
• Hypoglycemia—ruled out by measuring
• Most genetically affected dogs (>80%) will
• Episodes of collapse first occur between blood glucose during an episode.
5 months and 3 years of age. have at least one episode of collapse before
• Hypo- or hyperkalemia—ruled out by
• Collapse episodes occur only with extremes
they reach 3 years of age, but affected dogs
with a sedentary lifestyle or calm temperament measuring potassium during collapse.
of exciting exercise. • Hypoadrenocorticism (Addison’s disease)—
• Dogs can engage normally in hiking,
may never exhibit weakness or collapse.
can cause exercise-induced hypoglycemic
swimming, jogging, and other activities. collapse or seizures; should be ruled out with
Physical Examination Findings adrenocorticotropin hormone (ACTH)
Between weakness/collapse episodes, physical stimulation test.
and neurologic examinations are normal. DIAGNOSIS • Cataplexy—peracute, nonprogressive, brief
DIFFERENTIAL DIAGNOSIS episodes of flaccid paralysis.
Features of Weakness/Collapse • Heat stroke—collapse due to heat stroke is
Episodes • The episodic nature of the collapse,
association with exercise and excitement, usually associated with bleeding, shock, and
• Weakness occurs after 5–20 minutes of abnormal mentation. Acute renal failure,
intense exercise with excitement or stress. typical features of collapse including rear
limb weakness and normal mentation, disseminated intravascular coagulation (DIC),
• Rear limbs become weak and unable to and death are common. Recovery, if it does
support weight. progression of weakness during an episode,
and rapid complete recovery should lead to a occur, is prolonged.
• Rear limb muscles are flaccid during • Malignant hyperthermia—hypermetabolic
collapse and there is a loss of patellar reflexes. presumptive diagnosis of EIC in an otherwise
healthy Labrador retriever. Physical and state triggered by certain anesthetics, extreme
• Dogs may continue to run, dragging their heat, intense activity, or psychologic stress in
rear limbs in a crouched posture. neurologic examinations are normal; further
evaluation should be performed to eliminate genetically susceptible dogs. Hyperthermia,
• During a severe episode, all four limbs can be generalized skeletal muscle contraction,
affected; rarely the dog may become recumbent other causes of weakness and collapse.
Genetic testing is required to confirm the rhabdomyolysis, and DIC occur and many
and unable to move its limbs or raise its head. dogs die. Recovery, if it does occur, is
• Dogs remain conscious and fully alert diagnosis of EIC.
• The disorder most often confused with EIC
prolonged. In vitro contracture tests on
during episodes. muscle biopsies or identification of the
• There is no apparent pain or discomfort on is a focal seizure/movement disorder
characterized by brief episodes of abnormal causative genetic mutation of the ryanodine
palpation or manipulation of the muscles, receptor (RYR1) is required for diagnosis.
joints, or spine during or after collapse. crouched gait, disequilibrium, head-bobbing,
• Complete recovery occurs within 5–30 or incoordination. Episodes are often induced CBC/BIOCHEMISTRY/URINALYSIS
minutes. by exercise/excitement, leading to confusion Normal at rest and during collapse.
• Rectal temperature is elevated (mean with EIC. The onset of signs is peracute, the OTHER LABORATORY TESTS
>107 °F; >41.6 °C), but not different from episodes are short (usually less than 5 • Arterial blood gas—normal at rest,
Labradors without exercise-induced collapse minutes), all limbs are involved, and recovery respiratory alkalosis and metabolic acidosis
doing similar exercise. is immediate, helping to distinguish this during collapse identical to intensively
• A few dogs with exercise-induced collapse disorder from the more progressive gait exercising Labradors without EIC.
(EIC) have died during collapse—death is disturbance caused by EIC. Diagnosis can • Lactate and pyruvate—normal at rest, not
usually preceded by a short generalized only be made by ruling out other disorders different during collapse from exercising
seizure. The cause of death is uncertain, but (including EIC) with testing. Labradors without EIC.
weakness of the respiratory muscles and • Dogs with metabolic myopathies, • Thyroid evaluation—normal.
extreme hyperthermia are suspected. polymyositis, and myasthenia gravis are • ACTH stimulation test—normal.
typically much more exercise intolerant than
(continued) Exercise-Induced Weakness/Collapse in Labrador Retrievers
• Analysis for mutation in RYR1 causing CLIENT EDUCATION bred or should be bred only to known
malignant hyperthermia—negative. • Signs commonly worsen in the 3–5 minutes noncarriers to avoid producing affected
• Testing for acetylcholine receptor after exercise is terminated; some (<5%) offspring.
antibodies causing acquired myasthenia affected dogs die during collapse. • Carrier dogs (with one copy of the DNM1
gravis— negative. • All activity should be halted at the first sign mutation) should only be bred to known
of weakness or incoordination. noncarriers to avoid producing affected
E
IMAGING
Thoracic and abdominal radiographs, abdominal • Consider offering cool water orally, spraying offspring.
ultrasound, echocardiography—normal. with water, or immersing in water to lower ABBREVIATIONS
body temperature. • ACTH = adrenocorticotropin hormone.
• DIC = disseminated intravascular
ECG findings at rest and during collapse—
normal. coagulation.
• EIC = exercise-induced collapse.
DNA Testing
MEDICATIONS INTERNET RESOURCES
• Definitive diagnosis requires demonstration
that a dog has two copies of the causative DRUG(S) OF CHOICE https://www.vetmed.umn.edu/research/labs/
DNM1 mutation. There is no recommended drug therapy for canine-genetics-lab/genetic-testing/
• Testing can be performed on blood, cheek this disorder. exercise-induced-collapse
swabs, puppy dewclaws, or semen. Suggested Reading
• Approximately 6% of all tested Labrador Furrow E, Minor KM, Taylor SM, et al.
retrievers have two copies of the DNM1 Relationship between Dynamin-1 mutation
mutation (affected); >35% of all tested status and phenotype in 109 Labrador
Labrador retrievers have one copy of the
FOLLOW-UP retrievers with recurrent collapse during
Most affected dogs can be managed effectively
DNM1 mutation (carrier). exercise. J Am Vet Med Assoc 2013,
by avoiding trigger activities and carefully
• Finding two copies of the DNM1 mutation 242:786–791.
observing for the first signs of weakness.
confirms that a dog is EIC affected and Patterson EE, Minor KM, Tchernatynskaia
susceptible to collapse, but does not rule out AV, et al. A canine DNM1 mutation is
other causes of exercise intolerance or highly associated with the syndrome of
collapse. It is important to do the necessary exercise-induced collapse. Nat Genet 2008,
tests to rule out other causes of collapse that MISCELLANEOUS 40(10):1235–1239.
may be potentially more treatable. Taylor SM, Shmon CL, Adams VJ, et al.
PATHOLOGIC FINDINGS Evaluations of Labrador retrievers with
Dogs with EIC do not develop other
• Muscle histology—normal.
exercise-induced collapse, including
associated medical conditions as they age.
• Complete postmortem examinations of dogs
response to a standardized strenuous
AGE-RELATED FACTORS exercise protocol. J Am Anim Hosp Assoc
dying during collapse due to EIC—normal.
Episodes of collapse may become less 2009, 45:3–13.
frequent as dogs age, perhaps because Taylor SM, Shmon CL, Shelton GD, et al.
of less excitement associated with trigger Exercise induced collapse of Labrador
activities. retrievers: survey results and preliminary
TREATMENT PREGNANCY/FERTILITY/BREEDING investigation of heritability. J Am Animal
ACTIVITY • Animals should be tested to establish their Hosp Assoc 2008, 44:295–301.
Most affected dogs can live normal active lives EIC status prior to breeding. Author Susan M. Taylor
if specific trigger activities are avoided or • Affected dogs (with two copies of the
done in moderation. DNM1 mutation) should not be
Exocrine Pancreatic Insufficiency

with weight loss and loose stools. Other Exocrine Pancreatic Function
• Severity—varies depending on time until Tests
diagnosis and therapy. • Assays of fecal proteolytic activity using
BASICS casein-based substrates have been used to
Historical Findings
E DEFINITION • Weight loss with normal to increased diagnose EPI in both dogs and cats; however,
Syndrome that is caused by inadequate appetite. • Chronically loose stools or fecal proteolytic activity is associated with
amounts of pancreatic digestive enzymes in diarrhea. • Fecal volumes are larger than false-positive and false-negative test results
the small intestinal lumen. normal and may be associated with steator- and should only be used in exotic species for
PATHOPHYSIOLOGY rhea. • Flatulence and borborygmus are which a serum TLI test is not available. • An
• Most commonly caused by insufficient commonly reported, especially in dogs. assay for the measurement of fecal elastase has
synthesis and secretion of pancreatic enzymes • May show coprophagia and/or pica. • May been validated for the dog; however, this test
by the exocrine pancreas. • In rare cases can be accompanied by polyuria/polydipsia with is associated with a high rate of false-positive
be caused by an obstruction of the pancreatic diabetes mellitus as a sequel to chronic test results; therefore a positive test result,
duct or isolated lipase deficiency. pancreatitis. suggesting EPI, must be verified by measure-
• Insufficient synthesis of pancreatic digestive ment of a serum cTLI concentration.
enzymes can be due to destruction of acinar • Thin body condition. • Decreased muscle Screening Tests for Malassimilation
cells resulting from chronic pancreatitis mass. • Poor-quality hair coat. • Cats with Microscopic examination of feces for
(approximately 50% of cases in dogs and steatorrhea may have greasy “soiling” of the undigested food, assessment of fecal proteo-
almost all cases in cats) or can be due to hair coat in the perineal area, but this is seen lytic activity, and the plasma turbidity test are
idiopathic pancreatic acinar atrophy (PAA; in the minority of cases. unreliable and not recommended.
most common cause of exocrine pancreatic
insufficiency in German shepherd dogs). CAUSES Cobalamin and Folate
• Deficient exocrine pancreatic secretion • PAA. • Chronic pancreatitis. • Pancreatic • Often run as a panel with TLI. • Used to assess
results in maldigestion and nutrient malab- adenocarcinoma or other abdominal tumor for concurrent small intestinal dysbiosis or
sorption, leading to weight loss and loose leading to pancreatic duct obstruction concurrent small intestinal disease (such as
stools with steatorrhea. • Malabsorption RISK FACTORS inflammatory bowel disease [IBD]). • Cobalamin
contributes to small intestinal dysbiosis. • Breed—German shepherd dogs, rough- (vitamin B12) is frequently deficient in both dogs
coated collies, and Eurasians. • Any and cats with EPI and can lead to treatment
SYSTEMS AFFECTED failure or complications if not addressed.
Nutritional—protein-calorie malnourish- condition predisposing dogs or cats to chronic
ment. pancreatitis. IMAGING
GENETICS Abdominal radiography and ultrasonography
Assumed to be hereditary in the German are unremarkable unless the patient has
shepherd dog and probably transmitted by a concurrent conditions.
complex trait (early studies have suggested an DIAGNOSIS DIAGNOSTIC PROCEDURES
autosomal recessive trait, but this is no longer N/A
believed to be the case). DIFFERENTIAL DIAGNOSIS
• Secondary causes of chronic diarrhea and PATHOLOGIC FINDINGS
INCIDENCE/PREVALENCE weight loss (e.g., hepatic failure, renal failure, • Chronic pancreatitis—microscopically, acini and
• PAA is very commonly seen in the German hypoadrenocorticism, and hyperthyroidism in possibly islets are depleted and replaced by fibrous
shepherd dog; it is less commonly seen in cats). • Primary gastrointestinal disease (e.g., tissue; there may also be an active inflamma-
rough-coated collies and Eurasians. • Other infectious, inflammatory, neoplastic, tory infiltration. • PAA—marked atrophy/
causes of exocrine pancreatic insufficiency mechanical, or toxic). absence of pancreatic acinar tissue on gross
(EPI) may be seen in all dog and cat breeds. and histopathologic inspection in dogs with PAA.
• Less common in cats than in dogs. CBC/BIOCHEMISTRY/URINALYSIS
Usually normal.
None OTHER LABORATORY TESTS
SIGNALMENT Direct/Indirect Fecal Examinations
Negative for parasites. TREATMENT
Species
Dog and cat. Exocrine Pancreatic Function Tests— APPROPRIATE HEALTH CARE
Trypsin-Like Immunoreactivity (TLI) • Outpatient medical management.
Breed Predilections
• Diagnostic test of choice in both dogs and • Patients with concurrent diabetes mellitus
German shepherd dogs, rough-coated collies,
cats. • Principle of test—serum TLI can be may initially require hospitalization if ill (e.g.,
and Eurasians.
measured by an assay that detects trypsinogen diabetic ketoacidosis).
Mean Age and Range and trypsin that is directly released into the
• PAA in young adult dogs. • Chronic blood from pancreatic acinar cells; serum TLI NURSING CARE
pancreatitis in dogs and cats of any age. is detected in the serum of all normal dogs and N/A
Predominant Sex cats with a functional exocrine pancreatic mass. ACTIVITY
No sex predilection. • Serum TLI concentrations are dramatically No restriction.
reduced with EPI—dogs: cTLI ≤2.5 μg/L;
SIGNS DIET
cats: fTLI ≤8.0 μg/L. • The TLI tests are
• Type of diet does not play a role in the
General Comments species specific. • Advantages—simple; quick;
management of EPI in dogs and cats.
• Consider in young adult (age range approx- single serum specimen (fasted); highly sensitive
• However, low-fat and high-fiber diets
imately 1–4 years) German shepherd dogs and specific for EPI in both species.
should be avoided.
(continued) Exocrine Pancreatic Insufficiency

CLIENT EDUCATION can often be successfully managed by addition of AGE-RELATED FACTORS
• Discuss hereditary nature in German shepherd fish oil to the enzyme supplement or administra- Consider EPI in young adult German shepherd
dogs. • Discuss expense of pancreatic enzyme tion of raw beef, pork, or game pancreas. • Each dogs with weight loss and loose stools.
supplementation and need for lifelong therapy. teaspoon of pancreatic enzyme supplement ZOONOTIC POTENTIAL
• Discuss the possibility of diabetes mellitus in needs to be replaced with 1–3 ounces (approxi-
patients with chronic pancreatitis. mately 30–90 g) of raw chopped pancreas.
None E
• Raw pancreas can be kept frozen for months PREGNANCY/FERTILITY/BREEDING
SURGICAL CONSIDERATIONS Do not breed animals with EPI suspected to
Mesenteric torsion has been reported in without losing enzymatic activity.
be due to PAA.
German shepherd dogs with EPI in Finland,
but not North America. SYNONYMS
None
FOLLOW-UP SEE ALSO
• Cobalamin Deficiency.
PATIENT MONITORING
• Diarrhea, Chronic—Cats.
MEDICATIONS • Weekly for first month of therapy.
• Diarrhea, Chronic—Dogs.
DRUG(S) OF CHOICE • Diarrhea improves markedly—fecal
• Pancreatitis—Cats.
• Powdered pancreatic enzymes are the treat-
consistency typically normalizes within 1
• Small Intestinal Dysbiosis.
ment of choice (as a reference these products week. • Gain in bodyweight. • Patients that
should contain at least 70,000 USP of lipase per fail to respond after 2 weeks of enzyme ABBREVIATIONS
therapy and cobalamin supplemenation • cTLI = canine trypsin-like immunoreactivity.
teaspoon). • In Europe, microencapsulated
should be treated for secondary intestinal • EPI = exocrine pancreatic insufficiency.
products are available; because the lipase is
dysbiosis. • Once bodyweight and condition • fTLI = feline trypsin-like immunoreactivity.
protected from gastric inactivation a much
normalize, gradually reduce daily dosage of • IBD = inflammatory bowel disease.
smaller amount is needed for treatment.
enzyme supplements to a level that maintains • PAA = pancreatic acinar atrophy.
• Initially—mix enzyme powder in food at a
normal fecal quality and bodyweight. • TLI = trypsin-like immunoreactivity.
dosage of 1 teaspoon/10 kg body weight with
each meal; feed at least two meals daily to PREVENTION/AVOIDANCE INTERNET RESOURCES
promote weight gain. • Preincubation of Do not breed patients that belong to a breed http://www.vetmed.tamu.edu/gilab
enzymes with food does not improve the predisposed to PAA. Suggested Reading
effectiveness of oral enzyme therapy, but may POSSIBLE COMPLICATIONS Batchelor DJ, Noble PJ, Taylor RH, et al.
negatively impact owner compliance. • Approximately 20% of dogs fail to respond Prognostic factors in canine exocrine
• Approximately 85% of all dogs with EPI and to pancreatic enzymes and need further pancreatic insufficiency: prolonged survival
virtually all cats with EPI are cobalamin deficient evaluation and therapy. • Most patients with is likely if clinical remission is achieved. J
and require parenteral or oral cobalamin EPI have cobalamin deficiency and need to be Vet Intern Med 2007, 21:54–60.
supplementation (see Cobalamin Deficiency for managed accordingly. • Some dogs and cats German AJ. Exocrine pancreatic insufficiency
dosing). • Administration of a proton pump treated with pancreatic enzyme supplements in the dog: breed associations, nutritional
inhibitor (e.g., omeprazole at 0.7–1.0 mg/kg develop oral ulcerations; in most of these considerations, and long-term outcome.
q12h) may improve the condition in nonrespon- patients the dose of pancreatic enzyme Top Companion Anim Med 2012,
sive patients. • Most dogs and cats respond to supplements can be decreased, while maintain- 27:104–108.
therapy within 5–7 days; after a complete ing therapeutic response; in a few patients, the Steiner JM. Exocrine pancreas. In: Steiner
response has been achieved, the amount of dose of the pancreatic enzyme supplement JM, ed., Small Animal Gastroenterology.
pancreatic enzyme supplement may be gradually needs to be adjusted frequently to avoid Hanover: Schlütersche-Verlagsgesellschaft,
reduced to a dose that prevents return of clinical treatment failure and oral ulceration. • Two 2008, pp. 283–306.
signs. • Oral antibiotic therapy (tylosin: 25 mg/ cats with EPI and vitamin K–responsive Thompson KA, Parnell NK, Hohenhaus AE,
kg PO q12h) may be required for 4–6 weeks in coagulopathy have been reported; thus, patients et al. Feline exocrine pancreatic insuffi-
patients with concurrent dysbiosis, but in most that present with a bleeding diathesis should be ciency: 16 cases (1992–2007). J Feline Med
patients dysbiosis resolves spontaneously upon further evaluated and possibly treated with Surg 2009, 11:935–940.
commencement of enzyme replacement therapy. parenteral vitamin K supplementation. Westermarck E, Wiberg M. Exocrine
• Severely malnourished dogs may also require pancreatic insufficiency in the dog:
supplementation with tocopherol; body stores of EXPECTED COURSE AND PROGNOSIS
• Most causes are irreversible, and lifelong
historical background, diagnosis, and
other fat-soluble vitamins are probably also treatment. Top Companion Anim Med
decreased in dogs and cats with EPI, but therapy is required. • Patients with EPI alone
have a good prognosis with appropriate enzyme 2012, 27:96–103.
supplementation does not appear to be crucial. Xenoulis PG, Zoran DL, Fosgate GT, et al.
supplementation and supportive management.
CONTRAINDICATIONS • Prognosis is more guarded in patients with Feline exocrine pancreatic insufficiency: a
Avoid tablets and capsules, as mixing of EPI and concurrent diabetes mellitus. retrospective study of 150 cases. J Vet Intern
enzymes and chyme is unpredictable. Med 2016, 30:1790–1797.
PRECAUTIONS Author Jörg M. Steiner
N/A Consulting Editor Mark P. Rondeau
POSSIBLE INTERACTIONS MISCELLANEOUS

N/A Client Education Handout
ASSOCIATED CONDITIONS available online
ALTERNATIVE DRUG(S) • Dysbiosis. • Cobalamin deficiency. • IBD.
• The cost of pancreatic enzyme replacement is • Diabetes mellitus. • Associated vitamin
very high; also, some cats refuse to consume the K–responsive coagulopathy.
pancreatic enzyme supplement; these patients
Eyelash Disorders (Trichiasis/Distichiasis/Ectopic Cilia)

Ectopic Cilia Ectopic Cilia
• Unilateral or bilateral; typically central/ • Surgical treatment—en bloc resection of
upper eyelid. • Hair may be pigmented or the cilia and associated meibomian gland.
BASICS nonpigmented. • Severe blepharospasm. • Cryotherapy—may be used as sole treat-
OVERVIEW • Epiphora. • Conjunctivitis. • Recurrent ment or adjunct after resection. • May
E • Trichiasis—normal hair from the skin superficial corneal ulcers. develop ectopic cilia at other locations.
contacting corneal or conjunctival surface. • Recheck if clinical signs recur.
• Distichiasis—abnormal hairs that emerge • Trichiasis—often related to conformation.
from the meibomian glands along the eyelid • Secondary (acquired) entropion may be
margin; may contact corneal or conjunctival associated with pain (spastic entropion),
surface. • Ectopic cilia—abnormal hairs that scarring (cicatricial entropion), or
emerge through the palpebral conjunctiva
MEDICATIONS
enophthalmos; occasionally seen in cats.
several millimeters from the lid margin; • Distichiasis—considered to be inherited; DRUG(S) OF CHOICE
contact the corneal surface. many predisposed breeds. • Eyelid agenesis • Rarely indicated. • Lubricant ointments—
SIGNALMENT (eyelid coloboma)—may be hereditable or lessen irritation before surgical correction.
• Trichiasis: ◦ Facial fold trichiasis— due to in utero viral infection. • Ectopic • Soft contact lens—temporary relief of
brachycephalic dogs with prominent facial cilia—multiple breeds predisposed. clinical signs before surgical correction.
folds or a shallow orbit and prominent globe • Topical antibiotics—for ulcerative keratitis,
(e.g., Pekingese, pug, English bulldog). prophylactic following surgical eyelid
◦ Entropion—rolling in of eyelid margin; procedures.
conformational (primary) entropion common CONTRAINDICATIONS/POSSIBLE
in young dogs in predisposed breeds (shar pei, DIAGNOSIS
INTERACTIONS
retrievers, chow chow, English bulldog, DIFFERENTIAL DIAGNOSIS N/A
among others); secondary (acquired) • Other adnexal abnormalities.
entropion may occur in dogs and cats of any • Keratoconjunctivitis sicca. • Conjunctival
breed or age. ◦ Eyelid agenesis (eyelid foreign body. • Infectious or inflammatory
coloboma)—congenital in cats; sporadic conjunctivitis. • Diagnosis based on observation
occurrence. • Distichiasis— common in of abnormal cilia and lid/facial conformation. FOLLOW-UP
young dogs; rare in cats; some predisposed • Trichiasis—good prognosis; some corneal
breeds include spaniels, English bulldog, CBC/BIOCHEMISTRY/URINALYSIS changes may be permanent. • Distichiasis—
flat-coated retriever, and dachshund. • Ectopic N/A regrowth may occur; destructive procedures
cilia—common in young dogs, rare in cats; OTHER LABORATORY TESTS must be done conservatively to minimize lid
predisposed breeds include Pekingese, shih N/A damage. • Ectopic cilia—good prognosis;
tzu, and English bulldog. regrowth may occur.
IMAGING
SIGNS N/A
Facial-Fold Trichiasis DIAGNOSTIC PROCEDURES
• Commonly bilateral. • Epiphora. Ocular examination with magnification.
• Pigmentary keratitis (especially nasally). MISCELLANEOUS
• Often associated with lagophthalmos Suggested Reading
(incomplete blink). • Blepharospasm if Bettenay S, Mueller RS, Maggs DJ. Diseases
ulcerative keratitis present. of the eyelids. In: Maggs DJ, Miller PE,
TREATMENT
Trichiasis Associated with Entropion Ofri R, Slatter’s Fundamentals of Veterinary
• Bilateral if primary. • Blepharospasm. Trichiasis Ophthalmology, 6th ed. St. Louis, MO:
• Epiphora. • Conjunctivitis. • Keratitis • Conservative management—topical lubricating Saunders, 2018, pp. 127–157.
(vascularization, pigmentation, possibly ointments. • Clipping hair on facial folds may Gelatt KN, Plummer CE. Canine eyelids. In:
ulcerative). cause hairs to become stiffer and more irritating. Gelatt KN, Plummer CE, eds., Color Atlas
• Surgical correction of adnexal abnormalities of Veterinary Ophthalmology, 2nd ed.
Eyelid Agenesis (primary entropion, eyelid agenesis). • Reduce/ Wiley-Blackwell, 2017, pp. 67–85.
• Typically bilateral. • Absent portion of remove facial folds in contact with ocular surface. Author Renee T. Carter
dorsal-lateral eyelid margin. • Other • Medial canthoplasty—for nasal trichiasis; Consulting Editor Kathern E. Myrna
intraocular congenital abnormalities are reduces lagophthalmos and medial entropion. Acknowledgment The author and book
common. • Conjunctivitis. • Keratitis • Treat underlying cause (e.g., spastic entropion, editors acknowledge the prior contribution of
(vascularization, pigmentation; possibly enophthalmia); temporary eyelid tacking may be Filipe Espinheira.
ulcerative). • Lagophthalmos. indicated.
• Blepharospasm.
Distichiasis
Distichiasis • If asymptomatic, no treatment is required.
• Involves upper and/or lower eyelid margin; • Symptomatic—mechanical removal
unilateral or bilateral. • Soft hairs and those (periodic manual epilation) or surgical
directed away from the cornea: asymptomatic. destruction of hair follicles by cryoepilation,
• Stiff, stout cilia contacting the cornea: electroepilation, or transconjunctival electro-
blepharospasm, epiphora, conjunctivitis, and cautery. • Avoid lid-splitting and partial tarsal
keratitis (vascularization, pigmentation; plate excision techniques; may predispose to
possibly ulcerative). cicatricial entropion and impaired lid function.
Facial Nerve Paresis and Paralysis

• Facial asymmetry. • Neoplastic—aural cholesteatoma, squamous
• Eye—inability to close eyelids, rubbing, cell carcinoma.
ocular discharge, ulceration. • Trauma—fracture of petrous temporal bone,
BASICS direct injury to facial nerve by laceration, or
Physical Examination Findings compression by hematoma or other mass.
DEFINITION
• Facial asymmetry—lip and ear droop, wide
Dysfunction of the facial nerve (cranial nerve • Toxic—tick bite paralysis (Dermacentor spp.
palpebral fissure, collapse of nostril.
[CN] VII) causing paresis (weakness) or
• Decreased or absent palpebral reflex.
(humans), Ixodes holocyclus). F
paralysis of the muscles of facial expression, Bilateral Peripheral
• Decreased or absent menace response (may
which include the ears, eyelids, lips, and nostrils. • Idiopathic.
see eye retraction rather than lid closure).
PATHOPHYSIOLOGY • Inability to close eyelids. • Immune-mediated—polyradiculoneuritis
• Central—impairment of the facial nucleus • Excessive drooling or food falling from (coonhound paralysis), polyneuropathy,
within the rostral medulla (brainstem). mouth on affected side. myasthenia gravis.
• Peripheral—impairment of the facial nerve • Chronically, patients may have facial • Metabolic—paraneoplastic polyneuropathy
anywhere along its length or at the muscle contraction toward the affected side (e.g., insulinoma), hypothyroidism.
neuromuscular junction. due to muscle fibrosis subsequent to paralysis • Toxic—botulism.
SYSTEMS AFFECTED and denervation. CNS
• Nervous—facial nerve peripherally or its • Decreased Schirmer tear test, mucopurulent • Most unilateral.
nucleus centrally. discharge from affected eye, and exposure • Infectious—viral, bacterial, fungal,
• Ophthalmic—if parasympathetic conjunctivitis or keratitis with concurrent rickettsial, protozoal encephalitis.
preganglionic neurons that supply the KCS. • Inflammatory—meningoencephalitis of
lacrimal gland and gland of the third eyelid • Altered mentation (e.g., somnolence or unknown etiology (MUE).
that course with the facial nerve proximally stupor) and/or other cranial nerve • Neoplastic—primary such as meningioma,
are affected, keratoconjunctivitis sicca (KCS) abnormalities and gait disturbances may be choroid plexus tumor, lymphoma; metastatic
develops due to lack of tear secretion. noted when secondary to intracranial tumor such as hemangiosarcoma, carcinoma.
(brainstem) disease.
GENETICS • Hemifacial spasms (facial nerve tetanus) RISK FACTORS
N/A may be infrequently observed in lesions Chronic otitis externa and otitis media.
INCIDENCE/PREVALENCE affecting the facial nerve such as neuritis or
More common in dogs than cats. otitis media. These patients have sustained
contraction of the facial muscles, giving a
SIGNALMENT
“grinning” appearance to the affected side of DIAGNOSIS
Species the face. This is a dynamic process and at
Dog and cat. times the face will appear normal, only to DIFFERENTIAL DIAGNOSIS
begin the “grinning” appearance once again. If • Differentiate unilateral from bilateral
Breed Predilections involvement.
Idiopathic paralysis—cocker spaniel, beagle, one notices this clinical presentation, middle
ear disease should be investigated thoroughly. • Look for other neurologic deficits—
Pembroke Welsh corgi, boxer, English setter, behavior change, gait disturbance, other CN
golden retriever, and domestic longhair cats. • Intermittent facial paresis can be observed
in patients with a contralateral thalamocortical deficits.
Mean Age and Range lesion when patient is relaxed—due to • Idiopathic—diagnosis of exclusion; no
Adults “release” of upper motor neuron influence on historical or physical signs of ear disease and
lower motor neuron (CN VII). no other neurologic deficits.
Predominant Sex
• Concurrent heat tilt on ipsilateral side with • Hypothyroidism—with clinical evidence
N/A
concurrent otitis interna. (e.g., lethargy, poor hair coat, weight gain,
SIGNS anemia, hypercholesterolemia, ↓FT4, ↑canine
• Concurrent head tilt on ipsilateral side
General Comments with concurrent idiopathic vestibular thyroid-stimulating hormone [cTSH]).
• Assess strength of palpebral closure—there neuropathy. • Otitis media–interna—Horner’s syndrome,
should be full eyelid closure when a finger is • Abnormal tympanum (bulging, opaque, head tilt, and KCS may be simultaneously
gently passed over the eyelids. rupture) on otoscopic examination. Obvious present.
• Idiopathic—unaffected side may become external ear disease may not be present with • CNS disease—if there is somnolence, gait
affected within a few weeks to months; may otitis media. disturbances, or other CN deficits.
rarely occur bilaterally at first presentation; CBC/BIOCHEMISTRY/URINALYSIS
can have concurrent idiopathic vestibular CAUSES • Usually normal in idiopathic facial
neuropathy. Unilateral Peripheral paralysis.
• Most patients with bilateral nerve • Idiopathic. • Fasting hypercholesterolemia, normocytic/
involvement have polyneuropathy-associated • Metabolic—hypothyroidism. normochromic nonregenerative anemia may
systemic disease—look for other nerve deficits. • Infectious—otitis media–interna (dogs and be observed with hypothyroidism-associated
• May accompany other clinical signs and/or cats). facial paralysis.
neurologic deficits—always perform a full • Inflammatory—nasopharyngeal polyps • Hypoglycemia with insulinoma.
neurologic examination. (cats), neuritis. OTHER LABORATORY TESTS
• Ear droop is not always evident in cats and • Iatrogenic—secondary to surgical ablation • Indicated for patients with suspected
dogs with erect ears. of external ear canal or bulla osteotomy; underlying disease
Historical Findings secondary to exuberant ear cleaning; • Insulin : glucose ratio to detect insulinoma.
• Messy eating; food left around mouth. idiosyncratic reaction to potentiated • Acetylcholine receptor antibodies to
• Excessive drooling on affected side. sulfonamides (dogs). diagnose myasthenia gravis.
Facial Nerve Paresis and Paralysis (continued)
• Free T4 (ideally by equilibrium dialysis) and needed if animal is a breed with natural • Improvement may take weeks or months or
cTSH to diagnose hypothyroidism. exophthalmia; client must regularly check may never occur.
IMAGING eyes for redness, discharge, or pain that may • Lip contracture sometimes develops.
• CT—sensitive to evaluate middle–inner ear
indicate corneal ulcer. • Corneal ulcers may perforate and require
diseases, preferred modality to evaluate bony • Inform client that most animals tolerate enucleation.
structures in middle ear. this nerve deficit well; there is no significant
F • MRI—superior to CT for intracranial
impact on quality of life.
imaging, preferable for CNS disease; contrast SURGICAL CONSIDERATIONS
enhancement of facial nerve in dogs with Bulla osteotomy may be indicated for patients
idiopathic facial nerve paralysis; the greater with disorders of middle ear. MISCELLANEOUS
the extent of enhancement, the poorer the ASSOCIATED CONDITIONS
prognosis for return to function. Otitis
• Bullae radiographs—four views; two
obliques, 30° open mouth, dorso-ventral; not AGE-RELATED FACTORS
sensitive for middle–inner ear diseases. MEDICATIONS N/A
DIAGNOSTIC PROCEDURES DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING
• Schirmer test—evaluate tear production • Treat specific disease if possible (e.g., N/A
(normal >15 mm in 60 seconds), should thyroxine for hypothyroidism). SYNONYMS
always be performed when evaluating a • Idiopathic disease—no treatment required; • Facial neuritis.
patient with facial paresis/paralysis. efficacy of corticosteroids unknown and used • Facial palsy.
• Fluorescein test—evaluate for presence of commonly in humans to treat Bell’s palsy, • Idiopathic facial neuropathy.
corneal ulceration secondary to KCS. however are not recommended in veterinary
• Otoscopic examination—evaluate integrity medicine at this time. SEE ALSO
of tympanic membrane and for evidence of • Tear replacement if Schirmer test value low • Hypothyroidism.
otitis media. (<15 mm), in patients with KCS or with • Keratitis—Ulcerative.
• Cerebrospinal fluid (CSF)—evaluate for exophthalmic globes. • Keratoconjunctivitis Sicca.
evidence of intracranial disease; not sensitive • Otitis Media and Interna.
CONTRAINDICATIONS
if used alone, should be combined with If middle ear disease is suspected, and ABBREVIATIONS
diagnostic imaging (e.g., MRI). tympanic membrane may be ruptured, do not • CN = cranial nerve.
• Facial muscle electromyography—evaluate use topical ear cleaning solutions due to risk • CSF = cerebrospinal fluid.
for denervation and neuromuscular disease. of ototoxicity. • cTSH = canine thyroid-stimulating
• Facial and trigeminal nerve reflex hormone.
electrodiagnostic testing—evaluate peripheral PRECAUTIONS
• KCS = keratoconjunctivitis sicca.
nerve integrity, distinguish between N/A
• MUE = meningoencephalitis of unknown
peripheral and central lesions. etiology.
PATHOLOGIC FINDINGS Suggested Reading
Idiopathic—may see degeneration of large Cook LB. Neurologic evaluation of the ear.
and small myelinated fibers without evidence FOLLOW-UP Vet Clin North Am Small Anim Pract 2004,
of inflammation. 34:425–435.
PATIENT MONITORING
• Reevaluate early for evidence of corneal
de Lahunta A, Glass EN, Kent M. Veterinary
ulcers. Neuroanatomy and Clinical Neurology, 4th
• Reassess monthly (for 2–3 months) for
ed. St. Louis, MO: Elsevier Saunders, 2015,
TREATMENT menace responses, palpebral reflexes, and lip pp. 172–180.
and ear movements to evaluate return of Jeandel A, Thibaud JL, Blot S. Facial and
APPROPRIATE HEALTH CARE vestibular neuropathy of unknown origin in
• Outpatient—idiopathic facial paralysis.
function, condition of affected eye, and
development of other neurologic deficits that 16 dogs. J Small Anim Pract 2016,
• Inpatient—initial medical workup and 57:74–78.
management of systemic or CNS disease if would indicate progressive disease.
Kern TJ, Erb HN. Facial neuropathy in dogs
present. PREVENTION/AVOIDANCE and cats: 95 cases (1975–1985). J Am Vet
DIET N/A Med Assoc 1987, 191(12):1604–1609.
No change required. POSSIBLE COMPLICATIONS Varejao AS, Munoz A, Lorenzo V. Magnetic
• KCS. resonance imaging of the intratemporal
CLIENT EDUCATION facial nerve in idiopathic facial paralysis in
• Corneal ulcers.
• Clinical signs may be permanent; however, as the dog. Vet Radiol Ultrasound 2006,
• Permanent facial asymmetry (aesthetic
muscle fibrosis develops, there is a natural “tuck 47(4):328–333.
up” of the affected side that reduces asymmetry; only).
Author Andrea M. Finnen
drooling usually stops within 2–4 weeks. EXPECTED COURSE AND PROGNOSIS
• Inform client that other side can become • Depends on underlying cause if one is
affected. present. Client Education Handout
• Discuss eye care—cornea on affected side • Idiopathic disease—prognosis guarded for available online
may need lubrication; extra care may be full recovery.
False Pregnancy
SIGNALMENT • Mammary neoplasia.
• Mammary hyperplasia (queens).
Species
• Pyometra.
BASICS Dog and cat.
• Other causes of abdominal distension
DEFINITION Breed Predilections (organomegaly, ascites).
• Physical and behavioral changes resulting None • Hypothyroidism.
from normal hormonal changes during Mean Age and Range • Pituitary tumor causing hyperprolactinemia F
diestrus and early anestrus in the nonpregnant Any age. (rare).
bitch. The term false pregnancy is a misnomer, CBC/BIOCHEMISTRY/URINALYSIS
Predominant Sex
since the pattern of hormonal changes is • Normocytic, normochromic anemia—17–21%
Female only.
normal. decrease in hematocrit during late diestrus.
• Physical, hormonal, and behavioral changes SIGNS • Hypercholesterolemia—75–94% increase
following a nonfertile mating or spontaneous General Comments during diestrus.
ovulation in the queen. • Although all cycling bitches have similar OTHER LABORATORY TESTS
PATHOPHYSIOLOGY progesterone and prolactin hormone profiles Serum progesterone concentrations elevated if
• Hormone profile of pregnant and nonpregnant during late diestrus and early anestrus, they vary tested during diestrus.
bitch very similar following ovulation. in the magnitude of clinical symptoms associated
• All cycling bitches undergo a lengthy (2+ with the false pregnancy. This may be due in part IMAGING
months) diestrus following ovulation. to individual sensitivities to prolactin. • Ultrasonography—uterine enlargement;
• Mammary development and behavioral • Some bitches experience repeated overt false performed after 25 days from mating; can be
changes occur under the influence of pregnancies, while others have covert false used to evaluate for pregnancy and uterine
progesterone and prolactin in late diestrus. pregnancies. fluid accumulation.
• Galactorrhea (excessive production and • The magnitude of symptoms can vary • Radiography—normal; performed after 54
inappropriate excretion of milk) is seen during individual false pregnancies for the days from mating; can be used to detect presence
following a rise in serum prolactin at the end same bitch. of fetal skeletons and uterine fluid accumulation.
of diestrus, and also in dogs with severe • Overt symptoms are uncommon in queens. DIAGNOSTIC PROCEDURES
hypothyroidism due to resulting Historical Findings N/A
hyperprolactinemia. • Estrus—bitch: ~6–12 weeks previously; PATHOLOGIC FINDINGS
• False pregnancies in the bitch are thought queen: ~40 days previously. N/A
to occur as a holdover from a period in • OVE or OHE during diestrus, 3–14 days
evolution when females of a pack would cycle prior to presentation.
at the same time, but only dominant • Mammary gland development.
individuals would become pregnant. • Galactorrhea.
Nonpregnant pack members were available to • Weight gain. TREATMENT
nurse puppies of the more dominant females. • Behavior change including nesting, APPROPRIATE HEALTH CARE
• Any event that results in an abrupt drop in maternal behavior, aggression, lethargy. • Usually no treatment needed.
serum progesterone and rise in prolactin can • Inappetence. • Outpatient treatment for medical
lead to a clinically overt false pregnancy. Signs • Abdominal distension (rare). management of severe clinical signs of false
are frequently created iatrogenically when
Physical Examination Findings pregnancy.
ovariectomy (OVE) or ovariohysterectomy
(OHE) is performed during mid to late diestrus. • Mammary gland hypertrophy. NURSING CARE
• Queens that ovulate spontaneously or ovulate • Galactorrhea—fluid can be clear to milky • Prevent mammary gland stimulation from
following mating but do not become pregnant to brown in color. self-nursing with Elizabethan collar or body suit.
experience a 6–7-week period of diestrus due to CAUSES • Owners can cold pack mammary glands to
elevated progesterone concentrations; some • Decline in serum progesterone reduce mammary gland activity.
queens develop a clinically overt false pregnancy concentration and rise in serum prolactin ACTIVITY
during this time. concentration. Increase activity in sedentary dogs and cats to
SYSTEMS AFFECTED • Decline in serum progesterone increase caloric expenditure and decrease
• Reproductive. concentrations due to OVE or OHE during calories available for lactation.
• Behavioral. diestrus.
• Hyperprolactinemia—can be due to severe DIET
• Endocrine. Decrease caloric intake for several days to
hypothyroidism.
GENETICS reduce energy available for lactation.
N/A RISK FACTORS
• OHE or OVE during diestrus. CLIENT EDUCATION
INCIDENCE/PREVALENCE • Does not impact future fertility. • False pregnancies are normal in bitches and
• False pregnancies occur in 100% of bitches do not impact future fertility.
following ovulation. • Advise cat owners that pyometra can
• >60% of cycling bitches exhibit signs of develop following spontaneous ovulations.
false pregnancy. SURGICAL CONSIDERATIONS
• Spontaneous ovulation occurs frequently in DIAGNOSIS • OVE or OHE if bitch or queen is not
the queen (35–85%) depending on presence of DIFFERENTIAL DIAGNOSIS intended for use in a breeding program.
other queens and tom. False pregnancy occurs • Pregnancy. • Perform OVE or OHE during anestrus or
after every nonpregnant ovulation in the • Mastitis. early diestrus when possible.
queen, but overt symptoms are uncommon.
False Pregnancy (continued)
should be explained and owners should give • Bitches and queens should be evaluated for
informed consent prior to treatment. Do not possible pregnancy before treating for false
give to cats. pregnancy.
MEDICATIONS
SYNONYMS
DRUG(S) OF CHOICE • Pseudopregnancy.
• Dopamine agonists—reduce milk • Pseudocyesis.
F production and some maternal behaviors by
FOLLOW-UP • Pseudogestation.
inhibiting prolactin release. • Phantom pregnancy.
• Cabergoline 5 μg/kg PO q24h for 5–7 PATIENT MONITORING • False whelping.
days. Have owners monitor mammary glands for
• Bromocriptine 10 μg/kg PO q8h for 5–7 ABBREVIATIONS
inflammation and discoloration that could
days. • OHE = ovariohysterectomy.
indicate mastitis.
• OVE = ovariectomy.
CONTRAINDICATIONS PREVENTION/AVOIDANCE
Dopamine agonists can cause abortion if Suggested Reading
• Perform OVE or OHE during anestrus or
given to a pregnant bitch or queen, as Gobello C, De La Sota RL, Goya RG. A
early diestrus when possible.
prolactin is luteotrophic. Drugs that suppress review of canine pseudocyesis. Reprod Dom
• Estrus suppression.
prolactin will terminate pregnancy by Anim. 2001, 36:283–288.
reducing progesterone and can cause POSSIBLE COMPLICATIONS Kowalewski MP. Endocrine and molecular
premature parturition (abortion). Mastitis with significant mammary gland control of luteal and placental function in
hypertrophy, galactostasis, and ascending dogs: a review. Reprod Domest Anim 2012,
PRECAUTIONS infection. 47(Suppl 6):19–24.
• Incidence of vomiting with bromocriptine Lee WM, Kooistra HS, Mol JA, et al.
administration reduced if given with food; EXPECTED COURSE AND PROGNOSIS
• Typically resolves in 4–6 weeks without Ovariectomy during the luteal phase
cabergoline has fewer side effects and higher influences secretion of prolactin, growth
efficacy, but is more costly. treatment.
• Resolution in 10–14 days with dopamine hormone, and insulin-like growth factor-I
• Coat color changes in dogs possible with in the bitch. Theriogenology 2006,
prolonged dopamine agonist treatment agonist or mibolerone.
• May recur after any ovulation. 66(2):484–490.
(uncommon). Root AL, Parkin TD, Hutchison P, et al.
POSSIBLE INTERACTIONS Canine pseudopregnancy: an evaluation of
Avoid acepromazine and metoclopramide; prevalence and current treatment protocols
both can promote lactation and reduce in the UK. BMC Vet Res 2018, 14(1):170.
efficacy of dopamine agonists. MISCELLANEOUS Verstegen-Onclin K, Verstegen J.
Endocrinology of pregnancy in the dog: a
ALTERNATIVE DRUG(S) ASSOCIATED CONDITIONS review. Theriogenology 2008,
• Short-term therapy with diazepam can be N/A 70:291–299.
useful for bitches with extreme behavioral
AGE-RELATED FACTORS Author Milan Hess
signs.
N/A Consulting Editor Erin E. Runcan
• Mibolerone 16 μg/kg PO q24h for 5–7 days
to reduce symptoms of false pregnancy. Can ZOONOTIC POTENTIAL
also be used at 2.6 μg/kg/day PO starting at N/A Client Education Handout
least 1 month prior to the next heat cycle to PREGNANCY/FERTILITY/BREEDING available online
suppress estrus in bitches, which will prevent • The tendency to display overt false
recurrence. Side effect and risks of treatment pregnancies has no impact on fertility.
Familial Shar-Pei Fever

INCIDENCE/PREVALENCE • Elevations in serum alkaline phosphatase
• Estimated 23–28% of shar-pei dogs. (ALP) and alanine aminotransferase (ALT)
• Estimated 53% of shar-pei dogs with fever. activities and bilirubin concentration.
BASICS • Proteinuria—in cases of glomerular
SIGNALMENT
DEFINITION • Mean age—4 years.
amyloidosis.
A hereditary autoinflammatory disease in the • Bilirubinuria—secondary to cholestasis or
• Range—19 weeks–9 years.
Chinese Shar-Pei dog characterized by • Sex predisposition—female (female : male,
hepatic failure. F
episodic fever and progressive systemic 2.5 : 1). OTHER LABORATORY TESTS
amyloidosis. • Genetic tests are available for HAS2 and
SIGNS
PATHOPHYSIOLOGY MDM2 binding protein (MTBP) defects.
• Multifactorial disorder caused by genetic General Comments • Coombs’ test, antinuclear antibody test,
defects that induce chronic inflammation and Findings vary depending on distribution and and rheumatoid factor identify concurrent
reactive amyloidosis. Environmental factors severity of amyloidosis. underlying immune-mediated disease.
and gene modifiers play a role. Historical Findings • Prothrombin time (PT) and partial
• Associated with the thick skin phenotype, • Episodic anorexia, lethargy, stiffness, thromboplastin time (PTT)—can be
resulting from an excessive dermal deposition swollen hocks and/or muzzle—self-limiting prolonged with liver failure and disseminated
of hyaluronic acid (HA) by increased (12–36 hours) or responsive to nonsteroidal intravascular coagulation (DIC); DIC may
expression of hyaluronic acid synthase 2 anti-inflammatory drugs (NSAIDs). result in increased D-dimer concentration.
(HAS2). • Intermittent abdominal pain, vomiting, • Antithrombin activity—may be low
• Overabundant HA is degraded into low and/or diarrhea. (urinary loss).
molecular weight HA, triggering release of • Polyuria and polydipsia. • Thromboelastography/elastometry—
inflammatory interleukins. • Weight loss. hypercoagulability.
• Elevated inflammatory cytokines increase • IgA or IgG levels—may be low.
Physical Examination Findings • Urine protein : creatinine ratio (UPC)—
serum amyloid A (SAA) concentration. SAA
• Marked fever 39.4–41.7 °C (103–107 °F) severely elevated with glomerular deposition
is deposited extracellularly throughout the
of 12–36-hour duration. of amyloid.
tissues.
• Lethargy and dehydration.
• Amyloid deposition may cause organ IMAGING
• Edematous periarticular soft tissue
failure, particularly in kidneys and liver. • Abdominal radiography—hepatomegaly
swellings.
SYSTEMS AFFECTED • Joint effusion. or decreased detail due to peritoneal
• Musculoskeletal—nonerosive • Swollen muzzle. effusion.
polyarthropathy, frequently affecting the • Abdominal pain. • Thoracic radiography—pleural effusion.
tibiotarsal joints. • Reluctance to move/hunched posture. • Joint radiography—periarticular swelling of
• Skin—periarticular edema, especially • Tachypnea or dyspnea. the soft tissues without bony involvement.
around the tibiotarsal region, swollen muzzle, • Hepatomegaly, ascites, and icterus. • Abdominal ultrasonography—diffusely
icterus, skin sloughing. • Pale mucous membranes secondary to hypoechoic liver with rounded edges; kidneys
• Renal/urologic—amyloid deposition in chronic anemia or rarely hemoperitoneum. may appear hyperechoic with loss of
renal medulla, glomerular amyloidosis, renal corticomedullary distinction.
CAUSES
failure, proteinuria. DIAGNOSTIC PROCEDURES
Dysregulation of inflammatory processes in
• Hepatobiliary—impaired hepatic function; • Synovial fluid analysis—may reveal acute
the shar-pei dog induces reactive amyloidosis.
hepatomegaly; friable liver, hepatic rupture synovitis.
and hemoabdomen (rare). RISK FACTORS • Kidney and/or liver fine-needle aspiration
• Hemic/lymphatic/immune—inflammatory Stress may trigger a fever episode. or biopsy (pending coagulation testing,
response; anemia; coagulation defects; biopsy preferred)—amyloid deposition,
hypercoagulability; hyperglobulinemia; confirmed by Congo red staining and
occasionally decreased immunoglobulin (Ig) polarized light.
A or IgG levels. DIAGNOSIS
• Gastrointestinal (GI)—submucosal amyloid PATHOLOGIC FINDINGS
deposition; GI ulceration due to renal or DIFFERENTIAL DIAGNOSIS Deposition of amyloid in multiple organs,
hepatic failure. • Infectious or immune-mediated causes of associated primarily with vessels or within the
• Cardiovascular—venous thrombosis; polyarthritis (see Polyarthritis, Nonerosive, parenchyma.
systemic hypertension. Immune-Mediated, Dogs).
• Nervous—vascular accident; hepatic • Infectious or immune-mediated causes of
encephalopathy. fever (see Fever).
• Ophthalmic—retinal detachment. CBC/BIOCHEMISTRY/URINALYSIS TREATMENT
• Respiratory—pleural effusion; pulmonary • Nonregenerative anemia.
thromboembolism. APPROPRIATE HEALTH CARE
• Neutrophilia with or without left shift. • Minor episodes of pain and fever—
GENETICS • Acute kidney injury (e.g., azotemia, outpatient care.
• Autosomal recessive inherited disorder. hyperphosphatemia, metabolic acidosis, • Inpatient care required for severe fever,
Different modes of inheritance proposed. isosthenuria). anorexia, dehydration, lameness or
• A greater number of mutations in the • Hypoalbuminemia—secondary to nonspecific pain, vomiting and/or diarrhea.
“meatmouth” (or heavily wrinkled) shar-pei proteinuria or liver failure. • Intensive care may be required to treat organ
phenotype increases risk. • Hypercholesterolemia—consistent with failure or sequelae of thromboembolism.
nephrotic syndrome.
Familial Shar-Pei Fever (continued)
NURSING CARE CONTRAINDICATIONS SYNONYMS

• IV isotonic crystalloid fluids—for • NSAIDs contraindicated in patients with • Swollen hock syndrome.
dehydration, anorexia, vomiting and/or renal disease, GI upset, and in combination • Shar-pei autoinflammatory disorder.
diarrhea. with corticosteroid therapy. SEE ALSO
• Oxygen—to treat hypoxemia. • ACE inhibitors/ARBs contraindicated in • Hepatic Encephalopathy.
• Abdominocentesis/thoracocentesis—if dehydrated or hypovolemic patients. • Icterus.
F effusion causes respiratory compromise or PRECAUTIONS • Nephrotic Syndrome.
elevated intra-abdominal pressure. Colchicine can cause GI upset; chronic use • Proteinuria.
• Blood transfusions—to treat anemia.
can be associated with bone marrow ABBREVIATIONS
• Fresh frozen plasma—consider for suppression. • ACE = angiotensin-converting enzyme.
coagulopathies, DIC.
POSSIBLE INTERACTIONS • ALP = alkaline phosphatase.
DIET Concurrent use of colchicine and cyclo- • ALT = alanine aminotransferase.
• Protein and phosphorus restriction in
sporine increases risk of colchicine toxicity. • ARB = angiotensin receptor blocker.
accordance with IRIS renal staging. • DIC = disseminated intravascular
• Dogs with hepatic encephalopathy should coagulation.
be fed protein-restricted diet. • GI = gastrointestinal.
• Omega-3 fatty acids may be beneficial for • HA = hyaluronic acid.
glomerular disease. FOLLOW-UP • HAS2 =hyaluronic acid synthase 2.
CLIENT EDUCATION PATIENT MONITORING • Ig = immunoglobulin.
• There is no cure; therapy is palliative and • Body temperature. • MTBP = MDM2 binding protein.
lifelong. • Blood pressure measurement and fundic • NSAID = nonsteroidal anti-inflammatory
• Early therapy may decrease further examination—monitor for hypertension. drug.
deposition of amyloid. • Urinalysis and UPC. • PT = prothrombin time.
• Diagnostics should be performed to • Biochemistry panel—renal and hepatic • PTE = pulmonary thromboembolism.
ensure there is no underlying or concurrent parameters, including albumin. • PTT = partial thromboplastin time.
disorder. • CBC—to assess anemia and inflammation. • SAA = serum amyloid A.
• Affected dogs should not be bred; genetic PREVENTION/AVOIDANCE • UPC = urine protein : creatinine ratio.
testing available. Avoid puppies from lines that have a history INTERNET RESOURCES
of shar-pei fever. • www.drjwv.com
POSSIBLE COMPLICATIONS • www.iris-kidney.com
• Death—due to hepatic rupture or • www.wvc.vetsuite.com
MEDICATIONS pulmonary thromboembolism (PTE). Suggested Reading
DRUG(S) OF CHOICE • Neutrophilic vasculitis causing severe skin DiBartola SP, Tarr MJ, Webb DM, et al.
• Colchicine 0.03 mg/kg PO q24h; advised sloughing; streptococcal toxic shock Familial renal amyloidosis in Chinese Shar
early in course of disease to delay amyloid syndrome causing localized necrotizing Pei dogs. J Am Vet Med Assoc 1990,
deposition; unknown if beneficial once fasciitis and/or concurrent shock and 197:483–487.
amyloid has been deposited. multiorgan failure. May C, Hammill J, Bennett D. Chinese shar
• Corticosteroids—if concurrent EXPECTED COURSE AND PROGNOSIS pei fever: A preliminary report. Vet Rec
immune-mediated disease is present. • Waxing and waning, progressive disorder 1992, 26:586–587.
• Clopidogrel (1–2 mg/kg PO q24h) if with a fair to poor prognosis, depending on Metzger J, Nolte A, Uhde AK, et al. Whole
concerned about hypercoagulability. timing of diagnosis. genome sequencing identifies missense
• Angiotensin-converting enzyme (ACE) • Inevitably fatal due to chronic kidney mutation in MTBP in Shar-Pei affected
inhibitor (e.g., enalapril or benazepril disease or hepatic failure. with Autoinflammatory Disease (SPAID).
0.25–0.5 mg/kg PO q12–24h) or • Time course may be weeks to more than BMC Genomics 2017, 18(1):348.
angiotensin receptor blocker (ARB; e.g., 10 years. Olsson M, Tintle L, Kierczak M, et al.
telmisartan 1 mg/kg PO q24h) for Thorough investigation of a canine
proteinuria (may cause transient autoinflammatory disease (AID) confirms
worsening of azotemia). one main risk locus and suggests a modifier
• Anti-hypertensive therapy if indicated. locus for amyloidosis. PLoS One 2013,
• Antibiotics—for concurrent infection or MISCELLANEOUS 8(10):e75242.
sepsis. AGE-RELATED FACTORS Author Bianca N. Lourenço
• NSAIDs/analgesics for fever and pain, Most severe in cases diagnosed at an early age. Consulting Editor Melinda S. Camus
unless corticosteroids have been given. Acknowledgment The author and book
PREGNANCY/FERTILITY/BREEDING editors acknowledge the prior contribution of
• Gastroprotectants—if gastric ulcer
Do not breed affected dogs. Julie Armstrong.
suspected.
Fanconi Syndrome
• Azotemia if renal failure develops. CONTRAINDICATIONS/POSSIBLE
• Hypophosphatemia and hypocalcemia may INTERACTIONS
occur in affected young, growing animals. • Avoid drugs that are nephrotoxic or have
BASICS • Urine specific gravity usually low (1.005– potential to cause Fanconi syndrome (see
OVERVIEW 1.018); mild proteinuria common; ketonuria Causes & Risk Factors).
Defective proximal renal tubular reabsorption may be present. • Avoid potassium chloride if hyperchloremic.
of glucose, electrolytes, and amino acids. • Granular or lipid casts and bacteria were F
seen in 27–40% of dogs.
SIGNALMENT
Species
Hyperchloremic normal anion gap metabolic FOLLOW-UP
Dogs and rarely cats.
acidosis due to bicarbonaturia with urine pH • Monitor serum biochemistry at 14-day
Breed Predilections <5.5. Urine pH >6.0 in distal renal tubular intervals to assess treatment response;
Sporadically reported in several breeds, acidosis, which is key diagnostic difference to monitor serum potassium concentration
idiopathic Fanconi syndrome primarily affects proximal renal tubular acidosis (Fanconi regularly as bicarbonate therapy may
the basenji breed (approximately 75% of syndrome). aggravate renal potassium loss; once stable,
cases). In America, 10–30% of basenjis are monitor biochemistry at 3-month intervals.
IMAGING
affected. It is presumed to be inherited in this • Clinical course varies; some dogs remain
Radiography—young growing dogs may have
breed, but the mode of inheritance is stable for years, others develop rapidly
rickets and angular limb deformities; adults
unknown. progressive renal failure over a few months;
may have decreased bone density.
Mean Age and Range cause of death usually acute kidney injury
Age at diagnosis: 10 weeks–11 years. Affected with severe metabolic acidosis.
Urinary clearance studies to document
basenjis usually are >2 years of age; most • Some dogs (18% in one study) developed
excessive excretion of glucose, amino acids,
develop clinical signs from 4 to 7 years. seizures or other neurologic signs several years
and electrolytes needed for confirmation. Do
Predominant Sex after diagnosis.
not test animals <8 weeks of age because
None false-positive results may occur. Urine can be
SIGNS evaluated at PennGen for aminoaciduria.
• Depends on the severity of specific solute Fractional reabsorption of amino acids in
losses and residual renal function. affected dogs ranges from 50% to 96% MISCELLANEOUS
• Loss of amino acids and glucose—usually (normal 97–100%). SEE ALSO
not associated with clinical signs other than PATHOLOGIC FINDINGS • Acute Kidney Injury.
polyuria and polydipsia. Renal papillary necrosis may occur in late disease. • Chronic Kidney Disease.
• Weight loss.
INTERNET RESOURCES
• Uremia, lethargy, decreased appetite.
• https://www.vet.upenn.edu/research/
• Abnormal growth (rickets) may occur in
academic-departments/clinical-sciences-
young animals.
TREATMENT advanced-medicine/research-labs-centers/
CAUSES & RISK FACTORS • Discontinue any drug or treats that may penngen
• Inherited in basenjis and possibly Irish cause Fanconi syndrome or treat for specific • http://www.basenji.org/ClubDocs/
wolfhounds. intoxication. fanconiprotocol2003.pdf
• Acquired Fanconi syndrome has been • No treatment reverses transport defects in Suggested Reading
reported in dogs given gentamicin, dogs with inherited or idiopathic disease. Thompson M, Fleeman L, et al. Acquired
streptozotocin, maleic acid, amoxicillin, • Because magnitude of transport defects proximal renal tubulopathy in dogs exposed
chlorambucil (cats), and chicken or duck varies among affected animals, treatment to a common dried chicken treat:
jerky treats, many of which have originated must be individualized. retrospective study of 108 cases (2007–2009).
from China; also reported secondary to • Treat for metabolic acidosis if blood Aust Vet J 2013, 91(9):368–373.
primary hypoparathyroidism, copper bicarbonate concentration <12 mEq/L. Large Authors Joao Felipe de Brito Galvao and
associated hepatopathy, and lead toxicity. doses of alkalinizing agents may be required Stephen P. DiBartola
because decreased proximal tubular resorptive Consulting Editor J.D. Foster
capacity results in marked bicarbonaturia.
Goal of alkali therapy to maintain blood
DIAGNOSIS bicarbonate concentration 12–18 mEq/L.
• Young, growing dogs may require vitamin D,
DIFFERENTIAL DIAGNOSIS calcium, and phosphorus supplementation.
Primary renal glucosuria causes glucosuria
despite normoglycemia; documentation of
aminoaciduria, mild proteinuria, or a
hyperchloremic normal anion gap metabolic
acidosis suggests Fanconi syndrome. MEDICATIONS
CBC/BIOCHEMISTRY/URINALYSIS DRUG(S) OF CHOICE
• CBC usually normal. Use potassium citrate or sodium bicarbonate
• Hypokalemia. (start with low dosage) as dictated by blood
• Hyperchloremic metabolic acidosis. gas and electrolyte data.
Fear and Aggression in Veterinary Visits—Cats

Consider rescheduling to add oral sedative/
anxiolytics and/or divide treatment into shorter
visits with fewer procedures. • Place required
BASICS TREATMENT procedures in order of most important to least
DEFINITION APPROPRIATE HEALTH CARE in case not all are tolerated. • Place procedures
• Fear—involuntary, negative emotional in order of least to most aversive so early
Prior to Handling
F state caused by anticipation/awareness of Assess environment, patient, and veterinary
procedures do not inhibit completion of later
danger. • Aggression—warning/intent to ones. • Consider pain, invasiveness, number of
personnel. What cats see, smell, feel, taste,
cause harm/increase distance to perceived procedures, how patient is coping. • Use
and hear affects emotional state and can lower
threat. chemical restraint immediately, prior to any
aggression threshold.
necessary procedures in which fear may escalate
PATHOPHYSIOLOGY Assess Environment: Make Cat above mild. • Have chemical restraint prepared
See Causes and Risk Factors.
Comfortable for at-risk patients—use before arousal to
SYSTEMS AFFECTED • Reduce carrier/transport stress. • Eliminate/ promote efficacy, safety, reduce future fear.
• Behavioral—neurochemical input between avoid triggers. • Modify environmental stimuli— CC
limbic system and forebrain. • Sympathetic light, noises, sound level (stress at ≥80 DB), • Learning where cat’s negative emotional
nervous system arousal. movement, touch, temperature (30–36 °C). response (fear) to stimulus (veterinary setting) is
GENETICS • Comfortable exam site (no slippery, shiny, cold changed to positive one (pleasure). • Food is
Fearful/fractious temperaments are heritable. surfaces). • Allow cats to hide, feel secure. easiest/most powerful way to create this shift.
INCIDENCE/PREVALENCE Assess Animal: Anxiety/Fear/Arousal • Palatability must be high (e.g., meat baby food,
Up to 85% of cats stressed at physical exam. Fuel Aggression squeeze cheese, canned food) to maximize cat’s
• Body language interpretation is critical. interest/increase positive emotional response.
GEOGRAPHIC DISTRIBUTION • Offer food while cat relaxed/feels safe, then just
• Track willingness to approach, interact with
None before/during/after any (aversive) procedure.
environment and people. • Intervene early.
SIGNALMENT • Change in location (examination vs. • Stressed cats may need food for duration of
treatment area), interaction, procedure, handling to prevent escalation of fear/arousal.
Species
personnel can affect patient. • Barometer—stressed cats often reject food.
Cat
Assess Yourself: Avoid Perceived Guidelines for Restraint
Breed Predilections
• Create safe handling plan for each procedure;
Any Threats, Track Body Postures
use least restraint required. • Avoid over-
Mean Age and Range and Behavior restraint—causes more stress than procedure
Any • Avoid direct eye contact or putting face near itself. • If greater restraint needed, use balanced
fearful cat. • Avoid petting top of head, pressure with global support. • Prevent
Predominant Sex grabbing body, or reaching into carrier.
Any flailing—control head/rear. • Avoid scruffing—
• Remove carrier tops—do not pull or dump use only for cats comfortable with technique.
SIGNS cat. • Allow time to sniff your hand; gently • Avoid stretching—use lateral recumbency only
Fearful body language—dilated pupils, ears scratch under chin and side of head if postures if procedure requires. • Avoid multiple bouts of
back, crouching, hissing, growling, tail indicate safety; avoid petting beyond shoulder— restraint; adjust position by sliding hands along
thrashing, swatting. often overarousing. • Start exam at head or body instead of release/regrab. • Struggling 2
CAUSES middle and move back; save socially invasive seconds—stop, reposition, try again; wait for cat
• Previous frightening/painful experience.
(head, feet, rear, belly) or painful areas for last. to relax to resume. • Second attempt—if not
• Talk softly; work quietly; avoid sudden relaxed and/or starts to get fractious, stop; is
• Fearful temperament.
movements. • Often narrow window of procedure essential? • If essential—use chemical
RISK FACTORS opportunity before fear/arousal escalates. • Not restraint. • If nonessential—send home with
History of fearful/fractious behavior to approaching indicates use of social distance to handling plan and medication if indicated for
handling, unfamiliar people, travel, or at cope; anticipate approach may lead to aggressive return visit. • Owner presence—can provide
previous visits. response—make a plan. • Fear or frustration by secure base and reduce stress.
handler increases cat fear. • Use language that is
scientifically accurate and promotes patient Handling Tools
empathy—fearful, painful, confused; avoid Expedite procedures by reducing patient fear,
labels that result in poor handling and offend minimizing manual restraint, and increasing safety.
DIAGNOSIS
clients—evil, spiteful, mean, bad, stupid. Pheromones: F3 Cheek Gland (Feliway®
DIFFERENTIAL DIAGNOSIS • Strictly avoid punishment (verbal or physical).
• Pain. • Irritability from illness. • Forebrain
Classic)
Make Handling Plan • Diffusers—reception, exam rooms, wards.
lesion. • Cognitive dysfunction syndrome.
• Handling plans unique to individual cats, • Spray/wipes—travel, examination, cages.
CBC/BIOCHEMISTRY/URINALYSIS environment, and procedures and require
Stress leukogram; hyperglycemia; glucosuria.
Muzzles
adjustments based on patient response. • Make Toweling preferred.
IMAGING plan for safety, decreased handling time,
If indicated to rule out medical conditions, patient welfare, client satisfaction. • Maintain Towels
record of likes and dislikes to plan future visits. • Towel/thick bedding for immobilization—
e.g., pain.
protects cat from flailing, handler from bites/
DIAGNOSTIC PROCEDURES Patient Handling Plan Guidelines scratches. • Provides head/body control, avoids
If indicated to rule out medical conditions. • Determine cat’s preferred food/treat for visual stimuli, firm global pressure—can modify
distraction and counter-conditioning (CC). to gain head/jugular or front/back leg access.
PATHOLOGIC FINDINGS
• Select restraint for individual cat/procedures. • Allows auscultation, abdominal palpation.
Stress related increase in blood pressure, heart
• Select handling tools that increase safety and • Safe restraint of fleeing/fearful cats, removal
rate, temperature, respiratory rate.
decrease patient fear/arousal. • Critically from carrier/cage, chemical restraint injection.
consider procedures—must it be done today?
(continued) Fear and Aggression in Veterinary Visits—Cats

Music additional sedation can add ketamine 3–5 mg/kg such as aggression to owners or strangers,
Classical music and cat-specific music may mask IM. • Alternative—tiletamine/zolazepam undesirable elimination, and anxiety disorders.
stressful external sounds, relax patients, have 5–10 mg/kg IM. • Geriatric/ill—acepromazine AGE-RELATED FACTORS
potential calming effects on clients and staff. 0.01–0.05 mg/kg or dexmedetomidine 5–10 μg/ • Socialization period (2–7 weeks)—time
kg + opioid: for greater sedation add ketamine
Cat Carrier where positive early exposure minimizes fear.
3–5 mg/kg IM; hydromorphone 0.05 mg/kg + • Regular, gentle, brief exposure to handling
• Positively condition/train cats to carrier prior to
travel. • Select carrier that allows cat to easily exit
midazolam 0.1–0.2 mg/kg ± ketamine 3–5 mg/ paired with positive experience (food) leads to F
kg ± acepromazine 0.01–0.05 mg/kg; alfaxalone less fear/improved future handling.
or remain in lower portion for exam (removable
1–2 mg/kg + midazolam 0.2 mg/kg ± opioid ±
top). • Provides familiar area, prevents fleeing, ZOONOTIC POTENTIAL
acepromazine 0.01–0.05 mg/kg. • Can reverse
promotes hiding. • Soft-sided/mesh panels—can Bite wounds and associated infections.
dexmedetomidine—½ volume atipamezole to
press mesh against cat’s body for safe IM injection.
volume of dexmedetomidine administered IM. PREGNANCY/FERTILITY/BREEDING
• Place carrier in cage of hospitalized cat—offers
• Dexmedetomidine/ketamine protocols—to Fearful/aggressive temperaments are heritable.
familiarity, encourages faster return to eating.
avoid dysphoria wait 45–60 min to reverse.
Restraint Nets (EZ Nabber) • Opioid choices (full Mu agonist superior for SYNONYMS
• Provides safe option for catch/restraint for pain control)—butorphanol 0.2 mg/kg; • Fear aggression. • Defensive aggression.
prompt administration of IM injections. buprenorphine 0.01–0.03 mg/kg; morphine • Phobic behavior.
• Very effective for cats housed in wall unit 0.2 mg/kg; hydromorphone 0.05–0.1 mg/kg; SEE ALSO
cages. • Cover with towel once cat inside— oxymorphone 0.1 mg/kg. • Car Ride Anxiety—Dogs and Cats.
reduces visual stimulation, protects handler. • Fears, Phobias, and Anxieties—Cats.
CONTRAINDICATIONS
NURSING CARE Reports of acute hepatic necrosis with oral • Kitten Socialization and Kitten Classes.
N/A diazepam. ABBREVIATIONS
ACTIVITY • CC = counter-conditioning.
PRECAUTIONS
N/A • Have client perform drug trial at home to • OTM = oral transmucosal.
DIET determine response/ideal dose. • Agitation, INTERNET RESOURCES

N/A gastrointestinal upset, sedation, appetite Travel
changes possible with above oral medications. • https://catfriendly.com/be-a-cat-friendly-
CLIENT EDUCATION • Benzodiazepines—disinhibition of aggression
• Preventive counseling (start at first visit)— caregiver/getting-cat-veterinarian • www.
uncommon but possible. • Gabapentin— catalystcouncil.org/resources/health_welfare/
positive carrier training, travel, handling, caution with chronic renal disease.
feline communication, reward training, avoid cat_carrier_video/index.aspx
use of punishment. • Provide kitten classes in POSSIBLE INTERACTIONS Veterinary Visits
veterinary clinic. See Internet Resources. N/A • https://https://fearfreehappyhomes.com/
SURGICAL CONSIDERATIONS ALTERNATIVE DRUG(S) courses/how-to-prepare-your-pet-for-vet-visit/
N/A Natural products including pheromones and • https://fearfreehappyhomes.com/courses/
supplements containing l-theanine or how-to-make-trip-to-vet-fear-free/
alpha-casozepine. Body Language
• https://www.dacvb.org/page/cats • https://
MEDICATIONS fearfreehappyhomes.com/courses/
cat-body-language-101
DRUG(S) OF CHOICE
FOLLOW-UP General
Chemical Restraint • http://www.fearfreepets.com • http://www.
PATIENT MONITORING
• Allows safe handling, effective completion of
• Evaluate physiologic/behavioral parameters. catalystcouncil.org • https://www.
procedures. • Blocks/prevents fear, discomfort, partnersforhealthypets.org/practice_feline.
• Evaluate and record response to handling,
pain, further distress, and fear escalation. aspx • https://lowstresshandling.com
location, personnel, products, drugs.
• Minimal or no physical restraint.
• https://www.catvets.com/guidelines/
• Injectable sedation (IM) most effective for PREVENTION/AVOIDANCE
practice-guidelines/handling-guidelines
safe handling of fractious/highly fearful • Prevention—more effective, safer, less expense,
• https://www.aaha.org/aaha-guidelines/
patients. • Base protocol on age, temperament, improves healthcare compliance, avoids fear
behavior-management/behavior-
health. • Pre-travel oral anxiolytics/sedatives sensitization. • Low Stress handling and CC
management-home/ • http://www.
reduce fear, facilitate gentle handling, promote during all kitten and adult visits recommended.
catalystcouncil.org/resources/health_welfare/
safety for injection, reduce injectable doses. POSSIBLE COMPLICATIONS cat_friendly_practices • https://icatcare.org/
Oral Sedative/Anxiolytics Fearful and/or aggressive behavior negatively advice/cat-handling-videos
• Administer 60–90 min prior to travel for mild/ impacts frequency and level of veterinary care.
Suggested Reading
moderate fear, or to facilitate administering EXPECTED COURSE AND PROGNOSIS Herron M, Shreyer T. The pet friendly
chemical restraint. • May give first dose 12h in Effective implementation of Fear Free, Low veterinary practice: a guide for practitioners.
advance. • Also may be required for inpatients. Stress, and Cat Friendly visits reduces fear, Vet Clin North Am Small Anim Pract 2014,
• Gabapentin—10–20 mg/kg PO (50–150 mg/ anxiety, and stress and improves frequency 44:451–481.
cat). • Trazodone—25–50 mg/cat PO. and quality of veterinary care. Yin S. Low Stress Handling, Restraint, and
• Lorazepam—0.05–0.25 mg/kg PO (0.125–
Behavior Modification of Dogs and Cats.
0.25 mg/cat). • Buprenorphine— Davis, CA: Cattle Dog Publishing, 2009.
0.01–0.03 mg/kg oral transmucosal (OTM). Authors Meghan E. Herron and Traci A. Shreyer
• For additional sedation can add
MISCELLANEOUS Consulting Editor Gary M. Landsberg
acepromazine—0.5–2.2 mg/kg PO.
Injectable Sedation/Chemical Restraint ASSOCIATED CONDITIONS
• Young/healthy—dexmedetomidine 10–20 μg/ Fearful/fractious cats in veterinary setting often
kg or acepromazine 0.1 mg/kg + opioid; for have comorbid behavioral problems at home,
Fear and Aggression in Veterinary Visits—Dogs

plan for safety, decreased handling time, patient
welfare, and client satisfaction. • Maintain
record of likes and dislikes to plan further visits.
BASICS TREATMENT
Patient Handling Plan Guidelines
DEFINITION APPROPRIATE HEALTH CARE • Determine most motivating food/treats for
• Fear—involuntary, negative emotional state distraction and counter-conditioning (CC).
Prior to Handling
F caused by anticipation/awareness of danger. Assess environment, dog, and veterinary • Select restraint for individual dog/procedures.
• Aggression—warning/intent to cause harm/ personnel. What dogs see, smell, feel, taste, • Select handling tools that increase safety and
increase distance in response to perceived threat. and hear affects emotional state and lowers decrease patient fear/arousal. • Critically
PATHOPHYSIOLOGY aggression threshold. consider procedures—must it be done today?
See Causes and Risk Factors. Consider rescheduling to add oral sedative/
Assess Environment: Make Dog
anxiolytics and/or divide treatment into shorter
SYSTEMS AFFECTED Comfortable visits with fewer procedures. • Place required
• Behavioral—neurochemical input between • Eliminate known triggers. • Modify procedures in order of most important to least
limbic system and forebrain. • Activation of environmental stimuli including light, noises, in case not all are tolerated. • Place procedures
hypothalamic pituitary axis (HPA) and sound level (stress at ≥80 DB), movement, touch, in order of least to most aversive, so early
sympathetic nervous system. temperature (15–30 °C). • Owner presence— procedures do not inhibit completion of later
GENETICS can provide secure base, reduce stress. ones. • Consider pain, invasiveness, number of
Fearful temperament may be heritable. • Comfortable exam site (no slippery, shiny, cold procedures, how dog is coping. • Use chemical
surfaces). • Allow fearful dogs to hide, feel secure. restraint immediately for any necessary
Over 75% fearful when examined. Assess Dog procedures in which fear escalates beyond mild;
• Anxiety/fear/arousal leading to aggression. use before arousal to promote efficacy, safety,
SIGNALMENT • Body language interpretation critical. escalation, learning.
Species • Track willingness to approach, interact with CC
Dog environment/people. • Intervene early. • Learning where dog’s negative emotional
• Change in location (examination vs. response (fear) to stimulus (veterinary setting)
Breed Predilections
Any treatment area), interaction, procedure, is changed to positive one (pleasure). • Food
personnel can affect patients. easiest/most powerful way to create shift.
Mean Age and Range
Assess Yourself: Avoid Perceived • Palatability must be high (meat baby food,
Any
Threats, Track Body Postures squeeze cheese, canned food) to maximize
Predominant Sex dog’s interest/increase positive emotional
Any and Behavior
response. • Offer food while dog relaxed/feels
• Avoid direct eye contact, bending over, putting
SIGNS safe, then just before/during/after any
face near fearful dog, loud talking, sudden
Fearful body language—ears back, gaze (aversive) procedure. • Stressed dogs may
movements. • Bend at knee, turn to side, squat
avoidance, crouching, tail tucked, yawning, need food for duration of handling to distract
(when safe). • Avoid reaching out, petting top of
panting, lip licking, scanning. and prevent escalation of fear/arousal.
head, grabbing collar. • Encourage patients to
• Barometer—stressed dogs often reject food.
CAUSES approach or have handler they trust move them
• Previous frightening/painful experiences. to you. ◦ Hand at your side, pat your leg gently, Restraint
• Fearful temperament (genetics, peri/ soft verbal encouragement. ◦ Palm open with • Create safe handling plan for each procedure.
postnatal experience, socialization). valued treats. ◦ Allow dog to sniff/investigate. • Use least restraint required—increased restraint
◦ Gently pet under chin/neck. ◦ Test increases stress. • If greater restraint needed, use
RISK FACTORS acceptance—stop petting, does dog reengage. gentle, balanced pressure with global support.
History of fearful behavior to handling, ◦ If no: stop, make a plan. ◦ If yes: pet again, • Prevent flailing by controlling head/rear.
unfamiliar people, noises, environments, or slowly move to desired exam position. ◦ Start • Avoid lateral recumbency—only if procedure
previous visits. exam in middle, slowly work to rear, back to requires. • Avoid multiple bouts of restraint—
center, to head. ◦ Monitor/be prepared for any adjust positioning by sliding hands along body.
fear- or pain-evoking handling. • Not • Struggling 3 seconds—stop, reposition, try
approaching indicates use of social distance to again; wait for dog to relax to begin. • Second
DIAGNOSIS cope; approach may lead to aggressive attempt—if fear increases or starts to get
response—make a plan. • Avoid front-facing fractious, stop; is procedure essential?
DIFFERENTIAL DIAGNOSIS • Essential—use chemical restraint.
interactions or cover dog’s head; work at side,
• Pain. • Irritability from illness. • Nonessential:—send home with handling plan
just behind point of shoulder, facing same
• Forebrain lesion. • Cognitive dysfunction and pre-visit meds if indicated for return visit.
direction as dog. • Often narrow window of
syndrome.
opportunity before fear/arousal escalates. • Fear Handling Tools
CBC/BIOCHEMISTRY/URINALYSIS or frustration by handler or veterinary personnel Expedite procedures by reducing dog fear,
Stress leukogram; glucosuria. increases pet fear; use scientifically accurate minimizing manual restraint, and increasing
OTHER LABORATORY TESTS language that promotes patient empathy— safety.
As indicated to rule out medical conditions. fearful, painful, confused; avoid labels that result
in poor handling/offend clients—mean, bad, Music
DIAGNOSTIC PROCEDURES spiteful, dominant. • Strictly avoid punishment Music and sources of white noise may mask
As indicated to rule out medical conditions. (verbal or physical). stressful external sounds. Classical music may relax
dogs and have calming effects on clients and staff.
PATHOLOGIC FINDINGS Make Handling Plan
Stress-induced increase in blood pressure, • Handling plans unique to individual dogs, Dog-Appeasing Pheromone (Adaptil®)
heart rate, temperature, panting. environment, and procedure and require • Diffusers—reception, exam rooms, wards.
adjustments based on dog’s response. • Make • Spray/wipes—travel, examination, cages.
(continued) Fear and Aggression in Veterinary Visits—Dogs

Muzzles • Diazepam—0.5–2.2 mg/kg. • Alprazolam— POSSIBLE COMPLICATIONS
• For safety, assessment/evaluation, avoid 0.01–0.1 mg/kg. • For additional sedation can Dogs with fearful and/or aggressive behavior may
human fear response, injectable sedation. add acepromazine—0.55–2.2 mg/kg. • Can not receive adequate veterinary care including
• Home desensitization (DS)/CC—enters combine trazodone, clonidine, gabapentin, wellness care, diagnostics, and treatment.
wearing comfortably. • Basket muzzle benzodiazepines. • Avoid acepromazine as sole EXPECTED COURSE AND PROGNOSIS
preferred—allows panting: safer for longer agent—ineffective anxiolysis Effective implementation of Fear Free, Low
procedures/kenneling; allows CC: inserted food Injectable Restraint Stress care prevents and reduces fear, anxiety, F
or smeared along inside. • Nylon sleeve—short • Young/healthy—dexmedetomidine 10–20 μg/ and stress and improves frequency and quality
procedures or facilitate essential injection. kg + opioid: for additional sedation can add of veterinary care.
Elizabethan Collar ketamine 3–5 mg/kg IM. • Alternative—
Muzzle alternative for avoiding/reducing tiletamine/zolazepam 5–10 mg/kg IM (not
visual stimuli. practical for dogs >20 kg due to volume).
Towels • Geriatric/ill—acepromazine 0.01–0.05 mg/kg MISCELLANEOUS
or dexmedetomidine 5–10 μg/kg + opioid: for
• Towels/thick bedding can help immobilize— ASSOCIATED CONDITIONS
additional sedation add ketamine 2–5 mg/kg
especially small dogs: head/body control, Dogs with fearful/fractious behavior in veterinary
IM; alfaxalone 1–2 mg/kg (not practical for dogs
reduced visual stimuli, global pressure. • Roll setting often have comorbid behavioral problems,
>10 kg due to volume) + midazolam 0.2 mg/kg
towels (cervical collar)—head control. including aggression to owners or strangers, leash
± opioid ± acepromazine 0.01–0.05 mg/kg.
Eye Covers (e.g., ThunderCap®) reactivity, resource guarding, anxiety disorders.
• Can reverse dexmedetomidine—equivolume
Reduce visual stimuli/triggers for fear and atipamezole to volume of dexmedetomidine IM. AGE-RELATED FACTORS
anxiety during travel, exam, injections. • Dexmedetomidine/ketamine protocols—to • Socialization period (3–12 weeks)—sensitive
avoid dysphoria wait 45–60 min to reverse; period where positive exposure minimizes fear;
Compression Garments (e.g.,
opioid choices (full Mu agonist superior for pain gentle, brief handling paired with positive
ThunderShirt®) experience (food) leads to less fear and improved
control): butorphanol 0.2–0.4 mg/kg; morphine
Swaddles—may relax patients with balanced handling. • Fear period (8–10 weeks of age and
0.2–0.4 mg/kg; hydromorphone 0.05–0.2 mg/
body pressure. between 4 and 11 months)—susceptible to
kg; methadone 0.3–0.5 mg/kg.
NURSING CARE single-event learning, highly sensitive to negative
Oral Transmucosal (OTM) experiences. • Social maturity (1–3 years)—
N/A
• Young/healthy—dexmedetomidine 10–40
fearful puppies/adolescents may begin to show
ACTIVITY μg/kg ± opioid (e.g., morphine 10 mg/kg or fear and aggression at this time; prompt
N/A butorphanol 0.2 mg/kg) OTM; can reverse recognition and intervention essential at first
DIET dexmedetomidine with atipamezole (½ volume of signs of fear to establish handling plan.
N/A dexmedetomidine). • DS/CC to syringe in buccal
pouch. • Up to 1h to effect. • Mucosal contact ZOONOTIC POTENTIAL
CLIENT EDUCATION time improves absorption—mix with syrup. Bite wounds and associated infections.
Preventive counseling at first puppy visit ± PREGNANCY/FERTILITY/BREEDING
puppy classes in clinic to review positive travel, CONTRAINDICATIONS
Avoid clonidine with cardiovascular output issues. Fearful/aggressive temperaments heritable.
handling, communication, reward training, and
avoiding punishment. See Internet Resources. PRECAUTIONS SYNONYMS
• Have client perform oral medication trial at • Fear aggression. • Defensive aggression.
SURGICAL CONSIDERATIONS • Phobic behavior.
N/A home to determine dose/response. • Agitation,
gastrointestinal upset, sedation, appetite changes SEE ALSO
possible. • Benzodiazepines—disinhibition of • Car Ride Anxiety—Dogs and Cats.
aggression possible. • Gabapentin—caution • Fears, Phobias, and Anxieties—Dogs.
with chronic renal disease. • Puppy Socialization and Puppy Classes.
MEDICATIONS
POSSIBLE INTERACTIONS ABBREVIATIONS
DRUG(S) OF CHOICE Avoid combining oral acepromazine with • CC = counter-conditioning.
Chemical Restraint clonidine—potential blood pressure fluctuation. • DS = desensitization.
• Allows safe, effective, minimal handling and • HPA = hypothalamic pituitary axis.
ALTERNATIVE DRUG(S)
successful completion of procedures. • Blocks or • OTM = oral transmucosal.
Natural products including pheromones,
prevents distress, discomfort, pain, escalation, supplements containing l-theanine or INTERNET RESOURCES
and fear sensitization. • Injectable sedation alpha-casozepine and calming probiotic. • https://fearfreehappyhomes.com/courses/
(IM)—most effective for safe handling how-to-prepare-your-pet-for-vet-visit/
fractious/fearful dogs. • Base protocol on age, • https://fearfreehappyhomes.com/courses/
temperament, health. • Pre-travel oral sedative/ how-to-make-trip-to-vet-fear-free/ • https://
anxiolytics reduce fear, facilitate gentle handling, fearfreehappyhomes.com/courses/dog-body-
safety for injection, reduce injectable doses. FOLLOW-UP language-101 • http://www.fearfreepets.com
Oral Sedative/Anxiolytics PATIENT MONITORING • https://lowstresshandling.com/
• Administer 1.5–2 hours pre-travel for mild/ • Evaluate and monitor physiologic/ Suggested Reading
moderate fear or to facilitate restraint injection; behavioral parameters. • Maintain record Herron M, Shreyer T. The pet friendly
may give first dose 12 hours in advance; repeat of response to handling, location, personnel, veterinary practice: a guide for practitioners.
dosing as needed if patient is hospitalized. products, and drugs. Vet Clin Small Anim 2014, 44:451–481.
• Trazodone—4.0–10 mg/kg (up to 18 mg/kg); PREVENTION/AVOIDANCE Yin S. Low Stress Handling, Restraint, and
maximum 300 mg per dose. • Clonidine— • Prevention—more effective, safer, less expense, Behavior Modification of Dogs and Cats.
0.01–0.05 mg/kg. • Dexmedetomidine improved healthcare compliance, and avoids fear Davis, CA: Cattle Dog Publishing, 2009.
oromucosal gel—125 μg/m2. • Gabapentin— sensitization. • Also see Client Education. Authors Meghan E. Herron and Traci A. Shreyer
20–50 mg/kg. • Lorazepam—0.05–0.5 mg/kg. Consulting Editor Gary M. Landsberg
Fears, Phobias, and Anxieties—Cats

SIGNALMENT OTHER LABORATORY TESTS
Any age, sex, or breed. As indicated, including T4 in middle age and
SIGNS older.
BASICS
General Comments IMAGING
DEFINITION As indicated.
• Fear is the feeling of apprehension resulting • Signs of fear or anxiety can vary between
individuals and with different stimuli that
F from the nearness of some situation or object
may be specific (a particular individual,
presenting an external threat. The response of
the autonomic nervous system prepares the sound, etc.) or more generalized.
body for “freeze, fight, or flight.” As such, it is • In mild cases of anxiety or fear the cat may TREATMENT
a normal behavior, essential for adaptation become tense and more reactive to environ
ACTIVITY
and survival. mental stimuli. Some individuals may retreat
Normal social interactions and play should be
• Anxiety is the anticipation of dangers from to perceived safe hiding places or show little
encouraged, but contact should not be forced.
unknown or imagined origins that results in movement.
physiologic reactions associated with fear. • Cats in panic can become very aggressive or DIET
Anxiety may occur in the aftermath of a destructive in an attempt to retreat from the Placement of food, water, and litter box may
fear-producing event or as a result of fearful stimulus. need to be altered if anxious or fearful
unrelated environmental changes that are behavior is limiting access.
Historical Findings
unpredictable. • Clear description of the cat’s body language, CLIENT EDUCATION
• A phobia is a persistent and excessive fear of behavior, and events or situations that General Comments
a specific stimulus, such as a thunderstorm or consistently trigger anxiety or fear is helpful • Educate owners to read and understand cat
separation from an attachment figure. in setting up behavioral modification and communication language for early recognition
PATHOPHYSIOLOGY environmental management program. of signs.
• Stress responses become problematic when • Body postures associated with fearful • Discuss behavioral expectations. Owner
the individual is not able to control the behavior include ears flattened to back or side expectations in regard to social interactions
stressful situation by their actions or escape of head, crouched body posture when resting with humans or other cats may be contributing
from it through appropriate behavioral or moving, lowered head, tail tucked to the problem and could affect prognosis.
responses. alongside body or held low, piloerection, • Treatment plan involving case-tailored
• Chronic anxiety or fear can lead to dilated pupils, shaking, panting, drooling, behavioral modification, environmental
secondary behavior problems, such as “Halloween cat” silhouette. adjustments, and support material will help
overgrooming, spraying, or intercat • If fear is intense, cat may lose bladder and owner better understand situation and
aggression, or predispose the cat to health bowel control and express its anal sacs. implement treatment.
problems owing to a compromised immune • Vocalizations are usually minimal, unless
cat is showing defensive behavior in response Behavioral Therapy
system. • Identify and avoid exposure to fear-evoking
to perceived threat.
SYSTEMS AFFECTED • Cat may pace, vocalize, and solicit attention stimuli and situations. Provide ways for cat to
• Behavioral—hypervigilance, avoidance from owner. manage situation by creating “safe places” for
behaviors, possible aggression. • Urine spraying and destructive scratching cat to go to avoid the stimulus.
• Cardiovascular—increased heart rate and may be seen in anxious cats. • If cat must be handled while fearful, caution
blood flow to internal organs during and gentle physical restraint aids (cat muzzles,
fear-evoking incidents. Physical Examination Findings head covers, towel wraps, etc.) should be used
• Endocrine/metabolic—glucose release into Usually unremarkable unless cat has injured to prevent injury and decrease stress.
bloodstream, release of glucocorticoids. itself trying to escape or while seeking shelter. • Desensitization and counter-conditioning
• Gastrointestinal (GI)—decreased appetite. CAUSES & RISK FACTORS to help decrease reactivity to fear-producing
• Hemic/lymphatic/immune—chronic stress Fearful behavior in cats can be related to stimulus. Systematic desensitization is
effects on immune function. genetic influences on temperament; lack of program of slowly increasing exposure to
• Musculoskeletal—weight loss in response to positive early experience and socialization, fearful stimulus or situation. Counter-
chronic stress effects on appetite, decreased observational learning from fearful mother, conditioning consists of enhancing internal
food intake due to hiding behavior. other adult cats; learning from negative and external environment with food rewards
• Neuromuscular—decrease in activity due to experiences; social stress, population or other pleasurable stimuli such as playing
avoidance and hiding; fearful/anxious pressure. with toys.
reaction may also include pacing, trembling, • Address secondary problems such as
repetitive activity. strained social interactions subsequent to
• Ophthalmic—dilated pupils in response to defensive aggression directed toward humans
autonomic nervous system stimulation. or other cats, or elimination problems that
• Respiratory—increased respiratory rate
DIAGNOSIS may be result of fears or anxieties.
when anxious or frightened. DIFFERENTIAL DIAGNOSIS
• Skin/exocrine—overgrooming in response Thorough medical history and physical
to stressors. examination will help differentiate fearful
behavior from withdrawal due to illness.
GENETICS MEDICATIONS
• Genetic component possible. CBC/BIOCHEMISTRY/URINALYSIS
DRUG(S) OF CHOICE
• Breed/coat color and paternal personality As indicated to rule out medical conditions
• Medication can be helpful adjunct to
have been linked to individual personality and as baseline prior to medication use and as
behavioral modification, if animal’s fearful or
traits in cats. premedication screen.
(continued) Fears, Phobias, and Anxieties—Cats

anxious behavior is so intense that it interferes • Practitioner should verify safety when
with quality of life. combining psychoactive drugs with other
• No drug is approved by FDA for use in cats medications.
for fearful behavior; therefore, clients must be MISCELLANEOUS
ALTERNATIVE DRUG(S)
advised that information concerning efficacy, • Natural products that might aid in reducing ASSOCIATED CONDITIONS
contraindications, and side effects is limited. anxiety alone or in conjunction with drugs— • Stereotypic or compulsive disorders.
• If there are questions or concerns about a S-adenosylmethionine (SAMe) 100 mg PO • Urine marking, inappropriate elimination. F
specific patient or medication, consultation q24h; alpha-casozepine 75 mg (15 mg/kg or • Defensive aggression directed toward
with a veterinary behaviorist may be helpful. greater) PO q24h; l-theanine 25 mg PO daily. humans, other animals; may also make cat
• Selective serotonin reuptake inhibitors target for aggression from other cats.
• Cat-appeasing pheromone (Feliway®
(SSRIs)—fluoxetine or paroxetine 0.5–1 mg/ Multicat or Friends); F3 cheek gland ZOONOTIC POTENTIAL
kg PO q24h. Side effects—decreased appetite pheromone (Feliway). N/A except for bite and scratch wounds.
and irritability; paroxetine has anticholinergic • Calming and stress diets containing
effects. PREGNANCY/FERTILITY/BREEDING
alpha-casozepine and l-tryptophan.
• Tricyclic antidepressants (TCAs)— Drug use in pregnant animals should be avoided.
clomipramine 0.5 mg/kg PO q24h SEE ALSO
(2.5–5 mg/cat). Side effects—sedation, • Aggression, Overview—Cats.
anticholinergic effects, possible cardiac • Compulsive Disorders—Cats.
conduction disturbances in predisposed FOLLOW-UP • Fear and Aggression in Veterinary Visits—
animals. PATIENT MONITORING Cats.
• Buspirone—0.5–1.0 mg/kg q8–24h. Side Frequent follow-up either in person or by • Housesoiling—Cats.
effects—GI upset, mild sedation. telephone is necessary, especially during first • Marking, Roaming, and Mounting
• Benzodiazepines—oxazepam 0.2–0.5 mg/kg few months of treatment, to motivate client Behavior—Cats.
q12–24h; alprazolam 0.125–0.25 mg/cat q12h and monitor effectiveness of any adjunct drug
or as needed prior to event; lorazepam ABBREVIATIONS
treatment. • GI = gastrointestinal.
0.025–0.05 mg/kg (or 0.125–0.5 mg/cat)
q12h or as needed prior to event. Side effects— PREVENTION/AVOIDANCE • SAMe = S-adenosylmethionine.
sedation, increased appetite, agitation. • Early socialization to people, places, and things • SSRI = selective serotonin reuptake inhibitor.
• Buspirone and benzodiazepines might up to 7 weeks of age, and ongoing positive • TCA = tricyclic antidepressant.
reduce fear and build confidence in fearful cat exposure during first year, may help prevent INTERNET RESOURCES
that does not retaliate or fight back. some later problems with fearful behavior. • https://www.catvets.com
• Calm interactions and positive associations
CONTRAINDICATIONS • https://fearfreehappyhomes.com/courses/
with fear-producing stimuli may help keep cat-body-language-101
• Cats with renal or hepatic disease. fear-based reactions to minimum.
• Caution with TCAs and SSRIs in diabetics. Suggested Reading
• TCAs in patients with cardiac abnormalities. POSSIBLE COMPLICATIONS Herron, M. E., Horwitz, D., Siracusa, C., &
Secondary behavior problems may arise or Dale, S. (2020). Decoding your cat: The
PRECAUTIONS persist after fearful or anxious behavior has
• Laboratory screening tests suggested before ultimate experts explain common cat
diminished and will need specific treatment. behaviors and reveal how to prevent or
placing animal on psychotropic medication
for health assessment and baseline for EXPECTED COURSE AND PROGNOSIS change unwanted ones. Boston: Houghton
comparison. • Realistic “end point” depends on animal’s Mifflin Harcourt.
• Compounding medications in more background (socialization history, genetic and Landsberg G, Hunthausen W, Ackerman L.
palatable form can ease administration and individual differences in personality), home Behavior Problems of the Dog and Cat, 3rd
improve compliance. situation, and other confounding factors such ed. Edinburgh: Saunders Elsevier, 2013.
• Assess all medications and natural as frequency of natural exposure to fear- Levine ED. Feline fear and anxiety. Vet Clin
supplements being administered for potential producing stimuli. North Am Small Anim Pract 2008,
contraindications. • Medication may improve but not totally 38(5):1065–1079.
ameliorate signs. Overall KL. Manual of Clinical Behavioral
POSSIBLE INTERACTIONS Medicine for Dogs and Cats. St. Louis,
• TCAs and SSRIs should not be used together. MO: Elsevier Mosby, 2013.
• Mirtazapine should be used cautiously in Author Leslie Larson Cooper
combination with TCA or SSRI. Consulting Editor Gary M. Landsberg
Fears, Phobias, and Anxieties—Dogs

INCIDENCE/PREVALENCE IMAGING
• Separation anxiety—13–40%. • Sound CT or MRI if indicated to rule out CNS
aversion, fear, and phobia—up to 50%. disorder. Other imaging if indicated (e.g., pain).
BASICS • General fearfulness—26%. • Reactivity to DIAGNOSTIC PROCEDURES
DEFINITION people—7%. • Fear of veterinarian—up to • Thorough behavioral history and
• Fear—an emotion consisting of a 78.5%. observation of patient (video of behavior is
F physiologic stress response (PSR) and a SIGNALMENT helpful). • Exposure to stimulus if safe.
psychologic response to the presence of a No age, breed, or sex overrepresented.
stimulus perceived as dangerous (e.g., person,
animal, situation, sound, object, scent) SIGNS
inducing an adaptive, avoidance reaction. General Comments
• Phobia—marked, irrational, and excessive Hypervigilance, ANS arousal, catatonia, TREATMENT
fear of a stimulus (e.g., animal, situation, increased motor activity, elimination, APPROPRIATE HEALTH CARE
person, sound, object, scent) consisting of a destruction, vocalization, hypersalivation, • Typically outpatient. • Inpatient
PSR and psychologic response resulting in a panting, hiding, trembling, escape behaviors, (dayboarding/daycare)—if fear-/anxiety-/
maladaptive reaction. • Anxiety—reaction fearful body language. phobia-inducing stimulus unavoidable,
consisting of a PSR and psychologic response patient causing self-injury, medication not yet
Historical Findings
triggered by anticipation of future or memory effective, hospitalization to stabilize patient on
Traumatic experience, inadequate
of past dangers. medication. • Treatment includes owner
socialization, fearful/anxious dam or sire,
PATHOPHYSIOLOGY history of inability to escape stimulus education, safety, behavior modification to
• Information about a fear-inducing stimulus (e.g., locked in crate). change emotional state of patient,
is perceived by sensory organs and transmitted environmental modification to avoid triggers
Physical Examination Findings and distract patient during episodes, reduction
to the central nucleus of the amygdala; the
May be unremarkable; self-induced injuries of anxiety. • Diagnose and treat any
central nucleus sends output to the central grey
possible. conditions that may cause pain, discomfort, or
matter (musculoskeletal response), lateral
hypothalamus (autonomic nervous system CAUSES changes in mood as well as any injuries.
[ANS] response), and stria terminalis • Inadequate socialization, traumatic event, Safety
(hormonal response) causing a PSR. • The hereditary, cognitive dysfunction syndrome • Owner—should not push, pull, grab, or
PSR is graded based on the animal’s perceived (CDS), previous learning. • Illness or pain reach for dog showing clinical signs, as this
level of control, coping strategy, and level of may contribute to development of fears, can result in owner-directed aggression;
difficulty. • Any neutral stimulus in the phobias, and anxieties. instead, use food or toy to move patient.
environment can be paired with the PSR RISK FACTORS • Patient—if intense escape attempts or
through classical conditioning triggering a PSR General—existing fears, anxieties, and phobias; self-injury are present, avoid crating and limit
to the conditioned stimulus. • Hormones and inadequate socialization, rehoming, anxious/ dog’s access to windows, doors, electrical
neurotransmitters released during the PSR fearful/physically ill dam, traumatic event. wiring, and water lines; consider dayboarding.
enhance learning, memory consolidation, and • Public—avoid situations where stimulus is
retrieval. • There is evidence that while present until treatment is complete.
frightening memories can be significantly
reduced, they cannot be “erased.” Behavior Modification
DIAGNOSIS • Avoid stimulus for 2–8 weeks depending on
SYSTEMS AFFECTED severity of reaction while teaching coping skills
• Psychologic—immobility, restlessness, DIFFERENTIAL DIAGNOSIS to patient (e.g., sit, watch, look at that, leave it,
pacing, circling, hyperattachment, escape, • Psychologic—CDS; incomplete relaxation) and setting up safe spot. • Structured
avoidance, approach/retreat, destructiveness, housetraining; urine/fecal marking; territorial interactions with owner (e.g., sit for all
vocalization, aggression. • Cardiovascular— aggression; separation-related disorders; interactions). • Independence exercises—down/
tachycardia, hypertension. • Endocrine/ attention-seeking; storm, noise, or stay with food toy. • Punishment (e.g., shock/
metabolic—alterations in hypothalamic environmental phobias; generalized anxiety; choke collar correction, yelling, hitting)
pituitary–adrenal axis, increased blood neophobia; fear-induced aggression. contraindicated. • Client should distract dog
glucose. • Gastrointestinal—inappetence, • Medical—neoplasia (e.g., intracranial), and redirect to play or food toy when frightened
hypersalivation, vomiting, diarrhea, endocrinopathy (e.g., Cushing’s, or anxious. • Desensitization and counter-
defecation. • Hemic/lymphatic/immune— hypothyroidism), cystitis, pyelonephritis, conditioning (DS/CC)—can begin after coping
stress leukogram. • Musculoskeletal— diabetes, gastrointestinal disease (e.g., tools have been taught; can be attempted with
self-injury. • Neurologic—increased motor inflammatory bowel disease), neurologic supervision of highly qualified positive
activity, trembling, decreased pain perception, disease (e.g., seizures), dermatologic reinforcement trainer or veterinary behavior
catatonia, partial seizure. • Ophthalmic— (e.g., ALD, atopy, food allergies), toxicity technician; DS/CC can sensitize animal to
episcleral injection, mydriasis. • Renal/ (e.g., lead, recreational drugs). stimulus, causing behavior disorder to worsen.
urologic—urination. • Respiratory— CBC/BIOCHEMISTRY/URINALYSIS
tachypnea. • Skin/exocrine—traumatic Environmental Modification
Perform before initiating drug treatment. • Create safe spot/safe haven where exposure
injury, acral lick dermatitis (ALD).
OTHER LABORATORY TESTS to fear-producing stimulus can be limited.
GENETICS • Thyroid status. • Adrenal tests if indicated • Consider dayboarding/daycare. • Limit use
Heredity influences development of fears and by history, signalment, physical examination, of crate until dog uses readily and does not panic
phobias, although unclear at this time to what and laboratory tests. when confined. • Environmental enrichment
extent specific fears (e.g., noise) are heritable. (e.g., rotate toys, food toys, exercise).
(continued) Fears, Phobias, and Anxieties—Dogs
NURSING CARE Human Services recommendations. • Cardiac • Treatment duration varies from 2 to 12
Behavior treatment appointments can be conduction anomalies—use caution and months depending on severity and number
scheduled with veterinary technicians. Consider monitoring when giving TCAs. • Use of problems; only dogs who respond well
short-term or day boarding for regulation of caution when prescribing drugs to geriatric to behavior modification and
medications or avoidance of stimulus. patients or patients with hepatic or renal environmental management can be
ACTIVITY compromise—review metabolism and expected to be weaned off medication.
• Increased exercise will act as environmental
elimination of medication before prescribing. • Typically, treatment will continue to F
enrichment for patient but will not significantly • Clients should receive drug information some extent throughout dog’s life.
lower anxiety/fear disorders. • Exercise should handouts with potential side effects listed.
avoid any exposure to fear-inducing stimulus. • Mood-altering medications have potential
to increase agitation, fear, and aggression.
CLIENT EDUCATION
• Advise owners that patient is not spiteful or
POSSIBLE INTERACTIONS MISCELLANEOUS
• Use caution when prescribing multiple
guilty; may be long course of treatment; will AGE-RELATED FACTORS
most likely be managed, not cured. • Help medications concurrently that have same
CDS can present as nonspecific fear.
client understand subtlety of signs involved mode of action; review drug monographs
for each drug before prescribing. • Do not PREGNANCY/FERTILITY/BREEDING
and learn to recognize signs associated with
use SARIs, SSRIs, or TCAs with monoamine Most listed medications are not evaluated in
fear, anxiety, and stress.
oxidase inhibitor (MAOIs), including or contraindicated in pregnant animals.
but not limited to selegiline and amitraz. SYNONYMS
• Do not use SSRIs and TCAs together— • Generalized anxiety. • Neophobia.
possible risk of serotonin syndrome, which
MEDICATIONS can be fatal. SEE ALSO
• Aggression – Overview Dogs.
DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) • Fear and Aggression – Veterinary Visits Dogs.
• Should always be prescribed with complete Buspirone (daily)—0.5–1.0 mg/kg BID–TID. • Separation Anxiety Syndrome.
treatment plan in order to be compliant with • Thunderstorm and Noise Phobias – Dogs.
Supplements
standard of care. • Most treatment will be long
Natural products that may aid in reducing ABBREVIATIONS
term, possibly years; minimum treatment
anxiety—dog-appeasing pheromone • ALD = acral lick dermatitis.
generally 6 months with concurrent behavior
(Adaptil®); alpha-casosopene (Zykene®) alone • ANS = autonomic nervous system.
modification; if dog has significantly improved
or in diet together with l-tryptophan (Royal • CDS = cognitive dysfunction syndrome.
in 6 months, try slow weaning by reducing dose
Canin Calm® diet); l-theanine alone • DS/CC = desensitization and counter-
by 25–50% every 14 days. • Situational, mild
(Anxitane®) or in combination product conditioning.
PRN drug indicated, e.g., benzodiazepine,
containing whey protein, Phellodendron • MAOI = monoamine oxidase inhibitor.
serotonin reuptake inhibitor/antagonist (SARI)
amurense, and Magnolia officinalis (Solliquin®); • PSR = physiologic stress response.
either alone if stimulus is occasional and
melatonin; S-adenosylmethionine (SAMe); • SAMe = S-adenosylmethionine.
predictable, or more commonly concurrent with
Souroubea and Plantanus (Zentrol®), or a • SARI = serotonin reuptake inhibitor/antagonist.
selective serotonin reuptake inhibitor (SSRI) or
probiotic supplement (Calming Care®). • SSRI = selective serotonin reuptake inhibitor.
tricyclic antidepressant (TCA) prior to event.
◦ Best administered before any signs of • TCA = tricyclic antidepressant.
anxiety, fear, or panic; minimally 60–90 min INTERNET RESOURCES
before anticipated provocative stimulus. • https://www.dacvb.org • https://avsab.org
◦ Benzodiazepines—diazepam 0.50–2 mg/kg FOLLOW-UP • https://fearfreehappyhomes.com/courses/
PO up to q8h; clorazepate 0.50–2 mg/kg PO up PATIENT MONITORING dog-body-language-101
to q6h; alprazolam 0.01–0.1 mg/kg PO up to • Clients should contact veterinary healthcare
q4h. ◦ SARI: trazodone 3.0–10 mg/kg PO up Suggested Reading
team with updates at 2-week intervals for first Becker M, Radosta L, Sung W, et al. From
to q8h (up to 15 mg/kg). ◦ Alpha-2 agonist— 6–8 weeks of treatment; typically, treatment
clonidine 0.01–0.05 mg/kg PO up to q8h. Fearful to Fear Free. Irvine, CA: Lumina
plan will have to be altered. • CBC, biochemistry, Media, 2017.
• Dexmedetomidine oromucosal gel—125 μg/ urinalysis, T4, fT4, q12 months for animals
m2 onto oral mucosa 30–60 min prior to fear- Horwitz D, ed. Blackwell’s 5 Minute Consult
<8 years on daily administered medications; Clinical Companion: Canine and Feline
evoking event. • Generalized, stimulus senior dogs may require more frequent
unavoidable or severe—daily administered drug Behavior, 2nd ed. Chichester: Wiley, 2018,
reassessment based on age and health. pp. 253–388.
indicated. ◦ Both TCAs and SSRIs can take up
to 6 weeks to take effect; start at low end of PREVENTION/AVOIDANCE Horwitz D, Mills D, eds. BSAVA Manual of
dosing range and then slowly increase in • Proper socialization—8–12 weeks, Canine and Feline Behavioural Medicine,
2–4-week increments based on response to avoid including puppy classes starting at 8 weeks. 2nd ed. Gloucester: BSAVA, 2009.
side effects. ◦ TCA—clomipramine 1.0–3.0 mg/ • Structured relationship with owner (e.g., sit Landsberg G, Hunthausen W, Ackerman L.
kg PO q12h. ◦ SSRI—sertraline 1.0–3.0 mg/kg for all interactions). • Basic obedience. Behavior Problems of the Dog and Cat, 3rd
PO q24h; fluoxetine or paroxetine 0.5–2.0 mg/ • Treat traumatic experiences immediately. ed. Philadelphia, PA: Elsevier Saunders, 2013.
kg PO q24h. Author Lisa Radosta
POSSIBLE COMPLICATIONS Consulting Editor Gary M. Landsberg
PRECAUTIONS If left untreated or treated with medication
• All listed medications are extra-label except only, worsening clinical signs likely.
clomipramine and fluoxetine for treatment of EXPECTED COURSE AND PROGNOSIS Client Education Handout
separation anxiety and dexmedetomidine • Depends on response to medication, available online
oro-mucosal gel for noise aversion in dogs in suitability of environment, and client’s
the United States—follow Health and ability to perform behavior modification.
Feline Alveolar Osteitis

bone that looks similar to alveolar osteitis.
However, when biopsied, alveolar bone
expansion may show no signs of inflammation.
OVERVIEW FOLLOW-UP
Thickening of bone over the jugum of tooth CBC/BIOCHEMISTRY/URINALYSIS
No specific abnormalities seen related to PATIENT MONITORING
roots due to inflammation. Alveolar osteitis Recheck patient at 2 weeks postoperatively,
most commonly occurs over the maxillary alveolar osteitis.
F canine tooth roots of middle-aged and older IMAGING
with regular reevaluations depending on what
treatment was chosen.
cats (sometimes also called buttressing). This Intraoral dental radiographs typically show
process appears to be secondary to evidence of vertical periodontal bone loss PREVENTION/AVOIDANCE
periodontal inflammation. Tooth resorption along the long axis of the root on the palatal No known methods of prevention.
and extrusion (supereruption) may also be and buccal surface of the root. The expanded POSSIBLE COMPLICATIONS
seen in affected teeth. Feline alveolar osteitis bone may be less dense than normal adjacent Complications include those that may occur
should be distinguished from benign alveolar alveolar bone. when extracting teeth (perforation of
bone expansion (also called buccal bone mucogingival flap, dehiscence, iatrogenic
expansion), which is devoid of inflammation. oronasal fistula, etc.).
• Appropriate preanesthetic diagnostics when
SIGNALMENT indicated prior to procedure. EXPECTED COURSE AND PROGNOSIS
Although alveolar osteitis can occur in dogs, • Complete oral examination with periodontal Good with appropriate treatment, unless
it is far more common in cats. There are no probing—assess for periodontal pockets, neoplasia is diagnosed with biopsy.
established breed or sex predilections, and no gingival bleeding or tooth mobility; pay
established genetic basis. Middle-aged and particular attention to probing depth of
Suggested Reading
older cats are most commonly affected. Beebe DE, Gengler WR. Osseous surgery to
palatal surface of maxillary canine teeth.
augment treatment of chronic periodontitis
SIGNS • Intraoral radiographs under anesthesia—
of canine teeth in a cat. J Vet Dent 2007,
assess extent of osseous changes; assess root
History 24(1):30–38.
stability, attachment loss, and evidence of
• Owner may report thickening or bulging Author John R. Lewis
tooth resorption.
over the maxillary canine teeth roots, usually Consulting Editor Heidi B. Lobprise
• Consider biopsy if bone changes are
bilateral, but can be unilateral. unilateral or if aggressive osseous changes are
• Evidence of oral pain is not often noted by seen on dental radiographs.
pet owners.
◦ Discomfort may occur with mobile teeth.
◦ Discomfort may occur when extruded
maxillary canine teeth contact the lower lip
or the opposing canine, resulting in an TREATMENT
acquired malocclusion. • If mild periodontal changes are present
(moderate pocket depth, no tooth mobility,
Clinical Findings
minimal extrusion, no oronasal fistulation), a
• Bulging of alveolar bone on the buccal
professional ultrasonic dental cleaning with
surface of the root; variable degree of gingival
root planing and subgingival curettage ±
inflammation.
placement of periodontal pocket antimicrobial
• Patient may have abnormal periodontal
treatment ± osseous surgery.
pocket depths on probing (normal sulcus depth
• If extensive periodontal disease is present
for cats is 0–1 mm); patients often exhibit
(deep periodontal pocket, tooth mobility,
vertical bone loss with infrabony pockets.
extensive extrusion, patient discomfort, oronasal
• Patients may exhibit extrusion (supereruption)
fistula), consider extraction. Buccal attached
of one or more teeth; extended tooth length
gingiva may be very thin, making it difficult to
may cause trauma to lower lip or malocclusion
elevate a gingival flap. Ostectomy/osteoplasty of
with opposing mandibular canine tooth.
buccal alveolar bulge is necessary after raising
• May progress to tooth mobility and acquired
the gingival flap and prior to closure. Biopsy of
dental malocclusion due to contact between
buccal alveolar bone can be accomplished with
maxillary and mandibular canine teeth.
rongeurs once a mucogingival flap has been
CAUSES & RISK FACTORS elevated. Gently elevate palatal mucosal edge to
Cause is unknown, but buttressing in humans facilitate closure.
is considered to be an attempt by the body to
stabilize a diseased tooth. Cats that are prone
to periodontal disease may be at a higher risk
for developing alveolar osteitis.
MEDICATIONS
DRUG(S) OF CHOICE
Appropriate antimicrobials and pain
medications when indicated.
DIAGNOSIS
Alveolar bone expansion, also known as buccal INTERACTIONS
bone expansion, is an enlargement of alveolar N/A
Feline Calicivirus Infection

SIGNS CBC/BIOCHEMISTRY/URINALYSIS
General Comments No characteristic or consistent findings.
BASICS Severity of disease is dependent on host OTHER LABORATORY TESTS
immune status, virulence of infecting strain, Often diagnosed on clinical signs.
DEFINITION and presence of co-infections. Most common
A common viral respiratory disease of IMAGING
manifestation involves self-limiting upper Radiographs of lungs—consolidated lung
domestic and exotic cats characterized by respiratory tract disease and oral ulceration. tissue in cats with pneumonia.
F
upper respiratory disease and oral ulceration,
occasionally pneumonia or arthritis, and Historical Findings DIAGNOSTIC PROCEDURES
rarely a highly fatal systemic hemorrhagic • Sudden onset. • PCR—oropharyngeal swabs most likely to
disease (FCV–VSD). • Anorexia. detect virus; positive result does not prove
• Serous ocular or nasal discharge, usually that FCV is causative agent for disease due to
PATHOPHYSIOLOGY with little or no sneezing.
• Spread through ocular, nasal, and oral persistently shedding cats.
• Ulcers on tongue, hard palate, lips, tip of
secretions. • Cell cultures to isolate virus—oral pharynx;
nose, or around claws. lung tissue; feces; blood; secretions from nose
• Transmission typically occurs through • Dyspnea from pneumonia.
direct contact or fomite exposure; droplet and conjunctiva.
• Acute, painful lameness.
transmission possible within 4–5 feet; • Immunofluorescent assays of lung
replication takes place primarily in respiratory Physical Examination Findings tissue—viral antigen.
and oral tissues. • Ranging from generally alert and in good • Serologic testing on paired serum samples—
• Rapid cytolysis of infected cells results in condition to lethargy and decreased detect rise in neutralizing antibody titers
tissue pathology and clinical disease. mentation. against virus; vaccination interferes with
• Fever. results from serum neutralization testing.
SYSTEMS AFFECTED • Ulcers of tongue/mouth may occur without
• Gastrointestinal—ulceration of the tongue PATHOLOGIC FINDINGS
other signs. • Gross—upper respiratory infection; ocular
common; occasional ulceration of the hard • Hypersalivation.
palate and lips. and nasal discharge; pneumonia with
• Upper to lower respiratory tract disease— consolidation of large portions of individual
• Hemic/lymphatic/immune—hemorrhage; nasal discharge, or stertor; wheezes, crackles,
splenic necrosis (FCV–VSD). lung lobes; possible ulcerations on tongue,
or increased bronchovesicular sounds on lips, and hard palate; systemic hemorrhages.
• Hepatobiliary—hepatic necrosis (FCV– pulmonary auscultation,
VSD). • Histopathologic—interstitial pneumonia of
• Epistaxis or hematochezia with systemic large portions of individual lung lobes;
• Musculoskeletal—acute arthritis. hemorrhage (FCV–VSD).
• Ophthalmic—acute serous conjunctivitis ulcerations on epithelium of tongue, lips, and
• Facial and limb edema with crusting/ hard palate; mild inflammatory reactions in
without keratitis or corneal ulcers. ulcerations of face, pinnae, and feet due to
• Respiratory—rhinitis; interstitial nose and conjunctiva; systemic hemorrhages,
vasculitis (FCV–VSD). vasculitis, or necrosis.
pneumonia; ulceration of nose tip. • Icterus (FCV–VSD).
• Skin/exocrine—subcutaneous edema;
ulcerations of pinnae or pawpads; pancreatic CAUSES
necrosis (FCV–VSD). • A small, nonenveloped single-stranded
RNA virus, feline calicivirus (FCV).
GENETICS • Numerous strains exist in nature, with
TREATMENT
None varying degrees of antigenic cross-reactivity. APPROPRIATE HEALTH CARE
INCIDENCE/PREVALENCE • More than one serotype. Outpatient, unless severe pneumonia,
• Persistent infection common, resulting in • Relatively stable and resistant to many hemorrhage, or severe systemic disease.
virus-shedding carriers. disinfectants. NURSING CARE
• Clinical disease—common in multicat RISK FACTORS • Clean eyes and nose as indicated with warm
facilities, shelters, breeding catteries. • Lack of vaccination or improper water or saline.
• Routine vaccination—reduces incidence vaccination. • Provide access to steam, such as in a
and severity of clinical disease; has not • Multicat facilities. bathroom, to clear secretions.
decreased prevalence of the virus. • Concurrent infections with other • Provide palatable, soft foods.
GEOGRAPHIC DISTRIBUTION pathogens, e.g., feline herpesvirus (FHV), • Oxygen—with severe pneumonia.
Worldwide feline panleukopenia virus (FPV), feline ACTIVITY
immunodeficiency virus (FIV), feline Patients should be restricted from contact
SIGNALMENT
leukemia virus (FeLV). with other cats to prevent transmission of
Species • Poor ventilation. causative virus.
Cat • Stress.
DIET
Breed Predilections • No restrictions.
None • Special diets—to entice anorectic cats to
Mean Age and Range resume eating.
• Young kittens >6 weeks old—most DIAGNOSIS • Soft foods—if ulcerations restrict eating.
common. DIFFERENTIAL DIAGNOSIS CLIENT EDUCATION
• Cats of any age may show clinical disease. • FHV. Discuss need for proper vaccination and to
Predominant Sex • Chlamydiosis. modify vaccination protocol in breeding
None • Bordetella bronchiseptica. catteries to include kittens before they
Feline Calicivirus Infection (continued)
become infected (often at 6–8 weeks of age) days; follow-up vaccinations every 3–4 weeks • Limping kitten syndrome.
from a carrier queen. until 16 weeks of age. • Hemorrhagic calicivirus.
• Vaccination will not prevent virus infection
SURGICAL CONSIDERATIONS SEE ALSO
None in subsequent exposure, but can prevent • Chlamydiosis—Cats.
serious clinical disease caused by most strains; • Feline Herpesvirus Infection.
FCV–VSD can occur in vaccinated cats. • Feline (Upper) Respiratory Infections.
F • Environmental management—decrease • Rhinitis and Sinusitis.
housing density; isolate affected cats by >4 ft; • Stomatitis and Oral Ulceration.
MEDICATIONS beware of hygiene and fomites; disinfect with
dilute (1 : 30) bleach. ABBREVIATIONS
DRUG(S) OF CHOICE
• FCV = feline calicivirus.
• No specific antiviral drugs are clearly POSSIBLE COMPLICATIONS • FCV–VSD = feline calicivirus–virulent
indicated. • Interstitial pneumonia—most serious systemic disease.
• Broad-spectrum antibiotics—indicated for complication; can be life-threatening. • FeLV = feline leukemia virus.
treatment of secondary bacterial infections • Secondary bacterial infections of lungs or • FHV = feline herpesvirus.
(e.g., amoxicillin or amoxicillin–clavulanate upper airways. • FIV = feline immunodeficiency virus.
at 22 mg/kg PO q12h; doxycycline at 5 mg/
EXPECTED COURSE AND PROGNOSIS • FPV = feline panleukopenia virus.
kg PO q12h).
• Clinical disease—usually appears 3–4 days • MLV = modified live virus.
• Secondary bacterial infections of affected
after exposure. INTERNET RESOURCES
cats not nearly as important as with FHV-1
• With supportive care, infection usually
infections. http://www.abcdcatsvets.org/
self-limiting and cats with upper respiratory feline-calicivirus-infection-2012-edition
• Antibiotic eye ointments—to reduce
signs respond favorably within 7–10 days.
secondary bacterial infections of conjunctiva. Suggested Reading
• Oral ulcerations typically improve in 2–3
• Pain medication—as indicated for arthritis Afonso MM, Gaskell RM, Radford A. Feline
weeks.
pain or significant ulceration. upper respiratory infections. In: Ettinger SJ,
• Lameness usually resolves in 1–2 days.
CONTRAINDICATIONS • Prognosis excellent, unless severe pneumonia Feldman EC, Côté, E, eds. Textbook of
None or systemic hemorrhagic disease develops. Veterinary Internal Medicine: Diseases of
• FCV–VSD may be severe and fatal. the Dog and Cat, 8th ed. St. Louis, MO:
PRECAUTIONS
• Recovered cats—persistently infected for Elsevier, 2017, pp. 1013–1016.
None
long periods; will shed small quantities of Gaskell RM, Dawson S, Radford AD. Feline
POSSIBLE INTERACTIONS virus in oral secretions continuously. respiratory disease. In: Greene CE, ed.,
None Infectious Diseases of the Dog and Cat, 4th
ALTERNATIVE DRUG(S) ed. St. Louis, MO: Saunders Elsevier, 2012,
None pp. 151–162.
Pedersen NC, Elliot JB, Glasgow A, et al. An
MISCELLANEOUS isolated epizootic of hemorrhagic-like fever
ASSOCIATED CONDITIONS in cats caused by a novel and highly virulent
Affected cats may also be concurrently infected strain of feline calicivirus. Vet Microbiol
FOLLOW-UP with FHV-1, especially in multicat and breeding 2000, 73:281–300.
PATIENT MONITORING facilities. FCV has been implicated in develop- Scherk MA, Ford RB, Gaskell RM, et al.
• Monitor for sudden development of ment of feline chronic gingivostomatitis. 2013 AAFP Feline Vaccination Advisory
dyspnea associated with pneumonia. Panel Report. J Feline Med Surg 2013;
AGE-RELATED FACTORS
• No specific laboratory tests. 15:785–808.
Usually occurs in young kittens whose
Author Sara E. Gonzalez
PREVENTION/AVOIDANCE maternally derived immunity has waned.
• American Association of Feline ZOONOTIC POTENTIAL Acknowledgment The author and book
Practitioners—classifies FHV, FPV, and FCV None editors acknowledge the prior contribution of
as core vaccines; vaccinate all cats with either Fred W. Scott.
a modified live virus (MLV) or inactivated PREGNANCY/FERTILITY/BREEDING
core vaccine on initial visit (as early as 6 Generally no problem, because most cats have
weeks of age), repeat every 3–4 weeks until 16 been exposed or vaccinated before becoming
weeks of age, and booster 1 year after last pregnant.
available online
kitten vaccine; revaccinate every 3 years. SYNONYMS
• Breeding catteries—respiratory disease is a • Feline picornavirus infection—FCV
problem; vaccinate kittens at earlier age, originally classified as a picornavirus; older
either with additional vaccination at 4–5 literature refers to the infection by this name;
weeks or with intranasal vaccine at 10–14 no known picornavirus infects cats.
Feline Herpesvirus Infection

• Recurrent signs—carriers. IMAGING
• Abortion. • Radiography—open-mouth ventrodorsal
Physical Examination Findings and rostrocaudal (skyline) views of skull
BASICS reveal presence of chronic disease in nasal
• Fever—up to 106 °F (41 °C).
DEFINITION • Rhinitis—serous, mucopurulent, or cavity and frontal sinuses; infection cannot be
An acute disease in cats characterized by purulent discharge. reliably distinguished from neoplasia and
sneezing, fever, rhinitis, conjunctivitis, and • Conjunctivitis—serous, mucopurulent, or inflammatory polyps; no abnormal F
ulcerative keratitis. purulent discharge. radiographic findings with acute disease.
• Chronic rhinitis/sinusitis—chronic • CT provides more accurate assessment of
PATHOPHYSIOLOGY
purulent nasal discharge. disease in nasal cavity and frontal sinus
Feline herpesvirus-1 (FHV-1) causes acute
• Keratitis—ulceration, descemetocele, compared to radiographs; CT may
cytolytic infection of respiratory or ocular
panophthalmitis. differentiate neoplasia from inflammation
epithelium after oral, intranasal, or conjunctival
based on amount of bony destruction.
exposure. The intracellular virus travels from CAUSES
cell to cell and does not stimulate a strong FHV-1 DIAGNOSTIC PROCEDURES
immune response from the host. N/A
RISK FACTORS
SYSTEMS AFFECTED • Lack of vaccination for FHV-1, although PATHOLOGIC FINDINGS
• Integumentary—herpes dermatitis near the vaccines do not bestow sterilizing immunity. • Gross—ocular and nasal discharge,
nares. • Multicat facilities with overcrowding, poor mucosal edema of upper airway epithelium,
• Ophthalmic—conjunctivitis with serous or ventilation, poor sanitation, poor nutrition, tracheitis, sinusitis, ulcerative keratitis,
purulent ocular discharge; ulcerative keratitis or physical or psychologic stress. panophthalmitis.
or panophthalmitis. • Pregnancy and lactation. • Microscopic—submucosal edema,
• Reproductive—in utero infection (infected • Concomitant disease, especially owing to inflammatory cell infiltrates of upper
pregnant queen) may result in severe neonatal immunosuppressive organisms or other respiratory and conjunctival tissues, chronic
herpetic infection. respiratory organisms. sinusitis, intranuclear inclusion bodies in
• Respiratory—rhinitis with sneezing and • Kittens born to carrier queens—infected ~5 epithelial cells.
serous to purulent nasal discharge; chronic weeks of age.
sinusitis may result; tracheitis possible.
• Neurologic—latent virus found in optic
nerve, ciliary ganglion, brainstem, cerebellum, TREATMENT
and olfactory bulb.
DIAGNOSIS APPROPRIATE HEALTH CARE
GENETICS • Inpatient—nutritional and fluid support to
N/A DIFFERENTIAL DIAGNOSIS
• Feline calicivirus infection—less sneezing anorectic cats.
INCIDENCE/PREVALENCE than FHV-1, conjunctivitis, ulcerative • Outpatient—if eating and afebrile.
• Common, especially in multicat households keratitis; may cause ulcerative stomatitis, NURSING CARE
or facilities housing large numbers of cats; pneumonia. • Outpatient—keep patient indoors to
catteries and shelters are source of most • Feline Chlamydophila infection—more prevent environmentally induced stress,
infections. chronic conjunctivitis, which may be which may lengthen disease course.
• Perpetuated by latent carriers that harbor unilateral; pneumonitis; intracytoplasmic • Fluids—IV or SC; to correct and prevent
virus in nerve (especially trigeminal) ganglia. inclusions in conjunctival scrapings; dehydration; to keep nasal secretions thin.
GEOGRAPHIC DISTRIBUTION responds to tetracyclines or • Appetite stimulant as needed
Worldwide chloramphenicol. (mirtazapine—1.8 mg/cat PO q24–48h).
• Bacterial infection (Bordetella, Haemophilus,
SIGNALMENT ACTIVITY
or Pasteurella)—less nasal and ocular Isolate affected cats during acute phase
Species involvement; often respond to antibiotics.
All domestic and many exotic cats. because they are contagious.
CBC/BIOCHEMISTRY/URINALYSIS DIET
Breed Predilections • Nonspecific.
• Outpatient—encourage food consumption
• None. • Transient leukopenia followed by
• Brachycephalic breeds have more severe
to avoid anorexia; offer foods with appealing
leukocytosis may occur. tastes and smells; warming food may enhance
corneal disease and are more likely to have
corneal sequestra. OTHER LABORATORY TESTS smell.
• PCR testing from pharyngeal and • Inpatient—forced enteral feeding for
Mean Age and Range conjunctival swabs will identify presence of anorectic cats; remove nasal secretions (so
• All ages. virus; more sensitive than other diagnostic nasal breathing can occur) before starting
• Kittens most susceptible. modalities; may be transiently positive orogastric or esophagostomy tube feeding;
Predominant Sex following vaccination with modified live virus avoid nasoesophageal tubes because of
N/A (MLV) vaccine for FHV-1. rhinitis.
• Immunofluorescent assay—nasal or
SIGNS CLIENT EDUCATION
conjunctival scrapings; viral detection. • Inform client of contagious nature of
Historical Findings • Viral isolation—pharyngeal swab
disease.
• Acute onset of paroxysmal sneezing. sample. • Discuss proper vaccination protocols and
• Blepharospasm and ocular discharge. • Stained conjunctival smears—detect
early vaccination of cats in multicat facilities
• Anorexia (from high fever, general malaise, intranuclear inclusion bodies. and households.
or inability to smell).
Feline Herpesvirus Infection (continued)
• Inform client that early weaning and (FeLV) or feline immunodeficiency virus
isolation from all other cats except littermates (FIV).
may prevent infections. ALTERNATIVE DRUG(S) MISCELLANEOUS
SURGICAL CONSIDERATIONS • Lysine (500 mg PO q12h) might reduce
Surgically implanted feeding tubes (esopha viral shedding, clinical signs. ASSOCIATED CONDITIONS
gostomy tube, gastrostomy tube) may be • Lysine-lactoferrin (500 mg PO q12h) Simultaneous viral or bacterial respiratory diseases.
F needed to manage prolonged anorexia. more effective than lysine alone for AGE-RELATED FACTORS
treatment. More severe in young kittens.
• Penciclovir—effectively inhibits FHV-1,
ZOONOTIC POTENTIAL
doses unknown at this time.
None
MEDICATIONS PREGNANCY/FERTILITY/BREEDING
DRUG(S) OF CHOICE Pregnant cats with FHV infection may
• Antibiotics not recommended if nasal transmit FHV-1 to kittens in utero, resulting
discharge is serous and lacks purulent or FOLLOW-UP in abortion or neonatal disease.
mucopurulent component; antibiotics PATIENT MONITORING SYNONYMS
recommended only if fever, lethargy, or Monitor appetite closely; hospitalize for fluids • Coryza.
anorexia present concurrently with and tube feeding if anorexia develops. • Feline rhinotracheitis.
mucopurulent nasal discharge. PREVENTION/AVOIDANCE • Rhino.
• Doxycycline (10 mg/kg PO q24h) Can survive in environment for several hours;
recommended; amoxicillin (22 mg/kg PO/ SEE ALSO
drying and most disinfectants effectively kill Feline Calicivirus Infection.
IM/SC q8–12h) or ampicillin (10–20 mg/kg the virus.
IV/IM/SC q6–8h) for secondary bacterial ABBREVIATIONS
infections. Vaccines
• Famciclovir (40–90 mg/kg PO 12h) may • Routine vaccination with MLV or
• FHV-1 = feline herpesvirus type 1.
shorten course and severity of disease. inactivated virus vaccine—prevents • FIV = feline immunodeficiency virus.
• Ophthalmic antibiotics—for keratitis. development of severe disease; does not • MLV = modified live virus.
• Ophthalmic antivirals for herpetic ulcers in prevent infection and local viral replication
order of efficacy—trifluridine, cidofovir, with mild clinical disease and virus Suggested Reading
idoxuridine, ganciclovir, aciclovir; must be shedding. Bol S, Bunnik EM. Lysine supplementation is
instilled q2h for significant effect, except for • Vaccinate at 8–10 weeks, 12–14 weeks, and not effective for the prevention or treatment of
cidofovir which can be given q12h, making it 16–18 weeks of age and with annual boosters feline herpesvirus 1 infection in cats: a
ophthalmic drug of choice, although it must for reasonable protection, especially in systematic review. BMC Vet Res 2015, 11:284.
be compounded. high-risk populations. Horzinek MC, Addie D, Sándor B, et al. ABCD:
• Some evidence that administration of • Endemic multicat facilities or households— update of the 2009 guidelines on prevention
intranasal vaccine 2–6 days prior to exposure vaccinate kittens with dose of intranasal and management of feline infectious diseases. J
will result in lessening of clinical signs; may vaccine at 10–14 days of age, then Feline Med Surg 2013, 15:530–539.
be helpful in outbreak in multicat setting. parenterally at 6, 10, and 14 weeks of age; Lappin MR, Blondeau J, Boothe D, et al.
isolate litter from all other cats at 3–5 weeks Antimicrobial use guidelines for treatment
CONTRAINDICATIONS of age; then use kitten vaccination protocol to of respiratory tract disease in dogs and cats.
• Idoxuridine ophthalmic—may be painful; prevent early infections. J Vet Intern Med 2017, 31:279–294.
discontinue medication. Malik R, Lessels NS, Webb S, et al. Treatment
• Cidofovir ophthalmic—scarring of POSSIBLE COMPLICATIONS of feline herpesvirus-1 associated disease.
nasolacrimal duct reported in humans, • Chronic rhinitis or rhinosinusitis with
J Feline Med Surg 2009, 11(1):40–48.
rabbits. long-term sneezing and nasal discharge. Thiry E, Addie D, Belak S, et al. Feline
• Trifluridine, idoxuridine, acyclovir—toxic if • Herpetic ulcerative keratitis.
herpesvirus infection: ABCD guidelines on
given systemically. • Corneal sequestrum that must be removed
prevention and management. J Feline Med
• Systemic corticosteroids—may induce surgically. Surg 2009, 11(7):547–555.
relapse in chronically infected cats. • Permanent closure of nasolacrimal duct
Thomasy SM, Maggs DJ. A review of
• Ophthalmic corticosteroids—may with chronic ocular discharge. antiviral drugs and other compounds with
predispose to ulcerative keratitis EXPECTED COURSE AND PROGNOSIS activity against feline herpesvirus-1. Vet
• Nasal decongestant drops—0.25% • 7–10 days followed by spontaneous Ophthalmol 2016, 19(Suppl 1):119–130.
oxymetazoline HCl; decrease nasal discharge; remission, if secondary bacterial infections do Author Lisa Restine
contraindicated because some cats object and not occur. Consulting Editor Amie Koenig
some experience rebound rhinorrhea. • Prognosis generally good, if fluid and Acknowledgment The author and book
PRECAUTIONS nutritional therapy are adequate. editors acknowledge the prior contribution of
• Oral doxycycline tablets can cause • Correlation between severity of acute signs Gary D. Norsworthy.
esophageal ulceration. and degree of latent infection.
• Death usually result of inadequate • May become chronically affected and
nutritional and fluid support or immuno exhibit respiratory signs long term. Client Education Handout
suppression due to feline leukemia virus available online
Feline Hyperesthesia Syndrome

of spinal cord, nerve roots, epaxial muscles, or treat self-mutilation in cats. • Selective
vertebral column causing pain—degenerative serotonin reuptake inhibitors (fluoxetine
(intervertebral disc disease), inflammatory 0.5–2.0 mg/kg PO q24h), tricyclic
BASICS (discospondylitis, meningitis, myositis), antidepressants (clomipramine 0.5–1.0 mg/kg
OVERVIEW neoplastic, or traumatic; spinal radiographs PO q24h), or benzodiazepines (lorazepam
• Idiopathic disorder of cats characterized by helpful in evaluating for abnormalities; further 0.125–0.50 mg per cat PO q8–24h)
paroxysmal agitation, focal epaxial muscle diagnostics (e.g., advanced imaging, serology for recommended when primary behavioral disorder F
spasms, vocalization, and intense biting or infectious agents, cerebrospinal fluid [CSF] suspected. • Combination therapy often
licking of the back, tail, and pelvic limbs. analysis) may be necessary. • Forebrain disease required. • Treatment response variable; in cats
• Also known as atypical neurodermatitis, rolling causing behavioral changes and/or seizures— that respond, therapy often lifelong as episodes
skin disease, apparent neuritis, and twitchy cat metabolic (hepatic encephalopathy), infectious/ tend to resume after medication discontinued.
disease. • Pathophysiology unknown. inflammatory (feline leukemia virus, feline CONTRAINDICATIONS/POSSIBLE
• Organ systems affected—behavioral, nervous, immunodeficiency virus, feline infectious
peritonitis, cryptococcosis, toxoplasmosis), INTERACTIONS
neuromuscular, skin/exocrine.
neoplastic, vascular; complete diagnostic Fluoxetine inhibits the cytochrome P450
SIGNALMENT system and should be used cautiously with
evaluation including bile acid tolerance, testing
Species for infectious causes, CSF analysis, and brain other drugs that undergo extensive hepatic
Cat imaging may be indicated. • Behavioral metabolism, including phenobarbital,
condition—compulsive disorder; exclusion benzodiazepines, and tricyclic antidepressants.
Breed Predilections
Can be seen in any breed; Siamese, diagnosis.
Abyssinian, Burmese, and Himalayan may be CBC/BIOCHEMISTRY/URINALYSIS
predisposed. Frequently normal.
FOLLOW-UP
Mean Age and Range IMAGING
Most common at 1–7 years of age. None required aside from that necessary to PATIENT MONITORING
exclude differential diagnoses. Cats administered phenobarbital—check
SIGNS serum drug concentrations in 2–3 weeks and
• Episodes of twitching of skin over lumbar area, DIAGNOSTIC PROCEDURES adjust dosage as needed to maintain levels of
violent swishing of tail, vocalizing, and biting or • Diagnosis based on characteristic history 20–30 μg/mL (85–130 μmol/L); CBC and
licking of flank, pelvic region, or tail. • Pupils and clinical findings, and by excluding other biochemistry profile at 6–12-month intervals
often dilate, and cats can become aggressive or diseases that can cause similar signs. • No test to monitor for adverse effects.
appear agitated and run wildly about the or group of tests support definitive diagnosis.
environment. • Episodes are several seconds to • Electromyography (EMG)—evidence of EXPECTED COURSE AND PROGNOSIS
several minutes in length; cats are typically normal abnormal spontaneous activity in thora Prognosis depends on whether underlying
between episodes, but may be intolerant of being columbar epaxial muscles in one study of cause is identified, response to medication,
stroked along the back. • General physical affected cats. • Muscle biopsy—if EMG and frequency and severity of episodes.
examination often reveals no abnormalities aside changes; isolated report of vacuoles within
from possible alopecia and broken hair over epaxial muscles, with antibody labeling
lumbar area from self-mutilation; many cats resent characteristics similar to those described with
palpation of thoracolumbar musculature, and inclusion body myositis/myopathy in humans. MISCELLANEOUS
manipulation of area may elicit an episode; no
neurologic deficits present. ABBREVIATIONS
CAUSES & RISK FACTORS • EMG = electromyography.
• Not known whether this syndrome is TREATMENT Suggested Reading
manifestation of underlying behavioral • Outpatient. • Eliminate environmental
problem, dermatopathy, focal seizure disorder, Amengual Batle P, Rusbridge C, Nuttall T,
changes that can precipitate episodes.
or abnormal sensory state causing neuropathic et al. Feline hyperaesthesia syndrome with
• Behavioral modification has been successful
pain or itch; speculated that cause is self-trauma to the tail: retrospective study of
in reducing clinical manifestations in some
multifactorial, or that syndrome is not seven cases and proposal for integrated
cats. • In severe cases of self-mutilation,
distinct entity with single cause, but rather multidisciplinary diagnostic approach. J
Elizabethan collar or tail bandaging may be
can develop from variety of different factors. Feline Med Surg 2019, 21(2):178–185. doi:
necessary.
• Cats that tend to be nervous or 10.1177/1098612X18764246
hyperexcitable may be at increased risk; Author Karen R. Muñana
environmental stressors can serve as trigger.
MEDICATIONS
DRUG(S) OF CHOICE
• Several pharmacologic agents recommended,
DIAGNOSIS
based on suspected underlying cause.
DIFFERENTIAL DIAGNOSIS • Prednisolone indicated if pruritic dermatitis
• Dermatologic conditions causing pruritus— suspected. • Antiepileptic drugs often utilized;
parasitic (e.g., flea, Notoedres, Cheyletiella), phenobarbital (1–2 mg/kg PO q12h) effective
fungal (e.g., dermatophytosis), or allergic (e.g., in some cats; gabapentin (5–10 mg/kg PO
parasitic, inhalant, dietary); evaluate for q12h) can be used for both antiepileptic and
underlying dermatitis; skin scrapings and fungal analgesic properties; topiramate (5 mg/kg PO
cultures can help confirm diagnosis. • Diseases q12h) is antiepileptic that has also been used to
Feline Idiopathic Lower Urinary Tract Disease

• Uncommon in cats <1 and >10 years old. • Ultrasonography may exclude uroliths and
SIGNS thickening of bladder wall due to inflammation
or neoplasia.
BASICS Historical Findings • Contrast cystography may exclude small or
DEFINITION • Dysuria. radiolucent uroliths, blood clots, urethral
Idiopathic lower urinary tract disease, • Hematuria. stricture, vesicourachal diverticula, and
• Pollakiuria.
F commonly referred to as feline idiopathic cystitis
• Periuria.
thickening of bladder wall due to
(FIC), is a nonmalignant, sterile, inflammatory inflammation or neoplasia.
disease of the urinary bladder and urethra. It is • Urge incontinence.
• Outflow obstruction. DIAGNOSTIC PROCEDURES
the most common urinary disorder of young to • Cystoscopy may exclude uroliths and
middle-aged cats and is characterized by dysuria, Physical Examination Findings diverticula.
pollakiuria, hematuria, periuria, and in some Thickened, firm, contracted bladder wall. • Biopsies of urinary bladder wall may permit
cases urinary obstruction. Clinical observations morphologic characterization of inflammatory
CAUSES
suggest that FIC is associated with different or neoplastic lesions.
See Pathophysiology.
clinical phenotypes (acute self-limiting,
chronic, nonobstructive, and obstructive RISK FACTORS PATHOLOGIC FINDINGS
forms) and pathologic phenotypes (ulcerative, • Male, middle-aged, and overweight cats, • Cystoscopy may reveal petechial
inflammatory, hyperplastic, nonulcerative, and as well as cats housed indoors or living in hemorrhages (glomerulations) of urinary
noninflammatory forms). Regardless of form, a home with other cats, are at increased bladder mucosa.
the terms idiopathic lower urinary tract disease risk. • Mucosal ulceration or hyperplasia, submucosal
and FIC represent an exclusionary diagnosis • Feeding dry food has not been consistently edema, hemorrhage, neovascularization, fibrosis,
established only after known causes have been recognized as a risk factor. and mononuclear inflammatory cell infiltrates
eliminated. • Stress may play a role in precipitating or are prominent features of chronic FIC.
exacerbating signs.
PATHOPHYSIOLOGY
• Etiopathogenesis is uncertain.
• Urinary bladder abnormalities include
alterations in urothelial barrier structure and TREATMENT
function, differentiation and repair, signaling, DIAGNOSIS APPROPRIATE HEALTH CARE
eicosanoid biosynthesis, and innate immune DIFFERENTIAL DIAGNOSIS • Patients with nonobstructive lower urinary
and inflammatory responses. • Metabolic disorders including various types tract diseases—typically managed as outpatients;
• Association of FIC with stress (environ of uroliths/urethral plugs. diagnostic evaluation may require brief
mental, psychologic, physiologic, or comorbid • Urinary tract infection (UTI) from bacteria, hospitalization.
pathologic stressors) and identification of mycoplasma/ureaplasma, fungal agents, and • Patients with obstructive lower urinary tract
multiple abnormalities of nervous and parasites. diseases—usually hospitalized for diagnosis
endocrine systems have led to hypothesis that • Trauma. and management.
systemic psychoneuroendocrine factors may • Neurogenic disorders including reflex
have a role in the pathogenesis. DIET
dyssynergia, urethral spasm, and hypotonic or • Results of prospective, randomized, double-
• Clinical and morphologic features of atonic bladder.
chronic forms of FIC are similar to those of masked, controlled clinical trial provided
• Iatrogenic disease including reverse evidence that feeding specific multipurpose
an idiopathic cystopathy of humans called flushing solutions, indwelling and
interstitial cystitis/painful bladder syndrome therapeutic urinary food (Hill’s c/d Multicare)
postsurgical urethral catheters, and enriched with omega-3 fatty acids (EPA and
(IC/PBS). However, the extent to which the urethrostomy complications.
feline and human forms share pathogenic DHA) and antioxidants significantly reduced
• Anatomic abnormalities including urachal rate of recurrent episodes of FIC signs.
mechanisms has not yet been fully defined. anomalies and acquired urethral strictures. • Low-grade evidence that recurrence of signs
SYSTEMS AFFECTED • Neoplasia. may be minimized by feeding moist foods.
• Renal/urologic—lower urinary tract. • Clinical signs may be confused with • Appropriate dietary management for
• Persistent urethral outflow obstruction constipation. persistent crystalluria associated with matrix-
results in postrenal azotemia. CBC/BIOCHEMISTRY/URINALYSIS crystalline urethral plugs.
INCIDENCE/PREVALENCE • Hematuria and proteinuria without CLIENT EDUCATION
• Incidence of hematuria, dysuria, and/or significant pyuria or bacteriuria—usually • Hematuria, dysuria, and pollakiuria—often
urethral obstruction (UO) in domestic cats has present. self-limiting within 4–7 days in most cats.
been previously reported to be ~0.5–1% per year. • If UO persists, serum chemistry profiles Signs may recur unpredictably; up to 65% of
• Hospital morbidity rate for FIC in cats reveal azotemia, hyperphosphatemia, cats experience ≥1 episodes within 1–2 years.
with lower urinary tract signs is ~65%; it is hyperkalemia, and acidosis. • A lack of controlled studies demonstrating
the single most common cause of lower OTHER LABORATORY TESTS efficacy of most drugs used to treat this
urinary tract signs in cats. • Absence of bacteriuria—verify by quantitative disorder symptomatically.
SIGNALMENT urine culture; collect urine specimens by • Reduce environmental stress by minimizing
cystocentesis to avoid contamination. impact of changes in the home and
Species maintaining a constant diet. Environmental
• Transmission electron microscopy has revealed
Cat enrichment for indoor-housed cats consists of
calicivirus-like particles in some urethral plugs.
Mean Age and Range provision of necessary resources (food, water,
• May occur at any age, but most commonly
IMAGING litter boxes, space, play), providing a safe
• Survey radiography may exclude radiopaque place to hide, refinement of cat–owner
recognized in young to middle-aged adults
(mean 3.5 years, range: 2–7 years). uroliths or urethral plugs. interactions, and management of conflict.
(continued) Feline Idiopathic Lower Urinary Tract Disease

• Provide proper litter box hygiene. some because of their anti-inflammatory and EXPECTED COURSE AND PROGNOSIS
• Males should be monitored for signs of analgesic properties; the safety of NSAIDs in Hematuria, dysuria, and pollakiuria often
UO. the treatment of FIC has not been evaluated self-limiting within 4–7 days in most
SURGICAL CONSIDERATIONS by controlled clinical trials. patients. These signs often recur
• Antibiotics—no detectable effect on unpredictably.
Do not perform perineal urethrostomy to
minimize recurrent UO without localizing remission of clinical signs in cats demonstrated.
obstructive disease to penile urethra by CONTRAINDICATIONS F
contrast urethrography. • Phenazopyridine—may result in methemo
globinemia and irreversible oxidative changes MISCELLANEOUS
in hemoglobin resulting in formation of
AGE-RELATED FACTORS
Heinz bodies and anemia.
Frequency of recurrence appears to decline
• Methylene blue—may cause Heinz bodies
MEDICATIONS and severe anemia.
with advancing age.
DRUG(S) OF CHOICE • Bethanechol—do not use in patients with SYNONYMS
• Amitriptyline—empirically advocated to treat UO. • Feline idiopathic cystitis.
cats with severe recurrent or persistent signs; • Feline interstitial cystitis.
PRECAUTIONS
suggested dosage is 5–10 mg/cat q24h given at SEE ALSO
• Cats with UO and postrenal azotemia are at
night; not recommended for treatment of • Dysuria, Pollakiuria, and Stranguria.
increased risk for adverse drug events,
acute, self-limiting episodes of FIC. • Hematuria.
especially with drugs and anesthetics that
• Butorphanol, buprenorphine, and fentanyl—
depend on renal elimination or metabolism. • Lower Urinary Tract Infection, Bacterial.
have been empirically recommended for • Lower Urinary Tract Infection, Fungal.
• Indwelling transurethral catheters,
short-term analgesia in cats with FIC; there • Urolithiasis, Struvite—Cats.
especially when associated with fluid-
have been no reports of controlled studies to
induced diuresis, predispose patients to ABBREVIATIONS
evaluate their safety or efficacy.
bacterial UTIs. • FIC = feline idiopathic cystitis.
• Prazosin—may be used to minimize reflex
dyssynergia and functional urethral outflow • IC/PBS = interstitial cystitis/painful bladder
obstruction; suggested dosage is 0.25–0.5 mg/ syndrome.
cat PO q12–24h. • NSAID = nonsteroidal anti-inflammatory
• Tolteridine may be considered as an FOLLOW-UP drug.
anticholinergic and antispasmodic to minimize • UO = urethral obstruction.
PATIENT MONITORING • UTI = urinary tract infection.
hyperactivity of bladder detrusor muscle and Monitor hematuria by urinalysis;
urge incontinence; suggested dose is 0.05 mg/ cystocentesis may cause iatrogenic hematuria, Suggested Reading
kg PO q12h; there have been no controlled so naturally voided samples are preferred. Forrester SD, Towell TL. Feline idiopathic
studies to evaluate its safety or efficacy. cystitis. Vet Clin Small Anim 2015,
• Glycosaminoglycans—empirically recom- PREVENTION/AVOIDANCE 45:783–806.
mended to help repair glycosaminoglycan Best evidence suggests that multimodal Kruger JM, Lulich JP, MacLeay J, et al. A
coating of urothelium; results of controlled approach to managing cats with acute randomized, double-masked, multicenter,
clinical studies have not demonstrated any nonobstructive FIC is advised, including clinical trial of two foods for long-term
beneficial effects on reducing severity or multipurpose therapeutic urinary food proven management of acute nonobstructive feline
frequency of clinical signs in cats with FIC. to reduce rate of recurrent episodes of FIC idiopathic cystitis (FIC). J Am Vet Med
• Feline facial pheromone—empirically signs (Hill’s c/d Multicare); environmental Assoc 2015; 247:508–517.
recommended to decrease signs of stress in enrichment; feeding moist food; and short- Author John M. Kruger
cats with FIC; results of controlled clinical term administration of analgesics to control Consulting Editor J.D. Foster
studies have not demonstrated any beneficial signs of pain. Acknowledgment The author and book
effects in management of FIC. POSSIBLE COMPLICATIONS editors acknowledge the prior contributions
• Corticosteroids—no detectable effect on • Indwelling transurethral catheters—cause of Carl A. Osborne and Jody P. Lulich
remission of acute clinical signs demonstrated; trauma; predispose to ascending bacterial
predispose to bacterial UTIs, especially in cats UTIs.
with indwelling transurethral catheters. • Perineal urethrostomies—predispose to Client Education Handout
• Nonsteroidal anti-inflammatory drugs bacterial UTIs and urethral strictures. available online
(NSAIDs)—empirically recommended by
Feline Immunodeficiency Virus (FIV) Infection

GENETICS
No predisposition for infection, but may play
role in progression and severity.
BASICS DIAGNOSIS
DEFINITION United States and Canada—1–3% prevalence DIFFERENTIAL DIAGNOSIS
A complex retrovirus that causes in healthy cat populations; 9–15% in sick • Primary bacterial, parasitic, fungal, or viral
F immunodeficiency in domestic cats; same cats. infections, especially FeLV.
genus (Lentivirus) as human immuno • Toxoplasmosis—neurologic and ocular
deficiency virus (HIV). GEOGRAPHIC DISTRIBUTION manifestations may be the result of
Worldwide; variable seroprevalence. Toxoplasma infection, FIV infection, or both.
PATHOPHYSIOLOGY
SIGNALMENT • Nonviral neoplastic diseases.
• Infection causes immune dysfunction due
to cytokine alterations, nonspecific hyper • Chronic kidney disease.
Species
activation of B and T lymphocytes, and Cat CBC/BIOCHEMISTRY/URINALYSIS
apoptosis of T cells. • Anemia, lymphopenia, or neutropenia—
Mean Age and Range
• Strain or subtype influences pathogenicity; common; but neutrophilia may occur in
• Prevalence of infection increases with age.
subtypes A and B are most common in the response to secondary infections; may also be
• Mean age—6 years at time of diagnosis.
United States. normal.
• Acute infection—virus spreads from site of Predominant Sex • Urinalysis and serum chemistry profile—
entry to lymph tissues and thymus via Male—more aggressive; roaming. hypergammaglobulinemia, azotemia with
dendritic cells, first infecting T lymphocytes, SIGNS isosthenuria, proteinuria (immune-mediated
then macrophages. glomerulonephritis).
• Primary receptor is feline CD134; uses General Comments
• Diverse due to immunosuppressive nature. OTHER LABORATORY TESTS
chemokine receptor CXCR4 as co-receptor.
• CD4+ and CD8+ T cells can be infected; • Cannot be clinically distinguished from Serologic Testing
virus selectively and progressively decreases FeLV-associated immunodeficiency. • Detects antibodies to FIV.
CD4+ (T-helper) cells; inversion of the Historical Findings • ELISA—routine screening; point-of-care
CD4+ : CD8+ ratio (from ∼2 : 1 to <1 : 1) Recurrent minor illnesses, especially upper and diagnostic laboratory kits; confirm
develops slowly, with absolute decrease of respiratory and gastrointestinal. positive results with additional testing,
CD4+ T cells after several months of infection. especially in healthy, low-risk cats.
Physical Examination Findings • Western blot (immunoblot)—confirmatory
• Early infection and activation of CD4+
• Opportunistic infections. testing of ELISA-positive samples.
CD25+ regulatory T cells may limit effective
• Lymphadenomegaly—mild to moderate. • Kittens—when <6 months old may test
immune response to FIV infection.
• Gingivitis, stomatitis, periodontitis positive owing to passive transfer of anti
• Cats clinically asymptomatic until cell-
(25–50% of cases). bodies from FIV-positive queen; positive test
mediated immunity is disrupted; humoral
• Rhinitis, conjunctivitis, keratitis (30% of does not indicate infection; retest at 8–12
immune function declines in advanced stages
cases); often associated with feline herpesvirus months to determine infection.
of infection.
and calicivirus infections. • Vaccinated cats may test positive for FIV
• T cells and macrophages—main cellular
• Persistent diarrhea (10–20% of cases); antibodies.
reservoirs of virus in affected cats; lymphoid
bacterial or fungal overgrowth, parasite-
tissues are reservoirs throughout the body. Others
induced inflammation; direct effect of FIV on
• Astrocyte and microglial cells in brain and • Virus isolation and subtyping.
gastrointestinal epithelium.
megakaryocytes and mononuclear bone • Reverse transcriptase polymerase chain
• Chronic, nonresponsive, or recurrent
marrow cells may be infected; neuronal loss reaction (RT-PCR)—useful in vaccinated cats
infections of external ear and skin—bacterial
may occur. or kittens with maternal antibody.
infections or dermatophytosis.
• Co-infection with feline leukemia virus • CD4+ : CD8+ evaluation—helps
• Fever and wasting—especially in later
(FeLV) may increase expression of FIV in determine extent of immunosuppression.
stage.
many tissues, including kidney, brain, and
• Ocular disease—anterior uveitis; pars IMAGING
liver.
planitis; glaucoma. N/A
SYSTEMS AFFECTED • Neurologic abnormalities—disruption of
• Hemic/lymphatic/immune—loss of CD4+ DIAGNOSTIC PROCEDURES
normal sleep patterns; behavioral changes
T cells; lymphocytic/plasmocytic infiltrates in N/A
(pacing and aggression); motor and
tissues (especially gingiva, lymphoid tissues); neurocognitive deficits; peripheral PATHOLOGIC FINDINGS
lymphomas, mast cell tumors. neuropathies. • Lymphadenopathy—initially, follicular
• Gastrointestinal—panleukopenia-like hyperplasia and paracortical infiltration of
CAUSES
syndrome. plasmacytes; later, follicular hyperplasia with
• Cat-to-cat transmission—usually by bite
• Nervous—alterations in astrocyte function follicular depletion or involution; in terminal
wounds.
and neurotransmitter expression. stages, lymphoid depletion.
• Occasional perinatal transmission.
• Ophthalmic—anterior uveitis. • Lymphocytic and plasmacytic infiltrates—
• Sexual transmission uncommon, although
• Renal/urologic—nephropathy. gingiva, lymph nodes and other lymphoid
FIV has been detected in semen.
• Reproductive—fetal death or perinatal tissues, spleen, kidney, liver, and brain.
infections. RISK FACTORS • Perivascular cuffing, gliosis, neuronal loss,
• Cardiovascular—possible myocarditis. • Male. white matter vacuolization, and occasional
• Other body systems—secondary infections. • Free-roaming or feral. giant cells in the brain.
(continued) Feline Immunodeficiency Virus (FIV) Infection

• Intestinal lesions similar to those seen with • Corticosteroids or gold salts—judicious but AGE-RELATED FACTORS
feline parvovirus infection. aggressive use may help control immune- Kittens (up to 4–6 months old) may test
mediated inflammation. positive because of passive antibody transfer.
• Topical corticosteroids—for anterior
ZOONOTIC POTENTIAL
uveitis; long-term response may be • None known.
incomplete or poor; pars planitis often
TREATMENT • Potential transmission of secondary
regresses spontaneously and may recur. pathogens (e.g., Toxoplasma gondii) to F
• Glaucoma—standard treatment.
immunocompromised humans.
• Outpatient sufficient for most patients. • Vaccinate for respiratory and enteric pathogens
• Inpatient—with severe secondary infections based on individual risk assessment. Rabies PREGNANCY/FERTILITY/BREEDING
until stable. vaccination according to regulatory guidelines. FIV-positive queens—reported abortions and
stillbirths; transmission to kittens infrequent
NURSING CARE CONTRAINDICATIONS if queen is antibody-positive before
• Primary consideration—manage secondary • Griseofulvin—avoid or use with extreme
conception; rate of transmission may be
and opportunistic infections. caution in FIV-positive cats; may induce subtype or strain-dependent (>90% for
• Supportive therapy—parenteral fluids and severe neutropenia; neutropenia is reversible if experimental infections with some strains).
nutrition, as required. drug is withdrawn early enough, but
secondary infections can be life-threatening. SYNONYMS
ACTIVITY
Feline immunodeficiency syndrome.
Normal PRECAUTIONS
Systemic corticosteroids—use with caution; SEE ALSO
DIET
may lead to further immunosuppression. • Feline Calicivirus Infection.
Normal, may alter as necessary for cats with
• Feline Herpesvirus Infection.
diarrhea, kidney disease. ALTERNATIVE DRUG(S) • Feline Leukemia Virus (FeLV) Infection.
CLIENT EDUCATION • Propionibacterium acnes
• Feline Stomatitis—Feline Chronic
• Inform client that infection is slowly (ImmunoRegulin®)—0.5 mL/cat IV once or Gingivostomatitis (FCGS).
progressive and healthy antibody-positive cats twice weekly. • Gingival Enlargement/Hyperplasia.
may remain healthy for years. • Acemannan (Carrisyn®)—100 mg/cat PO
q24h. INTERNET RESOURCES
• Advise client that cats with clinical signs
https://catvets.com/public/PDFs/Practice
will have recurrent or chronic health
Guidelines/RetrovirusGLS-Summary.pdf
problems that require medical attention.
• Discuss importance of keeping cats indoors ABBREVIATIONS
to protect them from exposure to secondary FOLLOW-UP • FeLV = feline leukemia virus.
pathogens and to prevent spread of FIV. • FIV = feline immunodeficiency virus.
PATIENT MONITORING • HIV = human immunodeficiency virus.
SURGICAL CONSIDERATIONS Varies according to secondary infections and • RT-PCR = reverse transcriptase polymerase
• Oral treatment or surgery—dental cleaning, other manifestations of disease. chain reaction.
tooth extraction, gingival biopsy as needed;
gingivitis and stomatitis may be refractory to PREVENTION/AVOIDANCE Suggested Reading
treatment. • Prevent contact with FIV-positive cats. Hartmann K, Wooding A, Bergmann M.
• Quarantine and test incoming cats before Efficacy of antiviral drugs against feline
• Biopsy or removal of neoplastic lesions.
introducing into multicat households. immunodeficiency virus. Vet Sci 2015,
• Vaccine no longer available in the U.S. 2:456–476.
EXPECTED COURSE AND PROGNOSIS Levy JK, Crawford CP, Tucker SJ.
• Approx. 20% of cats die within 2 years of Performance of 4 point-of-care screening
MEDICATIONS diagnosis or 4.5–6 years after estimated time tests for feline leukemia and feline
DRUG(S) OF CHOICE of infection, but >50% remain asymptomatic. immunodeficiency virus. J Vet Intern Med
• Zidovudine (Retrovir®) 5–10 mg/kg PO • In late stages of disease (wasting and 2017, 31:521–526.
q12h—antiviral agent; most effective against frequent or severe opportunistic infections), Little S, Levy J, Hartmann K, et al. 2020
acute infection; monitor for bone marrow life expectancy ≤1 year. AAFP feline retrovirus testing and
toxicity. • Overall survival time and quality of life for management guidelines. J Feline Med Surg
• Immunomodulatory drugs—may alleviate many FIV-positive cats will be similar to 2020, 22:5–30.
some clinical signs: uninfected cats. Sykes JE. Feline immunodeficiency virus
◦ α-interferon (Roferon®-A)—diluted in infection. In: Sykes JE, ed., Canine and
saline at 30 units/day PO for 7 days, every Feline Infectious Diseases. St. Louis, MO:
other week; may increase survival rates and Elsevier Saunders, 2014, pp. 209–223.
improve clinical status. Author Margaret C. Barr
◦ Feline omega-interferon (Virbagen®
MISCELLANEOUS Consulting Editor Amie Koenig
Omega)—1 million units/kg/day SC q24h ASSOCIATED CONDITIONS
for 5 days at 3 intervals (d0–4, d14–18, • Secondary bacterial, viral, fungal, and
d60–64); lower-dose oral protocols may be parasitic disease. Client Education Handout
effective. • Lymphoid tumors. available online
• Antibacterial or antimycotic drugs—as • Immune-mediated disease.
indicated; prolonged therapy or high dosages
may be required.
Feline Infectious Diarrhea

Mean Age/Range primary GI neoplasia, pancreatic
Young cats more likely to develop diarrhea insufficiency, and hepatic or renal disease.
from FECV, FPV, Cryptosporidium, helminths; CBC/BIOCHEMISTRY/URINALYSIS
BASICS FIP has bimodal distribution (young and old). • Eosinophilia with intestinal parasitism or
DEFINITION Predominant Sex histoplasmosis.
• Diarrhea is defined as excess fecal water, FIP more frequent in males. • Leukopenia with FPV, sepsis from
F increased quantity of fecal material, or
SIGNS salmonellosis or translocation, bone marrow
increased frequency of bowel movements. involvement with histoplasmosis or FeLV.
• Etiologies include viral, enteropathogenic General Comments • Anemia and microcytosis suggest GI
bacterial, protozoal, fungal, or helminths; Range from mild to severe. hemorrhage or iron deficiency, particularly
small bowel, large bowel, or mixed bowel Historical Findings with high worm burden.
diarrhea. • Acute or chronic, small or large bowel diarrhea. • Elevated liver enzyme activities or creatine
• Secondary systemic signs likely with kinase with toxoplasmosis.
• Possibly lethargy, vomiting, weakness,
infection by feline immunodeficiency virus weight loss, hyporexia. • Hyperglobulinemia, elevated total bilirubin
(FIV), feline leukemia virus (FeLV), feline • Crowded environment. with FIP.
enteric coronavirus (FECV), feline parvovirus • Hemoconcentration, prerenal azotemia,
(FPV), histoplasmosis. Physical Examination Findings
electrolyte derangements with dehydration.
• Presence of organisms on diagnostic • Dehydration.
• Panhypoproteinemia if protein-losing
screening does not indicate causation; patient • Poor body condition.
enteropathy or GI blood loss.
factors (clinical signs, age, environmental • Fluid/gas-filled intestinal loops.
exposure) should be considered before • Signs of sepsis or systemic inflammatory IMAGING
treatment. response syndrome (SIRS) possible— • Abdominal radiographs if no response to
• Some cats will have self-resolution; tachycardia, hypotension, hyper/hypothermia, symptomatic care to rule out other causes of
diagnostic testing may be appropriate for tachypnea, pale mucous membranes. diarrhea.
more severely affected animals or if clinical • Abdominal masses or enlarged lymph nodes • Abdominal ultrasound recommended in
signs are persistent despite supportive care may be palpable (histoplasmosis, FIP). nonpediatric patients with diarrhea
and having ruled out other causes of acute or • With systemic infections may note nonresponsive to symptomatic care.
chronic diarrhea; kittens with acute diarrhea chorioretinitis, icterus, neurologic deficits. • Thoracic radiographs may show pulmonary
should be screened for FPV. disease or enlarged lymph nodes with
CAUSES histoplasmosis or toxoplasmosis.
PATHOPHYSIOLOGY • Viral—FECV, FPV, astrovirus, calicivirus,
• Typically, fecal–oral route of infection. FIV, FeLV, torovirus-like agent. DIAGNOSTIC PROCEDURES
• Diarrhea may result from decreased • Bacterial—Campylobacter spp., Clostridium • Fecal flotation—for intestinal parasitism;
intestinal absorption or increased intestinal perfringens enterotoxin A, Clostridium difficile false negatives are possible as ova are
secretion caused by enterotoxins, osmotic toxins, Salmonella spp., Escherichia coli, intermittently shed; cats suspected to have
forces, or epithelial damage. Yersinia spp. intestinal parasitism should have multiple fecal
• Immune response to infectious organisms • Helminth—Toxocara spp., Ancylostoma flotations or be treated with anthelmintics.
can contribute to development of diarrhea; spp., Strongyloides spp., Toxascaris leonine, • Fecal cytology—bacterial morphology
activated white blood cells release Spirometra spp., Trichuris vulpis. (frequent spirochetes, spores) or presence of
inflammatory mediators that stimulate • Protozoal—Giardia spp., Tritrichomonas fungal or protozoal organisms.
secretion and damage intestinal epithelium. foetus, Toxoplasma gondii. • Giardia ELISA.
• Coccidial—Cryptosporidium spp., • Tritrichomonas PCR using “colonic flush”
SYSTEMS AFFECTED Cystoisospora spp. technique.
• Cardiovascular—fluid balance. • Histoplasma enzyme immunoassay (EIA)—
• Fungal—Histoplasma capsulatum.
• Gastrointestinal (GI). urine.
RISK FACTORS • Toxoplasmosis immunofluorescence
GENETICS • Pediatric, young adult cats more commonly
Feline infectious peritonitis (FIP) more likely antibody test (IFA) for immunoglobulin (Ig)
affected, particularly with helminths, viral, G and IgM, rising titer between acute and
in purebred cats. and coccidial disease. convalescent samples.
INCIDENCE/PREVALENCE • Crowding, poor sanitation increase risk of
• FIV antibody, FeLV antigen ELISA.
• 84% of cats from shelters had entero transmission. • Infectious diarrhea PCR panels assess for
pathogens—no difference with or without
range of infectious causes of diarrhea; caution
diarrhea.
should be used in interpretation; positive
• FECV more common in cats with diarrhea.
results do not necessarily indicate causation
GEOGRAPHIC DISTRIBUTION DIAGNOSIS and false-negative results possible.
• Widespread.
DIFFERENTIAL DIAGNOSIS PATHOLOGIC FINDINGS
• Prevalence of etiologies varies by region.
• Acute diarrhea—dietary indiscretion, • Gross examination of intestinal mucosa
• Histoplasma more common in eastern
foreign body, GI neoplasia; non-GI diseases: may demonstrate parasites attached to
United States, Latin America.
hyperthyroidism, iatrogenic, hepatotoxicity, intestinal mucosa with multifocal
SIGNALMENT renal disease, and other systemic diseases hemorrhagic ulcerations, submucosal
Species (frequently have hyporexia, vomiting, congestion or hemorrhage, intestinal wall
Cat icterus). thickening, lymphadenopathy.
• Chronic diarrhea—chronic enteropathy • Histopathology of intestine may show
Breed Predilections (dietary responsive, antibiotic responsive, eosinophilic, neutrophilic, pyogranulomatous,
Purebred cats have higher prevalence of FIP. dysbiosis, or inflammatory bowel disease), or lymphoplasmacytic enteritis with varying
(continued) Feline Infectious Diarrhea

degrees of hemorrhage and necrosis, depending • Toxoplasmosis—clindamycin 10–17 mg/kg
on etiology; may visualize causative agent. PO/IM/IV q8–12h for 4 weeks.
• Trichomoniasis—ronidazole 30 mg/kg PO
q24h for 14 days. MISCELLANEOUS
• Patients with sepsis or leukopenia should be ASSOCIATED CONDITIONS
treated with broad-spectrum antibiotics. N/A
TREATMENT
• Cats with confirmed salmonella should not be
AGE-RELATED FACTORS F
treated with antibiotics unless systemically ill.
• Mildly affected cats treated as outpatients. Young animals more susceptible.
CONTRAINDICATIONS
• Moderate to severely affected cats may require ZOONOTIC POTENTIAL
N/A
IV fluids for dehydration/electrolyte management. • Toxoplasmosis—human abortion.
• Dextrose should be supplemented PRECAUTIONS • Giardiasis—low risk of transmission.
parenterally for hypoglycemia, • Metronidazole dose should be reduced in • Cryptosporidiosis.
animals with hepatic insufficiency. • Salmonellosis.
ACTIVITY
• Clindamycin should be given with food or • Campylobacter jejuni.
N/A
water to prevent development of esophageal • Toxocara spp. (ascarids)—visceral larval
DIET strictures. migrans, most common in children.
• Diets high in easily digestible protein, • Ronidazole can cause neurotoxicity and • Ancylostoma (hookworms)—cutaneous
including adequate taurine. should be discontinued if clinical signs larval migrans, most common in children.
• In anorexic pediatric patients, nasogastric including anorexia develop.
tube feeding of liquid diet recommended if PREGNANCY/FERTILITY/BREEDING
POSSIBLE INTERACTIONS Patients exhibiting clinical signs of illness
anorexia >48 hours.
Dependent on drug used; itraconazole has should not be bred. If illness develops while
CLIENT EDUCATION many interactions. pregnant, take caution regarding drug choice.
• For most infectious organisms,
environmental decontamination prevents SEE ALSO
reinfection and transmission to other pets/ • Acute Diarrhea.
humans; isolation during hospitalization may • Campylobacteriosis.
be warranted depending on cause. FOLLOW-UP • Clostridial Enterotoxicosis.
• Appropriate vaccination and deworming PATIENT MONITORING • Coccidiosis.
schedules should be followed. • Case-based, may include reassessment of • Diarrhea, Chronic—Cats.
• Cats with identified infectious causes of anemia, leukopenia, or electrolyte • Feline Infectious Peritonitis (FIP).
diarrhea should be isolated from other cats derangements as appropriate. • Feline Panleukopenia.
until clinical signs resolve; Histoplasma not • Persistent clinical signs after appropriate • Giardiasis.
directly transmitted from cat to other hosts. treatment suggest alternative cause of diarrhea. • Histoplasmosis.
• Patients with recurrent clinical signs should • Hookworms (Ancylostomiasis).
SURGICAL CONSIDERATIONS • Roundworms (Ascariasis).
Viral and parasitic enterocolitis can result in be retested, particularly if environmental
reinfection possible (e.g., giardiasis, • Salmonellosis.
intussusceptions. • Toxoplasmosis.
campylobacteriosis).
• Whipworms (Tricuriasis).
• Routine vaccination. ABBREVIATIONS
• Monthly flea and heartworm preventative • EIA = enzyme immunoassay.
MEDICATIONS with combination anthelmintic therapy. • FECV = feline enteric coronavirus.
DRUG(S) OF CHOICE • Maintain clean facilities and quarantine ill • FeLV = feline leukemia virus.
• Many cases self-resolve with supportive care patients. • FIP = feline infectious peritonitis.
and time. • Do not allow nonimmunocompetent • FIV = feline immunodeficiency virus.
• Empiric therapy, pending diagnostics if patients to contact other animals until • FPV = feline parvovirus.
clinical signs persist—probiotics (Visbiome® determined to be low risk. • GI = gastrointestinal.
112.5 billion bacteria/cat/day), or • IFA = immunofluorescence antibody test.
POSSIBLE COMPLICATIONS • Ig = immunoglobulin.
metronidazole 10 mg/kg PO q12h, with
• Sepsis. • SIRS = systemic inflammatory response
fenbendazole 50 mg/kg PO q24h for 5 days.
• Anemia. syndrome.
• Anthelmintics—fenbendazole 50 mg/kg
• Dehydration, electrolyte, acid-base
PO q24h for 5 days; pyrantel pamoate 10 g/ Suggested Reading
disturbances.
kg PO q24h for 3 days. Green CE. Infectious Diseases of the Dog and
• Coccidiostatic—sulfadimethoxine 50–60 EXPECTED COURSE AND PROGNOSIS Cat, 4th ed. St. Louis, MO: Elsevier
mg/kg PO q24h for 5–10 days; ponazuril 50 • Usually good to excellent; underlying Saunders, 2012.
mg/kg PO once. immunosuppressive conditions may increase Little SE. The Cat: Clinical Medicine and
• Campylobacteriosis with persistent clinical susceptibility to infection and worsen prognosis. Management. St. Louis, MO: Elsevier
signs—erythromycin 10–15 mg/kg PO q8h; • Infectious agents that cause systemic illness Saunders, 2012.
azithromycin 5–10 mg/kg PO q24h. likely have worse prognosis. Author Genna Atiee
• Histoplasmosis—itraconazole 5–10 mg/kg Consulting Editor Amie Koenig
PO q12–24h: do not use compounded
formulations.
Feline Infectious Peritonitis (FIP)

SIGNS • Reverse-transcription polymerase chain
General Comments reaction (RT-PCR) or immunohistochemistry
• Variable, depending on effectiveness of
on effusion or affected tissue confirmatory.
BASICS • No single diagnostic laboratory test.
cell-mediated immune response, and organ
DEFINITION system(s) affected. DIFFERENTIAL DIAGNOSIS
A systemic, immune-mediated, viral disease • Two classic forms—wet (effusive) and dry • Fever of unknown origin—infection,
F of cats characterized by insidious onset, (noneffusive); depends on presence of inflammation.
persistent fever, pyogranulomatous tissue effusion in body cavities; dry form may • Pleural effusion—cardiac disease; cardiac
reaction, exudative effusions in body cavities, become wet form with disease progression. effusion has low specific gravity and cell
and high mortality. count.
Historical Findings
PATHOPHYSIOLOGY • Neoplasia—lymphoma, other causing
• Insidious onset.
• The term feline coronavirus (FCoV) • Gradual weight loss and inappetence.
abdominal organ enlargement/effusion.
encompasses feline enteric coronavirus • CNS signs—neoplasia, toxoplasmosis.
• Stunted growth in kittens.
(FECV) and feline infectious peritonitis virus • Anemia and icterus—blood parasites
• Gradual increase in size of abdomen due to
(FIPV). effusion. causing hemolysis.
• FECV is common and highly infectious; • Pansteatitis (yellow fat disease)—classic feel
• Persistent fever—fluctuating, antibiotic
replicates locally in intestinal tract. unresponsive. and appearance of fat within abdominal
• FIPV infects monocytes/macrophages, cavity; pain on abdominal palpation; often a
which disseminate virus throughout body; Physical Examination Findings fish-only diet.
localizes at vein wall and perivascular sites. • Depression. • Leukopenia, enteritis—panleukopenia (see
• FIP is an immune-mediated disease— • Fever. Feline Panleukopenia).
perivascular accumulation of virus-infected • Poor condition.
• Stunted growth.
macrophages and inflammatory cells produces • Leukocytosis with neutrophilia and
pyogranulomatous inflammation in various • Dull, rough hair coat.
• Icterus.
lymphopenia.
organs. • Mild to severe anemia.
• Abdominal and/or pleural effusion.
SYSTEMS AFFECTED • High total plasma protein, specifically
• Palpable abdominal masses (granulomas or
• Multisystemic—pyogranulomatous or pyogranulomas). globulin fraction (serum albumin : globulin
granulomatous lesions on omentum, serosal • Ocular—anterior uveitis, keratic precipitates,
typically <0.8).
surface of abdominal organs, within • Hyperbilirubinemia and hyperbilirubinuria.
iris color change, irregularly shaped pupil.
abdominal lymph nodes, and submucosa of • Neurologic—seizure, ataxia, paresis/ OTHER LABORATORY TESTS
intestinal tract. paralysis, abnormal behavior, cranial nerve • Serum antibody tests—detect antibodies
• Nervous—vascular lesions throughout deficits. against FCoV; positive tests not diagnostic of
CNS, especially in meninges. FIP (indicate only previous FECV infection);
• Ophthalmic—uveitis, chorioretinitis, and CAUSES
• Prevailing theory is that FECV mutates to
likelihood of FIP increases with titers ≥1 : 3200,
iritis. but low titers do not exclude FIP.
• Respiratory—lesions on lung surfaces, FIPV during FECV infection in individual
• RT-PCR—detect viral genome; positive tests
pleural effusion. cats; weak cell-mediated immunity plays a
role in development of FIP. on blood or stool not diagnostic of FIP;
INCIDENCE/PREVALENCE • FCoV has two genomic types (FCoV type 1
positive tests on effusion or tissues confirm FIP.
• Prevalence of antibodies against FCoV— • Immunohistochemistry—detect virus in
and 2) and two biotypes (FECV and FIPV).
high, due to widespread presence of FECV, • FCoV type 1 is predominant (>85%); both
biopsy or tissue samples; excellent for
especially in multicat facilities. types 1 and 2 can cause FIP. confirming cause of specific lesions, especially
• Incidence of FIP—low in most populations, • FECV—enteritis; highly transmissible
abdominal disease, which often is not
especially in single-cat households. among cats. diagnosed as FIP.
• Because of difficulty in diagnosis, control, • FIPV—systemic, fatal disease (FIP); IMAGING
and prevention, outbreaks within breeding cat-to-cat transmission unlikely. • May confirm abdominal and pleural effusions.
catteries may be catastrophic; in endemic • May detect granulomatous lesions.
catteries, risk of FCoV antibody–positive cat RISK FACTORS
eventually developing FIP is usually <10%. • Contact with FECV-shedding cat; >30% of DIAGNOSTIC PROCEDURES
cats are chronic shedders. • Thoracocentesis and/or abdominocentesis—
GEOGRAPHIC DISTRIBUTION • Breeding catteries or multicat facilities. fluid pale to straw colored, viscous with flecks
Worldwide • Less than 2 years of age. of fibrin, specific gravity 1.017–1.047; fluid
SIGNALMENT • Feline leukemia virus (FeLV) or feline may be used for RT-PCR or immuno-
immunodeficiency virus (FIV) infection. histochemistry.
Species
• Certain cat breeds have higher incidence of • Laparoscopy—to observe specific lesions of
Cats—domestic and exotic.
FIP, especially dry form; some breeding pairs peritoneal cavity and obtain biopsy samples.
Breed Predilections are prone to producing litters that develop FIP. • Exploratory laparotomy—may be indicated
Some bloodlines or breeds of cats may be for difficult-to-diagnose patients.
more susceptible.
PATHOLOGIC FINDINGS
Mean Age and Range
Gross
Highest incidence in kittens 3 months–2 DIAGNOSIS • Variable, patient generally emaciated, with
years of age. • Wet form—straightforward clinical diagnosis. rough hair coat.
• Dry form—difficult to diagnose.
(continued) Feline Infectious Peritonitis (FIP)

• Abdomen and/or thoracic cavity—may ALTERNATIVE DRUG(S) ABBREVIATIONS
contain thick, viscous exudates. Direct-acting antiviral drugs for FIP have • FCoV = feline coronavirus.
• White, rough, pyogranulomatous plaques shown effectiveness in treatment and are • FECV = feline enteric coronavirus.
or granulomas—may be on serosal surface of under development. • FeLV = feline leukemia virus.
abdominal organs and omentum; fibrous • FIP = feline infectious peritonitis.
strands may extend between organs. • FIPV = feline infectious peritonitis virus.
• Discolored iris with anterior uveitis—may • FIV = feline immunodeficiency virus. F
see keratic precipitates. • RT-PCR = reverse-transcription polymerase
• Lesions in brain and/or spinal cord possible
FOLLOW-UP chain reaction.
PATIENT MONITORING
Histopathologic INTERNET RESOURCES
Monitor for development of pleural effusion
• Granulomas or pyogranulomas in any https://www.vet.cornell.edu/departments-
or neurologic disease.
affected tissue. centers-and-institutes/cornell-feline-health-
• Lesions—perivascular; increase in size, PREVENTION/AVOIDANCE center/health-information/feline-health-topics/
involving large portions of tissue; microscopic • Modified live intranasal vaccine—against feline-infectious-peritonitis
appearance suggests diagnosis. FIPV; low efficacy; cannot rely on vaccination
Suggested Reading
alone for control; will produce antibody-
Addie D, Belák S, Boucraut-Baralon C, et al.
positive cats, complicating monitoring in
Feline infectious peritonitis: ABCD
catteries or colonies; not generally
guidelines on prevention and management.
recommended.
TREATMENT • Mother/offspring—main method of
J Feline Med Surg 2009, 11:594–604.
Addie D, Jarrett O. Feline coronaviral
APPROPRIATE HEALTH CARE transmission appears to be from asymptomatic
infections. In: Sykes JE, Greene CE, ed.,
Inpatient or outpatient, depending on carrier queens to their kittens at 4–7 weeks of
Infectious Diseases of the Dog and Cat, 4th
severity of disease and owner’s willingness and age, after maternal immunity wanes; break
ed. St. Louis, MO: Saunders Elsevier, 2011,
ability to provide good supportive care. cycle of transmission by early weaning at 4–5
pp. 54–67.
NURSING CARE weeks of age and isolating litter from direct
Brown MA, Troyer JL, Pecon-Slattery J, et al.
• Therapeutic paracentesis—to relieve pressure/ contact with other cats, including queen.
Genetics and pathogenesis of feline
dyspnea from ascites or pleural effusions. • Routine disinfection to reduce FECV
infectious peritonitis virus. Emerg Infect
• Encourage cat to eat. transmission—premises, cages, and water/
Dis 2009; 15:1445–1452.
food dishes; common disinfectants readily
ACTIVITY Drechsler V, Alcaraz A, Bossong FJ, et al.
inactivate virus.
FIP transmission to other cats unlikely; no or Feline coronavirus in multicat
• Introduce only FCoV antibody–negative
low levels of FIPV shedding. environments. Vet Clin North Am Small
cats to catteries or colonies that are free of
Anim Pract 2011, 1133–1169.
DIET virus.
Hartmann K, Binder C, Hirschberger J, et al.
Any food that will entice patient to eat. • Avoid breeding pairs that are prone to
Comparison of different tests to diagnose
producing litters that develop FIP.
CLIENT EDUCATION feline infectious peritonitis. J Vet Intern
• Discuss various aspects of disease, including POSSIBLE COMPLICATIONS Med 2003, 17:781–790.
grave prognosis; once clinical FIP is confirmed, Pleural effusion may require thoracocentesis; Pederson NC. An update on feline infectious
nearly 100% of cats will die of disease. supportive care for other clinical signs. peritonitis: diagnostics and therapeutics. Vet
• Inform client of high prevalence of FECV EXPECTED COURSE AND PROGNOSIS J 2014b, 201:133–141.
infection but low incidence of FIP; <10% of • Clinical course—a few days to several Pederson NC. An update on feline infectious
FCoV antibody–positive cats <2 years of age months until euthanasia is warranted. peritonitis: virology and immunopathogenesis.
eventually develop clinical disease. • Prognosis grave once clinical signs occur; Vet J 2014a, 201:123–132.
mortality nearly 100%. Richards JR, Elston TH, Ford RB, et al. The
2006 American Association of Feline
• Generally none.
Practitioners Feline Vaccine Advisory Panel
• Rarely, inflammatory abdominal disease
Report. J Am Vet Med Assoc 2006, 229:
from FIP may cause intestinal obstruction.
1405–1441.
MISCELLANEOUS Scherk MA, Ford RB, Gaskell RM, et al.
ASSOCIATED CONDITIONS 2013 AAFP Feline Vaccination Advisory
FeLV or FIV-positive cats—more prone to Panel Report. J Feline Med Surg 2013,
MEDICATIONS developing FIP. 15:785–808.
DRUG(S) OF CHOICE Author Yunjeong Kim
PREGNANCY/FERTILITY/BREEDING Consulting Editor Amie Koenig
• No cure; only symptomatic treatment is FIPV transmission from mother to offspring
available. Acknowledgment The author and book
during pregnancy is presumed rare. editors acknowledge the prior contribution of
• Immunosuppressive drugs (e.g., oral
prednisolone)—may alleviate some SYNONYMS Fred W. Scott.
symptoms. • Feline coronaviral polyserositis.
• Feline omega interferon—unclear • Feline coronaviral vasculitis.
• Systemic feline coronavirus infection. Client Education Handout
effectiveness in symptomatic management. available online
• Antibiotics—generally not necessary.
Feline Ischemic Encephalopathy

SYSTEMS AFFECTED • Chemistry—occasionally elevated globulins
• Brain and less commonly spinal cord. or hyperglycemia.
• Larvae can also be found in skin, nasal passage, OTHER LABORATORY TESTS
BASICS pharynx, larynx, eye, trachea, and thorax of cats. • Serology for feline leukemia virus (FeLV),
DEFINITION GENETICS FIV, FIP—negative.
• Seasonal neurologic disease that occurs in None • Cryptococcal antigen titers—negative.
F outdoor cats or those with access to outdoors
INCIDENCE/PREVALENCE • Toxoplasma immunoglobulin (Ig) G and
in North America during late spring, summer, IgM—negative.
and early fall; usually results in sudden onset Not known.
of seizures, circling, altered mentation, and/or GEOGRAPHIC DISTRIBUTION IMAGING
blindness; however, any neurologic • MRI—diagnostic modality of choice;
• North America only.
abnormalities can be found in these cats. • Same distribution as Cuterebra botfly.
detect track lesion extending from cribriform
• Aberrant migration of Cuterebra larva in the • Disease not recognized in locations that do not
plate into olfactory bulb and frontal, parietal,
brain of a cat that often causes thrombosis or have Cuterebra botfly, such as Australia and Japan. and temporal lobes best recognized on dorsal
vasospasm of middle cerebral artery with sequences; may see abnormalities in ipsilateral
SIGNALMENT nasal passage; may also see area of ischemic
ensuing ischemic necrosis; degeneration of
superficial layers of cerebral cortex and Breed Predilections infarction in brain; if performed soon after
parenchymal destruction associated with None onset of signs, increased signal intensity on
physical migration of larva in brain T2 weighted, proton density weighted, and
Mean Age and Range fluid attenuated inversion recovery (FLAIR)
parenchyma. • Median age—2 years old.
• Must be differentiated from other causes of images associated with ischemia of superficial
• Range—1–7 years old. layers of cerebral cortex, or the area supplied
vascular diseases affecting brains of cats as
well as other neurologic diseases of cats. Predominant Sex by MCA; scant parenchymal enhancement in
None area of infarction after administration of
PATHOPHYSIOLOGY contrast. If MRI is done more then 2–3
• In feline ischemic encephalopathy (FIE), SIGNS
• Sudden onset of neurologic signs.
weeks after onset of signs, may find loss of
Cuterebra larva enters nasal passage of cat, overlying gray matter in region supplied by
migrates through cribriform plate into • Often preceded by upper respiratory signs
1–3 weeks prior to neurologic signs (due to MCA and associated hydrocephalus ex vacuo.
olfactory bulb of the brain, then along Magnetic resonance angiography (MRA; time
olfactory peduncle and sometimes continues migration of the parasite in the nasal passage).
• Often prosencephalic signs.
of flight or postcontrast) may be of some
in parenchyma of brain, or alternatively in utility in some cases.
subarachnoid space; parasite then, if still alive, • Most commonly—seizures, circling, altered
• CT—limited value.
migrates caudally, where it may compromise mentation, blindness.
the middle cerebral artery (MCA) physically • Sometimes multifocal neurologic signs. DIAGNOSTIC PROCEDURES
through spines on the larvae’s body, or • Rarely spinal cord signs. Cerebrospinal fluid—normal or nonsuppura-
possibly via chemical agent secreted by • May stop meowing/develop aphasia. tive inflammation with macrophages,
parasite causing vasospasm to vessel; or CAUSES lymphocytes, or eosinophils.
vasospasm may be secondary to hemorrhage Cuterebra larvae. PATHOLOGIC FINDINGS
caused by parasite; parasite may then die in • Local areas of malacia and hemorrhage
RISK FACTORS
subarachnoid space (SAS) or within involving olfactory bulbs and peduncles on
• Outdoor cats; access to outdoors.
parenchyma. brain transverse sections. Thorough
• Not reported in indoor only cats.
• Adult botfly lays eggs by entrance of examination of nasal passage, cribriform
• July, August, and September in northeast
rodent’s den; eggs hatch into L1 stage of plate, olfactory bulbs, and peduncles, as well
United States and southeast Canada; can be found
larva, which attaches to hair of mouse or as remaining parenchyma, meninges, and
in May and June in southeast United States.
rabbit and enters body through a normal overlying calvaria, may reveal the larva, which
• Hunting cats.
orifice (mouth, nose, eye, or anus) and is approximately 5–10 mm in length (stage 2
migrates into associated tissues (nasopharynx, larva), tan, and with concentric rings of
trachea, thoracic cavity, diaphragm, spines along length of body.
abdominal cavity); then larva continues its • Histopathologic features may include
migration to reach subcutaneous site in DIAGNOSIS necrosis and hemorrhage of parasitic track, or
inguinal or thoracic region where it matures DIFFERENTIAL DIAGNOSIS less specific findings such as superficial
first to L2 stage and then within warble to L3 • Other causes of vascular accidents in brain laminar cerebrocortical necrosis, cerebral
larval stage, emerges through skin, drops off such as renal disease and hyperthyroidism infarction, subependymal rarefaction, and
host, pupates in soil over winter, and then with hypertension. astrogliosis and subpial astrogliosis.
emerges in spring as an adult botfly. Adult • External trauma.
lays eggs near entrance of rodent’s den; eggs • Tumors—usually progressive rather than
hatch to form L1 larvae… When cat hunts sudden in onset.
near rodent’s den, L1 larva attaches to cat’s
hair and gains access to nasal passage of cat
• Infectious/inflammatory diseases—such as TREATMENT
those caused by Cryptococcus sp., Toxoplasma
and begins catastrophic pathway of FIE. gondii, feline infectious peritonitis (FIP) virus, NURSING CARE
• Occasionally larva does not migrate • Padded cage may be necessary if cat is
and feline immunodeficiency virus (FIV).
through cribriform plate but embeds in nasal having seizures.
passage or respiratory tract of cat, causing CBC/BIOCHEMISTRY/URINALYSIS • Swivel IV line can be used if patient
focal respiratory signs; larva has also been • Usually normal. exhibits propulsive/compulsive circling or loss
found in the eye and oropharyngeal region. • CBC—occasionally neutrophilia, of balance.
leukocytosis, or eosinophilia.
(continued) Feline Ischemic Encephalopathy

CLIENT EDUCATION for patients with clinical signs >1 week as AGE-RELATED FACTORS
• Only occurs in outdoor cats and those with parasite is likely already dead. N/A
access to outdoors; strictly indoor cats do not CONTRAINDICATIONS ZOONOTIC POTENTIAL
develop FIE. Do not use ivermectin in cats with known None; however, aberrant Cuterebra larva
• Only occurs in summer months, with sensitivity. migration has been reported in humans, most
majority of patients seen during July, August, commonly as ocular form in children.
PRECAUTIONS
and September in the northeast United States
No adverse effects from ivermectin have been SYNONYMS
F
and southeast Canada.
• May not occur in major metropolitan areas noted; however, anaphylactic or allergic CNS cuterebriasis.
that do not have normal appropriate hosts reaction could occur if Cuterebra larva ABBREVIATIONS
such as cottontail rabbit. suddenly dies and releases possible foreign • FeLV = feline leukemia virus.
antigens. • FIE = feline ischemic encephalopathy.
Successful removal of parasite from the brain/ ALTERNATIVE DRUG(S) • FIP = feline infectious peritonitis.
spinal cord has not been reported in cats, but Can use dexamethasone instead of • FIV = feline immunodeficiency virus.
may be possible if neuroimaging is available prednisone. • FLAIR = fluid attenuated inversion recovery.
early after onset of clinical signs. • Ig = immunoglobulin.
• MCA = middle cerebral artery.
• MRA = magnetic resonance angiography.
• SAS = subarachnoid space.
FOLLOW-UP
MEDICATIONS INTERNET RESOURCES
PATIENT MONITORING
http://www.neurovideos.vet.cornell.edu
DRUG(S) OF CHOICE Sequential neurologic evaluations.
Videos 14-8, 14-9, 12-20
• Supportive care including antiepileptic PREVENTION/AVOIDANCE
drugs and appropriate fluid supplementation, Suggested Reading
• Keep cat indoors.
which may include thiamine administration Bowman DD, Hendrix CM, Lindsay DS,
• Use of monthly fipronil, imidacloprid,
and additional potassium IV depending on et al. Feline Clinical Parasitology. Ames, IA:
selamectin, or ivermectin has been suggested
nutritional status of patient; typically Iowa State University Press, 2002, pp.
to prevent infections with Cuterebra parasite
phenobarbital is used at maintenance dose of 430–439.
in outdoor cats.
7.5–15 mg PO/IM/IV q12h/cat; in addition de Lahunta A, Glass EN, Kent M. Veterinary
phenobarbital can be loaded at a total loading POSSIBLE COMPLICATIONS Neuroanatomy and Clinical Neurology, 4th
• May continue to have uncontrolled seizures. ed. St. Louis, MO: Elsevier-Saunders, 2015,
dose of 16 mg/kg IV/PO/IM; this dose is
• May continue to circle compulsively/ pp. 433–436, 549–550.
usually divided over 24–48h (e.g., 4 mg/kg
q12h for 2 days); then maintenance dose is propulsively. Glass EN, Cornetta AM, de Lahunta A, et al.
• May have behavioral changes such as Clinical and clinicopathologic features in 11
started; diazepam can be used at 2.5–5 mg IV
to stop cluster seizures or status epilepticus; aggression, especially in cats with damage to cats with Cuterebra larvae myiasis of the
other anticonvulsants, such as levetiracetam, piriform lobe. central nervous system. J Vet Intern Med
• May stop meowing/develop aphasia in 1998, 12:365–368.
may also be utilized.
• Cocktail treatment has been proposed for
some cats. Williams KJ, Summers BA, de Lahunta A.
recently affected cats—diphenhydramine IM EXPECTED COURSE Cerebrospinal cuterebriasis in cats and its
at 4 mg/kg 1–2h before giving ivermectin SC association with feline ischemic
AND PROGNOSIS
at 200–500 μg/kg and prednisolone sodium encephalopathy. Vet Pathol 1998,
After initial onset, many patients improve and
succinate at 30 mg/kg IV; treatment is 35:330–343.
become acceptable pets; there may be
repeated at 24h and 48h after first injection Authors Eric N. Glass and Alexander de
persistent deficits, seizures, circling, and
of ivermectin; in addition patients receive Lahunta
undesirable behavior such as aggression; may
prednisone at 5 mg/cat q12h PO for 14 days develop aphasia; persistent clinical signs
and enrofloxacin at 22.7 mg PO q12h for 14 depend on damage caused by infarction and Client Education Handout
days. Because of concerns of blindness in parasitic migration. available online
some cats with administration of
enrofloxacin, pradofloxacin or other
antibiotics with broad-spectrum utility can be
considered; ivermectin is not approved for use
against Cuterebra larva so appropriate client MISCELLANEOUS
permission must be obtained prior to ASSOCIATED CONDITIONS
administration; this cocktail treatment is not None
Feline Leukemia Virus (FeLV) Infection

Worldwide
BASICS SIGNALMENT DIAGNOSIS
DEFINITION Species DIFFERENTIAL DIAGNOSIS
A simple retrovirus (Gammaretrovirus genus) Cat • FIV.
F that causes immunodeficiency and neoplastic Mean Age and Range • Other infections—bacterial, parasitic, viral,
disease in domestic cats. • Prevalence highest between 1 and 6 years or fungal.
of age. • Nonviral neoplastic diseases.
PATHOPHYSIOLOGY
• Four subgroups of feline leukemia virus • Mean—3 years. CBC/BIOCHEMISTRY/URINALYSIS
(FeLV)—A, B, C, and T; FeLV-A most Predominant Sex • Anemia—often severe, often nonregenerative;
transmissible and present in all isolates; Male : female ratio—1.7 : 1. regenerative anemias usually associated with
FeLV-B arises from recombination of FeLV-A Mycoplasma haemofelis or M. haemominutum
SIGNS
env gene with endogenous retroviral coinfections.
sequences (50% of isolates); FeLV-C (1% of General Comments • Lymphopenia or lymphocytosis.
isolates) arises from mutation in env gene • Onset of FeLV-associated disease—months • Neutropenia—sometimes cyclic; may be
sequences; FeLV-T infects only T cells. to years after infection. response to secondary infections or immune-
• Early infection (five stages)—(1) viral replication • Associated diseases—non-neoplastic or mediated disease.
in tonsils and pharyngeal lymph nodes; (2) neoplastic; most non-neoplastic or degenerative • Thrombocytopenia and immune-mediated
infection of circulating B lymphocytes and diseases result from immunosuppression. hemolytic anemia.
macrophages that disseminate virus; (3) replication • Regressive infections may be associated with • Biochemistry/urinalysis abnormalities
in lymphoid tissues, intestinal crypt epithelial cells, cardiomyopathies, lymphomas, leukemias, depend on affected organs.
bone marrow precursor cells; (4) release of infected anemia, other infections.
neutrophils and platelets from bone marrow; and • Clinical signs of FeLV-induced
• Immunochromatography (lateral flow) and
(5) infection of epithelial and glandular tissues, immunodeficiency cannot be distinguished
ELISA—point-of-care screening, detect
subsequent shedding of virus into saliva, urine. from FIV-induced immunodeficiency.
antigen in plasma, serum, saliva, tears; more
• Abortive infection—if virus replication Historical Findings sensitive than immunofluorescent antibody
terminated at stage 1; no viremia. • Outdoor cat. (IFA) for early or transient infection; single
• Regressive or nonproductive infection— • Multicat household. positive test does not predict persistent
immune response stops progression at stage 2 viremia (retest in 12 weeks); confirm positive
or 3 (4–8 weeks after exposure) and forces Physical Examination Findings
• Depend on type of disease (neoplastic or tests with another method.
virus into latency after transient viremia; may • IFA—identify FeLV antigen in leukocytes and
be reactivated with immune suppression or non-neoplastic) and secondary infections.
• Lymphadenomegaly—mild to severe. platelets in fixed smears of whole blood or buffy
other viral infections. coat; positive result indicates productive bone
• Progressive or productive infection—immune • Fever, wasting.
• Upper respiratory tract—rhinitis, marrow infection; 97% of IFA-positive cats
response not effective, persistent viremia (stages persistently infected and viremic for life; antigen
4 and 5) from 4–12 weeks after infection. conjunctivitis, keratitis.
• Persistent diarrhea—bacterial or fungal usually detected by 4 weeks after infection, but
• Tumor induction—DNA provirus may be up to 12 weeks; for leukopenic cats, use
integrates into cat chromosomal DNA in overgrowth, parasite-induced inflammation,
direct effect on crypt cells. buffy coat smears rather than whole blood
critical regions near oncogenes (e.g., c-myc or smears; confirm positive tests.
genes influencing c-myc expression); thymic • Gingivitis, stomatitis, periodontitis.
• Nonresponsive or recurrent infections of • FeLV vaccination does not interfere with
lymphosarcoma results. antigen testing.
• Feline sarcoma viruses—FeLV mutants; external ear and skin.
• Lymphoma—risk increased 62-fold in • PCR for proviral DNA in blood or
arise by recombination between FeLV and tissue—denotes exposure, confirm with
host genes; virus–host fusion proteins FeLV-infected cats; thymic and multicentric;
extranodal lymphoma can affect eye, antigen test; proviral DNA detectable 1–2
responsible for induction of fibrosarcomas. weeks after infection; proviral loads can
• Pathogenesis influenced by presence of nervous system.
• Erythroid and myelomonocytic leukemias. differentiate cats with regressive versus
other viruses (e.g., feline foamy virus, feline progressive infections.
coronavirus, feline immunodeficiency virus • Fibrosarcomas—coinfection with mutated
sarcoma virus; frequently young cats. • Reverse transcription PCR (RT-PCR) for
[FIV]) or endogenous retroviruses. viral RNA (virus circulating or replicating
• Peripheral neuropathies; progressive ataxia.
SYSTEMS AFFECTED within cells) in saliva or blood—denotes
• Hemic/lymphatic/immune—bone marrow CAUSES viremia and FeLV shedding; first test to
dyscrasia, neoplasia, immunosuppression. • Cat-to-cat transmission—close casual become positive as early as 1 week after
• Nervous—degenerative myelopathy, neoplasia. contact (grooming), shared dishes or litter infection.
• Other body systems—immunosuppression pans, bites. • Multiple tests over several months may be
with secondary infections or neoplasia. • Perinatal transmission—transplacental and needed to clarify FeLV status and whether
transmammary transmission in >20% of infection progressive or regressive; a few cats
GENETICS surviving kittens from infected queens.
N/A have persistently discordant ELISA-positive
RISK FACTORS and IFA-negative tests or test positive only
INCIDENCE/PREVALENCE • Age—kittens more susceptible than adults. sporadically.
• In United States, 2–3% in healthy cat • Male—result of behavior.
population; worldwide infection rate 1–8% in IMAGING
• Free-roaming. Thymic atrophy (fading kittens); mediastinal mass
healthy cats; 3–4 times greater in clinically ill cats. • Multicat household.
• Decline in US prevalence since 1980s.
and pleural effusion with thymic lymphoma.
(continued) Feline Leukemia Virus (FeLV) Infection

DIAGNOSTIC PROCEDURES ◦ α-interferon (Roferon®-A in saline 30 U/
Bone marrow aspiration or biopsy—arrest in day PO for 7 days every other week).
erythroid differentiation; true aplastic anemia ◦ Feline recombinant interferon omega
with hypocellular bone marrow may be seen; (Virbagen® Omega 1 million U/kg SC for MISCELLANEOUS
some cases of anemia result from myelopthesis. 5 days starting days 0, 14, 60)—may increase ASSOCIATED CONDITIONS
PATHOLOGIC FINDINGS survival rates and improve clinical status. • Secondary infections.
• Bone marrow hypercellularity with • Mycoplasma haemofelis infection—see • Neoplasia (lymphoid, fibrosarcoma). F
neoplastic disease. Mycoplasmosis for recommended treatment. • Immune-mediated disease.
• Lymphocytic and plasmacytic infiltrates of • Lymphoma—management with standard
AGE-RELATED FACTORS
gingiva, lymph nodes, other lymphoid tissues, chemotherapy protocols; remission periods
• Neonatal kittens—most (70–100%)
spleen, kidney, liver. average 3–4 months.
susceptible to infection.
• Intestinal lesions—feline panleukopenia- • Myeloproliferative disease, leukemias—
• Older kittens—<30% susceptible to
like syndrome. more refractory to treatment.
infection by 16 weeks of age; may develop
• Vaccinate for respiratory and enteric
regressive infections.
pathogens based on individual risk assessment.
Rabies vaccination according to regulatory ZOONOTIC POTENTIAL
guidelines. Probably low, but controversial.
TREATMENT CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING
APPROPRIATE HEALTH CARE Modified live vaccines—potential for disease • Abortions, stillbirths, and fetal resorptions
• Outpatient for most cats. in severely immunosuppressed cats. occur in about 80% of FeLV-positive queens.
• Inpatient—may be required with severe • Transmission from queen to kittens—in at
PRECAUTIONS
secondary infections, anemia, cachexia. least 20% of live births.
Systemic corticosteroids—potential for
• Blood transfusions—emergency support;
further immunosuppression. SEE ALSO
may need multiple transfusions; passive • Anemia, Nonregenerative.
antibody transfer (if vaccinated donor) POSSIBLE INTERACTIONS
• Feline Immunodeficiency Virus (FIV)
reduces level of FeLV antigenemia in some. N/A
Infection.
• Management of secondary and ALTERNATIVE DRUG(S) • Feline Stomatitis—Feline Chronic
opportunistic infections. Immunomodulatory drugs—Propionibacte- Gingivostomatitis (FCGS).
NURSING CARE rium acnes (ImmunoRegulin® 0.5 mL/cat IV • Lymphoma—Cats.
Supportive therapy (e.g., parenteral fluids, once or twice weekly); acemannan (Carrisyn® • Myeloproliferative Disorders.
nutritional supplements) as indicated. 100 mg/cat/day PO).
ABBREVIATIONS
ACTIVITY • FeLV = feline leukemia virus.
Normal • FIV = feline immunodeficiency virus.
DIET • IFA = immunofluorescent antibody.
Normal, may alter as necessary for cats with FOLLOW-UP • RT-PCR = reverse transcription polymerase
diarrhea, kidney disease. PATIENT MONITORING chain reaction.
CLIENT EDUCATION Varies according to clinical manifestations. INTERNET RESOURCES
• Keep cats indoors and separated from PREVENTION/AVOIDANCE http://www.abcdcatsvets.org/
FeLV-negative cats to protect from secondary • Prevent contact with FeLV-positive cats. feline-leukaemia-virus-infection
pathogens and prevent spread of FeLV. • Quarantine and test incoming cats before Suggested Reading
• Discuss good nutrition, routine husbandry introduction to multicat households. Little S, Levy J, Hartmann K, et al. 2020
to control secondary infections. • Screen blood donor cats for FeLV-regressive AAFP feline retrovirus testing and
SURGICAL CONSIDERATIONS infections using PCR for proviral DNA. management guidelines. J Feline Med Surg
• Biopsy or removal of tumors. Vaccines 2020, 22:5–30.
• Oral treatment or surgery—dental cleaning, • Most commercial vaccines induce virus- Sykes JE. Feline leukemia virus infection. In:
tooth extraction, gingival biopsy. neutralizing antibodies, reported efficacy ranges Sykes JE, ed., Canine and Feline Infectious
from <20% to almost 100%, depending on Diseases. St. Louis, MO: Elsevier Saunders,
methodology; canarypox–FeLV recombinant 2014, pp. 224–238.
vaccine does not contain adjuvant. Willett BJ, Hosie MJ. Feline leukaemia virus:
• Test cats for FeLV before initial vaccination. half a century since its discovery. Vet J
MEDICATIONS • Vaccinate kittens at 8–9 and 12 weeks of 2013, 195:16–23.
DRUG(S) OF CHOICE age; boost at 1 year of age; revaccinate every Author Margaret C. Barr
• Antiretroviral therapy not routinely 2–3 years if cat is in low risk environment; Consulting Editor Amie Koenig
indicated due to inconsistent evidence of annually if high risk..
efficacy and potential adverse effects; immune
EXPECTED COURSE AND PROGNOSIS Client Education Handout
modulator therapy also unproven.
Persistently viremic cats: >50% succumb to available online
◦ Zidovudine (Retrovir® 5–10 mg/kg PO
related diseases within 2–3 years after
q12h)—clinical improvement, does not
infection.
clear virus.
Feline Panleukopenia
SIGNS enteritis and panleukopenia, frequently
Historical Findings anemia; patient positive for FeLV antigen.
• Salmonellosis—can cause severe gastro
BASICS • History of recent exposure (e.g., from
shelter population). enteritis; white blood cell (WBC) count
DEFINITION • Newly acquired kitten.
usually high.
A viral infection of cats characterized by • Acute poisoning—similar to acute disease;
• Kitten 2–4 months old from premises with
F sudden onset, vomiting and diarrhea, severe history of feline panleukopenia (FP). depression; subnormal temperature; WBC
dehydration, and high mortality. • No vaccination history or last vaccinated
count normal.
• Many diseases cause mild clinical signs
PATHOPHYSIOLOGY when <16 weeks of age.
• Sudden onset, with vomiting, diarrhea,
hard to differentiate from mild FP; total
Feline parvovirus (FPV) infects and causes
depression, complete anorexia. WBC count always low during acute
acute death of rapidly dividing cells.
infection with FPV, even in subclinical
SYSTEMS AFFECTED Physical Examination Findings infections.
• Gastrointestinal—crypt cells of jejunum • Mental dullness/lethargy.
• Typical “panleukopenia posture”—
and ileum are destroyed causing blunted villi;
• Panleukopenia—most consistent finding;
malabsorption of nutrients; acute vomiting sternum and chin resting on floor, feet
tucked under body, top of scapulae elevated WBC counts usually between 500 and 3,000
and diarrhea; dehydration; and secondary
above the back. cells/μL during acute disease.
bacteremia.
• Biochemical findings usually nonspecific—
• Hemic/lymphatic/immune—severe • Dehydration—appears rapidly; may be
severe. hypoproteinemia, hypoalbuminemia,
panleukopenia; atrophy of thymus.
• Vomiting, diarrhea.
hypocholesterolemia possible.
• Nervous and ophthalmic—in neonates,
rapidly dividing granular cells of cerebellum • Body temperature—usually mild to OTHER LABORATORY TESTS
and retinal cells of eye destroyed; cerebellar moderately increased or decreased in early • CPV antigen fecal immunoassay (Cite
hypoplasia with ataxia and retinal dysplasia stages; becomes severely low as patients Canine Parvovirus Test Kit, IDEXX Labs)—
result. become moribund. not licensed for FP; detects FPV antigen in
• Reproductive—in utero infection in • Abdominal pain. feces.
nonimmune queens leads to fetal death or • Small intestine—either turgid or flaccid. • Chromatographic test strip—feces for FPV
neurologic abnormalities. • Subclinical or mild infections common, and CPV.
especially in adults. • Serologic testing—paired serum samples
GENETICS
• Ataxia from cerebellar hypoplasia—kittens detect rising antibody titer.
N/A
infected in utero or neonatally; evident at • PCR testing–confirms FPV in blood, feces,
INCIDENCE/PREVALENCE 10–14 days of age and persist for life: or tissue; positive result with recent modified
• Unvaccinated populations—most severe hypermetria; dysmetria; base‐wide stance; live virus (MLV) vaccination.
and important feline infectious disease. alert, afebrile, and otherwise normal; retinal DIAGNOSTIC PROCEDURES
• Routine vaccination—almost total control dysplasia sometimes seen. • Viral isolation from feces or affected
of disease.
CAUSES tissues (e.g., thymus, small intestine,
• Extremely contagious.
FPV spleen).
• Extremely stable virus, survives for years on
• Electron microscopy of feces—detects
contaminated premises. • Small, single‐stranded DNA virus.
• Single antigenic serotype.
parvovirus, presumably FPV.
• Antigenic cross‐reactivity with canine parvovirus PATHOLOGIC FINDINGS
Worldwide in unvaccinated populations.
(CPV) type 2 and mink enteritis virus. Gross
SIGNALMENT • Extremely stable against environmental • Rough hair coat, weight loss.
Species factors, temperature, and most disinfectants. • Severe dehydration.
• Felidae—all, domestic and exotic. • Requires a mitotic cell for replication. • Evidence of vomiting and diarrhea.
• Canidae—susceptible to canine parvovirus; CPV Types 2a, 2b, and 2c • Edematous, turgid small intestine.
some exotic canids may be susceptible to • CPV‐2a, CPV‐2b, and CPV‐2c can • Petechial or ecchymotic hemorrhages in
FPV. produce FP in domestic and/or exotic cats. jejunum and ileum.
• Mustelidae—especially mink; may be • Properties of CPV similar to FPV. • Thymic atrophy.
susceptible. • Gelatinous or liquid bone marrow.
RISK FACTORS
• Procyonidae—raccoon and coatimundi; • In utero or neonatal infection—gross
• Factors that increase mitotic activity of
susceptible. hypoplasia of cerebellum.
small intestinal crypt cells such as intestinal
Breed Predilections parasites or pathogenic bacteria. Microscopic
None • Secondary or coinfections—viral upper • Dilated small intestinal crypts with
Mean Age and Range respiratory infections. sloughing of epithelial cells.
• Unvaccinated and previously unexposed • Shortened and blunt intestinal villi.
cats of any age can become infected once • Lymphocytic depletion of follicles of lymph
maternal immunity has been lost. nodes, Peyer’s patches, spleen.
• Kittens 2–6 months of age—most • Neonatal and fetal infection—disorientation
DIAGNOSIS and depletion of granular and Purkinje cells
susceptible to develop severe disease.
• Adults—often mild or subclinical infection. DIFFERENTIAL DIAGNOSIS of cerebellum.
• Panleukopenia‐like syndrome of feline • Eosinophilic intranuclear inclusions in
Predominant Sex leukemia virus (FeLV) infection—chronic affected tissues during early infection.
N/A
(continued) Feline Panleukopenia

PREVENTION/AVOIDANCE ZOONOTIC POTENTIAL
• Contaminated environments (e.g., cages, None
floors, food and water dishes) should be PREGNANCY/FERTILITY/BREEDING
TREATMENT disinfected with 1 : 32 dilution of bleach. • Unvaccinated pregnant cats at great risk of
APPROPRIATE HEALTH CARE • FPV resistant to most commercial infection.
• Main principles of treatment—rehydration; disinfectants. • Fetuses almost always become infected with
antibiotic therapy; supportive care (antiemetics Vaccines fatal or teratogenic effects, even when dam F
and analgesics as needed). • FP vaccines are core vaccines—to be given has subclinical infection.
• Inpatient—severe cases. to all cats. • Fetal resorption, abortion, fetal mummi
• Outpatient—mild cases. • FP is preventable by routine vaccination of fication, stillbirth, or birth of weak, fading
NURSING CARE kittens. kittens.
• IV fluid therapy—essential in severe cases: • MLV vaccines are available for parenteral • Kittens may have cerebellar hypoplasia.
correct dehydration and provide electrolytes; injection or intranasal administration; MLV SYNONYMS
add dextrose if patient is hypoglycemic. vaccine is preferred, with exceptions, as it may • Feline distemper.
• SC fluids—mild cases without dehydration provide better protection. • Feline parvovirus infection.
or shock. • Inactivated vaccine is available for • Feline viral enteritis.
• Antiemetic therapy should be considered in parenteral injection.
vomiting patients. • Do not use MLV vaccines in pregnant cats ABBREVIATIONS
• Whole blood, packed red blood cells, or fresh or kittens younger than 4 weeks old. • CPV = canine parvovirus.
frozen plasma transfusions—if clinical signs of • Immunity—long duration, perhaps even • FeLV = feline leukemia virus.
anemia are present or serum albumin <2 g/dL. for life. • FP = feline panleukopenia.
• Kittens—vaccinate as early as 6 weeks of • FPV = feline parvovirus.
ACTIVITY • MLV = modified live virus.
age, then every 3–4 weeks until 16–20 weeks
Keep patient indoors during acute disease. • WBC = white blood cell.
of age; American Association of Feline
DIET Practitioners vaccination guidelines now Suggested Reading
Temporarily withhold food until vomiting is recommend the last vaccine to be given when Greene CE. Feline enteric viral infections. In:
controlled. kitten is at least 16 weeks old, instead of 12 Greene CE, ed., Infectious Diseases of the
CLIENT EDUCATION weeks, because maternal antibodies may not Dog and Cat, 4th ed. St. Louis, MO:
• Inform client that current and future cats in have waned until 16 weeks of age. Saunders Elsevier, 2012, pp. 80–91.
household must be vaccinated for FPV before • Boosters—1 year after last kitten vaccine; Kruse BD, Unterer S, Horlacher K, et al.
exposure. then repeat every 3 years. Prognostic factors in cats with feline
• Inform client that virus will remain POSSIBLE COMPLICATIONS panleukopenia. J Vet Intern Med 2010,
infectious for years unless environment can be • Shock, sepsis—severe dehydration, 24:1271–1276.
adequately disinfected with dilute bleach. hypoglycemia, hypoproteinemia bacterial Lappin MR, Veir J, Hawley J. Feline
translocation, electrolyte imbalance. panleukopenia virus, feline herpesvirus‐1,
• Chronic enteritis—fungal or other cause. and feline calicivirus antibody responses in
None
• Teratogenic effects (cerebellar hypoplasia seronegative specific pathogen‐free cats after
resulting in ataxia for life)—virus infection of a single administration of two different
fetus. modified live FVRCP vaccines. J Feline
• Concurrent infection with intestinal Med Surg 2009, 11:159–162.
MEDICATIONS parasites. Porporato F, Horzinek MC, Hoffman‐
Lehmann R, et al. Survival estimates and
DRUG(S) OF CHOICE EXPECTED COURSE AND outcome predictors for shelter cats with
Broad‐spectrum antibiotics (e.g., ampicillin PROGNOSIS feline panleukopenia virus infection. J Am
or ampicillin–sulbactam IV, amoxicillin or • Most cases acute, lasting only 5–7 days. Vet Med Assoc 2018, 253:188–195.
amoxicillin–clavulanate PO)—counter • Guarded prognosis during acute disease, Scherk MA, Ford RB, Gaskell RM, et al.
secondary bacteremia from intestinal bacterial especially if WBC count <2,000 cells/μL. 2013 AAFP Feline Vaccination Advisory
translocation. • Approximately 50% mortality has been Panel Report. J Feline Med Surg 2013,
CONTRAINDICATIONS reported. 15:785–808.
Oral medications until vomiting/ • If patient survives acute disease, recovery Truyen U, Addie D, Belák S, et al. Feline
gastroenteritis has been controlled. usually rapid and uncomplicated. panleukopenia: ABCD guidelines on
ALTERNATIVE DRUG(S) prevention and management. J Feline Med
None Surg 2009, 11:538–546.
Author Julie M. Walker
MISCELLANEOUS Consulting Editor Amie Koenig
ASSOCIATED CONDITIONS editors acknowledge the prior contribution of
FOLLOW‐UP Viral upper respiratory diseases—feline viral Fred W. Scott.
rhinotracheitis and feline calicivirus infection.
PATIENT MONITORING
• Monitor hydration and electrolyte balance AGE‐RELATED FACTORS
• Clinical—typically in kittens. Client Education Handout
closely.
• Subclinical—usually adults. available online
• Monitor CBC every 24–48h until recovery.
Feline Paraneoplastic Alopecia

• Telogen effluvium—not associated with
miniaturization of hair follicles.
• Skin fragility syndrome—markedly thin
BASICS skin with lacerations; not always associated MEDICATIONS
OVERVIEW with exfoliation. DRUG(S) OF CHOICE
• Rare condition characterized by cutaneous • Superficial necrolytic dermatitis—not N/A
F lesions that serve as markers of internal associated with marked exfoliation and
neoplasia. miniaturization of hair follicles.
• Most affected cats have pancreatic CBC/BIOCHEMISTRY/URINALYSIS
adenocarcinoma with metastases to liver, No consistent abnormalities; may be helpful
lungs, pleura, and/or peritoneum; reports of
FOLLOW-UP
in ruling out other differentials.
other neoplasias. EXPECTED COURSE AND PROGNOSIS
• Link between internal malignancies and OTHER LABORATORY TESTS • Progressive deterioration.
cutaneous lesions is unknown; may involve • Endocrine (thyroid profiles and • Supportive care—ultrasonography and
cytokines producing atrophy of hair follicles. dexamethasone suppression test)—endocrine thoracic radiographs may demonstrate
disease. progression of metastatic disease.
SIGNALMENT • Skin scrapings—demodicosis. • Death most often occurs within 2–20
• Domestic shorthair cats only reported cases. • KOH examination of hairs and/or fungal weeks after onset of skin lesions.
Median age—13 years; range: 7–16 years. culture—dermatophytosis.
SIGNS • Skin cytology—possible secondary
• Decrease in appetite followed by rapid Malassezia infection (causing pruritus).
weight loss and excessive shedding. IMAGING
• Pruritus—variable; sometimes with MISCELLANEOUS
• Ultrasonography—pancreatic mass and/or
excessive grooming. nodular lesions in liver, intestines, or SEE ALSO
• Hairs epilate easily leading to severe peritoneal cavity; failure to demonstrate Adenocarcinoma, Pancreas.
alopecia on ventral neck, abdomen, medial nodules does not exclude the diagnosis, Suggested Reading
thighs; rapidly progressive. neoplasia may be too small for detection. Caporali C, Albanese F, Binanti D, Abramos
• Stratum corneum may “peel,” leading to • Thoracic radiographs—metastatic lesions in F. Two cases of feline paraneoplastic alopecia
glistening appearance to skin. lungs or pleural cavity. associated with a neuroendocrine pancreatic
• Alopecic skin is shiny, inelastic, and thin,
DIAGNOSTIC PROCEDURES neoplasia and a hepatosplenic plasma cell
but not fragile. tumour. Vet Dermatol 2016, 27:508–513.
• Gray lentigines may develop in alopecic • Skin biopsy.
• Laparoscopy or exploratory laparotomy— Grandt LM, Roethig A, Schroeder S, et al.
areas. Feline paraneoplastic alopecia associated
• Footpads may be fissured and/or scaly; identify primary and metastatic tumors.
with metastasising intestinal carcinoma.
often painful. PATHOLOGIC FINDINGS J Fel Med Surg 2015,
CAUSES & RISK FACTORS • Skin—nonscarring alopecia; severe atrophy of 1(2):2055116915621582. doi:
• Majority of cases are associated with hair follicles and adnexa; miniaturization of 10.1177/2055116915621582
underlying pancreatic adenocarcinoma. hair bulbs; mild to severe acanthosis; variable Outerbridge CA. Cutaneous manifestations
• Other associated tumor types include absence of stratum corneum; variable mixed of internal diseases. Vet Clin North Am
cholangiocarcinoma, hepatocellular superficial perivascular infiltrates of neutrophils, Small Anim Pract 2013, 43:135–152.
carcinoma, intestinal carcinoma, neuro eosinophils, and mononuclear cells; some have Author Karen L. Campbell
endocrine pancreatic neoplasia, and secondary Malassezia infections. Consulting Editor Alexander H. Werner
hepatosplenic plasma cell tumor. • Primary tumor—usually pancreatic Resnick
adenocarcinoma, rarely primary bile duct
cholangiocarcinoma, hepatocellular or
intestinal carcinomas, other pancreatic
tumors (neuroendocrine), and hepatosplenic
DIAGNOSIS plasma cell tumor. • Metastatic nodules—
DIFFERENTIAL DIAGNOSIS common in liver, lungs, pleura, and
• Hyperadrenocorticism—polyuria, peritoneum.
polydipsia, and skin fragility.
• Hyperthyroidism—polyphagia.
• Feline symmetrical alopecia—hair loss
self-induced; not associated with easy epilation. TREATMENT
• Thymoma—skin is thick, scaly, and • Removal of tumor via surgery may be
fissured; lymphocytic interface dermatitis; curative; prognosis guarded, as majority of
radiographs reveal thoracic mass. cases have metastatic disease.
• Demodicosis—mites not associated with • Chemotherapy or other medications—no
paraneoplastic alopecia. reported response.
• Dermatophytosis—hair loss often • Affected animals rapidly deteriorate;
associated with breakage, not spontaneous euthanasia should be suggested.
shedding; inappetence and weight loss rare. • Supportive care—only if owners refuse to
• Alopecia areata—rarely involves entire consider euthanasia; feed highly palatable,
ventral surface; inappetence and weight loss nutrient-dense foods and/or tube feed.
rare.
Feline Stomatitis—Feline Chronic Gingivostomatitis (FCGS)
of moderate to marked caudal stomatitis; laser

helps to remove some of inflamed tissue and
bacterial load; laser is set to 4 W of
BASICS DIAGNOSIS continuous energy; after shielding airway
OVERVIEW DIFFERENTIAL DIAGNOSIS from laser energy with moistened gauze,
• Inflammatory response affecting the oral • Periodontal disease. inflamed areas can be rastered; relasering
cavity in cats. • Oral malignancy. recommended monthly for 3 months if F
• FCGS oropharyngeal inflammation is • Eosinophilic granuloma complex. inflammation persists.
classified by location as: • If patients do not respond to extraction of
◦ Alveolar mucositis (alveolar stomatitis)— teeth distal to canines, consider trial of
• Elevated globulin—polyclonal gammopathy
inflammation of alveolar mucosa (i.e., mucosa prednisolone 2 mg/kg every other day to
secondary to antibody production following
overlying the alveolar process and extending control the inflammation, or remove all teeth;
bacterial invasion into periodontal tissues.
from the mucogingival junction without when extracting teeth, pay meticulous
• Leukocytosis and eosinophilia may be
obvious demarcation to the vestibular sulcus attention to removing all dental hard tissue;
present.
and to the floor of the mouth). take intraoral radiographs before and after
◦ Caudal mucositis—inflammation of IMAGING surgery; postoperative application of
mucosa of the caudal oral cavity, bordered Intraoral radiographs to evaluate periodontal fluocinonide 0.05% (Lidex Gel) to gingival
medially by the palatoglossal folds and disease and tooth resorption. margin may help healing.
fauces, dorsally by the hard and soft palate, DIAGNOSTIC PROCEDURES • Refractory cases with extensive proliferative
and rostrally by alveolar and buccal mucosa. • Biopsy (especially unilateral lesions) to rule lesion in caudal oral cavity and pharynx
◦ Glossitis—inflammation of mucosa of the out neoplasia—primarily squamous cell warrant more guarded prognosis.
dorsal and/or ventral surface of the tongue. carcinoma.
◦ Stomatitis—inflammation of the mucous • Calicivirus, Bartonella, and oral bacterial
lining of any of the structures in the mouth; culture and sensitivity testing not
in clinical use the term should be reserved recommended. MEDICATIONS
to describe widespread oral inflammation
(beyond gingivitis and periodontitis) that DRUG(S) OF CHOICE
may also extend into submucosal tissues. • Medication and other therapies have been
used with limited long-term success; lack of
SIGNALMENT TREATMENT permanent response to conventional oral
• Cats. • Prognosis for cats whose lesions do not hygiene, antibiotics, anti-inflammatory drugs,
• Purebred breeds predisposed—Abyssinian, include caudal oral mucosa is better than and immunosuppressive drugs is typical;
Persian, Himalayan, Burmese, Siamese, and those affected by caudal stomatitis. medications should not be regarded as primary
Somali. • Initial therapy for early cases of alveolar method to control oropharyngeal inflammation.
SIGNS mucositis involves dental scaling above and • Antibiotics—clindamycin 5 mg/kg q12h,
• Ptyalism. below gingiva and treatment (extraction) for metronidazole, amoxicillin, ampicillin,
• Halitosis. teeth affected with grades 3 and 4 periodontal enrofloxacin, tetracycline.
• Dysphagia. disease and/or tooth resorption. • Corticosteroids—prednisone 2 mg/kg
• Anorexia—and/or prefers soft food. • For cases of focal vestibular and alveolar initially daily, followed by every other day;
• Weight loss. mucositis, extraction of locally affected teeth methylprednisolone acetate 2 mg/kg q7–30
• Scruffy hair coat from lack of grooming. in proximity to lesions usually results in days may also help control inflammation.
• Erythematous, ulcerative, proliferative resolution. • Gold salts—Solganal 1 mg/kg IM weekly
lesions affecting gingiva, glossopalatine • For cases of moderate to marked caudal until improvement (up to 4 months), then
arches, tongue, lips, buccal mucosa, and/or stomatitis, extraction of all maxillary and every 14–35 days.
hard palate. mandibular teeth (including root fragments) • Chlorambucil—2 mg/m2 PO every other
• Gingival inflammation commonly or those distal to canines (if no clinical day or 20 mg/m2 every other week.
completely surrounds the tooth, compared evidence of disease affecting canines and • Bovine lactoferrin—40 mg/kg applied to
with gingivitis, which usually occurs on incisors) resulted in resolution of oral mucous membranes.
buccal and labial surfaces. inflammation in ~60% of cases without • Interferon—alpha or omega 30 IU/day
• May extend to glossopharyngeal arches as further need for medication, with ~20% of 7 days on, 7 days off, indefinitely.
well as palate. cases requiring control with medication, and • CO2 laser to decrease inflamed tissue.
~20% refractory. • Cyclosporine—2 mg/kg BID.
• To aid extractions—create a gingival flap in
• Cause unknown; bacterial, viral, and
all quadrants for exposure; after completely
immunologic etiologies suspected.
elevating all roots, use high-speed drill with
• Significant findings of feline calicivirus;
water spray to create trough of bone where
however, calicivirus load does not correlate
roots were, removing most of keratinized FOLLOW-UP
with degree of inflammation or prognosis of
gingiva, periodontal ligament, and PATIENT MONITORING
positive therapy.
periradicular alveolar bone; before suturing, • Recommend 2- and 4-week postoperative
• Immunosuppression from feline leukemia
“smooth down” alveolar margin to remove examinations to determine success of surgical
virus (FeLV) or feline immunodeficiency
sharp edges with round or football-shaped procedure.
virus (FIV) can also lead to poorly responsive
diamond bur. • Soft diet should be encouraged for
infections; most affected cats are negative for
• CO2 laser has been effective as treatment 2 weeks postoperatively, though some cats
FeLV. Concomitant FIV infection is not
adjunct during initial care, especially in cases may not accept any dietary changes well.
uncommon.
Feline Stomatitis—Feline Chronic Gingivostomatitis (FCGS) (continued)
PREVENTION/AVOIDANCE Druet I, Hennet P, Relationship between

N/A Feline calicivirus load, oral lesions, and
POSSIBLE COMPLICATIONS outcome in feline chronic gingivostomatitis
MISCELLANEOUS (caudal stomatitis): retrospective study in
Wound dehiscence; inappetence, refractory
caudal inflammation. ASSOCIATED CONDITIONS 104 cats. Front Vet Sci 2017, 4:209. doi:
• Lymphocytic plasmacytic stomatitis. 10.3389/fvets.2017.00209
EXPECTED COURSE AND
F • Stomatitis. Wiggs RB, Lobrise HB. Veterinary Dentistry:
PROGNOSIS Principles and Practice. Philadelphia, PA:
ABBREVIATIONS
• Caudal mouth extractions have been Lippincott-Raven, 1997.
shown to greatly improve large percentage Author Jan Bellows
of patients; full-mouth extractions sometimes Consulting Editor Heidi B. Lobprise
warranted. INTERNET RESOURCES
• Refractory cases with extensive https://avdc.org/avdc-nomenclature
proliferative lesion in caudal oral cavity Suggested Reading Client Education Handout
and pharynx warrant more guarded Bellows, JE. Feline Dentistry. Oxford: available online
prognosis. Wiley-Blackwell, 2010.
Feline Symmetrical Alopecia

• Food elimination diet trial—adverse
reactions to food.
• Intradermal allergy testing—atopy.
BASICS • Skin biopsy—confirm/exclude presence of FOLLOW-UP
underlying cause (e.g., hypersensitivity • Frequent examinations are essential in
OVERVIEW
• Alopecia in a symmetrical pattern with no dermatitis vs. psychogenic, or rarely systemic confirming differential diagnoses.
• Successful identification of underlying
gross changes in the skin. disease).
cause offers best prognosis, if cause can be F
• Common clinical presentation in cats. • Cytology of papules or crusts, if present,
• Similar manifestation for many different may have large numbers of eosinophils. controlled (e.g., flea bites or food
underlying disorders. • Microscopic examination of skin hypersensitivity).
scrapings—ectoparasites.
SIGNALMENT
• Hair plucks (trichogram)—dermatophyte
No age, breed, or sex predilection reported.
arthrospores or Demodex mites adjacent to
SIGNS hair shafts. MISCELLANEOUS
• Total to partial hair loss; most often
PATHOLOGIC FINDINGS INTERNET RESOURCES
symmetrical but can occur in a patchy
• Histopathologic findings—vary depending https://indoorpet.osu.edu/cats
distribution.
on cause.
• Areas of the body commonly affected— Suggested Reading
• Feline psychogenic alopecia—hair follicles
ventrum, caudal dorsum, and lateral and Helton Rhodes KA, Werner A. Blackwell’s
and skin normal.
caudal thighs. Five-Minute Veterinary Consult Clinical
• High numbers of mast cells, eosinophils,
• Affected areas are often those accessible for Companion: Small Animal Dermatology,
lymphocytes, or macrophages suggest allergic
grooming. 3rd ed. Hoboken, NJ: Wiley-Blackwell,
dermatitis.
• Patchy areas of hair loss (unsymmetrical) on 2018.
• Alopecia areata—lymphocytic
distal extremities or body. Mertens PA, Torres S, Jessen C. The effects of
inflammation that encircles bulb portions of
CAUSES & RISK FACTORS hair follicles; rare. clomipramine hydrochloride in cats with
• Cutaneous hypersensitivity—flea allergic psychogenic alopecia: a prospective study.
dermatitis, food, atopy. J Am Anim Hosp Assoc 2006,
• Ectoparasites—flea bite dermatitis, 42(5):336–343.
Cheyletiellosis, Otodectes cynotis. Sawyer LS, Moon-Fanelli AA, Dodman NH.
• Infection—dermatophytosis.
TREATMENT Psychogenic alopecia in cats: 11 cases
• Management of underlying cause. (1993–1996). J Am Vet Med Assoc 1999,
• Neurologic or behavioral—“psychogenic
• Inform the owner of the diagnostic plan 214(1):71–74.
alopecia” (uncommon as primary cause of
symptoms). and the time it could take to see a response Waisglass SE, Landsberg GM, Yager JA, Hall
• Stress or metabolic—telogen effluvium.
(hair coat regrowth). JA. Underlying medical conditions in cats
• Environmental enrichment in cases of true with presumptive psychogenic alopecia.
• Neoplasia—pancreatic neoplasia
(paraneoplastic alopecia). psychogenic cause. J Am Vet Med Assoc 2006,
• Hyperadrenocorticism. 228(11):1705–1709.
• Alopecia areata. Author David D. Duclos
• Hyperthyroidism (early sign). Consulting Editor Alexander H. Werner
MEDICATIONS Resnick
DRUG(S) OF CHOICE
• Antihistamines—e.g., chlorpheniramine
DIAGNOSIS 0.5 mg/kg PO q8h; cetirizine 5 mg/cat
DIFFERENTIAL DIAGNOSIS q12–24h.
• Glucocorticosteroid—prednisolone 0.5 mg/
See Causes & Risk Factors.
kg PO, tapering/alternate-day therapy.
CBC/BIOCHEMISTRY/URINALYSIS • Amitriptyline—1–2 mg/kg PO daily.
Eosinophilia may occur with • Clomipramine hydrochloride—0.5 mg/kg
hypersensitivities. q24h.
OTHER LABORATORY TESTS • Cyclosporine, modified—5–7 mg/kg PO
Serum thyroxine—hyperthyroidism. daily; tapering therapy.
IMAGING CONTRAINDICATIONS/POSSIBLE
N/A INTERACTIONS
• Glucocorticosteroids—can cause alopecia,
• Flea combing—identify fleas, flea
diabetes mellitus, polydipsia, polyuria,
excrement, or both. polyphagia, and weight gain; can suppress
• Microscopic examination of hair—self-
pruritus, making it difficult to determine
induced hair loss results in broken blunt underlying cause.
• Withdraw antipruritic medications
shafts; endogenous hair loss results in tapered
ends (telogen hairs). (including glucocorticosteroids) as diagnostic
• Fecal examination—excess hair, mites, and
tests near completion (e.g., restricted-
ova (Cheyletiella), tapeworm, or fleas. ingredient food trials).
Feline Tooth Resorption (Odontoclastic Resorption)

while eating, reluctance to eat hard food, and
repetitive lower jaw motions (“chattering”).
BASICS Physical Examination Findings DIAGNOSIS
• Dental deposits, hyperplastic gingiva, and
DEFINITION granulation tissue often cover a clinically DIFFERENTIAL DIAGNOSIS
Tooth resorption (TR) is resorption of dental evident TR emerging at the gingival margin. Periodontal disease, stomatitis.
F hard tissues (cementum, dentin, and in late A dental explorer can be used under general IMAGING
stages also enamel). anesthesia to detect irregularities at the tooth • Without dental radiography, TR below the
PATHOPHYSIOLOGY surface near the gingival margin. gingival attachment (and thus the vast
• Odontoclasts deriving from hematopoietic • TR occurs more often on the labial and majority of TR) will not be detectable.
stem cells migrate to the external root surface, buccal aspects of premolar and molar teeth, • On a radiograph of a tooth with type 1
where they start resorption of cementum and and less commonly on canine and incisor resorption, a focal or multifocal radiolucency is
dentin. teeth. The mandibular third premolar teeth present in the tooth with otherwise normal
• TR is often preceded by dentoalveolar are usually the first teeth affected by TR. radiopacity and normal-appearing periodontal
ankylosis (fusion between alveolar bone and • Canine teeth (in particular maxillary) often ligament space. On a radiograph of a tooth
the root with disappearance of the periodontal appear to extrude excessively (abnormal tooth with type 2 resorption, there is narrowing or
ligament space). The alveolar bone (already in extrusion), leading to exposure of the root disappearance of the periodontal ligament space
a state of constant resorption and apposition) surface. Thickening of alveolar bone with in at least some areas and decreased radiopacity
will then include the tooth in its normal local osteomyelitis (alveolar bone expansion) of part of the tooth. On a radiograph of a tooth
remodeling process, which results in is often associated with this phenomenon. with type 3 resorption, features of both type 1
noninflammatory replacement resorption. If Classification of Tooth Resorption and type 2 resorptions are present in the same
TR progresses coronally and emerges at the • American Veterinary Dental College tooth; the affected tooth shows areas of normal
gingival margin, an inflammatory component (AVDC) currently suggests classification based and narrow or lost periodontal ligament space,
through contact with oral bacteria joins the on the severity (stages 1–5) and radiographic and there is focal or multifocal radiolucency in
initially noninflammatory process, and appearance of the resorption (types 1–3): the tooth and decreased radiopacity in other
inflamed granulation tissue may form to ◦ Stage 1 (TR1)—mild dental hard tissue areas of the tooth.
cover defects in the crown of the tooth loss (cementum or cementum and enamel). • For example, a clinically evident TR
(inflammatory resorption). ◦ Stage 2 (TR2)—moderate dental hard emerging at the gingival margin
• TR in cats most commonly starts anywhere tissue loss (cementum or cementum and (inflammatory resorption) will generally be
on the external root (not crown) surface and enamel with loss of dentin that does not visible as a notched radiolucency in the tooth
not just close to the cementoenamel junction. extend to the pulp cavity). with sharp or scalloped margins (type 1
SYSTEMS AFFECTED ◦ Stage 3 (TR3)—deep dental hard tissue resorption). The periodontal ligament space
Gastrointestinal—oral cavity. loss (cementum or cementum and enamel may be of normal width apical to the TR, but
with loss of dentin that extends to the pulp there will be horizontal or vertical loss of
INCIDENCE/PREVALENCE alveolar bone adjacent to the TR. Lesions on
cavity) with most of the tooth still retaining
At least one-third of cats may develop TR mesial and distal tooth surfaces or in the
its integrity.
during life, with the risk of developing TR furcation area usually are more obvious on
◦ Stage 4 (TR4)—extensive dental hard tissue
increasing with age. Reported prevalence radiographs than those on labial/buccal and
loss (cementum or cementum and enamel
(25–75%) greatly depends on the population lingual/palatal tooth surfaces.
with loss of dentin that extends to the pulp
of animals investigated (general practice • Fusion of the root and alveolar bone
cavity) with most of the tooth having lost its
versus dental specialist practice) and the (dentoalveolar ankylosis) results in focalized
integrity; there are substages TR4a (crown and
diagnostic methods applied (observation only, or generalized disappearance of the
root equally affected), TR4b (crown more
tactile exploration with an instrument, and/or periodontal ligament space and lamina dura
severely affected than root, and TR4c (root
use of dental radiography). on radiographs. Resorbed dental tissue will
more severely affected than crown).
SIGNALMENT ◦ Stage 5 (TR5)—remnants of dental hard gradually be replaced by bone (replacement
tissue are visible only as irregular resorption). The root will take on a striated or
Species moth-eaten appearance (“ghost roots”), and
Cats radiopacities with complete gingival
covering. the periodontal ligament space and lamina
Breed Predilections • See Imaging for additional classification dura will disappear on radiographs (type 2
Persian longhaired cats reported to have TR scheme (types 1–3). resorption). Unlike inflammatory resorption,
at a younger age compared with other breeds. adjacent bone usually is not resorbed.
CAUSES
Mean Age and Range • Etiology is unknown; possibly multifactorial
Rarely seen in cats less than 2 years of age; (e.g., nutritional, inflammatory, and hereditary).
first teeth usually affected at 4–6 years of age. • One hypothesis is that chronic dietary intake
SIGNS of excess vitamin D would lead to periodontal TREATMENT
ligament degeneration, hypercementosis, DIET
Historical Findings
hyperosteoidosis, narrowing of the periodontal Add water to hard kibble to soften it.
Most affected cats do not show clinical signs,
ligament space, dentoalveolar ankylosis, and
in particular when teeth are affected by CLIENT EDUCATION
replacement resorption. If such a process
replacement resorption only (which is Daily tooth brushing or other means of home
occurred close to the gingival attachment, an
asymptomatic) and the TR is located apical to oral hygiene may help control plaque and
inflammatory component would join the
the gingival attachment (not yet exposed to allow for earlier detection of teeth affected
initially noninflammatory disease.
oral bacteria); some show dropping of food by TR.
(continued) Feline Tooth Resorption (Odontoclastic Resorption)

SURGICAL CONSIDERATIONS extraction so that a flap can be used to close EXPECTED COURSE AND PROGNOSIS
• The treatment of choice for teeth with TR the wound. Additional teeth may develop TR in the
is complete extraction. Multirooted teeth are future, so monitoring with dental radiographs
sectioned after creation of a flap and removal is warranted.
of alveolar bone on labial and buccal aspects
of the roots so that each single-rooted crown–
MEDICATIONS
root segment can be elevated and removed.
Topical chlorhexidine or zinc ascorbate gel F
Resorbing root remnants under noninflamed
and intact gingiva (often appearing as a small
applied to the mouth once a day. MISCELLANEOUS
gingival bulge) and without periapical SYNONYMS
pathology on dental radiographs may be left Feline odontoclastic resorptive lesion
where they are. However, root remnants (FORL).
underneath inflamed gingiva with sinus tracts FOLLOW-UP ABBREVIATIONS
must be extracted. PATIENT MONITORING • TR = Tooth resorption.
• Teeth with dentoalveolar ankylosis and Author Alexander M. Reiter
• Recommend 2-week postoperative
replacement resorption can be treated by means examination to determine success of surgical Consulting Editor Heidi B. Lobprise
of crown amputation and intentional retention procedure. Acknowledgment The author and book
of resorbing root tissue. A flap is made, the • Soft diet should be encouraged for 2 weeks editors acknowledge the prior contribution of
crown is removed with a water-cooled round postoperatively, though some cats may not Jan Bellows.
bur to, or slightly below, the level of the alveolar accept any dietary changes well.
margin, and the wound is rinsed and closed by
suturing. Contraindications include PREVENTION/AVOIDANCE Client Education Handout
periodontitis, endodontic and periapical N/A available online
disease, and stomatitis. POSSIBLE COMPLICATIONS
• Canine teeth exhibiting moderate to severe Wound dehiscence.
abnormal extrusion and alveolar bone
expansion should be treated with an open
Feline (Upper) Respiratory Infections

• Ophthalmologic—conjunctiva. • C. felis—conjunctivitis, occasional sneeze,
• Musculoskeletal—FCV. fever.
• Integument/mucous membranes—FHV, • Mycoplasma spp.—conjunctivitis, ocular
BASICS Cryptococcus. and nasal discharge, dyspnea.
DEFINITION • Neurologic—Cryptococcus, lymph.
CAUSES
• Viral, bacterial, fungal etiologies. • VSD can affect many organ systems. • Viral—FHV, FCV, influenza.
F • Most cats harbor viral causes and become GENETICS • Primary bacterial—B. bronchiseptica, C.
clinical with stress. N/A felis, Streptococcus canis, Mycoplasma spp.
• Viral upper respiratory infection (URI) very • Secondary bacterial invaders—
common, secondary bacterial infections INCIDENCE/PREVALENCE
• FHV and FCV most common causes of
Corynebacterium spp., Escherichia coli,
common; primary bacterial rhinitis uncommon. Pasturella multocida, Pseudomonas aeruginosa,
• Most organisms spread through direct URI.
• Over 90% of cats are seropositive for FHV.
Streptococcus spp., Staphylococcus spp.
contact, air (droplets from coughing, • Fungal—Cryptococcus neoformans,
sneezing, or discharge), and contaminated • Conjunctivitis is most common disease
caused by FHV, most common feline Sporothrix schenckii, Aspergillus spp.,
surfaces (e.g., shared bowls, cages). Penicillium spp.
• Illness typified by rhinosinusitis, conjunctivitis, ophthalmic disease.
lacrimation, salivation, oral ulcerations. • Carrier states exist for FHV, FCV (10–75%). RISK FACTORS
• C. felis—1–5% for cats without signs of • Stress/steroids.
PATHOPHYSIOLOGY respiratory tract disease, 10–30% for cats • Decreased immune function, feline
• Feline herpesvirus (FHV) induces marked with conjunctivitis or URI. immunodeficiency virus (FIV)/feline
rhinitis, sneezing, and conjunctivitis, and may • Bordetella bronchiseptica—seroprevalence of leukemia virus (FeLV) infection.
lead to chronic signs; cats are infected for life, 24–79%, isolation rates up to 47% reported. • Multicat households, shelters, young cats.
with latent virus sequestered in trigeminal
nerve ganglion. GEOGRAPHIC DISTRIBUTION
• FHV infects epithelial cells of respiratory • Ubiquitous.
tract, conjunctiva, and/or cornea; during • Cryptococcus—worldwide, associated with
primary infection or recrudescence, direct pigeon guano. DIAGNOSIS
effect is cytolysis of infected cells and necrosis SIGNALMENT • Direct fluorescent staining of conjunctival
of affected tissues; inflammatory disease can • Species—cat. scraping—FHV.
occur via immune-mediated response to • Breed predilection—N/A. • PCR for B. bronchiseptica (controversial if
infection; turbinate lysis can occur. • Mean age/range—more common in positive), Chlamydophila felis, FCV, FHV,
• Feline calicivirus (FCV) has predilection for younger cats, though viral flare-ups can occur H7N2 influenza virus, influenza A virus
epithelial cells of oral cavity and upper through life. (including H7N2, H3N2, H1N1, H3N8),
respiratory tract; causes rhinitis, stomatitis, • Predominant sex—N/A. Mycoplasma felis.
oral ulceration: ulcers start as vesicles; some • Viral isolation.
SIGNS • Mycoplasma culture.
strains infect lungs and can cause focal
alveolitis and interstitial pneumonia; other Historical Findings • Cryptococcus—direct microscopic
strains cause “limping syndrome.” • Exposure to other cats common; stress, visualization of organisms in nasal discharge
• FCV–virulent systemic disease (VSD) steroids, immunosuppression may precipitate or tissue: cytology or histopathology, culture,
caused by hypervirulent strains that can infect clinical signs for viral causes. serology; latex agglutination to identify
endothelium of liver, lungs, and pancreas, • Caretakers may report upper respiratory antigen.
leading to severe systemic illness characterized signs, weight loss, anorexia, gagging, halitosis, DIFFERENTIAL DIAGNOSIS
by vasculitis; results in edema, alopecia, depression. • Nasopharyngeal polyps.
ulcers, and can cause multiple organ Physical Examination Findings • Nasopharyngeal stenosis.
dysfunction syndrome (MODS), systemic • Depend on organism. • Foreign body.
inflammatory response syndrome (SIRS), • Frequently—sneezing, nasal discharge, • Neoplasia.
disseminated intravascular coagulation, death. stertor, halitosis, ocular discharge, inappetence. • Dental disease—tooth root abscess.
• Chlamydophila felis predominantly infects • FHV—fever, sneezing, nasal discharge, • Anatomic defects.
conjunctiva and causes conjunctivitis; has also conjunctivitis, ulcerative stomatitis, ulcerative • Trauma.
been associated with URI. keratitis, blepharospasm, salivation, • Burn—caustic agent or electrical.
• Bacterial infection—often secondary to depression, anorexia.
viral disease, trauma, allergic rhinitis. CBC/BIOCHEMISTRY/URINALYSIS
• FCV—fever, salivation and ulceration of Generally normal with most etiologies—with
• Cryptococcus affects rostral nasal cavity tongue, hard palate, or nostrils, stomatitis,
resulting in rhinitis and turbinate lysis; virulent systemic FCV may see inflammatory
gingivitis, rhinitis, conjunctivitis, coughing, leukogram, thrombocytopenia, elevated liver
granulomatous protuberances can occur; dyspnea, lameness.
destruction of adjacent facial bones facilitates enzymes/total bilirubin.
• With VSD—peripheral edema, dermal
spread of infection to contiguous regions, such ulcers, icterus possible. OTHER LABORATORY TESTS
as bridge and side of nose, nasal planum, or • B. bronchiseptica—fever, sneezing, ocular • Culture of upper airways.
hard palate, resulting in facial distortion; discharge, nasal discharge, lymphadenopathy, • Lymph node cytology.
infection can spread through cribriform plate, coughing, dyspnea, cyanosis. • Nasal biopsies.
resulting in meningoencephalitis, cryptococcal • Cryptococcus—sneezing, nasal discharge, IMAGING
optic neuritis, secondary retinitis. ocular discharge, gagging, dysphagia, stertor, • Skull radiographs generally not helpful.
SYSTEMS AFFECTED upper airway obstruction, facial deformity, • Thoracic radiography—generally normal,
• Respiratory—nasal and upper airway, lymphadenopathy, neurologic abnormalities, may see pulmonary involvement if fungal
including sinuses, lower airway. optic neuritis, chorioretinitis. disease or pneumonia.
(continued) Feline (Upper) Respiratory Infections

• CT of head—may show mass, turbinate ◦ First choices—doxycycline 10 mg/kg PO EXPECTED COURSE AND PROGNOSIS
lysis, increased soft tissue within nasal q24h, usually effective for B. bronchiseptica, • Good to excellent; underlying immuno
passages, lymphadenopathy. C. felis, Mycoplasma spp.; amoxicillin suppression may increase susceptibility to
DIAGNOSTIC PROCEDURES 22 mg/kg, PO, q12h. infection, worsen prognosis.
◦ Other options—amoxicillin–clavulanate • FHV—generally, mortality low and prognosis
• Conjunctival scraping may identify FHV.
• Rhinoscopy—in cats with Cryptococcus.
15–20 mg/kg PO q12h, azithromycin good, except for young kittens and aged cats.
• Upper airway exam.
5–15 mg/kg PO q24h, marbofloxacin • FCV–VSD—poor, mortality >50%. F
• Bronchoalveolar lavage if pneumonia
2.5–5 mg/kg PO q24h, pradofloxacin
suspected. 5–10 mg/kg PO q24h.
• Antifungals—fluconazole 50 mg/cat PO
• FIV antibody, FeLV antigen testing.
q12–24h, itraconazole 10 mg/kg PO q24h;
PATHOLOGIC FINDINGS compounded formulations not recommended.
MISCELLANEOUS
Histopathology—lymphoplasmacytic stomatitis: • Antivirals—famciclovir 62.5 mg/cat PO AGE-RELATED FACTORS
FCV; vasculitis: FCV–VSD; bacterial rhinitis, q12h, cidofovir topical 0.5% 1 drop OU Young animals more susceptible.
suppurative inflammation; Cryptococcus q12h. ZOONOTIC POTENTIAL
organisms on nasal or lymph node biopsy.
CONTRAINDICATIONS • B. bronchiseptica rare cause of zoonotic
Use azole drugs with caution in patients with infections.
liver disease. • Human conjunctivitis caused by feline
chlamydia has been reported.
PRECAUTIONS
TREATMENT Doxycycline can cause esophagitis and PREGNANCY/FERTILITY/BREEDING
APPROPRIATE HEALTH CARE esophageal strictures—follow with food and/ Animals who are actively ill should not be
• Most cats managed as outpatient; isolate if or water. bred. FHV can cause abortions.
hospitalized, as many organisms highly SEE ALSO
contagious and airborne. • Chlamydiosis—Cats.
Azole antifungals have many drug
• Moderate to severely affected cats may
interactions. • Cryptococcosis.
require IV fluids for hydration. • Feline Calicivirus Infection.
• May require supplemental oxygen.
• Feline Herpesvirus Infection.
ACTIVITY • Mycoplasmosis.
N/A • Rhinitis and Sinusitis.
FOLLOW-UP
DIET ABBREVIATIONS
• Enteral feeding recommended if anorexia PATIENT MONITORING • FCV = feline calicivirus.
persists >48 hours. • Viral—most cases improve within 1 week;
• Nasogastric feeding may not be appropriate
could take up to 6 weeks to resolve. • FHV = feline herpesvirus-1.
if there is severe nasal discharge. • Persistent clinical signs after appropriate
• Cats with severe oral ulceration may need
treatment suggest alternative cause. • MODS = multiple organ dysfunction
enteric feeding while ulcers heal. PREVENTION/AVOIDANCE syndrome.
• Vaccination. • SIRS = systemic inflammatory response
CLIENT EDUCATION
• FCV, FHV—core vaccines; modified live syndrome.
Most agents are contagious.
and inactivated virus vaccines give reasonable • VSD = virulent systemic disease.
SURGICAL CONSIDERATIONS protection, mild clinical signs may be seen; • URI = upper respiratory infection.
Corneal ulcers can be deep, may require vaccines do not prevent infection or viral
surgical intervention. INTERNET RESOURCES
latency, although shedding post challenge https://catvets.com/guidelines/practice-
may be reduced. guidelines/feline-vaccination-guidelines
• Vaccination against C. felis and B.
bronchiseptica is noncore. Suggested Reading
• Do not allow non-immunocompetent Green CE. Infectious Diseases of the Dog and
MEDICATIONS Cat, 4th ed. St. Louis, MO: Elsevier
patients to contact other animals until
DRUG(S) OF CHOICE determined to be low risk. Saunders, 2012.
• Many cases will self-resolve. • Bleach diluted 1 : 30 with water mixed with Lappin MR, Blondeau J, Boothe D, et al.
• Antibiotics not recommended for cats with detergent is effective at eliminating most Antimicrobial use guidelines for treatment
only serous discharge; observation without respiratory pathogens from environment. of respiratory tract disease in dogs and cats.
antibiotics recommended for up to 10 days for J Vet Intern Med 2017, 31:279–294.
acute-onset mucopurulent/purulent discharge POSSIBLE COMPLICATIONS Little SE. The Cat: Clinical Medicine and
without systemic signs (fever, lethargy, • Pneumonia.
Management. St. Louis, MO: Elsevier
anorexia) or specific etiology identified by • Septicemia (rare).
Saunders, 2012.
exam or history; susceptibility profiles of Author Genna Atiee
organism may be helpful for chronic cases. Consulting Editor Amie Koenig
Fever
• Tachypnea. pyelonephritis, sepsis secondary to
• Hyperemic mucous membranes. immunodeficiency, leptospirosis, leishmaniasis,
• Dehydration. toxoplasmosis, Lyme disease, infection with
BASICS • Shock. Ehrlichia, Anaplasma, Bartonella, others.
DEFINITION • Immune-mediated disease (27%)—
CAUSES
Higher than normal body temperature polyarthritis, meningitis, vasculitis, others.
Infectious Agents
F because of changed thermoregulatory set
• Viruses—feline leukemia virus (FeLV),
• Bone marrow disease, including neoplasia
point in hypothalamus; normal body (16%).
temperature in dogs and cats 100.2–102.8 °F feline immunodeficiency virus (FIV), parvo, • Neoplasia (7%).
(37.8–39.3 °C). Fever of unknown origin distemper, herpes, calici. • Miscellaneous (10%)—hypertrophic
(FUO)—at least 103.5 °F (39.7 °C) on at • Bacteria—endotoxins, Mycoplasma, osteodystrophy, lymphadenitis, panosteitis,
least four occasions over 14-day period and Bartonella, Leptospira, Borrelia burgdorferi, portosystemic shunting, shar-pei fever.
illness of 14 days’ duration without obvious others. • Undiagnosed (12%).
cause. • Systemic fungi—Histoplasma, Blastomyces,
Coccidioidomyces, Cryptococcus. FUO—Cats
PATHOPHYSIOLOGY • Most virally mediated (e.g., FeLV, FIV,
• Vector borne—Rickettsia, Borrellia,
Exogenous or endogenous pyrogens reset Ehrlichia, Anaplasma, Neorickettsia. feline infectious peritonitis [FIP], less
thermoregulatory center to higher tempera- • Parasites and protozoa—Babesia,
commonly parvo, herpes, calici).
ture, activating physiologic responses to raise Toxoplasma, aberrant larva migrans, • Occult bacterial infection with atypical
body temperature. Physiologic consequences Dirofilaria thromboemboli, Leishmania, bacteria, sometimes secondary to bite wounds
include increased metabolic demands, muscle Cytauxzoon, Hepatozoon, Neospora. (e.g., Yersinia, Mycobacteria, Nocardia,
catabolism, bone marrow suppression, Actinomyces, Brucella).
heightened fluid and caloric requirements, Immune-Mediated Processes • Pyothorax.
and possibly disseminated intravascular Systemic lupus erythematosus, immune- • Additional causes—pyelonephritis, blunt
coagulation (DIC) and shock. mediated hemolytic anemia, immune- trauma, penetrating intestinal lesion, dental
mediated thrombocytopenia, pemphigus, abscess, systemic fungal disease, lymphoma,
SYSTEMS AFFECTED polyarthritis, polymyositis, rheumatoid solid tumors.
• Cardiovascular—tachycardia. arthritis, vasculitis, hypersensitivity reaction, • Immune disorders, endometritis,
• Hemic/lymphatic/immune—bone marrow transfusion reaction, infection secondary to discospondylitis, pneumonia, endocarditis
depression, DIC. inherited or acquired immune defects. rare.
• Nervous—cerebral edema, depression.
Endocrine and Metabolic RISK FACTORS
SIGNALMENT Hyperthyroidism, hypoadrenocorticism • Recent travel.
Species (rare), pheochromocytoma, hyperlipidemia, • Exposure to biologic agents.
Dog and cat. hypernatremia. • Immunosuppression.
Breed Predilections Neoplasia • Very young or old animals.
Some breed-associated conditions may result Lymphoma, myeloproliferative disease,
in FUO (e.g., shar-pei fever). plasma cell neoplasm, mast cell tumor,
malignant histiocytosis, metastatic disease,
SIGNS
necrotic tumor, and solid tumor, particularly DIAGNOSIS
General Comments in liver, kidney, bone, lung, lymph nodes.
• Fever lowers bacterial division and increases DIFFERENTIAL DIAGNOSIS
Other Inflammatory Conditions Differentiate fever from hyperthermia.
immune competence.
Cholangiohepatitis, hepatic lipidosis, toxic Temperatures up to 103 °F (39.4 °C) may be
• Prolonged fever >105 °F (>40.5 °C) leads
hepatopathy, cirrhosis, inflammatory bowel caused by stress or illness. Temperatures
to dehydration and anorexia.
disease, pancreatitis, peritonitis, pleuritis, >104 °F (>40 °C) almost always important.
• Fevers >106 °F (>41.1 °C) may lead to
granulomatous diseases, portosystemic Temperatures >107 °F (>41.7 °C) usually not
cerebral edema, bone marrow depression,
shunting, thrombophlebitis, infarctions, fever, more likely to be primary hyperthermia.
arrhythmia, electrolyte disorders, multiorgan
pansteatitis, panosteitis panniculitis,
damage, DIC. CBC/BIOCHEMISTRY/URINALYSIS
hypertrophic osteodystrophy, blunt trauma,
Historical Findings cyclic neutropenia, intracranial lesions, • CBC and blood smear—leukopenia or
• Clinical history (e.g., contact with pulmonary thromboembolism. leukocytosis, left shift, monocytosis,
infectious agents, lifestyle, travel, recent lymphocytosis, thrombocytopenia or
Drugs and Toxins thrombocytosis, spherocytes, organisms.
vaccination, drug administration, insect bites,
Tetracycline, sulfonamide, penicillins, • Biochemistry profile and urinalysis vary
previous illness, allergies) and physical
nitrofurantoin, amphotericin B, barbiturates, with organ system involved.
examination (including retinal examination)
iodine, atropine, cimetidine, salicylates,
may help identify underlying disease OTHER LABORATORY TESTS
antihistamines, procainamide, heavy metals.
condition. • If infectious disease suspected, attempt to
• Fever patterns (e.g., sustained, intermittent) FUO—Dogs culture an organism—urine culture, blood
rarely helpful. • Infection (28%)—discospondylitis, fungal cultures (i.e., three anaerobic/aerobic cultures,
infections, endocarditis, abscesses, bacteremia, taken 20 min apart; try to use as much
septic arthritis, septic meningitis, pyothorax, volume as possible to increase diagnostic yield;
• Hyperthermia.
pulmonary foreign body/abscess, stump use special blood culture bottles), fungal and
• Lethargy.
pyometra, pneumonia, osteomyelitis, cerebrospinal fluid cultures, synovial and
• Inappetence.
peritonitis, prostatitis, pancreatitis, prostatic fluid, biopsy specimens.
• Tachycardia.
(continued) Fever
• FeLV and FIV test, Snap 4DX test, NURSING CARE Glucocorticoids
serologic tests or PCR for Toxoplasma, • Fluid administration (IV) often lowers body • Do not use unless infectious causes have
Borrelia, Mycoplasma, Bartonella, Anaplasma, temperature. been ruled out.
Ehrlichia, Rickettsia, FIP, systemic mycoses. • Topical cooling if fever is severe (convection • May mask clinical signs, may lead to
• Fecal examination. cooling with fans, evaporative cooling with immunosuppression, and not recommended
• Tracheal wash or bronchoalveolar lavage. alcohol on foot pads, axilla, and groin). for use as antipyretics; administration of
• If immune disorders suspected—cytologic • Only use antipyretic treatment when fever corticosteroids to cats with intractable FUO
after ruling out infectious diseases may
F
examination of synovial fluid; Coombs’ test, is prolonged and life-threatening (>106 °F,
rheumatoid factor, antinuclear antibodies. >41.1 °C) and topical cooling is unsuccessful. promote favorable response.
• Pancreatic lipase immunoreactivity. Impaired patients (e.g., with heart failure, • Primarily indicated for fever associated with
• T4 in cats. seizures, or respiratory disease) require immune-mediated disease and certain steroid-
IMAGING antipyretic treatment earlier. Antipyretic responsive tumors (e.g., lymphoma).
treatment may preclude elucidation of cause, PRECAUTIONS
Radiography delay correct treatment, and complicate
• Abdominal radiographs—tumors and
Side effects of antipyretics include emesis,
patient monitoring (e.g., reduction of fever is diarrhea, gastrointestinal ulceration, renal
effusion. important indication of response to
• Thoracic radiographs—pneumonia,
damage, hemolysis, hepatotoxicity.
treatment).
neoplasia, pyothorax. POSSIBLE INTERACTIONS
• Survey skeletal radiographs—bone tumors, DIET Combination of nonsteroidal anti-
multiple myeloma, osteomyelitis, discospondylitis, Febrile patients in hypercatabolic state require inflammatory drugs and steroids raises risk of
panosteitis, hypertrophic osteopathy, high caloric intake. gastrointestinal hemorrhage.
hypertrophic osteodystrophy. CLIENT EDUCATION
• Dental/skull radiographs—tooth root abscess, Work-up of patients with FUO often
sinus infections, foreign bodies, neoplasia. extensive, expensive, and invasive, and may
• Contrast radiography (e.g., gastrointestinal not result in definitive diagnosis.
and excretory urography).
FOLLOW-UP
PATIENT MONITORING
Ultrasonography Surgery may be necessary in some animals
• Body temperature at least q12h.
• Abdominal (plus directed aspirate or (e.g., pyometra, peritonitis, pyothorax, liver
• If cause of fever not found, repeat history
biopsy)—abdominal neoplasia, abscess or abscess, neoplasms).
and physical exam along with screening
other site of infection (e.g., pyelonephritis,
laboratory tests.
pancreatitis, pyometra).
• If fever develops or worsens during
• Echocardiography if endocarditis suspected.
hospitalization, consider nosocomial infection
Nuclear Imaging MEDICATIONS or superinfection.
• Radionuclide scanning procedures to
DRUG(S) OF CHOICE EXPECTED COURSE AND PROGNOSIS
evaluate for bone tumors, osteomyelitis,
Do not use broad-spectrum (i.e., “shotgun”) Vary with cause; in some patients (more
pulmonary embolism.
treatment in place of thorough diagnostic commonly cats), underlying cause cannot be
• CT, MRI, or positron emission tomography
workup unless patient’s status is critical and determined.
scan if indicated.
deteriorating rapidly.
Antibiotics
• Arthrocentesis (culture and cytology).
• Based on results of bacterial culture or
• Bone marrow aspirate and biopsy if
malignancy or myelodysplasia suspected.
serology. MISCELLANEOUS
• In emergency situations, combination
• Lymph node, skin, or muscle biopsy if ASSOCIATED CONDITIONS
antibiotic therapy can be started after culture
clinically indicated. • Young animals—infectious disease more
specimens obtained (e.g., cephalothin 20 mg/
• Fine-needle aspirate or biopsy of any mass common; prognosis better.
kg IV q6–8h; combined with enrofloxacin
or abnormal organ. • Old animals—neoplasia and intra-abdominal
10 mg/kg IV q24h). Additional antimicrobials
• Central spinal fluid tap if neurologic signs. infection more common; signs tend to be more
depend on main clinical suspicion based on
• Endoscopy and biopsy if gastrointestinal nonspecific; prognosis often guarded.
preliminary laboratory and clinical evidence.
signs. SYNONYMS
• Do not give antibiotics longer than 1–2
• Exploratory laparotomy—last resort if all Pyrexia
weeks if ineffective.
other diagnostic tests fail to determine cause
and patient not improving. Antipyretics SEE ALSO
• Aspirin—dogs: 10 mg/kg PO q12h; cats: Heat Stroke and Hyperthermia.
6 mg/kg PO q48h. ABBREVIATIONS
• Deracoxib—dogs: 1–2 mg/kg/day. • DIC = disseminated intravascular coagulation.
• Carprofen—dogs: 2 mg/kg q12h. • FeLV = feline leukemia virus.
TREATMENT • Meloxicam—0.1 mg/kg/day. • FIP = feline infectious peritonitis.
APPROPRIATE HEALTH CARE • Dipyrone—dogs: 25 mg/kg IV. • FIV = feline immunodeficiency virus.
Goals of treatment—reset thermoregulatory • Flunixin meglumine—dogs: 0.25 mg/kg • FUO = fever of unknown origin.
set point to lower level; remove underlying SC once (give IV fluids). Authors Maria Vianna and Jörg Bucheler
cause. Consulting Editor Michael Aherne
Fiber-Responsive Large Bowel Diarrhea

CAUSES & RISK FACTORS 2–4 weeks and then the original diet can be
• Unknown; stress or abnormal personality slowly introduced. Some dogs develop
traits may play a role in some. diarrhea again, others can be maintained on
BASICS • Clinical response to dietary soluble fiber their original diet.
OVERVIEW supplementation suggests abnormal colonic • Hypoallergenic diet trial for 2–3 weeks; no
• A form of chronic idiopathic large bowel motility and/or dysbiosis. Dysbiosis is defined improvement in stool quality. During the
F diarrhea that occurs in dogs and usually as a microbial imbalance within the gastro food trial the dog must not receive any other
responds favorably to dietary soluble fiber intestinal tract. Soluble dietary fiber is a nutrients, including flavored heartworm
supplementation. prebiotic, fermented by colonic bacteria preventatives, vitamins, or any other
• At the author’s institution, chronic resulting in altered composition or activity of supplements. For this diet trial the author
idiopathic large bowel diarrhea is diagnosed bacteria. Prebiotics are not digested by recommends using a hydrolyzed diet. The
in approximately 25% of dogs referred for mammalian digestive enzymes and “feed” hydrolyzed protein in these diets is hypo
evaluation of chronic large bowel diarrhea. colonic bacteria, potentially correcting allergenic. If the dog’s stool becomes normal
• Exclusion diagnosis that requires dysbiosis. Soluble fibers also adsorb water, during this diet trial a diagnosis of dietary
eliminating known causes of chronic large improving stool quality. Fermentation of hypersensitivity or inflammatory bowel
bowel diarrhea and clinical response to soluble fiber by colonic bacteria produces disease can be made. These hydrolyzed diets
dietary fiber supplementation. volatile fatty acids, which are energy source are also highly digestible, low in fiber, and
• No pathophysiologic studies have been for colonic epithelial cells. restricted in fat. Some clinicians skip the
performed. highly digestible diet trial and go directly to
• Only 3 reports in dogs comprising 83 cases. the hydrolyzed diet trial. Without performing
• May overlap with a stress-associated poorly a highly digestible diet trial first, response to
defined syndrome that has been called irritable the hydrolyzed diet trial could also be due to
DIAGNOSIS digestibility, fat, and fiber content and not
bowel syndrome, also referred to as nervous
colitis, spastic colon, or mucus colitis. Some DIFFERENTIAL DIAGNOSIS due to dietary hypersensitivity. Many dogs
dogs with irritable bowel syndrome respond to • Dietary indiscretion. that respond to a hypoallergenic food trial can
dietary fiber supplementation, while others • Highly digestible diet-responsive diarrhea. be slowly switched back to their original diet
require stress alleviation, antispasmodic • Hypoallergenic diet-responsive diarrhea. after 12–14 weeks.
medications, and/or anti-anxiety drugs. • Whipworms. • Colonoscopy; usually within normal
• Clostridium perfringens–associated diarrhea. limits or only mild nonspecific findings
SIGNALMENT • Lymphocytic plasmacytic colitis. such as slight increases in mucosal
• Dogs of all ages (0.5–14 years); median 6 • Eosinophilic colitis. granularity or friability.
years. • Miscellaneous types of colitis.
• Many breeds, including mixed breeds; PATHOLOGIC FINDINGS
• Irritable bowel syndrome.
common breeds include German shepherd • Histopathologic evaluation of colonic
• Colonic neoplasia (adenocarcinoma,
dog, miniature schnauzer, cocker spaniel, and biopsy samples; within normal limits.
lymphoma, and adenoma are most common).
miniature or toy poodle. • Multiple biopsy samples should be
• Cecal inversion.
evaluated from throughout the colon from
SIGNS CBC/BIOCHEMISTRY/URINALYSIS the cecum to the rectum. Usually at least 5–6
• Chronic diarrhea (soft to liquid) with classic No consistent or specific abnormalities, locations are sampled.
large bowel characteristics; tenesmus, excess although can recognize peripheral eosinophilia
fecal mucus, hematochezia, increased frequency occasionally in dogs with colonic whipworms,
(median 3.5 times/day), and urgency. eosinophilic colitis, and food allergy.
• Diarrhea usually episodic alternating
with periods of normal stool; diarrhea may OTHER LABORATORY TESTS TREATMENT
be continuous in approximately 25% of Multiple fecal flotations by zinc sulfate; • Health care can be provided on an
dogs. negative for whipworms and other parasites. outpatient basis and consists of dietary fiber
• Less common signs include occasional IMAGING supplementation.
vomiting, decreased appetite during episodes • Abdominal radiographs within normal • Activity level does not have to be modified.
of diarrhea, abdominal pain, and anal limits. • A highly digestible “GI” diet should
pruritus. • Abdominal ultrasound within normal initially be supplemented with 1–3 tbsp daily
• Weight loss rare. limits. of psyllium hydrophobic mucilloid
• Stress factors or abnormal personality (Metamucil 10.2 g psyllium/tbsp).
traits in approximately 35% of dogs; DIAGNOSTIC PROCEDURES • Psyllium is a soluble fiber that adsorbs
• Clostridium perfringens enterotoxin fecal water, improving fecal consistency, and acts as
household visitation, travel, moving,
construction, instillation of an invisible ELISA; negative. a prebiotic promoting bacterial fermentation
• Therapeutic deworming for whipworms and production of volatile fatty acids, which
fence; recent adoption or considered
nervous, high-strung, sensitive, or (fenbendazole 50 mg/kg PO q24h for 5 are an energy source for colonic epithelial
aggressive; or possess noise phobia, anxiety, days); no improvement. cells. Psyllium comes from the seeds or husks
• Highly digestible diet trial for 2–3 weeks; of the plant ispaghul and consists of
or depressive disorders.
• Physical examination reveals no significant
no improvement in stool quality. During the approximately 90% soluble fiber. Psyllium
findings related to gastrointestinal tract. food trial the dog must not receive any other has been shown to be an effective treatment
• Digital rectal examination is usually
nutrients. These diets are highly digestible, in some children with chronic nonspecific
normal. Feces may be normal due to episodic low in fiber, and restricted in fat. If the dog’s diarrhea and in other people with several
nature of the disease. Loose stool may be stool becomes normal during this diet trial, diarrheal disorders.
present and it may contain hematochezia (red no further diagnostic tests are indicated. The • Median dose is 2 tbsp/day, or 0.13 tbsp/kg/
blood) or excess mucus. highly digestible diet can be fed for another day, or 1.3 g psyllium/kg/day.
(continued) Fiber-Responsive Large Bowel Diarrhea

• Initial response to lower amounts of fiber • Prognosis is very favorable, as approximately
supplementation or use of other types of fiber 85% of dogs have excellent or very good
is not as successful. long-term response to fiber supplementation.
• After 2–3 months without diarrhea, the MEDICATIONS
amount of fiber can be slowly reduced None indicated.
successfully in approximately 50% of dogs. CONTRAINDICATIONS/POSSIBLE
• After resolution of diarrhea with psyllium INTERACTIONS MISCELLANEOUS F
supplementation, owners may attempt to No known interactions of fiber supplementa- • There are no known associated conditions.
switch to a commercial high-fiber tion with commonly used drugs. • Age does not play a role in diagnosis or
(insoluble fiber) diet that may be more
treatment.
convenient to feed; however diarrhea may
• There is no known zoonotic potential.
return in 50% of dogs. Insoluble dietary
• There are no special considerations
fiber helps to distend the colonic lumen;
FOLLOW-UP regarding pregnancy, fertility, or breeding.
distention is necessary for normal fecal
storage and colonic motility. • Patient monitoring requires periodic Suggested Reading
• After resolution of diarrhea with psyllium assessment of stool quality, performed during Lecoindre P, Gaschen FP. Chronic idiopathic
supplementation, owners may be able to recheck office examinations or via telephone large bowel diarrhea in the dog. Vet Clin
switch from the highly digestible “GI” diet to interviews. North Am 2011, 41:447–456.
a high-quality maintenance dog food. • If stresses were initially identified, stress Leib M. Treatment of chronic idiopathic large
• Lack of initial response to fiber supple reduction should be attempted. bowel diarrhea in dogs with a highly
mentation suggests that chronic idiopathic • If abnormal personality traits were initially digestible diet and soluble fiber: a
large bowel diarrhea may be due to irritable identified, they should be modified. retrospective review of 37 cases. J Vet Int
bowel syndrome, and pharmacologic • Dietary soluble fiber supplementation can Med 2000, 14:27–32.
management of that disorder should be occasionally produce excessive flatulence, which Author Michael S. Leib
instituted. can be managed by reduction in fiber dosage. Consulting Editor Mark P. Rondeau
Fibrocartilaginous Embolic Myelopathy

• Severity of deficits—related to severity of swelling at embolic site; later, often normal or
infarction. Most display nonambulatory shows area of cord atrophy.
paresis, or plegia with intact nociception; • MRI—preferred imaging modality for
BASICS fewer patients display ambulatory paresis, or antemortem diagnosis: may see increased
DEFINITION plegia with absent nociception. T2 signal intensity within spinal cord at site
Acute ischemic necrosis of the spinal cord • Spinal pain—may be present briefly at of lesion; may see mild contrast enhancement.
F caused when fibrocartilaginous emboli onset of signs (owner report) and generally DIAGNOSTIC PROCEDURES
become lodged in the spinal vasculature. resolves by the time patient is examined.
CSF Analysis
PATHOPHYSIOLOGY CAUSES • Normal or nonspecific changes (mild
• Emboli—found in spinal cord vasculature; Unknown pleocytosis/elevated protein concentration).
histologically and histochemically identical to RISK FACTORS Profound elevations in cell count can
nucleus pulposus of the intervertebral disc. • Trauma/physical activity may precede the occasionally be observed with severe necrosis.
• Exact mechanism of entry into the spinal incident. • Results depend on location (lumbar vs.
vasculature unknown. • Hyperlipoproteinemia may be a cerebellomedullary cistern) and time of
SYSTEMS AFFECTED comorbidity in miniature schnauzers and collection in relation to onset of clinical signs.
Nervous Shetland sheepdogs. PATHOLOGIC FINDINGS
GENETICS • Gross—focal spinal cord swelling ±
N/A hemorrhage.
• Microscopic—emboli of fibrocartilage in
• Common cause of spinal cord disease in
DIAGNOSIS arteries and/or veins of spinal cord within
or near area of focal spinal cord swelling;
nonchondrodystrophic breeds of dogs. DIFFERENTIAL DIAGNOSIS
gray matter generally more affected than
• Rarely reported in chondrodystrophic breeds. • Acute noncompressive nucleus pulposus
white matter.
• Uncommon in cats. extrusion (ANNPE)—most important
• Histologic examination required for
SIGNALMENT clinical difference may be persistent spinal
definitive diagnosis. Presumptive
pain beyond 24 hours; differentiate with
Species antemortem diagnosis is based on typical
cross-sectional imaging; may be
Dog and cat. presentation and exclusion of other causes
indistinguishable but treated the same.
of acute myelopathy.
Breed Predilections • Thrombi/emboli from other sources can
• Giant- and large-breed dogs most common, cause similar ischemic injury to the spinal
but seen in small breeds as well. cord—consider underlying predisposing
• Miniature schnauzers overrepresented. conditions (cardiomyopathy, hypothyroidism,
hyperthyroidism, hyperadrenocorticism, TREATMENT
Mean Age and Range chronic kidney disease, hypertension,
• Median age 5 years. APPROPRIATE HEALTH CARE
hyperlipidemia; especially in cats). Inpatient—for immediate medical treatment
• Range: 8 weeks–14.5 years. • Intervertebral disc disease; discospondylitis; and diagnostic procedures.
Predominant Sex neoplasia; fracture and luxation—typically
Males overrepresented. painful with symmetric deficits; survey NURSING CARE
radiography, MRI, CT, and/or myelography • Keep recumbent patients on padded surface;
SIGNS turn frequently to prevent pressure sores.
help confirm the diagnosis.
Historical Findings • Intra- and extramedullary hemorrhage • Assist and encourage patients to ambulate
• May be associated with trauma or physical secondary to coagulopathy (e.g., anticoagulant as soon as possible.
activity at or immediately before onset of signs. rodenticide ingestion, thrombocytopenia, or • Assist bladder emptying (catheterize or
• Sudden onset, generally nonprogressive and disseminated intravascular coagulation)—rule express) several times daily if needed.
nonpainful. out by examining for underlying causes of • Physical rehabilitation therapy may improve
• Discomfort occasionally noted at onset but hemorrhage, performing platelet count, and recovery and reduce residual neurologic
resolves rapidly (minutes to hours). determining blood clotting times. deficits.
• Signs of paresis or paralysis develop over a • Infectious/immune-mediated focal • Sling or harness support for assisted
matter of seconds, minutes, or hours. myelitis—differentiate on progressive history walking at home.
• Condition typically stabilizes within 24 hours. and cerebrospinal fluid (CSF) analysis. ACTIVITY
Physical Examination Findings • Acute, nonprogressive, asymmetric, and • Restrict until diagnosis is made in case of
N/A nonpainful spinal cord disease—presence of vertebral column instability from other causes
these characteristics greatly helps in diagnosis such as intervertebral disc herniation or
Neurologic Examination Findings of fibrocartilaginous embolic myelopathy
• Localization—any spinal cord segment can
fracture/luxation.
(FCE). • Once FCE is confirmed, activity should be
be affected; T3–L3 and L4–S3 most
common; multifocal lesions may rarely be CBC/BIOCHEMISTRY/URINALYSIS encouraged, not restricted.
seen; may see spinal shock with T3–L3 Usually normal. DIET
lesions, which can give the appearance of a IMAGING Normal unless other general health comor-
multifocal spinal cord lesion. • Survey spinal radiograph—usually normal, bidities are present.
• Deficits—commonly lateralized (due to used to rule out other causes of myelopathy CLIENT EDUCATION
spinal vascular anatomy) but can be such as fracture, neoplasia, or discospondylitis. • Gradual recovery from paresis or paralysis;
symmetric; contralateral side may be mildly • Myelography and CT myelography—in acute most will recover ambulation, but residual
affected or normal. stage often demonstrates focal intramedullary neurologic deficits are common. Patients who
(continued) Fibrocartilaginous Embolic Myelopathy

are paraplegic with absent nociception have a POSSIBLE COMPLICATIONS Suggested Reading
more guarded prognosis for return of function. • Fecal and urinary incontinence. Bartholomew KA, Stover KE, Olby NJ,
• Most patients need considerable home care • Urinary tract infection. Moore SA. Clinical characteristics of canine
during recovery, including bladder management. • Urine scalding and pressure sores. fibrocartilaginous embolic myelopathy
SURGICAL CONSIDERATIONS EXPECTED COURSE AND PROGNOSIS (FCE): a systematic review of 393 cases
N/A • Generally good prognosis for recovery of (1973–2013). Vet Rec 2016, 179:650.
ambulation. De Risio L, Adams V, Dennis R, et al. F
• Most patients (85%) recover ambulation Magnetic resonance imaging findings and
within 3 weeks (range: 3 days–12 weeks). clinical associations in 52 dogs with
• Most patients retain some permanent suspected ischemic myelopathy. J Vet Int
MEDICATIONS neurologic deficits despite recovering Med 2007, 21:1290–1298.
DRUG(S) OF CHOICE ambulation. De Risio L, Platt SR. Fibrocartilaginous
No specific medications are indicated for the • Paraplegia with loss of pain perception at embolic myelopathy in small animals. Vet
treatment of FCE. Use of steroids such as presentation implies more guarded prognosis. Clin North Am Small Anim Pract 2010,
methylprednisolone sodium succinate is 233:129–135.
controversial and unlikely to be of benefit. Gandini G, Cizinauska S, Lang J, et al.
Fibrocartilaginous embolism in 75 dogs:
CONTRAINDICATIONS clinical findings and factors influencing the
Nonsteroidal analgesics should not be MISCELLANEOUS recovery rate. J Small Anim Pract 2003,
administered with methylprednisolone 44:76–80.
sodium succinate. ASSOCIATED CONDITIONS
Disorders that lead to compromise in Hawthorne JC, Wallace LJ, Fenner WR, et al.
PRECAUTIONS circulatory function may predispose or mimic Fibrocartilaginous embolic myelopathy in
N/A FCE—hyperadrenocorticism; hypothyroid- miniature schnauzers. J Am Anim Hosp
ism; high systemic blood pressure; hypervis- Assoc 2001, 37:374–383.
cosity syndrome; hyperlipidemia; bleeding Mikszewski JS, Van Winkle TJ, Troxel MT.
diathesis; bacterial endocarditis. Fibrocartilaginous embolic myelopathy in
five cats. J Am Anim Hosp Assoc 2006,
FOLLOW-UP AGE-RELATED FACTORS 42:226–233.
PATIENT MONITORING N/A Summers BA, Cummings JF, de Lahunta A.
• Sequential neurologic evaluations—during ZOONOTIC POTENTIAL Veterinary Neuropathology. St Louis, MO:
first 12–24 hours after initial examination. N/A Mosby, 1995, pp. 246–249.
• Neurologic status—at 2, 3, and 4 weeks Authors Kristen Bartholomew and Sarah A.
after onset of clinical signs. Moore
High-dose corticosteroid administration—
• Urinary incontinence—manually express Acknowledgment The authors and book
may cause premature delivery.
bladder in patients who are not voluntarily editors acknowledge the prior contribution of
urinating. Urinalysis and culture/sensitivity to ABBREVIATIONS Allen Franklin Sisson
detect urinary tract infection. • ANNPE = acute noncompressive nucleus
pulposus extrusion.
• FCE = fibrocartilaginous embolic
• Recurrence highly unlikely but possible.
myelopathy.
• No known method of prevention in most
cases.
Fibrosarcoma, Bone
• Metastatic bone tumors (transitional cell, • The benefit of adjuvant chemotherapy is
prostatic, mammary, thyroid, apocrine gland unknown, but it may be considered for
anal sac carcinomas). high-grade tumors; consult a veterinary
BASICS • Tumors that locally invade adjacent bone oncologist for current recommendations.
OVERVIEW (nasal carcinoma; oral squamous cell CONTRAINDICATIONS/POSSIBLE
• Primary bone fibrosarcoma (FSA) arises carcinoma, melanoma, fibrosarcoma,
INTERACTIONS
F from stromal elements within the marrow ameloblastoma; synovial sarcoma; histiocytic
• Use NSAIDs cautiously in all cats and in
cavity and is characterized by malignant sarcoma; digital squamous cell carcinoma,
melanoma). dogs with renal insufficiency.
spindle cells that produce varying amounts of
• Do not combine NSAIDs with corticosteroids.
collagen but not any osteoid or cartilage. • Hematopoietic tumors (myeloma,
• In dogs, FSA accounts for <8% of all lymphoma).
primary bone tumors, with 60% occurring in • Bacterial or fungal osteomyelitis.
the axial skeleton and 40% arising in the CBC/BIOCHEMISTRY/URINALYSIS
appendicular skeleton. Usually normal. FOLLOW-UP
• Bone tumors are rare in cats. FSA is the PATIENT MONITORING
second most common bone tumor in cats and IMAGING
• Radiographs of the primary lesion show Physical examination and thoracic radio-
can involve the maxilla, mandible, humerus, graphs every 2–3 months.
scapula, carpus, digits, ribs, and sacrum. features of an aggressive bone lesion (bone
lysis, cortical destruction, nonhomogenous EXPECTED COURSE AND PROGNOSIS
SIGNALMENT bone formation, ill-defined zone of • There is limited information regarding
• Dog and cat; no obvious breed or gender transition). long-term prognosis.
predilections in either species. • Thoracic radiographs are recommended to • Complete excision of the primary tumor
• Mean age of dogs 9.7 years (range: 2–15 years). screen for pulmonary metastasis can potentially provide long-term control.
• Affected cats tended to be older, but have (uncommon). • Patients with high-grade primary bone FSA
been reported as young as 1.5 years old. • CT is recommended for axial tumors to may be more likely to develop metastasis.
SIGNS plan for surgery and/or radiation therapy.
Historical Findings DIAGNOSTIC PROCEDURES
Appendicular FSA • Histopathology is needed for a definitive
• Lameness, usually progressive, but occasionally diagnosis. MISCELLANEOUS
acute if there is a pathologic fracture. • Primary bone FSA has been reported to
metastasize to a variety of locations—lungs, SEE ALSO
• A palpable swelling may be present. • Chondrosarcoma, Bone.
regional lymph nodes, other bones, skin,
Axial FSA kidneys, pericardium, and myocardium. • Osteosarcoma.
• Localized swelling with or without pain is Consider additional diagnostic evaluation as ABBREVIATIONS
common; however, anatomic site dependent. indicated to rule out metastasis to these or • FSA = fibrosarcoma.
• Tumors arising from the mandible or other locations. • NSAID = nonsteroidal anti-inflammatory
maxilla can be associated with halitosis, drug.
dysphagia, pain on opening the mouth, or
nasal discharge. Suggested Reading
• Vertebral tumors may induce neurologic Albin LW, Berg J, Schelling SH. Fibrosarcoma
deficits secondary to spinal cord compression. TREATMENT of the canine appendicular skeleton.
• Rib tumors are rarely associated with • Amputation is recommended for JAAHA 1991, 27:303–309.
respiratory signs unless large and causing appendicular tumors. Author Jenna H. Burton
space-occupying effects. Rib tumors can grow • For axial tumors, wide surgical excision is Consulting Editor Timothy M. Fan
asymmetrically, with majority of growth recommended whenever possible. If surgical Acknowledgment The author and book
occurring within the intrathoracic space. excision is incomplete, adjuvant radiation editors acknowledge the prior contribution of
therapy might help improve local control. Dennis B. Bailey
Physical Examination Findings • Palliative analgesic therapy is recommended
• For appendicular FSA, lameness and a for patients with nonresectable local disease
palpable swelling may be present. or gross metastasis, or when definitive therapy
• Physical examination findings may be is declined.
variable for FSA for the axial skeleton
depending on the size and location of the
tumor; a mass may be visible or palpable.
Unknown
MEDICATIONS
DRUG(S) OF CHOICE
• Nonsteroidal anti-inflammatory drugs
(NSAIDs).
• Tramadol (2–5 mg/kg PO q6–12h).
DIAGNOSIS • Gabapentin (3–10 mg/kg PO q8–24h).
DIFFERENTIAL DIAGNOSIS • Intravenous aminobisphosphonates
• Other primary bone tumors (osteosarcoma, (pamidronate, zoledronate) might alleviate
chondrosarcoma, hemangiosarcoma, bone pain and attenuate bone resorption.
histiocytic sarcoma, etc.).
Fibrosarcoma, Gingiva
• Tooth root abscess or osteomyelitis. CONTRAINDICATIONS/POSSIBLE
• Dentigerous cyst. INTERACTIONS
• Craniomandibular osteopathy (lion’s jaw). Use NSAIDs cautiously in all cats and in dogs
BASICS with renal insufficiency.
IMAGING
OVERVIEW • Skull radiographs recommended to evaluate
• Fibrosarcoma (FSA) is a malignant tumor for bone involvement (present in 60–70%).
of spindle cells that produce varying amounts • Thoracic radiographs to screen for F
of collagenous (fibrous) extracellular matrix pulmonary metastasis (uncommon).
and associated stroma. FOLLOW-UP
• CT imaging can more accurately determine
• Oral FSA arises most commonly in the extent of local disease and useful for planning PATIENT MONITORING
gingiva; occasionally involves lips and rarely surgery and/or radiation therapy. Physical examination every 2–3 months and
tongue; invasion into bone is common. thoracic radiographs every 3–4 months.
• In dogs, FSA is third most common oral DIAGNOSTIC PROCEDURES
• Histopathology required for definitive EXPECTED COURSE AND PROGNOSIS
malignancy (20% of all oral tumors). • Most patients die

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331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

Appendix I Normal Reference Ranges for Laboratory Tests 1441

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th

331 client education handouts are available at www.fiveminutevet.com/canineandfeline7th for

Drs. Tilley, Smith, Sleeper and Brainard

Larry P. Tilley, Francis W.K. Smith, Jr.,

TABATHA J. REGEHR, DVM WESLEY J. ROACH, DVM

MICHELLE C. TENSLEY, DVM, MS

NICOLE M. WEINSTEIN, DVM EWAN D.S. WOLFF, PhD, DVM

This book is accompanied by a companion website:

The website includes:

The password for the companion website: pl58ez690xle

Appendix I Normal Reference Ranges for Laboratory Tests 1441

(continued) Abortion, Spontaneous (Early Pregnancy Loss)—Cats A

(continued) Abortion, Spontaneous (Early Pregnancy Loss)—Dogs A

(continued) Abortion, Termination of Pregnancy A

(continued) Acetaminophen (APAP) Toxicosis A

(continued) Acidosis, Metabolic A

(continued) Acute Abdomen A

(continued) Adenocarcinoma, Nasal A

(continued) Adenocarcinoma, Thyroid—Dogs A

(continued) Aggression—Between Dogs in the Household A

(continued) Aggression to Unfamiliar People and Unfamiliar Dogs—Dogs A

(continued) Aggression, Intercat Aggression A

(continued) Aggression, Overview—Cats A

(continued) Aggression, Overview—Dogs A

BASICS INCIDENCE/PREVALENCE CBC/BIOCHEMISTRY/URINALYSIS

(continued) Amphetamine and ADD/ADHD Medication Toxicosis A

(continued) Anemia of Chronic Kidney Disease A

(continued) Anemia, Immune-Mediated A

(continued) Anemia, Regenerative A