Illustrated Surgery Road Map

Illustrated Surgery
A Road Map
Illustrated Surgery
A Road Map
Nilay Mandal MS (General Surgery)

Associate Professor
Department of Surgery
Bankura Sammilani Medical College
Bankura, West Bengal, India
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Illustrated Surgery—A Road Map
First Edition: 2016
ISBN 978-93-85891-20-5
Printed at
Dedicated
to
My teachers, my parents,
spouse Tapati and daughter
Tannistha, for their love and support
Contents 7
Preface
‘Books are the compass and telescopes and sextants and charts which other men have prepared
to help us navigate the dangerous seas of human life.’
I strongly believe that in the seas of life we all need some help in any moment from others. I
also believe that in midst of seas of medical science, all medical personnels particularly the medi-
cal students need a GPS and a philosopher. That GPS can come in his or her life in the form of a
teacher or a good book or both.
In my short period of teaching, I have experienced that most of the students can remember
the diseases and their management as a whole but without understanding the disease process, it’s
pathophysiology or the principles of treatment. From my understanding, the reason is so many
subjects in a too short period.
In this book I have attempted to describe the diseases in such a illustrative manner so that
the students can understand as well as recover his or her memories from the illustrations. Better
understanding , not a better memory make a average medical student to a good doctor.
As the book is based on illustrations, most of the diseases are described in a illustrative man-
ner, less text more illustrations.
I hope that the book will be more of a guide book for travelling in seas and mountains of
medical science than a reference book. Your safe journey can only make me happy.
Wish you a happy journey.
Nilay Mandal
Contents 9
Acknowledgments
‘Writing a book is a horrible, exhausting struggle,like a long bout with some painful illness. One
would never undertake such a thing if one were not driven on by some demon whom one can
neither resist nor understand.’
I am grateful to my teachers, my students and friends whose encouragement and emotional
support make me courageous to do this task.
I am also grateful to Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director)
and Mr Tarun Duneja (Director-Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd,
New Delhi, India, for publishing this book. I would also like to thank all staff members of Kolkata
production unit of Jaypee Brothers Medical Publishers (P) Ltd for their constant support and co-
operation to complete this book.
Contents
0Chapter 1 Wound Healing 1–12

Introduction 3
Wound healing involves any of the two processes 3
Classification of wound 4
Types of wound healing 4
Three phases of wound healing 5
Role of growth factors in healing 8
Factors affecting wound healing 8
Complications of abnormal wound healing 9
Wound closure techniques 11
Treatment of wound 12
0Chapter 2 Fluid, Electrolyte and Acid-base Balance 13–27

Fluid, Electrolyte and Acid-base Balance 15
Body fluids 15
Fluid input-output 16
Disturbances in fluid balance 16
Electrolyte imbalance 18
Acidosis and alkalosis 25
Chapter 3 Hemostasis-Coagulation-Hemorrhage 28–35

Hemostasis-Coagulation 30
Evaluation to assess risk of bleeding during surgery 30
Congenital hemorrhagic disorders 31
Acquired hemorrhagic disorders 31
Hemorrhage 32
Transfusion of blood and its components 33
Chapter 4 Gallbladder and Extrahepatic Biliary System 36–119

Anatomy of the Gallbladder and Extrahepatic Biliary System 38
Things to Remember 38
Pathologies of Gallbladder and Biliary System 40
Benign pathology 40
Malignant pathology 40
Gallstone 41
Risk factors 41
Varieties 41
xii Illustrated Surgery—A Road Map
Pathogenesis of Gallstone 42
Pathogenesis of cholesterol stone 42
Pathogenesis of black pigment stones 42
Pathogenesis of brown pigment stones 43
Things to Remember 43
Spectrum of gallstone disease 44
Spectrum of symptomatic gallstone disease 44
Complicated case scenario 48
Prepare for emergency cholecystectomy 48
Be prepared for partial cholecystectomy 48
More careful during cholecystectomy 48
Acute acalculous cholecystitis 58
Biliary dyskinesia 59
Choledocholithiasis 60
Acute cholangitis 67
Choledochal cyst 69
Recurrent pyogenic cholangitis (cholangiohepatitis) 76
Primary sclerosing cholangitis 77
Gallbladder carcinoma 78
Cholangiocarcinoma 86
Anomalous Anatomy 96
Anomalous gallbladder anatomy 96
Variations of cystic duct insertion with common hepatic duct 97
Variations in arterial supply of gallbladder 97
Endoscopic Therapeutic Approaches to Biliary System 98
Percutaneous transhepatic approach 98
Removal of retained cbd stone through T-tube tract 99
Removal of cbd stones by endoscopic sphincterotomy 99
Surgical Approaches to Gallbladder and Biliary System 101
Cholecystectomy 101
Open cholecystectomy 105
Why bile duct injury? 107
Bile duct injury recognized at operation 108
Injuries recognized in immediate postoperative period 110
Injuries presenting at an interval after initial operation 111
Laparoscopic management of cbd stones 112
Management of cbd stone (open approach) 115
Choledochoduodenostomy 117
Roux-en-y hepaticojejunostomy 118
Contents xiii
Chapter 5 Liver 120–172
Diseases of the Liver 122
Couinaud system of segmental nomenclature 122
Segmental anatomy of the liver by ct scan 123
Benign pathology 124
Malignant pathology 124
Pyogenic abscess of liver 125
Amebic liver abscess 131
Hydatid cyst 136
Congenital liver cyst 148
Polycystic liver disease associated with polycystic kidney disease 150
Cystadenoma 151
Solid benign neoplasm 152
Hepatocellular carcinoma 153
Liver metastases 161
Portal hypertension 162
Chapter 6 Pancreas 173–206

Diseases of the Pancreas 175
Anatomy 175
Acute pancreatitis 175
Chronic pancreatitis 187
Cystic neoplasms of pancreas 195
Pancreatic carcinoma 199
Chapter 7 Spleen 207–217

Splenic Pathologies 209
Anatomy 209
Functions of spleen 211
What is accessory spleen? 212
What is ectopic spleen (wandering spleen)? 212
What is splenosis? 212
When to do splenectomy? 213
Cyst and tumors of spleen 214
Iatrogenic splenectomy 215
Incidental splenectomy 215
Postsplenectomy blood picture 217
Chapter 8 Abdominal Wall, Peritoneum, Mesentery, Retroperitoneum 218–240

Abdominal Wall 220
Congenital defect 220
Acquired abnormalities of the abdominal wall 227
Peritoneum and Peritoneal Cavity 229
Abdominal abscess 230
xiv Illustrated Surgery—A Road Map
Malignant peritoneal mesothelioma 233

Pseudomyxoma peritonei 233
Mesentery 234
Mesenteric cyst 234
Acute mesenteric lymphadenitis 234
Mesenteric panniculitis 235
Malignancies of the mesentery 235
Omentum 235
Omental infarction 235
Omental cyst 235
Omental graft and transpositions 236
Retroperitoneum 236
Retroperitoneal abscess 236
Retroperitoneal hematoma 236
Retroperitoneal fibrosis 237
Retroperitoneal neoplasm 239
0Chapter 9 Stomach 241–291

Diseases of the Stomach 243
Anatomy 243
Peptic ulcer disease 243
Pathophysiology 246
Clinical presentations of gastric ulcer 247
Investigations 248
Treatment 251
Perforation 258
Bleeding peptic ulcer 262
Gastric outlet obstruction 263
Gastritis 266
Malignant neoplasms of stomach 267
Gastrointestinal stromal tumor (gist) 280
Gastric lymphoma 283
Other gastric lesions 284
Postvagotomy syndromes 287
Chapter 10 Intestine 292–375

Diseases of the Intestine 294
Intestinal obstruction 294
Small intestinal obstruction 294
Clinical features of intestinal obstruction 297
Diagnostic evaluation 299
Treatment 300
Principles of surgery in intestinal obstruction 301
Contents xv
Treatment 304
Intussusception 306
Crohn’s disease 309
Typhoid enteritis 320
Intestinal tuberculosis 321
Jejunal and ileal diverticula 324
Duodenal diverticula 325
Meckel’s diverticulum 326
Neoplasm of small intestine 330
Short bowel syndrome 331
Diverticular disease of colon 333
Volvulus of the colon 339
Ileosigmoid knotting 344
Large bowel obstruction 344
Ulcerative colitis 345
Colorectal polyp 353
Familial adenomatous polyposis (fap) 359
Cancer of colon 361
Chapter 11 Appendix 376–392

Acute Appendicitis 378
How it develops? 378
How appendix looks in acute appendicitis 380
Clinical presentation 380
Risk factors for perforation 381
Investigations to confirm diagnosis 381
How diagnostic laparoscopy helpful 382
Think other possibilities also 382
Special consideration in 383
What is alvarado scoring? 384
Treatment 385
Appendiceal Mass (Appendicular Lump) 390
During appendectomy if these things happen 391
Neoplasm of the Appendix 392
Carcinoid tumor (argentaffinoma) 392
Chapter 12 Rectum and Anal Canal 393–431

Prolapse of the Rectum 395
Associated with some anatomical changes 396
How will you differentiate complete rectal prolapse from mucosal prolapse? 397
Investigation 398
Treatment 398
xvi Illustrated Surgery—A Road Map
Solitary Rectal Ulcer Syndrome 399

Fissure-in-ano 400
Location of fissure 400
How fissure develops? 401
Treatment 402
Anorectal Abscess 404
Sites of anorectal abscess 404
Investigations 404
Treatment 405
Fistula-in-ano 406
Classification of fistula 406
How to examine a fistula? 408
Investigation 409
What is Goodsall’s rule? 410
Treatment 410
Hemorrhoids or Piles 413
What is hemorrhoids? 413
What is anal cushion? 413
Types 414
How to examine a patient with hemorrhoids? 415
Treatment 416
Principles of hemorrhoidectomy 419
Postoperative complications 420
Pilonidal Sinus 420
Treatment 421
Rectal Cancer 423
Spread of rectal carcinoma 423
Assessment of tumor 424
Preoperative staging 425
Treatment 425
Cancer of the Anus 429
Risk factors 429
Pathology 430
Assessment of the tumor and investigations to confirm diagnosis 430
Treatment 431
Contents xvii
Chapter 13 Breast 432–472
Diseases of the Breast 434
Inflammations and infections of breast 434
Other uncommon infections of the breast 441
Breast lump 441
Chapter 14 Thyroid 473–513

Diseases of the Thyroid Gland 475
Different thyroid pathologies 475
Thyroiditis 491
Neoplasm of thyroid 496
Surgical approaches to thyroid 509
Chapter 15 Parathyroid, Adrenal, Endocrine Pancreas and MEN 514–562

Parathyroid 516
Sites of ectopic parathyroid 516
Under microscope 517
How ca2+ level maintains? 517
Diseases of parathyroid 518
Diseases of Adrenal Gland 531
Anatomy and anatomical variations 531
Variant drainage of right adrenal vein 532
Microscopic features of adrenal gland 533
Hyperaldosteronism 534
Hypercortisolism [Cushing syndrome] 537
Adrenogenital syndrome 543
Adrenal insufficiency 544
Adrenal crisis 545
Diseases of adrenal medulla 546
Principles of adrenal surgery 552
Endocrine Pancreas 553
Pancreatic endocrine neoplasms 554
Multiple Endocrine Neoplasia (MEN) Syndromes 560
Multiple endocrine neoplasia type I 561
Multiple endocrine neoplasia type II 562
Chapter 16 Trauma 563–673

Introduction 565
Types of injury 565
Head injury 582
Assessment of severity of brain injury 595
Maxillofacial injuries 597
Neck injury 602
Thoracic trauma 612
xviii Illustrated Surgery—A Road Map
Abdominal injuries 624

Damage control surgery 670
Abdominal compartment syndrome 673
Chapter 17 Burn 674–693

Introduction 676
Different mechanisms of burn injury 676
When you refer a burn patient to a dedicated burn center? 677
Management of burn injury 677
Prognosis 680
Management 681
Systemic changes in burn 688
Electric burn 689
Chemical burn 692
Late complications of burn 692
Chapter 18 Arterial Diseases, Venous Diseases and Diseases

of Lymphatics 694–773
Diseases of the Arteries 696
Arterial occlusive diseases 696
Acute arterial occlusion of the extremity 701
Chronic occlusive disease of the extremity 709
Arterial occlusive disease of the upper extremity 712
In aortoiliac occlusive disease 716
In femoral, popliteal and tibial occlusive disease 716
Upper extremity occlusive diseases 716
Thromboangiitis obliterans 717
Chronic visceral ischemia 718
Aneurysmal vascular disease 724
Diseases of thoracic aorta 738
Vascular trauma 746
Venous Diseases 749
Different types 749
Deep vein thrombosis (dvt) 750
Venous insufficiency 754
Venous ulcer 765
Disorders of Lymphatic System 765
Acute lymphangitis 766
Lymphedema 766
Chapter 19 Hernia 774–812

Introduction 776
Different types of hernia 778
Nyhus classification of groin hernia 783
Contents xix
Anatomy of the groin 783
Inguinal hernia 785
Special types of inguinal hernia 795
Some unusual types of hernia 796
Fermoral hernia 797
Umbilical hernia 799
Epigastric hernia 801
Incisional hernia 802
Unusual hernia 808
Chapter 20 Diseases of the Testes, Scrotum and Penis 813–831

Diseases of the Testes 815
Undescended testis 815
Torsion of the testis (syn. Torsion of the spermatic cord) 822
Varicocele 823
Hydrocele 825
Hematocele 828
Pyocele 828
Chylocele 828
Other scrotal swellings 828
Other scrotal diseases 829
Phimosis 830
Paraphimosis 831
Chapter 21 Diseases of the Esophagus 832–863

Hiatus hernia 834
Gastroesophageal reflux disease (gerd) 837
Esophageal motility disorder 841
Esophageal diverticula 846
Esophageal perforation 849
Cancer of esophagus 857
Chapter 22 Diseases of the Salivary Gland 864–878

Salivary Gland Pathologies 866
Inflammatory pathologies 866
Obstructive pathology 868
Salivary gland tumors 871
Surgical procedures for salivary gland pathology 875
Chapter 23 Skin and Adnexal Lesion 879–911

Diseases of the Skin and its Adnexa 881
Cystic lesions of the skin 881
Ganglion 883
Vascular lesions of the skin 884
xx Illustrated Surgery—A Road Map
Benign tumors 890

Skin infection 895
Benign pigmented lesions 898
Premalignant lesions 900
Malignant lesions 901
Other malignancies of the skin 910
Chapter 24 Ulcer, Sinus and Fistula 912–928

Ulcer 914
Basic priniciples of ulcer dressing 926
Sinuses and Fistula 927
Sinus 927
Fistula 927
Chapter 25 Urology 929–1036

Diseases of the Kidney 931
Urinary symptoms 931
Diseases of Kidney and Uretzer 936
Congenital malformations 936
Cystic disease of kidney 943
Other malformations 946
Hydronephrosis 948
Renal stone 950
Percutaneous nephrolithotomy 959
Open surgery for renal stone 961
Infections of kidney 963
Tuberculosis of kidney 972
Kidney tumors 975
Diseases of Ureter 984
Ureteral calculi 984
Urothelial tumors of renal pelvis and ureter 985
Urinary Bladder 988
Congenital anomalies 988
Bladder calculi 990
Schistosomiasis of the urinary bladder 994
Bladder tumor 996
Diseases of Prostate 1000
Benign prostatic hyperplasia 1000
Prostate 1010
Prostatitis 1010
Carcinoma of prostate 1011
Urethra 1016
Urethral stricture 1016
Hypospadias 1019
Contents xxi
Priapism 1022
Peyronie's disease 1024
Carcinoma of penis 1025
Neoplasms of Testis 1031
Chapter 26 Minimally Invasive Surgery, Robotic Surgery 1037–1053

Minimally Invasive Surgery 1039
Different minimal access techniques 1039
Physiology of pneumoperitoneum 1041
Access 1042
Port placement 1045
Instrumentation 1045
Advantages and disadvantages 1049
Examples of laparoscopic procedures 1049
Contraindications 1050
Complications 1050
New techniques of minimally invasive surgery 1050
Robotic surgery 1051
Chapter 27 Nerve Injury 1054–1062

Introduction 1056
Classification of nerve injuries 1056
Sunderland's classification 1058
Clinical features 1058
Management of nerve injury in closed injury 1059
Management of nerve injury in open injury 1059
Principles of nerve repair 1059
Chapter 28 Surgery of Hand 1063–1071

Introduction 1065
Infections in hand 1067
Injuries in hand 1069
Chapter 29 Neck Swelling 1072–1082

Neck 1074
Anatomy of neck 1074
Neck swellings 1075
Chapter 30 Cleft Lip and Palate 1083–1089

Cleft lip 1085
Cleft palate 1088
xxii Illustrated Surgery—A Road Map
Chapter 31 Anesthesia 1090–1103

Introduction 1092
Types of anesthesia 1092
Preoperative evaluation 1101
Intraoperative management 1102
Complications of general anesthesia 1103
Chapter 32 Instrument 1104–1131

Surgical Instruments 1106
Parts of an instrument 1106
Instruments used for antiseptic dressing and draping 1106
Instruments used for fixation 1107
Instruments used for giving incision over the skin 1107
Instruments used for hemostasis 1108
Instruments used for holding tissues 1112
Instruments used for suturing 1115
Other methods of skin closure 1119
Index 1133–1140
Chapter 1
Wound Healing
Important Topics
zzProcess of Wound Healing

zzClassification of Wound
zzPhases of Wound Healing
zzGrowth Factors in Wound Healing
zzFactors Affecting Wound Healing
zzComplications of Wound Healing
zzTreatment of Wound
‘It is a most gratifying sign of the rapid progress of our time that our best textbooks become antiquated so quickly.’
Christian Albert Theodor Billroth (1829 –1894)
Austrian Surgeon
Wound Healing 3
Introduction
SS Wound healing is the normal body response to injury (surgical/traumatic) to restore the normal structure and
function.
Wound Healing Involves Any of the Two Processes

4 Illustrated Surgery—A Road Map
Classification of Wound
Types of Wound Healing

Wound Healing 5
Three Phases of Wound Healing
zz Inflammatory (reactive) phase

zz Proliferative (reparative) phase [The 3 phases often overlap]
zz Maturational (remodeling) phase
Inflammatory (Reactive) Phase

Day 1
SS Immediately after injury, blood vessels are disrupted, resulting in exposure of subendothelial collagen to platelets,
leads to platelet aggregation and activation of coagulation pathway.
SS The end product of coagulation cascade is fibrin, which plays an important role in clot formation and wound
healing. This fibrin acts as scaffold for migration of PMN and monocytes into the wound. It also serves as a reservoir
for cytokines.
SS Platetet and granulocytes release a number of substances, such as platelet derived growth factor (PDGF),
transforming growth factor-β (TGF-β), fibronectin, serotonin and histamine.
Day 1–4
SS Leukocytes begin to migrate out from the vessels to the wound. The release of histamine and serotonin causes
increased vascular permeability and various chemotactic factors facilitate migration.
SS PMNs are the first inflammatory cells to enter the wound. Increased vascular permeability and presence of
chemotactic substancs (e.g. IL-1, TNF-α, TGF-β, PDGF) facilitate migration of PMNs. In the first 24–48 hours,
neutrophils make about 50% of all cells in the wound.
These PMNs phagocytize bacteria, foreign material and devitalized tissue. They also release TNF-α2 (an important
cytokine for angiogenesis and collagen synthesis) and collagenases. Over time, neutrophils are removed by
apoptosis or macrophage phagocytosis.
SS Macrophages start to migrate in the wound after about 48 hours of injury, and present till healing proces is
completed. Macrophages also participate in phagocytosis. They synthesize oxygen radical and nitric oxide, release
cytokines and growth factors such as TGF-β, VEGF, Insulin-like growth factor (IGF), epithelial growth factor (EGF) and
thereby regulate cell proliferation, matrix synthesis, remodelling and angiogenesis.
SS T lymphocyles also migrate to the wound usually about 5–7 days after injury. They take part in wound healing by
producing stimulatory cytokines (e.g. IL–2) and inhibitory cytokines (e.g. TGF-β, TNF-a).
SS Mast cells are also recruited in this phase. Degranulation of mast cells release histamine, TNF-α , prostaglandins and
protease resulting in increased vascular permeability, cellular activation.
Proliferative (Reparative) Phase
SS It is the second phase of healing.

SS This phase involves angiogenesis, fibroplasia and epithelialization, and spans from day 4 to day 12.
SS Angiogenesis—Endothelial cell migration, its replication and new capillary tube formation result from complex
interaction of extracellular matrix material (e.g. fibronectin, hyaluronic acid) and cytokines (e.g. TGF-β, IL-8, VEGF).
The angiogenesis is regulated by TNF-α, TGF-b, VEGF, PDGF those are derived from platelets, macrophages, damaged
epithelial cells.
Metabolic environment of the wound also influences angiogenesis. Increased lactate, decrease pH and oxygen
tension result in reduction of NAD+ (inhibitor or angiogenesis).
SS Fibroplasia— The quiscent fibroblasts are chemoattracted to the injury site, where it replicates and proliferates,
being stimulated by macrophage and platelet derived cytokines (e.g. TGF-β, EGF, IGF–1). PDGF is the most potent
chemotactic and mitogenic factor for fibroblasts.
The activated fibroblasts now synthesize collagen and other components of extracellular matrix (ECM). ECM
consists of fibroblast-derived collagen monomer, proteoglycans and fibronectin. Two types of collagen are
important for wound repair, Type I and Type III. Among them, Type III collagen plays significant role. Collagen
synthesis significantly begins about 1 week postinjury. Oxygen, vitamin C, iron are cofactors for cross-linkge of
collagen fibers. Fibroblasts also produce matrix metalloproteinases (MMP) which helps to degrade matrix substances
resulting in smooth migration of fibroblasts.
SS Epithelialization—Epithelialization of wound develops due to migration of epithelial cells from the edges of
wound, mediated by EGF, TGF-β, PDGF, IGF-1.
Migration of epithelial cells occur at the rate of 1 mm/day and it begins within hours after injury. The attachments
between hemidesmosomes of the basal cells and the laminin of the basal lamina are broken down, leading to
migration of epithelial cells.
Reepithelialization is completed within 48 hours in approximated incised wound.
[If epithelium and superficial dermis is only damaged, then the repair process involves reepithelialization without
any fibroplasia (no scar formation at all).]
Wound Healing 7
Maturational (Remodeling) Phase
SS Wound contraction:
zz This process involves movement of the wound edge toward the center of the wound by the action of
myofibroblasts.
zz The process starts 4–5 days after injury and continues for 12–15 days.
zz Matrix metalloproteinases (MMPs) are important factors for wound contraction.
SS Remodeling:
zz The process begins about 21 days after injury.
zz Collagen synthesis is downregulated, collagen (type III) is broken down by MMPs and replaced by denser
collagen (collagen I) that is organized along the lines of stress. An early wound consists of about 30% type
III collagen (uninjured connective tissue composed of 80–90% type I collagen and 10–20% type III collagen).
Higher concentration of type III collagen in matrix, more weaker the wound.
With time, the ratio of type I and III collagen changed to the ratio of intact connective tissue.
zz Cellularity of the wound decreases.
zz As a result, a mature, avascular, acellular collagen rich scar develops.
zz This process reaches a steady state after 12–18 months. By about 6 months, the wound regains 80% of the
strength of an unwounded tissue.
[A well-healed wound never achieves the strength of an unwounded tissue. By 3 weeks, the tissue strength reaches
30% of original strength. After 3 months, the strength reaches the maximum, about 80% of its original strength.]
SS Healing by secondary intention:

zz The pathological process and phases are almost same, the differences are quantitative.
Role of Growth Factors in Healing
SS Differentgrowth factors are:

zz Platelet-derived growth factor (PDGF)
zz Transforming growth factor α and β (TGF-α, TGF-β)
zz Fibroblast growth factor (FGF)
zz Vascular endothelial growth factor (VEGF)
zz Granulocyte-macrophage colony-stimulating factor (GM-CSF)
zz Insulin-like growth factor (IGF-1, IGF-2).
SS Growth factors act on cells by surface receptor binding.
SS Growth factors have different actions on different cells:
zz Chemotaxis of PMNs, macrophages, fibroblasts
zz Stimulation of angiogenesis
zz Stimulation of fibroblasts leads to replication and proliferation
zz Stimulation of collagen synthesis
zz Regulation of ECM synthesis.
Factors Affecting Wound Healing
Factors affecting wound

healing
Systemic factors Local factors
Systemic Factors
SS Malnutrition—Normal healing process is delayed and impaired, leads to weak scar formation.
SS Hypoxic wound environment—Optimal collagen synthesis for wound healing requires oxygen as a cofactor.
Factors causing hypoxia in wound (e.g. cardiac failure, arterial insufficiency, excessive tension on tissue) affect
proper wound healing.
SS Diabetes mellitus—The lack of insulin (insulin restores collagen synthesis and granulation tissue formation) and
hyperglycemia (by affecting the migration and phagocytic function of inflammatory cells and proliferation of
fibroblasts and endothelial cells) leads to impaired wound healing.
Wound Healing 9
The micro and macroangiopathy, associated nephropathy—All adversely affect wound healing.
Diabetic wound also lacks adequate growth factors.
SS Chronic renal and hepatic disease—Decreased collagen synthesis leads to weak scar formation.
SS Collagen vascular disease—The disease itself as well as medications are responsible for impaired inflammatory
cell migration and collagen deposition.
SS Smoking—Impairs wound healing by causing cutaneous vasoconstriction, nicotine impairs collagen synthesis.
SS Steroid and antineoplastic drugs—Steroids inhibit the inflammatory phase of wound healing. It impairs collagen
synthesis, inhibit epithelialization and wound contraction.
Antineoplastic drugs impair proliferation of fibroblasts as well as inhibit the inflammatory phase of wound
healing.
SS Vitamin and mineral deficiency— Vitamin C deficiency leads to failure in collagen synthesis as well as cross-linking.
Vitamin A increases the inflammatory responses after injury increases the migration of macrophages, helps its
activation. It also increase collagen synthesis.
Vitamin A can restore wound healing that are impaired by diabetes, radiation, cyclophosphamide.
Zinc deficiency leads to decreased fibroblast proliferation, delayed epithelialization, decreased collagen synthesis.
Local Factors
SS Infection: Presence of infection delays wound healing. Infection alters the effects of cytokines, leads to delayed
healing.
SS Wound hypoxia: Local damage to the vessels following trauma, edema around the wound, excessive tension due
to suturing lead to wound hypoxia.
Hypoxia leads to impaired fibroblast proliferation and collagen synthesis.
SS Edema: Leads to increased tendency to skin breach and development of infection.
SS Ionizing radiation: Leads to abnormal wound healing.
SS Chemical agents: Chlorhexidine or povidone-iodine impairs inflammatory cell migration, leads to delayed wound
healing.
Complications of Abnormal Wound Healing
SS Poor alignment: When a wound crossed the definite anatomical structure such as vermilion border of lip, without
proper alignment during repair, defect in alignment develops.
SS Contracture: If a linear wound crosses flexor creases vertically, there is development of scar contracture.
Deep and extensive burn scar also causes scar contracture.
SS Altered pigmentation: Most of the scars are hypopigmented, hyperpigmentation may also occur.
SS Tattooing: Dirt or soot particles may become implanted in untidy wounds and results in tattooing of scar.
SS Hypertrophic scar: Raised scar that confines of the original wound.
zz Both increased collagen production and collagen breakdown, but the final result is excess collagen in tissue.
zz Stretched collagen bundles are aligned in same plane of epidermis, whereas the collagen bundles are randomly
arranged and relaxed in normal scar.
zz More cellular and vascular than normal scar, also contains aggregates of abundant fibroblasts, vessels and
collagen fibers.
zz A hypertrophic scar can develop anywhere in the body and frequently regress spontaneously.
zz The development of hypertrophic scar can be minimized by choosing appropriate direction of incisions
(hypertrophic scar usually occur at areas of tension and flexor surface).
zz Custom made pressure garments aids collagen maturation, increases collagenase activity and makes the scar
less cellular.
SS Keloid: Keloids are proliferative scar that grows beyond the limits of the wound.
zz Thicker, more abundant stretched collagen bundles aligned in the same place of the epidermis, as well as
acellular.
zz Rarely regress spontaneously.
zz Genetic predisposition is present.
zz More common in darker-pigmented peoples—African and Asian population.
zz May develop after surgery, burn, tattoos, ear piercing.
zz Certatin body parts have increased tendency of keloid formation—Presternal, deltoid, earlobe, upper back.
zz Treatment: Intralesional corticosteroids (e.g. triamcinolone acetate) is the first line of treatment.
zz Surgery and postoperative interstitial radiotherapy is the another option.
SS Chronic nonhealing wound—e.g. diabetic ulcer, pressure sore.

Wound Healing 11
Keloid Hypertrophic scar
Intrakeloidal triamcinolone injection
Wound Closure Techniques
SS Suturing— e.g. skin suturing with nonabsorbable, monofilament suture

SS Stapling—Allows quick closure
SS Steri-strips—
zz Least invasive way of skin closure
zz Particularly used after suture or staple removal.
SS Skin adhesive (octyl-cyanoacrylate)—
zz Provide a waterproof, antimicrobial barrier
zz No need of removal of suture or staples.

Treatment of Wound
SS History taking
SS Examination of wound—
zz To assess depth
zz To identify foreign bodies, dirt
zz Presence of nonviable tissue.
SS Tetanus prophylaxis
SS Local care of the wound—
zz Irrigation of the wound with normal saline
zz Removal of foreign body
zzDebridement of nonviable tissues

zzAll hematomas are evacuated and bleeding points are secured
zz Wound edges must be debrided to get a fresh edge for suturing
zz In case of tissue loss, skin graft or flap may be required.
SS Antibiotics—Choice of antibiotic depends on organisms most likely to be found in the wound and patient's
immune status.
SS Dressing—
zz The goal of dressing is to provide an ideal environment for wound healing
zz Characteristics of ideal dressing—
Cost effective
Permeable to gases and water vapor
Impermeable to microorganisms
Comfortable
Nonirritant
Minimal pain during change of dressing.
zz Different types of dressing—
Occlusive and semiocclusive dressing
Hydrophilic and hydrophobic dressing
Medical dressing
Alginates
Absorbent dressing.
Chapter 2
Fluid, Electrolyte and

Acid-base Balance
Important Topics
zzHypovolemia
zzVolume Overload
zzElectrolyte Imbalance
zzMetabolic Acidosis
zzMetabolic Alkalosis
zzRespiratory Acidosis
zzRespiratory Alkalosis
‘There is a strange disparity between the sciences of inert matter and those of life. Astronomy, mechanics, and physics are
based on concepts which can be expressed, tersely and elegantly, in mathematical language. ………….Those who investigate
the phenomena of life are as if lost in an inextricable jungle, in the midst of a magic forest, ………… but are incapable of
defining in algebraic equations.'
Alexis Carrel (1873 – 1944)
French-born American Surgeon
Disorders of Fluid, Electrolyte and Acid-base Balance
Body Fluids
SS Total body water (TBW)—

zz 50–60% of total body
weight.
zz Muscles and solid organs
have higher water content
than fat and bones.
zz In males: TBW is 60% of total
body weight.
zz In females: TBW is about
50% of total body weight
(higher adipose tissue and
less muscle mass).
zz In newborn: TBW is about
80% of total body weight.
SS Composition of fluid compartments—
Water is freely diffusible, where as movements of ions and protein are restricted through the fluid compartments.
Fluid Input-output
Disturbances in Fluid Balance
SS Volume overload
SS Hypovolemia (generally means both water and salt loss).
Hypovolemia
Causes
Clinical Manifestations
SS Fatigue— ↓jugular venous pressure

SS Weakness—Diminished skin turgor
SS Thirst—Dry mouth, sunken eyes
SS Oliguria
SS Tachycardia
SS Hypotension
SS Mental obtundation.
Blood Parameters
SS ↑blood urea nitrogen (BUN)

SS ↑creatinine
SS Acid-baseimbalance
SS ↑urine osmolality.
Treatment
SS Replacement of fluid with isotonic, 'normal' saline (0.9% NaCl) solution

SS Amount of fluid needed is guided by clinical signs and urinary output.
Volume Overload
Causes
SS Excessfluid infusion
SS Renaldysfunction
SS Congestive heart failure.
Clinical manifestations
SS Peripheral edema
SS Distended neck vein
SS ↑CVP
SS Pulmonery edema
SS Cardiac failure.
Treatment
SS Restriction of fluid intake
SS Diurectic (e.g. furosemide) may be required.
Electrolyte Imbalance
Sodium
SS Sodium is the principal cation of ECF
SS Bone is a big source of sodium. When abnormal loss of sodium develops, storage in bone compensates it
SS Charges in TBW is inversely proportional to serum sodium.
Hyponatremia
Plasma Na+ concentration < 135 mEq/l.
Causes
Clinical features
SS Headache, confusion, seizures, ↑ intracranial pressure

SS Weakness, fatigue, muscle cramp
SS Lacrimation, salivation.
Treatment
SS Inmost cases, calculated sodium is administered in isotonic solution
SS Insevere hyponatremia (<120 mEq/l) causing mental obtundation, hypertonic saline is indicated
[Rapid correction of Na+ may cause osmotic demyelination syndrome (the increase of Na+ should not exceed 10–12
mEq/l/hour).]
Hypernatremia
Plasma Na+ concentration < 145 mEq/l.
Causes
Clinical features
SS Restlessness, irritability, delirium, seizure, coma.

SS ↓salivation and lacrimation
SS Oliguria.
Treatment
SS Underlying cause is to be corrected
SS Wateris to be administered by mouth or by nasogastric tube
SS Hypotonic saline (1/4 or 1/2 NS) may be needed depending on patient's clinical status.
[The plasma Na+ should be corrected by no more than 10 mM/day to avoid development of cerebral edema.]
Potassium
SS Potassium is 98% intracellular, only 2% is in ECF

SS Three-fourth of total body potassium is found in skeletal muscles.
Hypokalemia
Plasma K+ concentration < 3.6 mEq/l.
Causes
SS Decreased intake— e.g. dietary, K+-free IV fluid infusion, TPN without potassium replacement.
SS Increased renal loss—e.g. diuretics that cause increased K excretion, penicillin (causes ↑ tubular loss of K ),
+ +
hyperaldosteronism.
SS Increased GI loss—e.g. diarrhea, nasogastric output, high output biliary and intestinal fistula.
SS Increased intracellular shift— e.g. in metabolic acidosis, insulin therapy.
Clinical features
SS Most of the patients are asymptomatic

SS Slurredspeech, abdominal distension (due to paralytic ileus), depressed reflexes, hypotonia
SS Cardiac arrest.
Characteristic ECG changes
SS T wave inversion or flattening

SS Prolonged QT interval
SS Depression of ST segment
SS U wave.
Treatment
SS Correction of the cause of hypokalemia

SS Potassium supplementation
zz Oral supplementation
Foods rich in potassium (e.g. milk, coconut water, fruit juices, meat extracts, honey)
As effervesent tablet or syrup.
zz Intravenous supplementation
Potassium concentration in IV solution should be ≤ 40 mEq/l.

Intravenous potassium should be administered in saline solutions rather than dextrose, since dextrose-
induced increase in insulin can actualy exacerbate hypokalemia.
Rapid IV supplementation caries risk of dysrrhythmia and cardiac arrest.
Serum potassium should be checked daily.
[be sure, urine output is adequate.]
SS Severe hypokalemia should be treated in intensive care setup.
SS Serum magnesium should be measured in all hypokalemic patients, as coexistent hypomagnesemia may present.
Hyperkalemia
Plasma K+ concentration ≥ 5.5 mEq/l.
Causes
Clinical features
SS Weakness, paralysis
SS Sinus bradycardia, ventricular tachycardia, ventricular fibrillation and asystole.
SS Peaked T waves
SS Widening of QRS complex
SS Depression of ST segment.
Treatment
Hyperkalemia is a medical emergency and should be treated urgently if (evidenced by ECG findings).
SS Insulin in dextrose solution— Insulin shifts the K into intracellular compartment.
+
SS IV calcium gluconate—Calcium raises the action potential threshold and reduces the excitability.
IV calcium should be used very cautiously in patients taking digoxin.

SS Cation exchange resin.
SS Hemodialysis (if hyperkalemia is a manifestation of renal failure).
Calcium
SS Calcium is an extracellular cation.

SS Most of the body calcium present within the bone matrix (>90%).
SS Serum calcium is present in 3 forms—
zz Protein-bound form—About 40% (albumin)
zz Complexed to phosphate or other anions (10%)
zz Ionized form (50%).
The ionized form is responsible for blood coagulation and neuromuscular stability.
SS The normal serum calcium level is monitored by—
zz Vitamin D
zz Parathyroid hormone
zz Calcitonin.
Hypocalcemia
Causes
SS Hypoparathyroidism
SS Hypomagnesemia
SS Renal failure
SS Crush injuries
SS Necrotizing fascitis
SS Malignancies associated with osteoclastic activity (e.g. breast carcinoma, prostate carcinoma).
Clinical features
SS Paresthesia of face and extremities.

SS Muscle cramp.
SS Carpopedal spasm.
SS Tetany.
SS Hyperreflexia.
SS Chvostek's sign (twitching of the circumoral muscles in response to tapping of the facial nerve just anterior to the
ear).
SS Trousseau's sign (carpal spasm is initiated if blood pressure cuff is inflated to 20 mmHg above the patients systolic
blood pressure for 3 minutes).
SS T wave inversion
SS Ventricularfibrillation
SS Prolonged QT interval.
Treatment
SS Acutehypocalcemia needs IV calcium, gluconate. (after parathyroidectomy)

SS Chronic hypocalcemia required oral calcium, vitamin D (due to hypoparathyroidism).
3
Hypercalcemia
Causes
SS Primary hyperparathyroidism
SS Ectopic parathormone production
SS Malignancy with bony metastases
SS Prolonged immobilization.
SS T wave flatening
SS AV block
SS Shortened QT interval
SS Prolonged PR and QRS interval.
Treatment
SS 4–6 liters of saline infusion is required over the first 24 hours (hypercalcemia leads to dehydration)
SS Zoledronic acid, pamidronate and etidronate are recommended for hypercalcemia of malignancy in adults.
Magnesium
SS An intracellular cation
SS Also present in bone.
Hypomagnesemia
Causes
SS Inadequate intake— e.g. prolonged IV infusion, TPN without magnesium supplementation

SS Increased renal excretion— e.g. diuretics, alcohol
SS Increased GI loss— e.g. diarrhea, nasogastric suction, intestinal fistula.
Clinical features
SS Tremor
SS Hyperreflexia
SS Tetany
SS Seizure
SS Chvostek's sign and Trousseau's sign.
Treatment
SS Oral replacement
SS In severe deficiency, IV magnesium (magnesium sulfate in IV fluid).
[ECG monitoring should be done during magnesium supplementation.]
Hypermagnesemia
Causes
SS Impaired renal function

SS TPN.
Clinical features
SS Vomiting
SS Hypotension
SS Weakness
SS Cardiacarrest
SS Hyporeflexia.

SS Elevated T
wave
SS Increased
PR interval
SS Widened QRS complex.
Treatment
SS Treatment of the cause
SS IV infusion of isotonic saline.
Acidosis and Alkalosis
Metabolic Acidosis
Causes
SS Increased acid intake—Salicylates, methanol, ethylene glycol.

SS Endogenous acid production—Diabetic ketoacidosis, lactic acidosis, renal failure.
SS Excessive loss of bicarbonate—Severe diarrhea, ulcerative colitis, high intestinal fistula, acetazolamide
administration, patient with ureterosigmoidostomies.
Clinical features
SS Rapid, deep breathing (Kussmaul respiration).

Treatment
SS Correction of tissue hypoxia

SS Treatment according to cause.
Metabolic Alkalosis
Causes
SS Lossof HCL from stomach (due to repeated vomiting or nasogastric aspiration)

SS Excess alkali administration—Antacids, bicarbonate, blood transfusion (citrate)
SS Excess bicarbonate production— Mineralocorticoid excess.
Clinical features
SS Mental obtundation
SS Seizures
SS Muscular cramp
SS Tetany
SS Cheyne-Stokes respiration.
Treatment
SS Correction of initiating factor for HCO3– generation

SS Isotonic saline infusion
–
SS Acetazolamide—Increases renal loss of HCO .
3
Respiratory Acidosis
Increase in PaCO and decrease in pH.

2
Causes
SS Inadequate ventilation at the recovery phase of anesthesia
SS Acuteairway obstruction
SS Chronic obstructive pulmonary disease (e.g. chronic bronchitis, emphysema).
Clinical features
SS Rapidincrease in PaCO2 can cause confusion, psychosis, hallucination and may progress to coma
SS Chronic increase may cause sleep disturbances, memory loss, impairment of coordination.
Treatment
Rapid correction of hypercapnia should be avoided.

SS Tracheal intubation and assisted mechanical ventilation.
SS Oxygen administration (should be properly titrated)
SS Improvement of lung function.
Respiratory Alkalosis
Causes
SS Anxiety related cause

SS Hypoxemia
SS Salicylates.
[Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients.]
Clinical features
SS Dizziness
SS Mental confusion
SS Seizures.
Treatment
SS Treatment of the underlying cause

SS Patient with hyperventilation syndrome may benefit from reassurance, relieving the stress factors.
Chapter 3
Hemostasis-Coagulation-
Hemorrhage
Important Topics
zzEvaluation of Risk of Bleeding

zzHemorrhagic Disorders
zzTypes of Hemorrhage
zzManagement of Hemorrhage
zzTransfusion of Blood
zzComplication of Transfusion
'The best physician is also a philosopher.’

Galen (129 – C. 216)
Greco-Roman Physician
Hemostasis and Coagulation
SS Hemostasis is a complex process that involves four events:
}
zz Vascular constriction
zz Platelet plug formation Endothelial cells, platelets, coagulation factors and anticoagulants
zz Formation of fibrin are involved in this process.
zz Fibrinolysis
Evaluation to Assess Risk of Bleeding during Surgery
Proper history and physical examination before the elective surgery are the most valuable evaluation tool regarding
the risk of bleeding.
SS History includes:
zz Easy bruising
zz Spontaneous mucosal bleeding, epistaxis
zz Menorrhagia
zz Past history of significant bleeding during invasive procedures
zz History of liver dysfunction
zz Hematologic malignancies, multiple myeloma
zz Aspirin, anticoagulant or NSAID intake.
SS Physical examination includes:
zz Petechiae
zz Ecchymosis
zz Lymphadenopathy
zz Hepatosplenomegaly.
SS Screening tests:
zz For minor operation, operations not requiring extensive dissection, no history suggestive of coagulation
difficulties or no family history—Preoperative screening tests are not indicated.
zz For major procedures, operations requiring extensive dissections, history or physical findings suggestive of
coagulopathy or positive family history—Need preoperative screening tests.
zz Commonly used screening tests:
Platelet count
Activated partial thromboplastin time (aPTT)
Bleeding time
Platelet count: Identified number of platelets
Prothrombin time (PT): Measures the function of factor VII, factor X, prothrombin-thrombin, fibrinogen and
fibrin.
[Warfarin therapy and vitamin K deficiency prolong the PT.]
INR is used to standardize PT value between different laboratories. The INR is the ratio of measured PT to a mean labora-
tory control PT.
Hemostasis-Coagulation-Hemorrhage 31
aPTT: Detects decreased level of kininogen, prekallikrein, factor VIII, IX, XI, XIII, fibrinogen, prothrombin and
factor V.
Heparin therapy causes prolongation of aPTT without alteration of PT.
A prolonged PT with normal aPTT suggests deficiency of vitamin K-dependant factors (factor II, VII, IX, X).
An abnormal aPTT with normal PT suggests deficiency of proximal intrinsic pathway factors.
Bleeding time: A screening test for platelet function as well as endothelial cell function.
Congenital Hemorrhagic Disorders
SS Hemophilia: Congenital coagulation disorder (X-linked recessive) characterized by deficiency of factor VIII.
zz If affects exclusively in males.
zz Laboratory investigation reveals prolonged aPTT with decreased factor VIII: C, normal PT, bleeding time.
zz Desmopressin temporarily raise factor VIII level.
SS Hemophilia B (Christmas disease): Congenital X-linked disorder characterized by deficiency in factor IX.
zz Laboratory investigation reveals prolonged aPTT with decreased factor IX, normal PT, platelet count and
bleeding time.
zz Prothrombin complex concentrate of high-purity factor IX concentrate is the replacement therapy.
SS von Willebrand's disease: Most common congenital bleeding disorder.
zz Desmopressin increases plasma levels of vWF, factor VIII.
Acquired Hemorrhagic Disorders
SS Vitamin K deficiency—
zz Causes—
Obstructive jaundice
Biliary fistula
Antibiotics (e.g. cephalosporin, quinolones, doxycycline).
zz Vitamin K is administered parenterally (IM/IV).
SS Anticoagulant drugs—
zz Warfarin—
Acts by inhibiting the synthesis of vitamin K-dependant clotting factors
Prolongs the PT, slightly prolong aPTT
Warfarin induced bleeding is treated by vitamin K, plasma infusion and administration of rF VIIa.
zz Unfractionated heparin—
Blocks the activation of factor X
All coagulation profiles are affected by UFH. aPTT is the most sensitive test to detect it.
zzLow molecular weight heparin (LMWH)—Less bleeding complications than UFH

PT is not altered by LMWH therapy
If heparin induced thrombocytopenia develops, fondaparinux is the treatment of choice
SS Liver diseases—
zz Liver synthesizes all coagulation factors except factor VIII
zz Laboratory investigation reveals prolonged PT, slightly increased aPTT
SS Thrombocytopenia—
zz Due to infection (many of the viral and bacterial infections), drugs (e.g. linezolid, piperacillin, vancomycin, etc.)
or heparin induced.
zz Careful history of drug intake (including herbal remedies) should be obtained.
[Drug are the most common cause thrombocytopenia].
Hemorrhage
SS Types of hemorrhage—
SS Local measures—
zz Pressure application
By digital pressure
By packing
By balloon tamponade.
zz Elevation of limb.
zz Mechanical
By using hemostatic forceps, vascular clamps.
By ligature.
Using Harmonic scalpel—This device converts electrical energy to mechanical energy. The vibration (55 kHz)
of the blade causes denaturation of collagen resulting in coagulum formation.
zz Thermal—
Heat causes denaturation of protein that results in coagulum formation.
Transfusion of Blood and Its Components

Indications
SS Replacement due to loss
zz Following trauma
zz Due to pathological lesions (e.g. hematemesis, meleana, hematuria).
SS For correction of anemia
zz Preoperatively
To correct anemia where there is inadequate time for other therapies of anemia.
zz Postoperatively
To replace the blood loss during surgery.
SS Replacement of clotting factors—In hemorrhagic disorders (e.g. hemophilia, Christmas disease).

Whole Blood and Its Fractions
SS Whole blood— Stored in blood bank in special refrigerators (4°C ± 2°C).

zz The shelf life of CPD blood is 3 weeks. During storage, intracellular ADP and 2, 3–DPG is reduced, resulting in
shifting of oxygen-Hb dissociation curve, thus decreasing oxygen transport.
zz Stored blood is a poor source of platelets, clotting factors (factor V and VIII).
zz Ideal component for patients having acute hemorrhage amounting ≥25% of total volume of blood.
SS Packed RBC—
zz Packed RBC are prepared by certifugation. The supernatant plasma is removed.
zz Indicated in pediatric patients, in elderly, patient with chronic anemia.
zz Most of the packed RBCs are now leukocyte-reduced to avoid post transfusion fever, CMV infection,
alloimmunization.
SS Platelet concentrates—
zz Indicated in both qualitative and quantitative platelet disorders.
zz Should be transfused within 120 hours of collection.
zz Is prepared either as random donor (RD) platelets or single donor apheresis platelets (SDAP).
zz Chance of allergic reaction and transmission of infectious diseases are same as whole blood transfusion.
SS Fresh-frozen plasma—
zz Is the source of vitamin K-dependant factors and the only source of factor V.
zz Indicated in congenital hemorhagic disorders, thrombotic thrombocytopenic purpura, during surgery in patient
with liver failure.
SS Cryoprecipitate—
zz Is a source of fibrinogen, factor VIII, von Willebrand factor.
zz Is an alternative to factor VIII concentrate.
Complications of Blood Transfusion
SS Immune-mediated reactions—
zz Allergic reaction —
One of the common type of transfusion reactions
Patient develops urticarial rash, itching. Rarely, bronchospasm develops
Treatment involves temporary stopping of the transfusion and administration of antihistaminics and steroids.
zz Febrile nonhemolytic transfusion reaction—
Most common type of reaction associated with transfusion of cellular blood components
Patient develops chills, rigor and rise of temperature
Due to antibodies against donor leukocyte and HLA antigens
Leukoreduction before storage can prevent this type of reaction.
zz Acute immune hemolytic reaction—
It is due to ABO or Rh incompatibility.
Always due to human error (mislabelling the sample or transfusion in a wrong patient).
Patient presents with fever, chill, discomfort at the infusion site, chest or flank pain, tachypnea, hypotension,
hemoglobinuria.
In anesthetized patient, excessive bleeding from incision or mucus membrane is alarming sign.
Immediately the details of the patient and the documents relating to donor blood should be checked.
Transfusion
–– should be stopped immediately.
The transfused blood sample and unused blood unit should be sent for analysis and blood bank should be
––
informed about the reaction.
Diuresis should be induced with IV fluids, frusemide or mannitol.
––
zz Anaphylactic reaction—
Patient presents with nausea, vomiting, hypotension, bronchospasm and even shock.
Transfusion should be stopped immediately. Epinephrine is given subcutaneously. In severe cases, steroid is
indicated.
zz Transfusion-related acute lung injury (TRALI)—
Patient presents with acute respiratory distress and signs of noncardiogenic pulmonary edema.
Treatment is supportive and usually patient recovers without any sequelae.
zz Postransfusion purpura—
Patient presents with thrombocytopenia 7–10 days after platelet transfusion.
Occurs predominantly in women.
Treatment is IV immunoglobulin or plasmapheresis.
SS Transmission of disease—
zz Viral infection—
Hepatitis C
Hepatitis B (risk of transmission is more than hepatitis C)
HIV 1
Cytomegalovirus (CMV)—Leukocyte-reduced cellular component transfusion can decrease the risk of CMV
transmission.
zz Bacterial infections—
As PRBCs and FFPs are stored at cold temperature, they are not common sources of bacterial contamination
(except Yersinia, Acinetobacter, Pseudomonas, Escherichia species).
As platelet concentrates are stored at room temperature, it is a common source of bacterial contamination.
zz Other infectious diseases—
Malaria
Babesiosis
Chagas disease
Dengue.
SS Other complications—
zz Fluid overload— Rate of transfusion as well as volume should be monitored to avoid overload.
In this setting, diuretic can solve the problem.

zz Electrolyte imbalance—
Hyperkalemia—Neonates and patient with renal failure are at risk. Fresh or washed RBC are the solution to
avoid this complications.
Hypocalcemia—Citrate (used as anticoagulant in stored blood) chelates calcium and thereby hypocalcemia
develops. No definite treatment is required.
zz Iron overload—
Can affect hepatic, cardiac and endocrine system.
Using alternative therapies (e.g. erythropoietin) and chelating agents (e.g. desferoxamine) are the solution.
zz Immunomodulation—is related to transfused leukocytes.

CHAPTER 4
Gallbladder and Extrahepatic

Biliary System
Important Topics
z Anatomy
zGallstone
zAcute Cholecystitis
zChronic Cholecystitis
zGallstone Pancreatitis
zGallstone Ileus
zCholecystoses
zAcute Acalculous Cholecystitis

zBiliary Dyskinesia
zCholedocholithiasis
zCholedochal Cyst
zCholangiohepatitis
zPrimary Sclerosing Cholangitis

zGallbladder Carcinoma
zCholangiocarcinoma
zAnomalous Anatomy
zSurgical Approaches to Biliary System
zBile Duct Injury
zManagement of CBD Stones
‘Science is not, as so many seem to think, something apart, which has to do with telescopes, retorts, and test tube and
AOLA?E=HHUSEPDJ=OPUOIAHHO >QPEPEO=S=UKBOA=N?DEJCKQP>UK>OANR=PEKJ PNE=H=J@?H=OOEł?=PEKJ EPOGAUJKPAEO
accuracy and its goal is truth.’
Archibald Garrod (1857– 1936)
British Physician and Biochemist
Anatomy of the Gallbladder and

Extrahepatic Biliary System
Things to Remember
S Gallbladder, average capacity 30–50 ml, can distend

upto 300 ml.
S Gallbladder differs S The left hepatic

histologically from duct is longer than
the rest of the the right and has a
gastrointestinal greater propensity
tract in that it for dilatation.
lacks muscularis
mucosa and
submucosa.
S The gallbladder S Contracted

mucosa has the sphincter of Oddi
greatest absorptive p
power per unit Pressure in CBD n
area than any other
p
structures in the
body. Retrograde flow of
bile through cystic
duct.
Gallbladder and Extrahepatic Biliary System 39
S About 250–1000 ml
of bile are secreted
by hepatocytes
everyday
S Gallbladder is supplied by
cystic artery, a branch of the
right hepatic artery (> 90%)
S Gallbladder is divided into four

anatomic areas: the fundus,
the body, the infundibulum,
the neck
Must Know S Gallbladder lymphatics drain into

nodes at the neck of the gallbladder.
Frequently, a visible lymph node
overlies the insertion of cystic artery
into gallbladder wall (Lund’s node
or Mascagni’s lymph node)
S Course of the cystic artery may vary, S Common bile duct is about 7–11 cm in
but it nearly always found within length:
the hepatocystic triangle, the area z Upper third (supraduodenal part)
bound by cystic duct, common z Middle third (retroduodenal part)
hepatic duct and liver margin z Lower third (pancreatic part)
Pathologies of Gallbladder and Biliary System
Benign Pathology
S Gallstone
S Calculous cholecystitis (acute and chronic)

S Acalculous cholecystitis
S Cholesterosis
S Biliary dyskinesia
S Gallbladder polyp
S Choledochal cyst
S Biliary atresia
S CBD stone
S Recurrent pyogenic cholangitis
S Biliary stricture
S Primary sclerosing cholangitis
S Gallstone pancreatitis.
Malignant Pathology
S Cholangiocarcinoma
S Gallbladder carcinoma
S Malignant biliary stricture.
Gallstone
Risk Factors Varieties
Cholesterol Stones
Pure cholesterol stones are rare. This type of stone presents as

single large stone
Black Pigment Stones
Brown Pigment Stones
S Earthy in texture
S Brownish-yellow
S Associated with bacterial and parasitic infection
Operated specimen of gallbladder shows multiple stones of varying S Usually found in bile ducts.
sizes
S Risk factors for brown pigment stone:

z Biliary strictures
z Choledochal cyst
z Sclerosing cholangitis
z Chronic pancreatitis.
Pathogenesis of Gallstone
Pathogenesis of Cholesterol Stone
Pathogenesis of cholesterol stones involves 3 stages:

S Cholesterolsupersaturation in bile
S Crystalnucleation
S Stone growth.
Pathogenesis of Black Pigment Stones
S Black pigment stones most often secondary to hemolytic disorders such as hereditary spherocytosis and sickle
cells disease, cirrhosis.
S Black pigment stones usually not associated with infected bile and primarily present in gallbladder.
Pathogenesis of Brown Pigment Stones
S Brown pigment stones

usually occur as primary
duct stones, associated
with bacterial infection and
stasis, parasite infestations
(Clonorchis sinensis, Ascaris
lumbricoides).
Things to Remember
1. 2.
S secretes E-glucuronidase that causes hydroly- S Cholesterol stones cast strong acoustic shadows on
sis of soluble conjugated glucuronide to produce USG.
insoluble free bilirubin, which then precipitates with
calcium.
USG of the gallbladder shows stone with acoustic shadow
3. 4.
S Black pigment stones composed of bilirubin S Brown pigment stones contain calcium bilirubinate,
polymers without calcium palmitate, small amount calcium palmitate, small amount of cholesterol,
of cholesterol, matrix of organic material. matrix of organic material.
5.
S Biliary
sludge composed of mucin, calcium, Spectrum of Gallstone Disease
monoconjugated bilirubin and cholesterol and
thought to be precursor of gallstones.
Spectrum of Symptomatic Gallstone Disease
Acute Cholecystitis
How it develops (pathophysiology)
S About 50% of patients have positive bile culture, E.

coli is the most common isolated organism.
Clinical presentation
S Pain in right hypochondrium/epigastrium

z May radiate to right upper part of back/interscapular area.
z Much longer in duration in comparison to previous episodes of

biliary colic.
S Nausea
S Vomiting
S Fever
S Anorexia
S Murphy’s sign—
z On deep palpation of right hypochondrium, an inspiratory

arrest.
S Tenderness in right hypochondrium
S Guarding
S If tender mass is palpable in right hypochondrium— Elicitation of Murphy’s sign
z Think of empyema gallbladder, omental phlegmon, abscess

due to localized perforation.
Investigations
Think other possibility (differential diagnosis)
S Mild leukocytosis.
S Serum bilirubin may be elevated.
S AST, ALT, alkaline phosphatase may be normal
or mildly elevated.
If significant elevation of serum bilirubin, then think of:

S Associated choledocholithiasis
S Mirizzi syndrome.
Do a Ultrasonography
S Thickened gallbladder wall (> 4 mm) and

pericholecystic fluid.
S Calculus with acoustic shadow.
S Sonographic Murphy’s sign (more sensitive than

clinical Murphy’s sign because probe is accurately
placed over the gallbladder site).
Treatment
Complicated Case Scenario
Prepare for Emergency Cholecystectomy
S Except mucocele gallbladder and cholecystoduodenal fistula, all others need broad spectrum antibiotics including
anaerobic coverage and emergency cholecystectomy.
Be Prepared for Partial Cholecystectomy
Anatomy of Calot’s triangle not clear in most of the cases.
More Careful during Cholecystectomy
S Chance of bile duct injury is more in the setting of complications.

Chronic Cholecystitis
S Acalculous cholecystitis causes same morphologic

changes.
Clinical presentation Think other possibilities (differential diagnosis)
S Pain in (epigastrium/right hypochondrium)
S Radiation of the pain to the right upper back or

between scapula.
S Usually appear after a fatty meal.
S Nausea.
S Vomiting.
S Don’t expect any physical findings.

S Don’t expect any abnormality in laboratory
findings in most of the patients.
Do a ultrasonography
z Contracted gallbladder with calculi

z Thickened gallbladder wall
z Sometimes, only sludge.
Treatment
Common case scenario
S Prepare the patient for elective laparoscopic

cholecystectomy.
S Give priority to diabetic patients as they are more prone to develop acute cholecystitis with complications.
Unusual case scenario
S Tellyour patient that you will be glad if she suffers from typical biliary colic rather than symptoms of dyspepsia as
results of cholecystectomy is more satisfactory in former group.
Gallstone Pancreatitis
How it develops
Anatomical variant
+
This pathophysiology
leads to gallstone pancreatitis.
Suspect gallstone pancreatitis
If
If
Signs of cholecystitis
Symptoms of cholecystitis +
+ S IPS—Sluggish/absent.
S Pain radiates to back. S p breath sound (specially on it
S Pain relieves on leaning side).
forward. S Shock (tachycardia, hypotension).
S Voluntary or involuntary guarding.
S Patient previously suffered from biliary colic, previous USG showed multiple stones in GB, now complaining of
more severe pain with some systemic manifestations (tachycardia, hypotension, p breath sound), suspect biliary
pancreatitis.
0A=N?DBKNKPDANłJ@EJCO
Investigations
S n hematocrit, Hb, blood urea nitrogen, creatinine

Pancreatitis
p
Diffuse capillary leak + vomiting
p
Hypovolemia
S p hematocrit (in hemorrhagic pancreatitis)
S nWBC count with shift to left
S If > 12,000/ml
p
Think of suppurative complications
S nserum bilirubin
Due to—
z Biliary tract stone
z Pancreas causing bile duct obstruction
z Nonobstructive cholestasis
S n alkaline phosphatase
z Think of gallstone pancreatitis
Investigations to confirm pancreatitis S Clinically

pancreatitis, but serum amylase normal:
Think the possibilities—
z Already 3–4 days have passed after an attack
z Necrotic pancreatitis
z Acute on advanced chronic pancreatitis.
S Send blood for lipase if patient present after 2–3

days of onset of symptoms.
S Also think of urinary amylase level, (level become
elevated for several days).
S So when patient present after 3–4 days. Send blood
S Send blood for amylase and lipase if patient present for—
within 2 days after the onset of symptoms. z Serum lipase and measure urinary amylase
S > 3 fold elevations from normal value
z Serum lipase> 3 fold of normal value

S In favor of pancreatitis
S 2–3 fold elevations

z In favor of pancreatitis

S n serum amylase, but normal serum lipase
z? Hollow viscus perforation S Think of other possibilities (e.g. peptic perforation).
z ? Acute cholecystitis
z ? Bowel obstruction
S n serum amylase – Mild

pancreatitis
S nnn serum amylase – Severe
pancreatitis
} Don’t think like
that
Do a Ultrasonography
z Pancreatic edema
z Pancreatic swelling
z Peripancreatic fluid collection.
Not always gives you satisfactory results due to presence

of gas.
Is Early CT Necessary
S Diagnosis of pancreatitis is uncertain.

S Suspecting severe pancreatitis, necrotizing pancrea-
Treatment titis.
S Otherwise not in early cases as it will not alter the
Treatment of pancreatitis
line of management.
S Management of pain by narcotic analgesics.

Treatment of biliary tract-
stone
MORPHINE IS PREFERABLY AVOIDED
S Fluid and electrolyte management

S Nasogastric decompression Endoscopy + stone clearance
S Nutrition (? enteral/? parenteral)
S Parenteral antibiotics.
In Mild Pancreatitis
In Severe Pancreatitis
Gallstone Ileus
S Elderly people with no history

of surgery or no features of
obstructed hernia, presenting
with intestinal obstruction,
think of gallstone ileus besides
malignancy.
S Distended abdomen
S Absolute constipation
S Diffuse tenderness
S Pain abdomen
S Peristaltic sound absent.
S Vomiting.
Do a straight X-ray abdomen Treatment
S Search for evidence of intestinal obstruction. S Resuscitation
S Is there any radiopaque shadow in right iliac fossa? z Nasogastric suction

(radiopaque gallstone). z IV fluid
z IV antibiotics.
The Cholecystoses
S Cholesterosis (strawberry gallbladder)

S Cholesterol polyposis of the gallbladder
S Adenomyomatosis
S Cholecystitis glandularis proliferans.
Cholesterosis (strawberry gallbladder)
Usually diagnosed after sectioning operated specimen.
Cholesterol polyposis of the gallbladder

Adenomyomatosis
Acute Acalculous Cholecystitis
Where it Develops
S Elderly person.
S Critically ill, after trauma and burn.
S Prolonged parenteral nutrition.
S After operations like abdominal aneurysm repair,

cardiopulmonary bypass.
Treatment
S Suspect acute acalculous cholecystitis if a critically

ill patient presenting with features of cholecystitis.
S Firstly, do a ultrasonography
z At bedside

Same findings like calculus cholecystitis except
stones
S HIDA Scan—
z Absent gallbladder filling.

Biliary Dyskinesia
Think of biliary dyskinesia
Do a HIDA scan
HIDA scan with 99mTc radionuclide (me-

brofenin) IV.
S Fatty meal is administered after 1 hour.

S Minimal contraction of gallbladder in response to
fatty meal represent—
z Nonfunctioning gallbladder.
S Ejection fraction < 35% at 30 minutes.

HIDA scan showing functioning gallbladder
Treatment
Nonfunctioning gallbladder in HIDA laparoscopic cholecystectomy.
Choledocholithiasis Primary Bile Duct Stone
Secondary Bile Duct Stone
S Primarily originated in gallbladder, subsequently

passed into the CBD.
S Mostly cholesterol stones, rest black pigment stones.
S Primarily originated in bile duct.

S Usually brown pigment stones.
S Often associated with intrahepatic stones.
S Stasis and infection are the main causative factors.
S Associated with benign biliary stricture, sclerosing

cholangitis, choledochal cyst, sphincter of Oddi
dysfunction.
So many presentations!
S Asymptomatic. S Gallstone pancreatitis (second most common

presentation).
S Incomplete obstruction leading to biliary colic

(most common presentation). S Secondary biliary cirrhosis with hepatic failure (rare).
S Complete obstruction leading to obstructive

jaundice with or without cholangitis.
Clinical features
S Biliary colic
S Nausea
S Vomiting
S Icterus—First in sclera (sclera rich in elastin, elastin has high affinity for bilirubin)
S Mustard-colored urine
S Clay-colored stool
S Elevated temperature with chill and rigor (if cholangitis develops)
S Tenderness in epigastrium/right hypochondrium
S Specially ask for fever with chill and rigor, if present, think of cholangitis.
Jaundice, mustard-colored urine and clay-colored stool are characteristics of obstructive jaundice.
Yellowish discoloration in sclera

Investigations
S Totalleukocyte count.
z Usually normal
If marked leukocytosis is present, then think of—
z Cholangitis
z Associated acute cholecystitis.
S Serum bilirubin n (usually < 10 mg/dl)
nn – think of malignant obstruction

S nnalkaline phosphatase (think of obstruction)
S n AST nALT.
Firstly, do a ultrasonography
S Stone in CBD not always visible (due to

bowel gas).
S Dilated CBD (> 8 mm).
Sensitivity of ultrasonography for detection

of CBD stones is low (about 30–50%).
USG shows stone in gallbladder
A patient with biliary colic and jaundice, USG

shows calculus in gallbladder with dilated
CBD, think of choledocholithiasis.
USG shows stone in CBD

Choose any one
ERCP showing narrowing at the lower end of CBD MRCP showing stone in gallbladder and common bile duct
S At the time of diagnosis, option for therapeutic Excellent anatomic detailing

intervention. High specificity for diagnosis of bile duct stones.
S Chance of complications (cholangitis, pancreatitis).
Endoscopic ultrasound is also a option but it is less sensitive.

Choose ERCP, not MRCP, if your patient having claustrophobia or with cardiac pacemakers, metallic implants, cochlear
implant or aneurysm clip.
So, what is your choice?

So, judge considering the patient’s socioeconomic status, physiological status, disease status and also institutional
protocol if any.
Treatment
Firstly, treat the complications aggressively.

Then, you have many options for management of ductal stone, choose any one:
1.
Your patient have associated problems/complications
Minimally invasive procedure is preferred

ERCP picture showing Dormia

basket in CBD
2.
S Bileduct stones detected preoperatively but endoscopic clearance unsuccessful
or
S Duct stones detected intraoperatively on intraoperative cholangiography
and
You have proper instrumentation, expertise and dedicated team
then,
Laparoscopic common bile duct exploration is a preferred approach.
3.
S Stones impacted in ampulla
or
S ERCP facility is not available or unsuccessful
or
S Laparoscopic expertise is not available.
Management of retained and recurrent duct stone
S Recurrent stones (stone in CBD detected <2 years after cholecystectomy) = Endoscopic sphincterotomy and
stone retrieval.
Management of primary duct stones
Acute Cholangitis
Suspect Cholangitis
S If you found a patient of choledocholithiasis with fever with chill and rigor.
Triad or pentad?
Treat Aggressively
S Biliary decompression by any one approaches.

Choledochal Cyst S Congenitalanomaly of bile duct.
S Abnormal, disproportionate cystic dilatation of bile
How it Develops duct.
So Many Variations
S Todani modification of Alonso-Lej classification.
Clinical Presentation
Investigations
First, do a ultrasonography
Type II, IV, V—Easily recognized

Type III—Not visualized due to bowel gas.
Then, do MRCP
Search for
S Type of cyst
S Extent of cyst
S Stone in biliary/pancreatic duct
MRCP showing Type I choledochal cyst
Surgeon must know the proper anatomic delineation of pancreatic-biliary duct junction.
Do CECT if
S USG report suspects intrahepatic cystic dilation
S Suspicion of associated hepatobiliary pathology.
Why we operate choledochal cyst?

S Because patient with choledochal cyst have increased risk of gallbladder or bile duct malignancy
S Methods of screening for malignancy in choledochal cyst are not still effective.
Now, make a plan for surgery

Consider:
S Is your patient fit for surgery or willing for biliary reconstructive surgery?
z If no, then do cholecystectomy/endoscopic treatment.
S Is your patient also suffering from associated complications (pancreatitis, cholangitis)?
z If yes, then first manage complications.
S What type of cyst it is?
z Plan specifically according to the type of cyst.
Treatment
Type I cyst
Type II cyst
Type III cyst

Type IV cyst
Type V cyst
OR
S Patient with cirrhosis or liver failure—Liver transplantation.
Regular Follow-up the Patient

S Because of long-term risk of:
z Recurrent cholangitis
z Postoperative biliary stricture
z Intrahepatic stones
z Pancreatitis
z Malignancy.
Recurrent Pyogenic Cholangitis (Cholangiohepatitis)

How it Develops
S Recurrence of pain in right upper quadrant, fever and jaundice — Characteristic, clinical presentation.
S Ultrasound can detect stones, but MRCP and PTC more specific for detecting strictures and stones.
Treatment
OR
Primary Sclerosing Cholangitis

S Associated with ulcerative colitis, Riedel’s thyroiditis and retroperitoneal fibrosis

S Cyclic
remissions and exacerbations of abdominal pain, jaundice, pruritus and fatigue are typical presentations
S Symptoms of bacterial cholangitis are uncommon
S Suspect associated sclerosing cholangitis in any patient of ulcerative colitis, so liver function should be assessed.
Investigations
S Cholangiography (ERCP)
z nn Alkaline phosphatase
z Multifocal strictures and dilations (beading) of intra and extrahepatic ducts.
S Brush cytology (? benign/? malignant)
S Liver biopsy
z Degree of hepatic fibrosis
z ? Cirrhosis.
Management PSC with endstage liver disease
No cirrhosis/significant fibrosis Liver transplantation

S Medical therapy
z Ursodoxycholic acid (? long-term benefit).
S Minimally invasive approach
z Endoscopic/percutaneous route o Dilation rstenting.
S Surgical approach
z Resection of extrahepatic biliary tree with bilateral hepaticojejunostomy.
Gallbladder Carcinoma
Risk Factors
Pathology
%EOPKHKCE?=HHU $=HH>H=@@AN =N?EJKI==NA H=OOEłA@EJPK
S Adenocarcinoma (most common)

S Papillaryadenocarcinoma
S Mucinous adenocarcinoma
S Squamous cell carcinoma
S Others (adenosquamous, oat cell carcinoma).
How it Spreads
S Pain in right upper quadrant (similar to pain of cholecystitis)

S Vomiting
S Weight loss
S Lossof appetite
S Jaundice
S Abdominal mass.
} Signs of advanced disease
S Clinical presentation in most of the patients is almost

similar to chronic cholecystitis.
Patients older than 70 years with history of recent weight loss and persistent rightupper quadrant pain, think of gall-
bladder carcinoma.
Investigations
}
S n serum bilirubin usual findings in advanced cases
S n alkaline phosphatase
S p Hb
First, do a ultrasonography
S Mural thickening of gallbladder wall
S Gallbladder mass > 1 cm
S Loss of normal gallbladder wall—Liver interface.

Always do a CT scan if gallbladder cancer is suspected
S Mass protruding into the gallbladder lumen or completely replacing the gallbladder
S Regional lymph node involvement
S Local invasion into the liver and porta hepatis
S Presence or absence of distant metastases.
How MRI will give you added advantage

More detailed information regarding regional lymph node involvement, local invasion and vascular involvement.
Is biopsy and cytology necessary?
S Mass suspicious for gallbladder carcinoma by imaging

z No need of biopsy before definite exploration and resection.
S Patient needs ERCP or PTC for obstructive jaundice
z Bile should be collected for cytology.
S Unresectable disease needs tissue diagnosis for palliative chemotherapy
z Tissue collection by USG or CT guided FNAC.
S Endoscopic USG guided fine needle aspiration is the best option for obtaining tissue.
Treatment
1.
2.
3.
4. Preoperatively diagnosed gallbladder carcinoma
Stage IIA (T3 No MO)

Or
IIB (T1–3 N1MO)
5. Stage III (T4 any NM0)
6. Stage IV (any T any N M1)
Role of adjuvant therapy
No improved survival is still observed with adjuvant chemotherapy or radiation therapy.

Cholangiocarcinoma
Perihilar Cholangiocarcinoma
Risk Factor
S Primary sclerosing cholangitis (160 times

risk).
S Genetic conditions
z Lynch syndrome II
z Multiple biliary papillomatosis.
S Caroli’s disease.
S Intrahepatic stones.
S Liver flukes (Opisthorchis viverrini, Clonorchis

sinensis).
S Choledochal cyst.
S Anomalous pancreatic-biliary duct junction.
S Biliary-enteric anastomosis.
S Patient with hepatitis C infection.
S Exposure to thorotrast.
Pathology
Histological Types
S Adenocarcinoma (> 90%)
S Sarcoma
S Small cell cancer
S Lymphoma.
S Painless progressive S Distended gallbladder (present as

jaundice (most palpable gallbladder)
common presentation) S Jaundice
S Pruritus
S Abdominal pain
S Weight loss
S Clay-colored stool
S High-colored urine
S Palpable liver
S Abdominal pain
S Weight loss
Investigations
S nn conjugated bilirubin
S nn alkaline phosphatase
S nnGGT
S nAST and ALT
S nn CA 19-9 [CA 19–9 is mildly elevated in

benign biliary tract diseases]
S nn alkaline phosphatase
S Bilirubin—Normal
S nn CA 19–9
First, Do a Ultrasonography
S Intrahepatic biliary radicles dilated

S Significant dilation proximal to narrowing of duct
S No stone in CBD.
Then, think of biliary or pancreatic malignancy

Do MRCP (magnetic resonance cholangiopancreatography)
S T2-weighted images of liver and pancreas
S Projection images of bile duct and pancreatic duct
S Associated masses and malignant thickening can be defined
S Location of biliary obstruction
S Proper delineation of biliary tract proximal and distal to obstruction.
How CT scan will help?

S Regional lymphadenopathy can be assessed
S Distant metastases present or not
S Presence or absence of local vascular invasion
S Liver atrophy is present or not
S Useful in diagnosis of intrahepatic bile duct carcinoma.
Diagnosis of Hilar cholangiocarcinoma should be suspected in a patient with painless jaundice whose CT scan reveals
dilated intrahepatic biliary radicles with a normal gallbladder and extrahepatic biliary tree.
Take Decision
Consider
S Is patient fit for surgery?

S Is the tumor resectable?
S Is preoperative stenting necessary?
z Bilateral hepatic duct involvement upto secondary radicals.

z Bilateral hepatic artery involvement.
z Encasement of portal vein proximal to its bifurcation.
z Unilateral extension to 2° biliary radicles with contralateral

portal vein branch involvement and or hepatic labor
atrophy.
Tumor unresectable
Distant metastasis
Palliation (relieve the symptoms of jaun-

dice, pruritus and malaise)
Percutaneous transhepatic stenting Endoscopic stenting

(Selfexpandable metal stent) (Selfexpandable metal stent)
OR
MRCP or CT guided selective unilateral stenting
Consider preoperative stenting if

S Serum bilirubin > 15 mg/dl
S Neoadjuvant therapy is planned
But
S Chance of cholangitisnn
S Incidence of perioperative infectious complicationsnn
So, is preoperative stenting beneficial?

-=PEAJPEOłPBKNOQNCANU=J@EPEO=NAOA?P=>HADEH=N?DKH=JCEK?=N?EJKI=
S Plan RO resection
S Plan type of surgery according to Bismuth-Corlette classification.
Type II and Type III—Associated caudate lobectomy??

Perihilar cholangiocarcinoma diagnosed unresectable peroperatively

Distal cholangiocarcinoma diagnosed unresectable peroperatively
S Cholecystectomy
S Roux-en-Y hepaticojejunostomy proximal to the tumor
S Gastrojejunostomy.
Anomalous Anatomy
Anomalous Gallbladder Anatomy

Variations of Cystic Duct Insertion with Common Hepatic Duct
Variations in Arterial Supply of Gallbladder

Endoscopic Therapeutic Approaches to Biliary System
Percutaneous Transhepatic Approach
S Useful
for removal of ductal stones in proximal bile duct
S Temporary stenting in proximal bile duct obstruction (benign or malignant)
S Permanent stenting in unresectable proximal biliary stricture.

Removal of Retained CBD Stone Through T-tube Tract
Removal of CBD Stones by Endoscopic Sphincterotomy

S Difficultyin removal, if:

z Stone > 1.5 cm
z Stone proximal to stricture
z Multiple impacted stones.
&B!EBł?QHPUEJ/AIKR=HKB0PKJA
Options
S Mechanical lithotripsy
S Electrohydraulic or laser lithotripsy
S Extracorporeal or shock wave lithotripsy
S Stent placement.
Plastic stent in CBD
Selfexpandable metal stent (wire-mesh stent)

Surgical Approaches to Gallbladder and Biliary System
Cholecystectomy
Operative picture of lap cholecystectomy
Indications of Lap Cholecystectomy
S Gallstone with biliary colic.

S Chronic calculous cholecystitis.
S Acute cholecystitis.
S Gallstone pancreatitis.
S Asymptomatic cholelithiasis in certain
circumstances.
Absolute Contraindications
S Unable to tolerate GA
S Refractory coagulopathy
S Suspected or confirmed gallbladder carcinoma.

Relative Contraindications
S Frozen upper abdomen due to previous surgery

S Portal hypertension
S Cholecystoenteric fistula
S Chronic obstructive pulmonary disease
S Pregnancy (Ist and 3rd trimester).
Operative Room Setup
S In Europe, surgeon stands in between legs.

Pneumoperitoneum
Why pneumoperitoneum?
How pneumoperitoneum?
Open technique
Closed technique
Port position
S A (10 mm)—Umbilical port—For camera (10 mm) and laparoscope

S B (10 mm)—Epigastric port—For surgeon’s right hand
S C (5 mm)—Right subcostal port at midclavicular line—For surgeon’s left
hand
S D (5 mm)—Right lateral port at anterior axillary line—For retraction of
gallbladder.
Exposure of structure in calot’s triangle
Dissection of gallbladder from its fossa
A = Anomalous anatomy—Keep in mind the possibility

B = Bile duct—Keep away from duct
C = Conversion to open—It is not failure, but a wise decision
D = Dissection—Good dissection to define cystic duct and artery
E = Expect—Expect uneventful postoperative recovery.
Open Cholecystectomy
Indications
S Poor pulmonary or cardiac reserve

S Conversion from an attempted laparoscopic cholecystectomy
S Suspected or known gallbladder cancer
S Cirrhosis and portal hypertension
S 3rd trimester pregnancy.
Incision
Exposure of Calot’s Triangle
S Retraction of fundus—Anteriorly and superiorly.

S Retraction of Hartmann’s pouch—Inferiorly and
laterally.
S Retraction of duodenum and colon—by retractor or
assistant’s left hand.
Dissection in Calot’s Triangle
S Dissection should be close to gallbladder.

S Identify the junction between gallbladder and cystic
duct, not the junction between cystic duct and CBD.
S Dissect the cystic artery pathway towards the
gallbladder to see its final distribution into gallbladder
wall — Unwanted ligature of aberrant right hepatic
artery can be avoided.
Dissection of Gallbladder from its Fossa
S Dissection of gallbladder from its fossa by sharp

dissection or diathermy.
S Dissection should be kept close to gallbladder within
the cystic plate—In order to avoid damage to liver
parenchyma.
Placement of Drain and Closure
S Use of drain (optional)

S Closure (in layers).
Evidence-based medicine does not support the

use of drain in routine cholecystectomy
What is Partial Cholecystectomy?
S Fundus can be recognized but infundibulum can’t be

delineated.
S Fundus opened, stone removed.
S Anterior visible wall of gallbladder is excised.
S Posterior wall in contact with the liver is left in place.
Why Bile Duct Injury?
S Compromised surgery
z Insufficient experience
z Inadequate incision and exposure
z Inadequate assistance.
S Anomalous anatomy
z Short cystic duct
z Narrow common bile duct
z Aberrant junction of cystic duct and common hepatic duct.
S Inflammatory pathology
z Chronic inflammation resulting in obscured anatomy of Calot’s triangle.

Mistaking the common bile duct for the cystic duct is a frequent visual misperception.
Bile Duct Injury Recognized at Operation

Keep in Mind
S Each failed repair is associated with some loss of bile duct length
S Each failed repair makes further repair more difficult.
Aim
S Maintaining ductal length

S Avoid uncontrolled postoperative bile leakage.
Definite reconstruction should not be attemped if expertise is not available.
S Chance of stricture is more in end to end anastomosis

S Long-term result is satisfactory in Roux-en-Y hepaticojejunostomy.
z Length maintained
z Defect is bridged by serosa
z Fistula between bile duct and jejunum is created after removing T-tube.
Injuries Recognized in Immediate Postoperative Period
Avoid early reoperation. S Patientseriously ill with signs of sepsis

S Take control of situation S May present with biloma without sepsis
S Maintain fluid and electrolyte balance S Needs drainage of bile and control of bile leak
S Maintain nutrition S Delayed definite repair is the best option
S Treat infection
S Fistulography
S Wait for at least 2–3 weeks
Most of the fistulas will close or output decrease after

that
Injuries Presenting at an Interval after Initial Operation
Principle
S Exposure of healthy bile duct proximal to stricture
S Preparation for Roux-en-Y biliary-enteric anastomosis
Outcome of repair and technique of repair depends on type of injury and stricture location.
Different Types of Stricture and their Management

z Difficult to expose the

left hepatic duct
z Technically demanding
procedure
Laparoscopic Management of CBD Stones
1. Transcystic Duct Exploration (without Choledoscope)
S Irrigationtechnique
S Balloon technique
S Basket technique.
S Clip applied at the junction of gallbladder and
cystic duct.
S Incision made on the larger portion of cystic
duct.
S Catheter introduced.
S Cholangiogram performed.
S Duct should be dilated.
2. Transcystic Duct Exploration (with Choledochoscope)
S Direct vision —Chance of accuracy more.

S No need of fluoroscopic guidance—Radiation exposure can
be avoided.
S Dormia basket is manipulated through scope.
3. Laparoscopic Choledochotomy
Indications
S Stones > 1 cm
S Multiple stones
S Require lithotripsy for impacted stones in proximal biliary tree.
Advantages
S Surgeon can use a larger scope
S Direct visualization of proximal and distal ductal system.

Management of CBD Stone (Open Approach)
1. 2.
S Calot’striangle dissected S Site of choledochotomy must be in the lowest part of
S Gallbladder not removed supraduodenal CBD.

S Two stay sutures (3-0 Vicryl) to lift the anterior wall
z Gallbladder can be used as a useful aid of
retraction. of CBD.
z Choledochotomy in the lower part leaves a
provision for choledochoduodenostomy.
z Lifting of the anterior wall almost removes the
chance of injury to the posterior wall.
z Lifting makes the wall tense, thereby making a
incision becomes easy.
Choledochotomy is done after lifting the anterior wall of CBD by

two stay sutures
3.
S Desjardins forceps introduced through choledo-
chotomy.
S Stone is grasped by the forceps. 4.
S Rubber catheter is fed into the duct.
S Saline flushing of the proximal and distal duct.
z Flushing clears the duct from smaller stones and
debris.
z Free passage of saline without reflux indicates
adequate clearance of distal duct.
Desjardins forceps is introduced to grasp the stone in CBD

5. 6.
Refashioning of T-tube Placement of T-tube
S T-tube size should be at least 14 Fr S T-tube should not enter the right or left hepatic duct
z More narrow tract makes further interventional or duodenum.

procedure impossible.
T-tube is placed in the CBD

S A strip of wall (half the diameter) is removed
z Prevents obstruction and helps easy removal.
8.
S T-tube brought out from the right flank.
7.
S T-tube protrudes from the lower end of
choledochotomy incision.
9.
T-tube cholangiogram normal
Removal of tube by smart pull

S T-tube cholangiogram on 5–7 days after opera-
tion.
Choledochoduodenostomy
Indications
S Retained or recurrent calculi in CBD or hepatic ducts
S Primary CBD stone
S Multiple stones (>15)
S Ampullary stenosis
S Stricture in transpancreatic part of CBD due to chronic pancreatitis.
Contraindications
S Duodenal ulcer
S Acute pancreatitis
S CBD <1.2 cm.
Choledochoduodenostomy should not be performed with duct < 1.5 cm.
1. 2.
S Kocherization of duodenum S Incision in CBD about 2.5 cm
z For a tension-free anastomosis. S Incision usually extended upto common hepatic duct
S Incision in postbulbar duodenum—Slightly smaller.
a–a1 = Midpoint of choledochal incision—

3.
Distal corner of duodenal incision.
b–b1 = Midpoint of choledochal incision—
Proximal corner of duodenal incision.
c–c1 = Lower corner of choledochal inci-
sion—Midpoint of duodenal incision.
4. 5.
S Posterior suture completed. S Stoma size at least 2.5 cm.
S Sutures should be placed close enough so that
no evidence of bile leakage.
Roux-en-Y Hepaticojejunostomy
1. 2.
Fashioning of Roux loop S Closed distal end is brought up through a window in
S Jejunum is transected 25–30 cm distal to DJ the transverse mesocolon to the right of middle colic
flexure. artery.
3.
S Incision in the Roux loop of jejunum.
4.
S Posterior row of sutures completed.
5.
S Completed hepaticojejunostomy.
6.
S Completed Roux-en-Y hepaticojejunostomy.
Chapter 5
Liver
Important Topics
z Anatomy
zRadiological Anatomy
zPyogenic Liver Abscess
zAmebic Liver Abscess
zHydatid Cyst of Liver
zLiver Cyst
zBenign Neoplasm of Liver
zHepatocellular Carcinoma
zPortal Hypertension
‘Medicine is a science of uncertainty and an art of probability.’

William Osler (1849 –1919)
Canadian Physician
Diseases of the Liver
S Largest solid organ in the

body.
S Weight about 1.5 kg in
adult.
Couinaud System of Segmental

Nomenclature
S Right lobe (V + VI + VII + VIII).

S Left lobe (II + III + IV).
S Caudate lobe (I).
S The plane of middle hepatic vein and the primary

bifurcation of the portal vein divide the liver into
right and left lobe.
S Right lobe is divided into anterior and posterior

sectors by the plane of right hepatic vein.
z Right anterior sector (V, VIII)
z Right posterior sector (VI, VII).

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S Left medial sector (III, IV)
S Left lateral sector (II).
Segmental Anatomy of the Liver by CT Scan
S Segments cephalad to portal vein bifurcation.
S Segments caudal to portal vein bifurcation.

Benign Pathology
S Congenital cyst
S Polycystic liver disease
S Neoplastic cyst
S Bile duct cyst
S Pyogenic liver abscess
S Amebic liver abscess
S Hydatid cyst
S Hepatic adenoma
S Focal nodular hyperplasia
S Hemangioma.
Malignant Pathology
S Hepatocellular carcinoma
S Intrahepatic cholangiocarcinoma
S Hepatoblastoma
S Angiosarcoma
S Metastatic tumor.
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Pyogenic Abscess of Liver
How it Occurs
Liver has dual circulation, so it has a greater probability of developing abscesses of hematogenous origin.
Biliary route
Invasive procedures in the biliary tract (cholangiography, stent placement, biliary-enteric anastomosis) also lead to
abscess formation.
Portal venous route
Hepatic artery route

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Direct extension of infective process and trauma
Site and Number of Abscess
Right lobe or left lobe? Solitary or multiple?

Investigation
S ? USG
S ? CT scan.
Is chest X-ray helpful?

S Elevated hemidiaphragm.
S Right-sided pleural effusion.
S Atelectasis.
S Air-fluid level within the abscess (if gas-forming

organisms present).
USG reveals
S Round or oval area less echogenic than liver.
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USG and CT scan are the two most useful
modality for diagnosing hepatic abscess.
CT is more sensitive than USG, can more
easily detect multiple small abscesses.
CT scan shows multiple abscesses in liver
Treatment
Most likely the culture report will show:

S E. coli
S Klebsiella pneumoniae } Gram (–ve) aerobic bacilli
S Bacteroides fragilis Gram (–ve) anaerobe

S Enterococcus
S Microaerophilic streptococcus } Gram (+ve) aerobes

Different options for treatment of pyogenic abscess:
1.
2.
USG guided aspiration of liver abscess
3.
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4.
Amebic Liver Abscess
How it Develops
Glisson’s capsule is resistant to liquefaction necrosis process. Abscess cavity is criss-crossed by vascular and
biliary portal structures as they are covered by intrahepatic covering of Glisson’s capsule.
What About the Abscess
S Mostly solitary abscess.

S Commonly in right lobe.
S Posterior-superior part of right lobe—Most common

location.
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S A young male patient who resides in an endemic area or has recently traveled an endemic area, complaining of fever
with chill, pain in right upper abdomen; on examination, tenderness in right hypochondrium and hepatomegaly—
Think of amebic liver abscess.
S Children specially neonates, pregnant women and women in postpartum period are in increased risk group and
disease may become fatal in this group.
What Happens if Abscess Ruptures? Diagnosis
Is chest X-ray helpful?
S Chest X-ray is abnormal in about half of the cases

S Elevated right hemidiaphragm
S Pleural effusion
S Atelectasis
}Findings suggestive of
liver abscess
USG
S Peripheral location.
S Oval or rounded, clearly defined from surrounding
liver parenchyma with distal sonic enhancement.
S Poor rim echoes.
S Contents of abscess cavity hypoechoic and

nonhomogeneous.
CT is more sensitive than USG and helpful in differen-

tiating amebic from pyogenic abscess.
S Peripherally located
S Rim is nonenhancing.
nonenhancing
Is serology helpful?
ELISA is positive in >90% cases of amebic liver abscess, but it may reflect old infection particularly in endemic areas.
Management
1. Clinical features, imaging and serology suggestive of amebic abscess:

Metronidazole:
z 750 mg orally 3 times per day for 10 days
z Clinical improvement is usually seen within 3 days
z Other nitroimidazoles (secnidazole, tinidazole) are also effective.
2. Imaging and serology inconclusive, but clinically amebic abscess:

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Management of complicated scenario
Septa running across the cavity are blood vessels and bile ducts traversing the abscess cavity.
Intercostal drain tube should be placed close to axilla as right diaphragm is significantly elevated.
Hydatid Cyst
How it Develops
Liver acts as first line of defense

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What happens if the hexacanth embryo enters into pulmonary and systemic circulation?
About the Cyst

S Pericyst
z Fibrous tissue layer

z Represents an adventitial reaction to parasitic infection
z Acts as a mechanical support of the cyst
z Parasite derives its nutrition through this layer.
S Ectocyst or laminated membrane
z Acts as a barrier for bacteria.
S Endocyst or germinal membrane
z Responsible for the production of hydatid fluid, ectocyst, brood capsules, scoleces and daughter cyst.
Do you know
S Freed brood capsules, freed protoscoleces, calcerous bodies form ‘hydatid sand’.
S ‘Hydatid sand’ contains about 400,000 scoleces in 1 ml of fluid.
S The development of brood capsules from the germinal layer is a sign of complete biologic development of the cyst.
S Daughter cysts are replicas of the mother cyst.
S Daughter cyst formation is considered a defense reaction.
S Infection, the most common type of noxious agent induce daughter cyst formation.
S Cyst cavity is filled with a bacteriologically sterile, colorless fluid. This fluid contains salts, enzymes, proteins, toxic
substances, has antigenic properties.
Simple, uncomplicated liver cyst
Complicated scenario
Liver 139
Diagnosis
Is serology helpful?
S Casoni’stest is no longer used

S ELISA gives positive result in >90% of patients.
USG
S USG is superior to CT in the investigation of hydatid cyst.
WHO H=OOEł?=PEKJKB%U@=PE@ UOP
CL CE1
S Unilocular S Pure fluid collection
S No cyst wall (snow-flake sign)

S Parasite status—Active. S Parasite status—Active.
CE2 CE3
S Visible cyst wall S Detachment
S Internal septation of laminated
S Parasite status— membrane (Water
Active. lily sign)
S Parasite status—
Transitional.
USG of Liver shows characteristic

appearance of hydatid cyst
CE4 CE5
S Heterogeneous hypo/ S Thick calcified wall
hyperechogenic S Parasite status—
degenerative contents Inactive?
S No daughter cyst
S Parasite status—
Inactive.
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Type I — Pure fluid collection

Type II — Fluid collection with a split wall
Type III — Fluid collection with septa
Type IV — Heterogeneous appearance
Type V — Reflecting thick walls.
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Is USG alone sufficient for planning therapy?
S It is very important to localize the cyst in respect to liver segments and important vascular and biliary structures,
specially the hepatic veins. So, USG alone cannot provide all these informations.
Is CT helpful?
S CT reveals the most accurate information regarding the number, position in relation to segments as well as extent
of intraabdominal diseases.
S Eggshell or mural calcification on CT, is diagnostic of E.granulosus infection and differentiate it from carcinoma, liver
abscess or hemangioma.
S CT scan can demonstrate exogenous vesiculation, an important cause of recurrence in conservative surgery.
z Cysts full of daughter cyst

z Segment II, IVA part of VIII
involved.
CT abdomen shows cyst with daughter CECT abdomen showing hydatic cysts different
cysts in liver intraabdominal organs
IS ERCP necessary?
S When USG or CT detect hydatid material in CBD
S Patient with hydatid cyst presents with cholangitis and or jaundice.
ERCP followed by papillotomy facilitates clearance of bile duct.
Management
Consider following factors to choose treatment option

S Size of the cyst
S Location of the cyst
S Type of the cyst
S Patient’s general condition.

1.
P A I R
Percutaneous Aspiration Infusion of scolicidal agent Reaspiration
Do PAIR if
S Patienthave refused surgery

S Inoperable patient
S CL, CE1, CE2 and CE3
S Multiple cyst more than 5 cm in different liver segments.
Don’t do PAIR if
Technique of PAIR
S Albendazole (15 mg/kg daily in two divided doses) at least 4 days before PAIR procedure and to be continued for at
least 4 weeks afterwards.
Liver 143
No cystobiliary communication
[I] Infusion of scolicidal agent
[R] Reaspiration
Cyst obliteration usually occurs in 9–12 months.
PAIR is an acceptable treatment option because

S Safe
S Minimally invasive
S Easy to perform
S Low morbidity and mortality
S Shorter hospital stay
S Cost-effective.
2.
Do surgery in
Don’t do surgery if
S Patient refuses surgery

S Extreme age
S Pregnant women
S Comorbid illness
S Numerous cysts
S Cyst difficult to access
S Cysts partially or totally calcified
S Very small cysts.
Different operative procedures

Liver 145
Incision and exposure
Safe decompression of the cyst

Sterilization of the cyst
S The most frequently used and effective protoscolicidal agents:

z 15–20% saline
z 75–95% ethanol
z 0.1–0.5% cetrimide solution
z 10% povidone-iodine.
S Exposure time is important for 100% protoscolicidal effect.
Management of bile duct communication
Suspect cystobiliary communication if
S Cyst> 10 cm
S Occupies several liver segments
S Cholangitis.
Liver 147
Packing of cyst with white gauze pack
Wait for several minutes—Whether bile staining appear

or not—
S In most cases, the communication is with a peripheral
duct, simple suturing is sufficient.
Management of residual cavity
S Leavingthe cyst open

S Marsupialization
S Capitonnage
S Omentoplasty.
S Capitonnage: Infolding the redundant cyst wall

into the depths of the cyst with successive layers of
S Omentoplasty is best option. sutures.
S If cavity has a large volume, placement S Increased chance of venous injury due to their
of drain is beneficial. presence in adjacent to cyst walls.
Laparoscopic management
S Different
steps are almost same as open approach
S Majordrawback of laparoscopic approach is the risk of spillage
S Many devices have been constructed to ensure safe cyst penetration and evacuation.
Pharmacotherapy
S Pharmacotherapy is indicated in:

z Inoperable patients
z Patients with multiple cysts in two or more organs
z Multiple small cysts in liver
z Prevention and management of secondary hydatidosis
z Management of recurrent hydatidosis
z Combination with surgery and PAIR.
S Albendazole is the only drug that is ovicidal, larvicidal, vermicidal.
Congenital Liver Cyst
S Simple cyst
S Polycystic liver disease.
Simple Cyst of the Liver

How it develops
S Unilocularcyst
S Contain serous fluid
S No communication with intrahepatic biliary tree
S Size ranges from few mm to >20 cm
S In about 50% cases, single cyst
S Female to male ratio is 9:1.
Female patient of over 50 years having large liver cyst —Think of simple cyst of the liver.
Liver 149
Investigation
If patient is living in an area where

hydatid disease is endemic or any
possibility of being hydatid cyst, do
serological test for hydatid disease.
CECT abdomen showing simple cyst in liver
Treatment
Deroofing the cyst by laparoscopic approach is now a well-accepted method.

Polycystic Liver Disease Associated with Polycystic Kidney Disease
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S Multiple round or oval cysts with sharp

margins in liver and kidneys.
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Treatment
S Laparoscopic deroofing of large cysts
S Liver resection, if needed.
Resection should include most cysts with least loss of hepatic function.
Cystadenoma
A neoplastic cyst
S Rare tumor.
S Presents as a large cystic mass (10–20 cm).
S Strong tendency to recur.
S Malignant potential.
S Globular external surface with multiple protruding cysts and locules

of varying sizes.
S Contains mucinous fluid.
Clinical Presentation Diagnosis

USG
S Abdominal pain or discomfort
S Single, large, anechoic, fluid-filled avoid or
S Anorexia
globular area with irregular margins.
S Nausea
S Internal echoes are seen.
S Abdominal swelling.
Malignant degeneration is typically suggested on

imaging by large projections and markedly thickened
wall.
Hydatid disease must always be considered in the
differential diagnosis.
Cystadenoma and cluster of contiguous cyst of liver
must be differentiated, because their prognosis and
treatment are completely different.
Treatment
S Complete excision (even in asymptomatic patient)

S Leaving any disease increases the chance of recurrence and
development of cystadenocarcinoma.
Solid Benign Neoplasm
Liver Cell Adenoma Focal Nodular Hyperplasia
S Benign proliferation of hepatocytes.

S Second most common benign tumor of liver.
S Usually solitary nodule.
S Predominantly in young women.
S Size may extends upto 30 cm.
S Solitary, well-defined nodular mass involves right and left lobe
S Large blood vessels are often prominent
on the surface and also within the tumor. equally.
S Mass is characterized by a central fibrous scar with radiating
S Tumor is well-demarcated from the
surrounding liver. septa, central scar often contains a large artery.
S Mostly diagnosed incidentally at laparotomy or imaging.
S Predominantly in women of 20–40 years.
S CECT and MRI are diagnostic.
S Malignant degenerations still not reported.
S Often associated with OCP use.
S Only symptomatic FNH or enlarging FNH needs resection.
S Common presenting symptom is upper
abdominal pain.
S CT and MRI scan are diagnostic. If
inconclusive, 99Tc-MAA liver scan is
helpful.
S Two major complications are —1) Rupture
leads to intraperitoneal hemorrhage,
2) malignant transformation.
S In patient presenting with acute
hemorrhage, hepatic artery embolization
as a emergency procedure is effective.
S Symptomatic masses should be resected.
Anatomical or segmental resections are
the best option.
Liver 153
Hemangioma
S Most common benign tumor of the liver.

S Small capillary hemangiomas are of no clinical significance.
S Cavernous hemangiomas are associated with FNH.
S Usually < 5 cm, > 5 cm are described as giant hemangioma.
S Microscopically, they are large blood-filled spaces separated by incomplete

fibrous septa.
S Mostly discovered incidentally on imaging studies.
S Large liver hemangioma, thrombocytopenia and consumptive coagulopathy—Known as Kasabach-Merritt

syndrome.
S CT and MRI are diagnostic.
S Malignant degeneration never reported.
S Asymptomatic patient with definite diagnosis can be observed.
S Rupture, change in size and Kasabach-Merritt syndrome are indications for resection.
S Associated with recognized syndromes:
z Klippel-Trenaunay-Weber syndrome (hepatic hemangioma + congenital hemiatrophy).
z Osler-Rendu-Weber syndrome (hemangioma of liver, pancreas, cerebellum and retina).
Hepatocellular Carcinoma
How it Develops
How it Looks
Hanging type
S Attached to the normal liver parenchyma by small
vascular stalk.
S Easily resectable with little loss of parenchyma.
Pushing type
S Well-demarcated and encapsulated
S Displace major vessels rather than invasion
S Often resectable.
Infiltrative type
S Indistinct tumor—Liver interface.
S Vascular infilitration and invasion.
S Resection difficult with increased chance of positive

margin.
Growth patterns are of no significance in terms of prognosis except fibrolamellar variant of HCC.
Fibrolamellar HCC
S Well-demarcated and encapsulated with a central fibrotic area.
S Commonly found in young patient without underlying cirrhosis.
S AFP is not usually elevated.
S Increased resectability with prolonged survival rate due to well-circumscribed nature and absence of underlying
cirrhosis.
S Triad of dull aching abdominal pain, weight loss, stony hard hepatic mass.
Liver 155
S Decompensated cirrhosis S Sudden onset of abdominal pain with swelling.
z Male patient with previously well-controlled S Tender abdomen with guarding and rebound
cirrhosis develops ascites, recurrent variceal tenderness.
hemorrhage, encephalopathy. S Hemodynamically unstable and usually in
hypovolemic shock.
Obstructive jaundice
S Massive ascites S Direct growth of the tumor into bile duct.
z Involvement of hepatic vein IVC causing S Extrinsic compression of extrahepatic bile
Budd-Chiari syndrome. duct by lymph nodes.
S Paraneoplastic syndromes (presents in less than 1% patients with HCC):

z Erythrocytosis
z Hypercalcemia
z Hypoglycemia
z Gynecomastia.
Diagnosis
Doppler USG
S Hypoechoic ill-defined lesion.

S Doppler study can assess the patency of portal and
hepatic veins.
S Helpful in distinguishing HCC from metastatic tumors
because HCC has a typical ring sign when <2 cm.
Particularly useful for screening of cirrhotic patients
for the development of HCC.
CECT
Triple phase helical thin slice CT

z Early vascular or arterial phase
z Portal phase
z Delayed phase
CECT is helpful to define:

}Triple phase
S Size and site of lesion
S Relationship to portal and hepatic veins
S Extent of biliary involvement
S Nodal and peritoneal metastases.
Contrast enhancement in arterial phase (about 30s

after contrast administration) and rapid washout in por-
tovenous phase (about 90s after contrast administration)
is typical pattern of HCC.
In some centers, lipiodol (oily derivative of poppy
seed) is combined with iodine contrast medium—Mix-
ture is retained by the tumor and has been used in CT to
evaluate small HCCs.
MRI
Is good at detecting intrahepatic lesions, specially T2-weighted studies?
Don’t forget to do a CXR!! HCC commonly metastasize to lungs and bone.

Liver 157
How serum AFP is helpful
S Hypervascular mass consistent with HCC and AFP > 400 ng/ml PIVKA II (desgammacarboxy prothrombin
protein induced by vitamin K absence) is also
Think of HCC positively increased in HCC.
S Increased level is also found in chronic hepatitis, following liver
resection or injury, seroconversion following Hep B infection.
S Serum AFP monitoring is helpful to detect recurrence.
Is pathologic diagnosis necessary?
S Detection of a hepatic mass within a cirrhotic liver is highly suspicious

of HCC.
S Patients with suspected liver lesion suggestive of HCC on imaging
(CT or MRI) and candidates for potentially curative surgical therapy
do not require preoperative biopsy.
S Do percutaneous needle biopsy only, if patient is a candidate for
palliative therapy.
CT guided FNAC from liver SOL
Plan for Appropriate Treatment
Staging laparoscopy—Additional in-

formation about extent of disease, ex-
traheptic disease and cirrhosis.
AJCC/TNM staging
Tumor + lymph node metastasis +
distant metastasis
Bercelona clinic liver cancer (BCLC) sys-
tem— Performance status (by ECOG
PS tool) + Child-Pugh grading + tumor
stage
CLIP staging
Morphology + Child-Pugh score +
AFP (ng/ml) + portal vein thrombosis
Okuda staging
Tumor size + ascites + serum albumin
Pugh’s modification of Child’s grading of cirrhosis— + serum bilirubin
Bilirubin (mg/dl) + prothrombin time prolongation (in secs) + INR + al-
bumin (g/dl) + ascites + encephalopathy.
2. Determination of functional liver reserve—

By Child-Pugh grading of cirrhosis
A. Well-compensated cirrhosis
B. Decompensating cirrhosis
C. Decompensated cirrhosis.
Treatment strategies are more dependent on the under-

lying liver disease than stage of the tumor.
A multidisciplinary team consisting of hepatologist, In-
terventional radiologist, surgical oncologist, transplant
surgeon, medical oncologist is essential for comprehen-
sive management of HCC.
Partial hepatectomy
Principles of resection—Principle 1: Resection of tu-

mor with free margin of at least 5 mm Principle 2: Little blood loss
Principle 3: Minimal blood transfusion Principle 4: Maximal preservation of nontumorous liver

Principle 5: Minimal manipulation of tumor
Liver 159
Portal vein embolization
Liver transplantation
Ideal candidate
Milan criteria are the most commonly used criteria for liver transplantation.
S Child-Pugh Class B or C
S Tumor d5 cm
S No macrovascular involvement
S No identifiable extrahepatic spread of tumor to surrounding lymph nodes, lungs, abdominal organs or bone.
What is MELD score?

S MELD—Modified end stage liver disease.
S Developed as a result of limited allograft availability.
S Complex equation includes creatinine, bilirubin, INR.
S Patient with highest MELD—Highest risk of dying—Highest priority in transplantation.
Radiofrequency ablation
4-prong needle electrode Multiple array needle electrode
Ethanol injection
Indications
S Tumor < 3 cm
S Isolated tumor recurrence after operation.
Absolute alcohol induces cellular dehydration, coagula-

tive necrosis and vascular thrombosis leads to death of
tumor cells.
Transarterial chemoembolization (TACE)

Transarterial radioembolization (TARE)
S Based on the principle of preferential tumor blood
S Microspheres made of glass or gelatin loaded
supply from hepatic artery.
with radioactive yttrium (emits E radiation).
Groups for Surveillance for HCC [as per American As- z All cirrhotic hepatitis B carriers
sociation for Study of Liver Disease (AASLD) guide- z Patient with high HBV DNA.
line]: S Nonhepatitis B cirrhosis
S Hepatitis B carriers
z Hepatitis C
z Asian men > 40 years
z Alcoholic cirrhosis
z Asian women > 50 years
z Genetic hemochromatosis and cirrhosis
z Africans > 20 years
z Primary biliary cirrhosis (stage 4)
z Family history of HCC
z D–1 antitrypsin deficiency and cirrhosis.
Surveillance with 6 monthly ultrasonography and AFP level.

Liver 161
Liver Metastases
S Most metastases originate from gastrointestinal primary tumors. (colorectal,

stomach, pancreas, biliary system).
S Other common primary sites:
z Eye
z Breast
z Neuroendocrine tumor
z Cancer of kidney, prostate
z Melanoma
z Lung.
Most relevant metastatic primary tumor is colorectal carcinoma because of

well-documented potential for long-term after resection.
How it Looks
Peroperative picture of liver metastases
Triphasic MDCT is crucial for evaluating liver metastases.

S Hypodense lesion in portal venous phase—
Metastases from primary tumors of GI tract.

S Homogeneous enhancement in early arterial phase
with isoattenuation in portal venous phase—
Primary tumors are:
z Renal cell carcinoma
z Neuroendocrine tumor
z Breast carcinoma
z Melanoma.
Multiple metastatic lesion in liver

Treatment
Ablation therapies (e.g. radiofrequency

ablation, ethonol injection are other
alternative approaches.
Portal Hypertension
Know the Anatomy
S Normal portal venous pressure 5–7 mmHg.

S Portal venous system is entirely devoid of
valves.
Liver 163
What Happens When Portal Hypertension Develops
S Numerous small tributaries drain into portal and systemic veins.

S Resistance to portal venous flow at any site leads to increased pressure in portal system resulting in opening of
collaterals at various sites of portal-systemic communications.
Why Portal Venous Obstruction
S In western countries, the

most common cause of portal
hypertension is cirrhosis.
S In India, noncirrhotic portal
fibrosis and extrahepatic
portal venous obstruction
account for about 50% of
cause of portal hypertension.
Noncirrhotic Portal Fibrosis
S Etiology—Not known
Extrahepatic Portal Vein Obstruction (EHPVO)
S Portalvein replaced by multiple branches —Portal cavernoma

S About 75% of children with portal hypertension having EHPVO.
S Common causes—
z Neonatal peritonitis
z Umbilical vein catheterization
z Hypercoagulable states
P. rubra vera
Myelofibrosis
Protein C deficiency
Protein S deficiency.
Budd-Chiari Syndrome
Type I
S Major hepatic vein obstruction
S Patient IVC.
Type II
S IVC obstruction above the level of hepatic venous opening.
Liver 165
Type III
S IVC obstruction
S Hepatic vein obstruction.
Causes of Budd-Chiari syndrome:

S In western countries
z Primary myeloproliferative disorders
z Paroxysmal nocturnal hemoglobinuria
z Protein C, protein S, antithrombin III deficiency.
S In India
z Pregnancy related hypercoagulability
z Infections
z IVC web or membrane.
Cirrhosis
Etiology
S Alcohol
S Posthepatitis (B and C)
S Primary biliary cirrhosis.
What is left-sided portal hypertension (sinistral portal hypertension)?
S Isolated splenic vein thrombosis results into development of isolated varices in fundus.
Investigations
Liver 167
Management
Pharmacotherapy
Balloon tamponade
S Used in acute life-threatening

bleeding from esophageal
or gastric varices that not
responding to medical therapy,
endoscopic hemostasis.
S Immediate endoscopic sclero-
therapy not possible due to ex-
cessive bleeding obscuring the
view.
How Balloon tamponade system works?
S Used only in emergency situations.
Endoscopic treatment
S Sclerosants used—
z 1.5% sodium tetradecyl sulfate
z 0.5–1% polidocanol
z 5% sodium morrhuate.
Causing necrotizing inflammation and secondary throm-

bosis of varices.
Liver 169
Indication of endoscopic treatment
S In acute bleeding episode
S Prevention of recurrent hemorrhage.
TIPS (transjugular intrahepatic

portosystemic shunt)
S Image guided radiological procedure.

S It is the procedure of choice in patient with
poor liver reserve as a bridge to liver transplant.
S Indicated
z For control of acute esophageal/gastric

variceal bleeding after failure of pharmaco-
therapy.
z For control of recurrent variceal bleeding
despite endoscopic treatment.
Surgical treatment
Nonselective shunts
End to side portocaval Side to side portocaval

S Portal vein is divided S Maintain the continuity of portal vein
S End of portal vein is anastomosed to side of IVC. S Shunt of choice in Budd-Chiari syndrome.
S Interposition
z Mesocaval
z Mesorenal.
S Interposing a conduit of autologous vein graft/
synthetic graft between superior mesenteric vein and
IVC/renal vein.
S Internal jugular vein as autologous vein graft.
S Dacron/PTFE as synthetic graft.

Liver 171
Splenorenal (proximal)
S Splenectomy done
S Hilar end of splenic vein is anastomosed to renal vein.
Selective shunts
Distal lienorenal shunt (Warren shunt)

S Distal end of splenic vein is anastomosed to side of
left renal vein.
S To maintain selectivity, important is to ligation of it
gastric vein, right and left gastroepiploic vein and
retrogastric collaterals.
Partial shunt
S Small diameter shunt between portal vein and IVC using PTFF ring supported 8 mm graft.
Devascularization procedures
Chapter 6
Pancreas
Important Topics
zzAnatomy
zzAcute Pancreatitis
zzChronic Pancreatitis
zzCystic Neoplasm of Pancreas
zzPancreatic Carcinoma
‘Seeing is an experience. A retinal reaction is only a physical state ……. People, not their eyes, see. Cameras and eye-balls,
are blind …….. there is more to seeing than meets the eyeball.’
Norwood Russell Hanson (1924 – 1967)
American Philosopher of Science
Pancreas 175
Diseases of the Pancreas
Anatomy
Acute Pancreatitis
How it Develops
SS Mildto severe continuous pain in upper abdomen

zz Radiates to back.
zz Sudden onset.
zz Pain relieved in sitting and leaning forward position, aggravated

by coughing, deep breathing.
zz Usually associated with nausea and vomiting.
zz Localized epigastric tenderness of variable intensity.
zz Epigastric fullness.
zz Gross distension of abdomen.
zz Tympanic abdomen.
zz Voluntary and involuntary guarding.
zz Tachycardia and hypotension.
Diagnosis
Pancreas 177
Blood tests
SS Estimation of serum amylase and/or lipase is still the gold standard for diagnosis of acute pancreatitis
SS Raised amylase or lipase level do not predict etiology, prognosis or severity of pancreatitis
SS Values 3 times above normal are almost specific
SS Not raised in:
zz Severe necrotic pancreatitis
zz Acute on chronic pancreatitis.
SS Severe amylase raised in many abdominal and extraabdominal conditions (e.g. peptic perforation)
SS Serum lipase is only secreted by pancreas—Better specificity and sensitivity
SS If patient presents after 3–4 days, serum lipase and urinary amylase is diagnostic, not serum amylase.
Imaging
Ultrasonography is the initial imaging technique for evaluating

patients with acute pancreatitis.
Common findings in USG
SS Biliary sludge or stone in gallbladder, dilatation of CBD
SS Increased pancreatic volume
SS Changes of pancreatic parenchyma
SS Presence of peripancreatic fluid collections.
Limitations of USG
SS Pancreasnot visible in many patients due to overlying gas filled bowel loops
SS Cannot assess organ perfusion, so diagnosis of pancreatic necrosis is difficult.
When to perform CECT?
SS Patients with acute pancreatitis not improving after 3–4 days of conservative therapy
SS Patient’s condition deteriorating even after treatment.
How CECT helpful?
SS Evaluate severity of inflammatory pancreas.

SS Detect complications such as pancreatic
abscess, pancreatic necrosis.
SS CT guided fine needle aspiration to detect
presence of infected pancreatic necrosis.
When CT guide FNAC is indicated?
SS Patient of acute pancreatitis with CECT suggestive of pancreatic necrosis, now in a unfavorable clinical state and
with features of toxicity.
Is straight X-ray abdomen is necessary?
SS Clinical features of acute pancreatitis and perforative peritonitis are similar in many aspects. To rule out perforation,
X-ray abdomen, X-ray chest is helpful.
SS Classic ‘Sentinel loop’ [due to localized ileus of duodenum and proximal jejunum] and ‘Colon cut off sign’ [ localized
ileus upto midpoint of transverse colon] if present, is suggestive of acute pancreatitis.
SS ‘Ground glass’ appearance (due to retroperitoneal fluid accumulation) is also a suggestive X-ray finding.
Is MRI helpful?
SS MRI is comparable to CECT regarding assessment of severity.
Assessment of Severity
SS To predict prognosis
SS To identify those patients whom need more intensive care.
Pancreas 179
CT grading system
SS Grade A— Normal pancreas.
SS Grade B—Focal or diffuse enlargement.
SS Grade C—Mild peripancreatic inflammation.
SS Grade D—Single fluid collection.
SS Grade E—Two or more fluid collection or gas within

pancreas or within peripancreatic inflammation.
Management
Medical management
SS Treat agressively with IV fluid and electrolyte replacement.

SS Analgesia—Narcotic analgesics, e.g. pentazocin, tramadol
zz Avoid morphine – Causing spasm of sphincter of Oddi.
SS Antibiotics—Value of prophylactic antibiotics remains controversial.
SS Nutritional support—Early enteral feeding help to reduce the actue phase response and gut derived complications
of pancreatitis.
SS Nasogastric suction—Indicated only if persistent vomiting, ileus.
Endoscopic management
SS Endoscopic sphincterotomy + stone/sludge extraction (if it is biliary pancreatitis)
Surgical management
1. In mild pancreatitis (stone induced)
2. In severe pancreatitis (stone induced)
3. Infected pancreatic necrosis

Pancreas 181
Complications
Acute fluid collection
SS Lack of wall of granulation or fibrous tissue.

SS Most are peripancreatic, some are intrapancreatic.
SS More than half regress spontaneously.
SS Rarely detectable clinically, diagnosed by imaging.
SS Represent an early point in the development of

acute pseudocyst or pancreatic abscess.
SS No specific treatment is required.
SS Attempting to drain fluid collection may lead to

infection.
CT scan showing acute fluid
collection
Sterile pancreatic necrosis
SS Nonviable pancreatic or peripancreatic tissue.

SS Most of the sterile pancreatic necrosis will eventually
recover nonoperatively.
Infected pancreatic necrosis

SS Nonviable pancreatic or peripancreatic tissue with
infection.
SS Necrosectomy is indicated.
Pancreatic abscess
SS Circumscribed intraabdominal collection of pus,
closely to the pancreas.
SS Contains little or no necrotic tissue.
SS Truly a infected pseudocyst.
Pancreatic fistula
SS Result of ductal disruption associated with

pancreatic necrosis.
SS Most of the fistulas will close nonoperatively.
SS Some may require operative repair—Anastomosis

between pancreatic duct and Rous-en-Y limb of
jejunum.
Pseudocyst
CT scan showing acute pseudocyst of pancreas

Pancreas 183
Waiting for spontaneous resolution?
Management
SS Thinks to keep in mind:

zz Be sure, it is a pseudocyst, not a neoplastic cyst
zz No history of acute or chronic pancreatitis or trauma, then think twice
zz Take time to allow the pseudocyst to mature
zz Cyst symptomatic–causing compression of contiguos organs-think of intervention regardless of size
zz Be sure, you are not operating on a pseudoaneurysm.

Cystogastrostomy
SS Pseudocyst adheres to stomach and indenting it.
Operative picture of pseudocyst–cyst is confirmed after aspira-

tion of clear fluid
Cystoduodenostomy
Cyst cavity is opened
SS Pseudocyst adherent to duodenum and indenting it.

Pancreas 185
Roux-en-Y cystojejunostomy
SS Pseudocyst arising from the body and tail of

pancreas.
SS Cyst not adherent to stomach and bulging through
left transverse mesocolon.
Resection of tail of pancreas
SS Pseudocyst arising from tail of pancreas.
Percutaneous catheter drainage
SS Particularly useful in the management of immature symptomatic pseudocyst.

Endoscopic treatment
Pancreas 187
Chronic Pancreatitis
What Happens at Cellular Level?
SS Most common symptom.

SS Usually epigastric in location with radiation
to back.
SS Pain typically steady and boring.
SS Persists for hours or days, taking food or

alcohol usually exacerbate pain.
SS Patient with pain typically sit in a bending
forward position or lie on their side in a
fetal position.
Pancreas 189
Malabsorption and steatorrhea
}
SS Trypsinogen (inactive) Enterokinase Trypsin (active)
SS Chymotrypsinogen (inactive)
Enterokinase Chymotrypsin (active) Proteolytic enzymes
SS Proelastase (inactive)
Enterokinase Elastase (active)
SS Phospholipase A2 (inactive)
SS Pancreatic lipase (active)
Phospholipase A2 (active)
} Lipolytic enzymes
SS Pancreatic amylase (active)
SS Steatorrhea
zz Bulky, foul smelling, loose stool pale in color

and float on the surface of water.
SS Frank diabetes in about 20% patients.

SS Ketoacidosis and diabetic nephropathy are
relatively uncommon.
Pancreatogenic diabetes SS Distal pancreatectomy and whipple procedure
have a higher incidence of diabetes than drainage
operations.
SS Enhanced peripheral sensitivity to insulin and
decreased hepatic sensitivity to insulin.
SS Patients become hyperglycemic when insulin
replacement is insufficient (due to unsuppressed
hepatic glucose production).
SS Patients become hypoglycemic when insulin
replacement is barely excessive (due to enhanced
peripheral insulin sensitivity and a deficiency of
pancreatic glucagon secretion to counteract the
hypoglycemia).
SS The main goals of treatment of chronic pancreatitis is not the treatment of disease itself, rather management
of usual manifestations and complications.
Diagnosis
SS Fordiagnosis
SS Evaluation of severity of disease
SS Detection of complications
SS Determining treatment options.
USG
SS Initial imaging in patients with abdominal symptoms
SS Heterogeneous echotexture of pancreas

SS Pancreatic duct dilatation
SS Intraductal filling defects
SS Cystic changes.
CECT
SS Pancreatic calcifications are diagnostic of chronic

pancreatitis.
SS Pancreatic duct dilatation.
SS Cystic changes.
SS Pseudocyst.
Pancreas 191
MRCP
SS Useful imaging technique for detecting ductal

abnormalities.
SS Ability to image the duct proximal to obstruction.
SS Noninvasive.
SS Contrast not required.
SS No exposure to ionizing radiation.
EUS
SS Can detect small neoplasm in the setting of chronic

inflammation.
SS Small intraductal lesion, intraductal mucus, cystic
lesions, subtle ductular abnormalities are detected.
SS Tissue samples can be obtained under image
guidance.
ERCP
SS Is indicated only if diagnosis is uncertain despite use

of other imaging modalities.
SS Placement of pancreatic duct stent to relieve
obstruction.
SS For draining pseudocyst.
SS For taking biopsy or brushing for cytology.
Conservative management
Treatment Total abstinence from alcohol

SS Dietary alterations
Frequent small meals
SS Pancreatic enzyme supplement
zz [Nonenteric coated] — For pain management
zz [Enteric coated] — For steatorrhea management.
SS Pain management—NSAIDs
⇓ Not controlled
Opioid analgesics
Endoscopic management
SS Management of pseudocyst.
SS Management of CBD Stenosis.
Surgical management
Drainage procedures
SS Puestow procedure
SS Partington and Rochelle’s modifica-
tion of Puestow procedure.
Puestow procedure
SS Originally described by Puestow and Gillesby.
SS Body and tail of pancreas was mobilized.

SS Tailof pancreas was resected.
SS Splenectomy was done.
SS Gland longitudinally opened.
SS Gland was invaginated into a Roux-en-Y

limb of jejunum.
Pancreas 193
Partington and Rochelle’s modification of Puestow procedure
Limited resection and drainage

SS Freyprocedure
SS Beger procedure } Can be performed whether or not pancreatic duct is dilated.
Frey procedure
SS Coring of the head of pancreas.
Beger procedure
SS Duodenum preserving resection of the head of pancreas.
Resection procedures:
SS Distal pancreatectomy
SS Pancreaticoduodenectomy—
zz Standard
zz Pylorus preserving.
SS Central pancreatectomy
SS Pancreatic resection with islet cell autotransplantation.
Distal pancreatectomy
Pancreas 195
Pancreaticoduodenectomy
SS Nondilated pancreatic duct.

SS Enlarged head of pancreas with cyst
and calcifications.
SS Previous ineffective ductal drainage.
SS Suspicion of malignancy.
Pylorus preserving pancreaticoduodenectomy
Cystic Neoplasms of Pancreas
SS Benign
zz Serous cystadenoma
zz Mucinous cystadenoma (most common)
zz Intraductal papillary-mucinous adenoma (second common)
zz Mature cystic teratoma.
SS Borderline
zz Mucinous cystic tumor with moderate dysplasia
zz Intraductal papillary-mucinous tumor with moderate dysplasia
zz Solid pseudopapillary tumor.
SS Malignant
zz Duct adenocarcinoma
zz Serous/mucinous cystadenocarcinoma
zz Intraductal mucinous papillary tumor.

Facts that Must Keep in Mind

SS Solid component in a cystic lesion, septations in a cyst—Think of cystic neoplasm
SS Pseudocysts should be biopsied at the time of internal drainage—
zz to rule out benign or malignant neoplastic lesion.
SS Dilated pancreatic duct should be biopsied at the time of decompression procedure to rule out ductular neoplasm
SS In a patient without history of pancreatitis, cystic lesion in pancreas is a cystic neoplasm until proved otherwise
SS Any cystic pancreatic lesion with malignant potential should be resected.
Mucinous Cystadenoma
Diagnosis
SS Multiplelarge cystic spaces at the region of tail of

pancreas.
Treatment
Pancreas 197
Intraductal Papillary Mucinous Tumor: IPMN
Diagnosis
SS IPMN follows adenoma–carcinoma sequence

SS Pan IN-1 Pan IN-2 Pan IN-3
(minimal dysplasia) (moderate dysplasia) (severe dysplasia or CIS)
Treatment
SS Pancreaticoduodenectomy/Central pancreatectomy/Distal pancreatectomy—Based on location of the cyst.

Serous Cystadenoma
Diagnosis
Treatment
SS Asymptomatic patient—Follow up (only if diagnosis is very much certain)

SS Symptomatic or any doubt in diagnosis—Resection.
Pancreas 199
Pancreatic Carcinoma
Pathology
SS Ductal adenocarcinoma of pancreas develops

from a initial intraepithelial neoplasm, termed as
pancreatic intraepithelial neoplasm (Pan IN), graded
into 1A, 1B, 2 and 3.
SS Ductal adenocarcinoma is the most common histologic type (about 85%)– arises from ductal epithelial cells.
SS Others:
zz Acinar cell carcinoma—Presents as larger tumor but a better prognosis.

zz Adenosquamous carcinoma
zz Undifferentiated carcinoma with osteoclast-like giant cells
zz Colloid carcinoma
zz Signet ring cell carcinoma.
SS Ductal adenocarcinomas infiltrate along nerve sheath (perineural growth), lymphatics.
SS Lymph node metastasis and distant metastasis (e.g. liver) are commonly present.
SS Fibrosis is a characteristic finding in both chronic pancreatitis and ductal adenocarcinoma. Image guided tissue
biopsy is therefore often misleading and inconclusive.
SS Elderly patient who present with pancreatitis

but without history of alcoholism or
gallbladder stone — Search for pancreatic or
periampullary carcinoma.
SS Recent-onset diabetes in elderly patient
specially if combined with vague abdominal
pain—Search for pancreatic carcinoma.
SS Cancer involving the body and tail of
pancreas—Only present with abdominal
pain and weight loss.
Advanced Carcinoma Presents With

Pancreas 201
Investigations
Serum markers
SS CA 19-9 (carbohydrate antigen 19-9) elevated in about 75% of patients with pancreatic cancer
SS Also elevated in benign conditions of pancreas, liver and bile ducts
SS ↑↑CA 19–9 is suggestive of advanced disease or metastatic disease
SS Postresection ↑CA 19–9 indicates recurrence.
USG
Multiphase multidetector helical CT
CT is an important diagnostic modal-

ity to determine resectability of the
tumor.
Magnetic resonance imaging
SS Intraand extrahepatic ductal dilation on imaging

SS No discrete mass lesion on CT
MR imaging–
zz Information about tumor size and extent
zz Intraductal anatomy of biliary and pancreatic ductal system
zz Status of the adjacent vascular structures.
MRCP
Endoscopic ultrasonography
zz When tissue diagnosis is necessary for neoadjuvant therapy or palliative chemoradiotherapy, EUS guided FNAC
is helpful.
Pancreas 203
ERCP
SS When stenting is needed for preoperative biliary decompression or palliative purpose.

SS When tissue diagnosis is needed.
SS Classic findings in ERCP:
zz Long irregular stricture in pancreatic duct with distal obstruction.
zz Cutoff of both the pancreatic duct and distal bile duct at the level of genu of the pancreatic duct— ‘Double duct
sign’.
Is tissue diagnosis necessary?
Tissue diagnosis is necessary when—

SS Tumor appears unresectable
SS High operative risk
SS Need neoadjuvant or palliative chemoradiation
SS Lymphoma is suspected.
Role of Laparoscopic Staging
SS Role controversial.
SS In pancreatic head lesion, laparoscopy is not justified because if tumor founds unresectable per operatively, only
palliative bilioenteric and gastroenteric bypass is beneficial, to relief jaundice and duodenal obstruction.
SS In left sided lesions (in body and tail) where there is no role of surgical bypass, staging laparoscopy is justified to
avoid unnecessary laparotomy.
Treatment
Borderline resectable tumor:

SS Tumor abutment of SMA (superior mesenteric artery)
SS Severe unilateral SMV or portal vein impingement
SS Gastroduodenal artery encasement upto its origin from the hepatic artery
SS Colon and mesocolon invasion.
Treatment of resectable tumor
Criteria of resectability:
SS Absence of extrapancreatic disease
SS Patient SMPV confluence
SS No direct tumor extension to celiac axis of SMA
SS No radiographic evidence of SMV and PV abutment, distortion, tumor thrombus or venous encasement.
Pancreas 205
Steps of resection
Steps of reconstruction
Palliative treatment
SS 3clinical problems that require palliation:

zz Jaundice
zz Duodenal obstruction
zz Pain.
Surgical palliation of jaundice and duodenal obstruction
Surgical palliation of pain
Nonoperative palliation of obstructive jaundice and duodenal obstruction

Chapter 7
Spleen
Important Topics
zzAnatomy
zzFunctions of Spleen
zzIndications of Splenectomy
zzSplenectomy
‘I would never use a long word, even, where a short one would answer the purpose. I know there are professors in this coun-
try who ‘ligate’ arteries. Other surgeons only tie them and it stops the bleeding just as well.’
Oliver Wendell Holmes (1809 –1894)
American Writer, Physician and Physiologist
Spleen 209
Splenic Pathologies
Anatomy
Care must be taken during splenectomy to avoid injury

to the pancreas.
Care must be taken during splenectomy to avoid injury to the adjacent structures.
Types of Distribution of Splenic Artery
Distributed type 70%
Magistral type 30%
Keeping in mind the different types of distribution of splenic artery helps to avoid difficulty during splenectomy.
SS Ligaments are nothing but duplications of peritoneum.

SS Gastrosplenic ligament contains short gastric vessels that runs from greater curvature to splenic hilum.
SS The other ligaments are generally avascular except in portal hypertension or myeloproliferative disorders.
SS During dissection of ligaments, extra care should be given regarding hemostasis in patient with portal hypertension
or myeloproliferative disorders.
Spleen 211
Functions of Spleen
SS Removal of senescent and defective red blood cells, red cell inclusion bodies —In the red pulp
SS Synthesis of antibodies—IgM, tuftsin, opsonin, properdin, interferon—In the white pulp
SS Removal of antibody-coated bacteria and antibody-coated blood cells from the circulation.
What is Accessory Spleen?
Operative picture showing accessory spleen
Failure to identify accessory spleen may lead to recurrence of certain hematologic disorders for which splenectomy is
performed.
What is Ectopic Spleen (Wandering Spleen)?
SS Torsion of pedicle — Emergency splenectomy.

SS Pelvic spleen — Elective splenectomy.
What is Splenosis?
In a few percentage of patients with splenic rupture
SS Ectopic splenic tissue may cause pain or

gastrointestinal obstruction.
SS Must be distinguished from peritoneal nodules of
metastatic carcinoma, accessory spleen.
Spleen 213
When to do Splenectomy?
SS Diffuse enlargement of spleen by neoplastic disorders, hemopoietic disorders, metabolic and storage disorders
SS Autoimmune disorders
SS Trauma to the spleen
SS Splenic vein thrombosis and splenic artery aneurysm
SS Cyst, tumor, abscess in spleen
SS Iatrogenic splenectomy
SS Incidental splenectomy
SS Staging splenectomy.
In Chronic Myelogenous Leukemia

SS Splenectomy does not affect natural history of disease
SS Removal of spleen makes patient more comfortable
SS Significantly reduce transfusion requirements.
In Hairy Cell Leukemia and Prolymphocytic Leukemia

SS Significanttumor regression in bone marrow and other sites of disease following splenectomy
SS Corrects thrombocytopenia in 70–85% of case and anemia in 60–75% of cases.
In Idiopathic Myelofibrosis
SS Splenectomy is indicated in
zz Major hemolysis unresponsive to medical management
zz Massive splenomegaly causing symptoms
zz Life-threatening thrombocytopenia
zz Portal hypertension with variceal hemorrhage.
In Hereditary Spherocytosis
SS Splenectomy is the treatment even the patient is asymptomatic and anemia is compensated.
SS If associated cholelithiasis (pigment stone), cholecystectomy should be performed along with splenectomy.
SS Unless the clinical manifestations are severe, splenectomy should be delayed until age six.
SS Children under age 5 with high transfusion requirements, partial splenectomy (80%) may correct while maintaining
normal immune functions.
SS Splenectomy cures the anemia and jaundice in all patients.
In Thalassemia Major
SS Splenectomy is indicated for
zz Excessive transfusion requirements > 200 ml/kg/year
zz Discomfort
zz Painful splenic infarction.
SS Careful assessment of risk: benefit ratio is essential.

Idiopathic Thrombocytopenic Purpura

SS Indicated in—
zz Patients who do not respond to steroids
zz Relapse after an initial remission on steroids
zz Steroid dependent patients.
Staging of Hodgkin’s Disease
SS Noninvasive staging is not a reliable basis for treatment decision.

SS Staging affects treatment as early stage patients who have no splenic involvement may be candidates for
radiotherapy alone, those with splenic involvement generally require chemotherapy or multimodality therapy.
CT scan showing abscess in both spleen and liver
Cyst and Tumors of Spleen
SS Hydatidcysts
SS Dermoid cysts
SS Epidermoid cysts
SS Endothelial cysts
SS Pseudocyst.
CT scan showing large cyst in spleen
Spleen 215
Iatrogenic Splenectomy
SS Chance of injury during mobilization of spleen and

pancreas in left adrenalectomy, left nephrectomy
SS Increased chance of injury during mobilization of
splenic flexure of colon.
SS Whenever possible, splenorrhaphy should be
attempted instead of splenectomy.
Incidental Splenectomy
SS Only contraindication to splenectomy is

the presence of marrow failure, in which
enlarged spleen is the only source of
hemopoietic tissue.
Prophylaxis
SS Routine revaccination of immunocompetent persons who are previously vaccinated with PPV 23 not recommended
SS Onlyone PPV23 revaccination is recommended in high-risk individuals

SS Long-term penicillin prophylaxis is not recommended.
Advice to Splenectomized Patient

SS Consider any unexplained fever as a medical emergency and prompt medical attention is necessary
SS Avoid areas where babesiosis is endemic
SS Use medical bracelet noting asplenia.
Splenectomy
SS Platelets should not be administered preoperatively in ITP patients because these cells will not survive.
SS Patient with myeloproliferative disorders who have a tendency to develop thrombosis, low dose heparin therapy
is beneficial.
SS Nasogastric tube is placed during operation to decompress the stomach.
1. Incision
SS Left subcostal incision about 2–5 cm below the
costal margin.
2. Transection of ligamentous attachments [by blunt/sharp dissection]
SS Ligaments are avascular except in portal hypertension.

Spleen 217
3. Ligation of ligament
Operative picture showing ligation of short gastric vessels
4. Ligation of splenic pedicle
SS Care must be taken to avoid injury to the tail of

pancreas.
SS Axial rotation of the spleen should be avoided
because this may lead to disruption of splenic artery
or vein.
5. Observation to check hemostasis
SS Thorough exploration to detect any accessory

spleen.
SS Initial ligation of the splenic artery and vein into the
lesser sac—If marked lymphadenopathy in splenic
hilum precludes safe dissection of the vessels.
Postsplenectomy Blood Picture
SS Immediate period
zz Leukocytosis, thrombocytosis. Within 2–3 weeks, counts and survival of each lineage become normal.
SS Permanent picture
zz Anisocytosis
zz Poikilocytosis
zz Howell-Jolly bodies (nuclear remnant)
zz Heinz bodies (denatured Hb)
zz Basophilic stippling.
SS This type of blood picture in a patient having spleen—Think of splenic infiltration by tumor–tumor is interfering the
normal culling and pitting function.
Chapter 8
Abdominal Wall,
Peritoneum, Mesentery,
Retroperitoneum
Important Topics
zzCongenital Defects of Abdominal Wall

zzAcquired Anomalies of Abdominal Wall
zzAbdominal Abscess
zzPseudomyxoma Peritonei
zzMesenteric Cyst
zzAcute Mesenteric Lymphadonitis
zzMesenteric Panniculitis
zzMalignancies of the Mesentery
zzOmental Infarction
zzRetroperitoneal Abscess
zzRetroperitoneal Hematoma
zzRetroperitoneal Fibrosis
zzRetroperitoneal Neoplasm
‘Every one is fond of comparing himself to something great and grandiose, ………… , I am a mere street scavenger (chiffo-
nier) of science. With my hook in my hand and my basket on my back, I go about the streets of science, collecting what I find.’
Francois Magendie (1783–1855)
French Physician and Physiologist
Abdominal Wall
Congenital Defect
Exomphalos
Exomphalors
SS Due to failure of the lateral folds of the body wall to fuse during formation of the body of the embryo.
SS Associated with 50–60% incidence of other congenital anomalies of skeleton, GI tract, nervous system, genitourinary
system and cardiopulmonary system (most common).
SS Associated with Beckwith-Wiedemann syndrome [omphalocele + hyperinsulinemia + macroglossia] postnatal
hypoglycemia due to pancreatic islet hyperplasia, Cantrell’s pentalogy, karyotype abnormalities (trisomy 13, 18, 21).
Abdominal Wall, Peritoneum, Mesentery, Retroperitoneum 221
Gastroschisis
Gastrochisis
SS Nonrotated bowel is matted, thickened, covered by a fibrinous ‘peel’ due to exposure of amniotic fluid.
SS Liver herniation is absent.
SS Incomplete mesenteric rotation and fixation leads to the infant at risk for mesenteric volvulus with resultant
intestinal ischemia and necrosis.
SS Concomitant congenital anomalies occur in about 10% of patients (mostly in GI system)—Intestinal atresia most
common abnormality.
Antenatal management
SS ↑ maternal serum α-fetoprotein provide the first clue.

SS Antenatal USG is diagnostic.
SS Gastroschisis and nonsyndromic exomphalos are not indications for termination of pregnancy because the
prognosis is excellent.
SS Termination should be considered for exomphalos with associated severe anomalies.
SS Delivery at a specialist center is recommended.
Postnatal management
SS Immediate problems are heat and fluid loss from the eviscerated bowel.
SS Every baby with exomphalos must be examined for signs of Beckwith-Wiedemann syndrome (macrosomia,
macroglossia, omphalocele) because severe hypoglycemia may occur due to pancreatic islet hyperplasia resulting
in cerebral damage.
SS Wrapping up the whole of the trunk in plastic bag minimizes both heat and fluid loss.
SS Fluid deficit is corrected by crystalloids, 2–3 times the maintenance requirement.
Operative repair
SS Operative repair may be primary or staged.

SS If possible, primary closure after returning the herniated viscera.
SS If primary closure not possible, plastic spring-loaded silo can be placed onto bowel and allows graduated reduction
daily. Surgical closure can be tried after that.
Infantile Umbilical Hernia
SS Most of the hernias resolve within the first two years

of life.
SS If hernia persists beyond the age of 3 or 4 years,
operative repair is indicated.
SS Rare chance of strangulation.
SS Caused by weakness in adhesion between remnant

of umbilical ring and umbilical cord.
If Omphalomesenteric Duct Persists
SS During fetal development, midgut communicated with the yolk sac through the vitelline or omphalomesenteric
duct
Usually the duct obliterates
1. SS Persistent omphalomesenteric duct resulting

enterocutaneous fistula.
SS Passage of meconium and mucus through the

umbilicus in the first few days of life.
SS Increased chance of mesenteric volvulus around the
persistent duct.
SS Treatment is—
zz Early laparotomy and excision of the fistulous
tract.
2. SS Duct near the umbilicus unobliterated.

Treatment is—
SS Excision of umbilicus along with band.
3.
Treatment is—
SS Excision of cyst with obliterated duct (fibrous band).
4.
Operative picture showing patent vitellointestinal duct
Treatment is—
SS Excision of the diverticulum.
SS Excision of the diverticulum along with band (if

band presents).
If Urachus Persists
1.
2.
Patent urachus
3.
Treatment
Acquired Abnormalities of the
Abdominal Wall
Diastasis Recti
SS Acquired condition in advancing age, obesity
or following pregnancy.
SS Don’t be mistaken as a ventral hernia.
Management
zz Reassurance of the patient and family.
zz Plication of the anterior rectus sheath in

severe diastasis.
Rectus Sheath Hematoma

Treatment
SS Small, unilateral and contained hematoma—Observation only.

SS If expanding hematoma, free bleeding or clinical deterioration —Emergency surgical intervention consists of evac-
uation of hematoma and ligation of bleeding vessel.
Desmoid Tumor (Aggressive Fibromatosis)
SS Sporadic occurrence or part of inherited syndrome (FAP).

SS Extra abdominal (e.g. shoulder girdle), abdominal wall and intraabdominal (mesenteric and pelvic desmoids) are
the different sites of tumor.
SS Sporadic abdominal wall desmoid tumors occur particularly in young women during gestation or within a year of
childbirth. OCP use is associated with this condition.
SS Estrogen receptor is detected in tumor.
SS Painless enlarging mass.
SS MRI provides information regarding extent of disease and its relationship to intraabdominal organs.
SS Though a low-grade fibrosarcoma, it is diffusely infiltrative and has increased tendency of local recurrence. Systemic
metastasis is extremely rare.
SS Complete resection with tumor-free margin is the treatment. Even with complete resection, chance of local
recurrence is very high.
SS Chemotherapy (doxorubicin, actinomycine, dacarbazine, carboplatin) is usually reserved for unresectable, sympto-
matic, clinically aggressive disease).
Peritoneum and Peritoneal Cavity
SS Peritoneal cavity is divided into

several potential spaces.
SS Knowledge about the peritoneal space helps

to predict the route of infection.
SS Communication from the left paracolic
gutter with the pelvis is limited due to
sigmoid colon.
SS Communication from the left paracolic
gutter with the left subphrenic space is
limited due to phrenicocolic ligament.
Abdominal Abscess
SS Intraperitoneal
SS Retroperitoneal
SS Visceral.
Diagnosis
SS USG is a useful tool for diagnosis of

intraabdominal abscesses.
Disadvantages of USG
zz Image is distorted by bowel gas.
zz Staples, dressing, stomas may impede

ultrasound.
zz Cannot differentiate abscess from
hematoma, lymphocele, biloma,
seroma.
SS CT is more accurate in evaluation specially
for retroperitoneum and pancreas.
SS One of the drawbacks is inability to
differentiate between subphrenic abscess
and pulmonic fluid.
About Different Intraabdominal Abscess
Management
Percutaneous drainage
SS Successful outcome in
Subphrenic abscess
Paracolic abscess
Superficial pelvic abscess.
Surgical drainage
Surgical drainage is first choice in:

SS Interloop abscess
SS Ill-defined abscess
SS Infected hematoma.
Can be used in other abscess when percutaneous drain-

age is unsuccessful.
SS Midline incision
SS Abscess cavity should be widely opened
SS Closed suction drain should be placed in dependent position.
Pelvic Abscess
Characteristic symptom
zz Passage of mucus in the stool
in a patient recovering from
peritonitis or bowel surgery.
zz Diarrhea.
zz Fever.
Treatment
SS For superficial abscess
zz Percutaneous drainage.
SS For deep seated abscess
zz TRUS guided drainage
zz TVS guided drainage.

Malignant Peritoneal Mesothelioma
SS Most common primary malignant peritoneal neoplasm.

SS Patient presents with abdominal pain, ascites and weight loss.
SS 50–70% of patients have a history of asbestos exposure.
SS Local invasion of liver, intestine and abdominal wall is common.
SS Complete surgical resection is technically demanding and requires peritonectomy with resection of involved
organs.
Pseudomyxoma Peritonei
Mesentery
Mesenteric Cyst
SS Twice as common in women.

SS Clinically,midabdominal mass
is palpable.
SS USG or CT is diagnostic.
SS Cyst deroofing or marsupialization

is not recommended due to high
propensity of recurrence.
Acute Mesenteric Lymphadenitis

Mesenteric Panniculitis
SS Most of the patients are
asymptomatic.
SS Spontaneous resolution of the
symptom is very common.
SS Symptoms improve after
administration of corticosteroids
and immunosuppressive agents.
Malignancies of the Mesentery

SS Most common neoplasm involving the mesentery is metastatic disease from an intraabdominal adenocarcinoma
SS Most common primary malignancy of the mesentery is desmoid tumor.
Mesenteric Desmoid
SS Commonly associated with FAP (familial adenomatous polyposis).
SS Increased chance of complications (intestinal obstruction, ischemia, perforation, aortic rupture) due to its close
relationship to vital structures and tendency to infiltrate adjacent organs.
SS Patient with minimal symptoms may be managed with watchful waiting, sulindac and antiestrogen therapy.
SS Imatinib mesylate can arrest disease progression.
Omentum
Omental Infarction
SS May be primary or secondary (associated with

hernia, adhesion, tumor).
SS Two times more common in men.
SS Patients present with acute onset of severe pain

most commonly in right side.
Treatment
SS Resection of involved omentum and management
of related cause.
Omental Cyst
SS USG or CT shows fluid filled complex,

cystic mass with internal septations.
Treatment
SS Excision of cyst (open/laparoscopic
approach)
Omental Graft and Transpositions
Retroperitoneum
Retroperitoneal Abscess
SS Clinicalfeatures
zz Abdominal or flank pain
zz Fever with chill
zz Malaise
zz Weight loss.
SS CT is the investigation of choice
SS Treatment
zz Antibiotics and CT guided drainage in

unilocular abscess.
zz Antibiotics and open drainage in multilocular
abscess.
Retroperitoneal Hematoma
SS Patient present with abdominal or flank pain.
SS Palpable abdominal mass is present.

SS CT is the diagnostic modality of choice—
High density mass in the retroperitoneum with

surrounding stranding in the retroperitoneal tis-
sue planes.
SS Treatment
zz Restoration of blood volume
zz Correction of coagulopathy
zz Embolization of the bleeding vessel
zz Surgical exploration.
Retroperitoneal Fibrosis
Etiology
SS Idiopathic
retroperitoneal fibrosis is also called
‘Ormond disease’.
Idiopathic (70%)
Etiology SS Drugs (methysergide, b-blockers, hydralazine,

a-methydopa, entacapone).
SS Infections.
Secondary to SS Trauma.
SS Retroperitoneal hemorrhage.
SS Radiation therapy.
SS Autoimmune disorders (ankylosing spondylitis,

SLE, Wegener’s granulomatosis, polyarteritis
nodosa).
SS Malignancies (prostate, NHL, sarcoma, carcinoid
tumor, gastric carcinoma).
Idiopathic Retroperitoneal Fibrosis (Ormond Disease)
SS Belongs to the group of fibrozing syndromes (other diseases: mediastinal fibrosis, sclerosing cholangitis, Riedel’s
thyroiditis, Peyronie’s disease).
SS No etiological factor found.
SS Usually affects men in the fifth or sixth decade of life.
SS Antibodies to ceroid, a lipoproteinaceous by-product of atheromatous plaque oxidation, are present in more than
90% of patients.
SS Allergic or autoimmune mechanism has been postulated.
Clinical features
SS Nonspecific symptoms including abdominal or flank pain, weight loss, loss of appetite, malaise
SS In advanced stage of the disease, bilateral ureteric obstruction lead to renal failure
SS Hypertension may be present.
Diagnosis
SS IVU shows hydronephrosis and hydroureter

associated with delayed excretion and medial
deviation of the ureter.
SS CT shows fibrous plaque that is isodense or slightly
hyperdense compared with surrounding muscle.
SS Mass should be biopsied to rule out malignancy.
Treatment
SS First,
to rule out whether the disease is secondary to
malignancy, drugs or infectious etiologies or not.
SS Corticosteroids is the mainstay of medical therapy.
SS Patient with moderate or massive hydronephrosis

warrants surgical intervention.
Wrapping of the ureter

with omentum
Retroperitoneal Neoplasm
SS Patients with Von Recklinghausen’s disease and Li-Fraumeni syndrome have an increased incidence of sarcoma.
SS Mutations of p and RB-1 genes have a predilection for the development of sarcoma.
53
SS Most patients present with asymptomatic abdominal mass.
SS Abdominal pain, GI hemorrhage, early satiety, nausea, vomiting, weight loss, lower extremity swelling are usual
clinical manifestations.
SS CT and MRI are useful imaging modality to determine size and location of the tumor and its relation to important
structures.
SS Treatment is en bloc resection of the tumor and any involved organs. Radical lymphadenectomy is not indicated.
SS Local recurrence even after complete resection is common.

Chapter 9
Stomach
Important Topics
zzAnatomy
zzPeptic Ulcer Disease

zzGastric Outlet Obstruction
zzGastritis
zzMalignant Neoplasms of Stomach

zzGastrointestinal Stromal Tumor
zzGastric Lymphoma
zzOther Gastric Lesions
zzPostvagotomy Syndromes
‘The extraordinary development of modern science may be her undoing. Specialism, now a necessity, has fragmented the
specialities, themselves in a way that makes the outlook hazardous. The workers lose all sense of proportion in a maze of
minutiae.’
William Osler (1849 –1919)
Canadian Physician
Stomach 243
Diseases of the Stomach
Anatomy
Peptic Ulcer Disease

Factors Responsible
SS Helicobacter pylori
SS NSAID
SS Acid
SS Others.
H. pylori
H. pylori can also found in:

SS Heterotopic gastric mucosa in proximal esophagus and Barrett’s espophagus
SS Gastric metaplasia in duodenum
SS Meckel’s diverticulum
SS Heterotopic gastric mucosa in the rectum.

Stomach 245
How NSAID damage mucosal defense mechanism
Role of acid
Linear relationship between MAO and parietal cell number.
Other factors responsible
↑ gastric acid secretion

SS Smoking
↓ gastroduodenal prostaglandin and bicarbonate production

SS Burninjury may cause — Peptic ulcer [Curling’s ulcer]
SS Head injury may cause— Peptic ulcer [Cushing ulcer].
Pathophysiology
Pathophysiology of Duodenal Ulcer
Pathophysiology of Gastric Ulcer
SS On the lesser curvature near the incisura

SS Normal/low acid output
SS Impaired mucosal defense
SS Ulcer at the body of stomach associated with

duodenal ulcer
SS ↑↑ acid secretion
Stomach 247
SS On the prepyloric region

SS Behave like duodenal ulcer
SS ↑↑ acid secretion
SS On the lesser curvature near the GE junction

SS Normal acid secretion
SS Impaired mucosal defense
SS Exact pathogenesis not known.
Clinical Presentations of Gastric Ulcer

Complicated Scenario
SS Bleeding gastric ulcer are prognostically not good in comparison to bleeding duodenal ulcer
SS Hemorrhage is frequently observed in type II, III and IV gastric ulcers
SS It is often difficult to differentiate between gastric carcinoma and benign ulcer
SS Duodenal ulcer never turns malignant.
Investigations
Stomach 249
SS Benign ulcer crater extend beyond the luminal
margin of the stomach and have radiating gastric
folds.
SS Malignant ulcers do not extend beyond the luminal
margin and have parallel gastric folds.
SS Radiographic study showing gastric ulcer must be
followed by endoscopy and guided biopsy.
Upper GI Endoscopy
Endoscopic pictures of stomach and duodenum
Benign peptic ulcer
Upper GI endoscopy is the most sensitive and specific

approach.
Malignant gastric ulcer
Resected specimen of stomach showing malignant

gastric ulcer
H. pylori Testing
Noninvasive tests
Stomach 251
Invasive tests
Treatment
Acid Neutralizing/Inhibitory/Cytoprotective Drugs
Proton pump inhibitors require an acidic environment within the gastric lumen to become activated. So antacids or H2
receptor antagonists should not be used in combination with PPIs.
Other mechanisms by which sucralfate helps in ulcer

healing—
SS Concentrate fibroblast growth factor
SS Enhance prostaglandin synthesis
SS Stimulate mucus and bicarbonate secretion.

Stomach 253
H.Pylori Eradication
SS H.pylori should be eradicated in all patients with documented PUD

SS No single agent is effective for eradication
SS Combination therapy for 14 days provided the highest efficacy
SS Triple therapy is recommended
[Antibiotic + PPI/H2 blocker/Bismuth compound]

SS Quadruple therapy is recommended when there is infection with a resistant organism
SS The test of choice for documenting eradication is urea breath test.
When to do Surgery?
Management of Intractable Peptic Ulcer
First, think why the ulcer is intractable or nonhealing:

Exclude the possibilities:
SS Gastric carcinoma
SS Persistence of H.pylori infection
SS Noncompliant patient
SS Zollinger-Ellison syndrome
If the ulcer is truly intractable or nonhealing duodenal ulcer
Highly selective vagotomy — Surgery of choice

(Parietal cell vagotomy)
Taylor procedure [anterior seromyotomy + posterior truncal vagotomy]

A simple alternative to highly selective vagotomy
Operative picture of truncal vagotomy

Stomach 255
Recommended technique of pyloroplasty
Management of Intractable or Nonhealing Gastric Ulcer

Type I ulcer
Typically present at the junction of antral and fundic mucosa.
Vagotomy is not recommended [because acid output is normal/low].

Stomach 257
Type II ulcer and Type III ulcer
Highly selective vagotomy is not recommended.
Type IV ulcer
Perforation
SS H.pylori (about 60%), NSAID use, smoking, alcohol consumption are associated with perforated peptic ulcer
SS Mortality rate is higher in perforated gastric ulcer.
Patient Presents with
SS History of chronic epigastric discomfort, NSAID use

SS Diffuse abdominal tenderness
SS Guarding
SS Card-board rigidity
SS Peristaltic sound —Absent or sluggish.
Diagnosis
SS Free air is present in 70% of patient with perforated

peptic ulcer in chest X-ray.
[So, absence of free gas can’t exclude the diagnosis of
perforation].
SS If free air is seen in X-ray, other investigations are of
any value or not?
zz The answer is no, but if USG is done, it will
demonstrate free air and occasionally ‘fish-eye’
sign (if anterior wall of duodenum is perforated.
Is CT necessary?
SS When the clinical diagnosis is preforated peptic Chest X-ray showing free gas under diaphragm
ulcer but in X-ray or USG, free air is not detected.
SS CT is very much accurate in detecting very small
amount of extraluminal free air. Fluid collection may Treatment
be detected in right subhepatic space or in lesser sac
in about 75% of patient with perforated ulcer.
SS Ruptured sigmoid diverticulitis can be diagnosed SS Resuscitation with IV crystalloids.
preoperatively, allowing the surgeon to use an ideal SS Nasogastric suction —To decompress the GI tract.
incision for laparotomy. SS Catheterization —To monitor urine output, so that
fluid resuscitation can be properly maintained.
SS IV broad-spectrum antibiotics.
A patient with sudden onset of severe upper abdominal SS Use of invasive hemodynamic monitors (central ve-
pain associated with pneumoperitoneum in X-ray, the nous catheter, arterial/pulmonary artery catheter)—
diagnosis is perforated peptic ulcer primarily duodenal, If indicated.
until proved otherwise.
Stomach 259
Operative or conservative?
zz Nasogastric suction
zz IV fluid
zz Parenteral antibiotics + intensive monitoring of vital parameters
zz Proton pump inhibitors
zz H.pylori eradication.
SS If subhepatic or subdiaphragmatic abscess develops offer conservative management
⇓
USG/CT guided percutaneous drainage of abscess
SS Conservative management is effective in properly selected patients.
Surgical Intervention of Perforated

Duodenal Ulcer
Options are
SS Simple omental patch closure
SS Patch closure with parietal cell vagotomy
SS Patch closure with Truncal vagotomy and drainage.
Simple omental patch closure [Graham’s patch]
Operative picture showing perforation at D1

Operative pic showing repair of perforation with

omental patch
SS Care must be taken during introduction of needle so that

SS In patient with hemodynamic instability. posterior duodenal mucosa is not entrapped within the
SS In patient with exudative peritonitis (> 24 hours bile
of contamination) SS Sutures should be tied loosely enough so that blood
supply to the omentum is not compromised.
Patch closure with parietal cell vagotomy
SS Patient known to be H.pylori negative

SS Presents with chronic history of peptic ulcer
SS Patient who needs long-term NSAID use
SS Risk of noncompliance with H.pylori eradication therapy
SS Hemodynamically stable
SS Early presentation [< 24 hours of contamination].
Patch closure with truncal vagotomy and

drainage procedure
SS Pyloroplasty is not justified as drainage procedure,

in the setting of duodenal ulcer perforation due to
excessive duodenal scarring.
Stomach 261
Surgical Intervention of Perforated Gastric Ulcer
Type I ulcer
SS Vagotomy is not recommended.
Type II and III ulcer
SS As they behave like duodenal ulcer, operative management is same as perforated duodenal ulcer.
Bleeding Peptic Ulcer
SS Concomitant use of steroid and NSAIDs increases

the risk of ulcer bleeding many times.
SS Alcohol and smoking are also related with ulcer
bleeding.
SS Patient presents with any of the following or
together—
zz Hematemesis
zz Melena
zz Hematochezia.
SS Patient without any history suggestive of

liver disease or chronic alcoholism, bleeding
peptic ulcer should be considered as the
most likely cause of upper GI hemorrhage.
Stomach 263
Emergency Surgery of Bleeding Gastric Ulcer
Type I Ulcer Type II and Type III Ulcer
Gastric Outlet Obstruction

Causes
SS Gastriccarcinoma
SS Duodenal ulcer and type III gastric ulcer
SS Chronic pancreatitis
SS Carcinoma of head of pancreas.
History of long standing peptic ulcer disease may be present.

Distended stomach with visible peristalsis
Investigations
SS Elevatedhematocrit—Due to dehydration
SS Hypokalemic, hypochloremic metabolic alkalosis
SS Hypoalbuminemia—In advanced disease.
Diagnosis
CT scan is only indicated, if

obstruction is due to malignant
lesion
CECT showing dilated contrast filled stom-

ach with old food debris
Treatment
SS Nasogastric suction—To decompress the stomach and prevent aspiration

SS Fluid resuscitation with NS and correction of hypokalemia with IV potassium supplement
SS Catheterization—To monitor urine output
SS Nutritional support with TPN (if necessary)
SS H.pylori eradication therapy.

Stomach 265
Many cases of outlet obstruction particularly acute obstruction will resolve with such conservative management

If not resolves
Surgical management
Preoperative management
SS Decompression of stomach with NG tube

SS Salineirrigation through NG tube to remove the gastric contents
SS Correction of dyselectrolytemia
SS Prophylactic IV antibiotics.
Surgery of chronic GOO due to duodenal ulcer
Surgery of obstructing type II and type III gastric ulcer

Antrectomy + truncal vagotomy + H. pylori eradication
Gastritis
SS Type A gastritis SS Ménétrier’s disease

SS Type B gastritis SS Lymphocytic gastritis
SS Reflux gastritis SS Eosinophilic gastritis
SS Erosive gastritis SS Granulomatous gastritis
SS Stress gastritis SS Phelgmounous gastritis
Type A Gastritis
SS An autoimmune condition (antibodies to the parietal cell develops)
SS Hashimoto’s thyroiditis, Addison’s disease may be associated.

SS Patients with Type A gastritis are at increased risk of developing gastric cancer —Screening by endoscopy is justified.
Type B Gastritis Reflux Gastritis
SS Associated with H.pylori infection SS Caused by enterogastric reflux

SS Mainly involves the antrum SS Common after gastric surgery
SS Patients are prone to PUD SS Bile chelating or prokinetic agents are useful in
SS Patient with pangastritis are at increased risk of treatment.
gastric carcinoma.
Stress Gastritis
SS Occurs following serious illness or injury.

Erosive Gastritis SS Due to decrease in blood supply of superficial
mucosa of stomach.
SS NSAIDs and alcohol are causative agents, by SS Prevention of stress ulceration and bleeding episode
disturbing the mucosal defense mechanism. is more effective rather than treating it.
Stomach 267
Ménètrier’s Disease Lymphocytic Gastritis
SS Chronic hypertrophic gastritis. SS Infiltration

of gastric mucosa by T cells
SS Characterized by gross hypertrophy of the gastric SS Associated with H.pylori infection.
mucosal folds, mucin production, hypochlorhydria.
SS Mainly affects the fundus and body.
SS Antrum is not affected. Eosinophilic Gastritis

SS Patient may present with hypoproteinemia, anemia.
SS The disease is premalignant.

SS Probably due to allergy.
SS Caused by over expression of transforming growth
factor alpha (TGF-alpha).
Phlegmonous Gastritis Granulomatous Gastritis
SS Rare bacterial infection of the stomach in patient SS Associated with tuberculosis and Crohn’s disease.
with severe intercurrent illness.
Malignant Neoplasms of Stomach
Adenocarcinoma of stomach
GIST of stomach
Adenocarcinoma of Stomach
Risk factors
Pathology
Stomach 269
Borrmann’s Classification System Lauren Classification System
(based on macroscopic appearance) (based on histology)
Intestinal type
SS Arises from precancerous lesion (e.g. gastric atrophy,
intestinal metaplasia).
SS More commonly in men.
SS More common in older age group.
SS More common in stomach cancer endemic zone.
SS Hematogeneous spread.
Diffuse type
SS Not arises from precancerous lesions
SS More commonly in women and younger patients
SS Higher familial occurrence (Blood group A)
SS Transmural/lymphatic spread
SS Tends to spread submucosally
SS Early metastasis
SS Prognosis less fovorable.

What is leather bottle stomach?

SS Also called Linitis plastica.
CT scan showing leather bottlle stomach
What is early gastric cancer?

SS When gastric cancer is confined to the mucosa and submucosa irrespective of lymph node involvement.
This type of gastric cancer is common in particularly Japan, where there is intense surveillance program.
Genetic events in gastric cancer

Stomach 271
Patterns of spread
Local extension
Lymphatic metastases
SS Japanese system of classification.

SS Sixteen lymph node stations have been mapped

around the stomach. (1 – 16)
SS 1–6 stations – (N )—First echelon
1
7–12 stations – (N2)—Second echelon
13–16 stations – (N3)—Third echelon
1 + 3 + 5
[along lesser curvature]
+
2 + 4 + 6 N1
[along greater curvature]
7–12
N2
N3 In this classification, involvement of station 2 in an-

SS Posteriorto pancreatic head (13) tral carcinoma is regarded as M1 disease, as involve-
SS Along the superior mesenteric vessels (14) ment of station 2 lymph node is rare and also carries
SS Along the middle colic artery (15)
poor prognosis.
SS Paraaortic lymphatics (16)
Stomach 273
Any of the following: Obstructive symptoms

SS Nonspecific symptom
Early satiety may indicated diffusely infiltrative tumor
Presents with GI bleeding Visible peristalsis in gastric outlet

obstruction
With Palpable Virchow’s node (in left supraclavicular area)

or lymph node in left axilla (Irish’s node)
Melena is more often encountered than hematemesis
[Indicates lymphatic spread of tumor via thoracic duct]

Advanced disease
Uncommon presentation
SS Transverse colon is a potential site of fistula formation and obstruction resulting from involvement of tumor
SS Intestinal obstruction may develop due to diffuse pertoneal spread of tumor.
Investigations for confirmation of diagnosis and staging
SS Flexibleupper GI endoscopy considered to be the best method to diagnose gastric cancer

zz Endoscopy directly visualizes the lesion
zz Endoscopy allows biopsy of the tissue for H/P
zz Endoscopy allows to assess the size, location and morphology of the tumor
zz Multiple biopsy specimens (seven or more) should be taken to achieve a high diagnostic accuracy
zz Addition of direct brush cytology increase the diagnostic accuracy.
Triphasic CT with oral and IV contrast

CT abdomen and pelvis—Important part of staging.
SS Assessment of perigastric lymphadenopathy, retroperitoneal
lymphadenopathy, peritoneal metastases (> 5 mm) and liver
metastasis.
SS Assessment of tumor penetration through the gastric wall.
SS With multiphase, multidetector spiral CT imaging, the accuracy of

assessment of extragastric disease and tumor penetration is more.
SS MRP-MDCT (multiplanar reconstruction-multidetector CT) with
combined air and water distension is superior to conventional
axial imaging, but has almost no role in detection of early gastric
cancer and small metastases (<5 mm) in liver or peritoneum. CT abdomen showing distended stomach with old
food particles
Stomach 275
SS Endoscopic ultrasonography (EUS): Ultrasound

transducer mounted on endoscope.
SS A cross section of the gastric wall can be demonstrated
ultrasonographically.
SS Useful tool for identify early gastric carcinoma.
SS Capable of defining the depth of invasion, an

important factor in choosing the type of surgery [e.g.
endoscopic resection, laparoscopic approach, open
approach]
Staging laparoscopy
SS Laparoscopy allows direct inspection of the peritoneal and visceral surfaces for detection of CT-occult metastases
SS Allows assessment of peritoneal cytology
SS Laparoscopic ultrasound may detect small deep metastases in liver.
[At laparoscopy, if metastatic disease is found, the disease is considered as incurable and laparotomy can be avoided.]
Newer diagnostic approaches to detect gastric carcinoma in early stage

SS Digital chromoendoscopy [helps to detect mucosal abnormalities through using short wavelength (blue) light].
SS Optical coherence tomography (OCT)— Principle is similar to EUS, except it uses infrared light instead of ultrasound.
It allows virtual ‘optical biopsy’.
SS Pepsinogen assay.
SS CA 72-4.
SS CEA.
SS Virtual gastroscopy.
SS Confocal laser endomicroscopy—It alows 3D visualization of lumen including subserosal structures, using laser and
contrast agent (e.g. fluorescein). It also allows real time ‘optical biopsy’.
SS Magnification endoscopy—Magnifies the endoscopic field by 1.5 to 150 fold.
Treatment
Assess—
SS Disease is curable or incurable (distant metastasis)?
SS Curative resection or palliative resection (for bleeding or GOO)?
SS Is patient fit for surgery?

Principles of curative resection
If RO resection can be achieved by partial gastrectomy, it is preferred over total gastrectomy, so that the sequele of
total gastrectomy can be prevented (e.g. early satiety, vitamin B12 deficiency).
Stomach 277
Type of gastrectomy depends on location of the lesion
Patient with distal lesion

Patient with GE junction lesion or proximal stomach

Stomach 279
Patient with midbody or fundal lesion
Extent of lymphadenectomy
16 or more lymph nodes are required to determine
the pathologic N stage.
SS D dissection: Removal of the involved part of the
1
stomach including greater and lesser omentum.
Perigastric lymph node.
SS D dissection: Entire omental bursa is removed
2
along with the front leaf of the transverse
mesocolon and clearance of vascular pedicles
of stomach. En bloc removal of second echelon
lymph nodes.
SS D dissection: Dissection of lymph nodes along
3
the hepatoduodenal ligament and the root of
mesentery in addition to D2 lymphadenectomy.
*Controversy present whether D1 or D2 dissection is
better in respect of postoperative mortality, morbidity
and 5-year survival rate.
In high-volume centers, spleen and pancreas pre-
serving D2 dissection can be performed.
What is endoscopic mucosal resection?

A recently developed endoscopy guided resection technique, without gastrectomy or lymphadenectomy, for treatment
of a group of early gastric cancer patients.
Tumor invading the submucosa are not suitable candidate for EMR, because of increased risk of lymph node
metastasis.
Gastrointestinal Stromal Tumor (GIST)
GIST comprises majority of mesenchymal tumors of the GI tract [other mesenchymal tumors of GI tract—Leiomyo-
ma, leiomyosarcoma, schwannoma, melanoma].
ICC cells are present in the myenteric plexus and regulate the gut peristalsis by coordinating the smooth muscle cells
of the gut with the autonomic nervous system.
Stomach 281
Histopathology
Spindle cell type of GIST is most common (about 70%) followed by epthelioid or round cell type.
SS Gastric GIST usually presented with abdominal pain, anorexia, weight loss or GI bleeding (in the form of melaena,
hematemesis, hematochezia or occult blood).
SS Rarely, tumor may ulcerate and cause significant intraperitoneal bleeding.
Immunology
SS KIT (CD117) expression is characteristic of most of the GIST. Other stromal tumors outside the GI tract do not
express KIT.
SS Other tumor markers are CD34, Desmin, Actin and S100 [CD34 is also expressed in desmoid tumors].
SS Not all KIT positive tumors are GIST.
[The diagnosis of GIST is based on clinical presentation, radiologic findings and tumor cell morphology. The KIT positiv-
ity supports the diagnosis of GIST.]
KIT mutations can be detected in about 85% of GIST. About 10% GIST harbor mutations in PDGFRA (mostly this
mutation is found in gastric GIST). About 5% GIST have no detectable kinase mutations. They are called wild type GIST.
Rarely, GIST harbor mutations in BRAF kinase.
Mutations are found in exon 11 of KIT (most common), followed by exon 9, exon 13, exon 17. Mutation in exon 9 is
almost always present in small bowel GIST.
Other tumors may express immunohistochemically detectable CD117: Ewing sarcoma, angiosarcoma, desmoid tu-
mor, melanoma, seminoma.
Investigations
CECT showing characteristic peripheral

entrancement pattern in GIST
Percutaneous biopsy
Indicated only when the mass seems to be irresectable and neoadjuvant imatinib therapy is planned. Endoscopic
ultrasound guided FNAC is the preferred approach.
Prognostic Factors
SS Sizeof the tumor → >10 cm— High risk of metastasis and recurrence
SS Site— Small bowel and rectal GIST have worse prognosis than gastric GIST
SS Mutation— GIST harboring PDGFRA mutations have very favorable prognosis
SS Mitotic rate of primary tumor—Increased mitotic rate carries more risk of metastasis or recurrence.
Stomach 283
Treatment

SS Surgery is the mainstay of therapy.
SS Goal of surgery is RO resection with en bloc resection of adjacent
organ if involved.
SS Rupture of tumor should be avoided to prevent dissemination of
tumor cells in peritoneal cavity.
SS Extended lymphadenectomy has no added benefit as lymph node
metastases are rare.
SS Palliative resection (R2 resection) is also beneficial for palliation of
pressure symptoms. Operative picture showing resection of gastric GIST
SS Imatinib therapy is indicated in recurrent and metastatic GIST.
SS Imatinib mesylate is a tyrosine kinase inhibitor which selectively

inhibits all ABL-tyrosine kinase (c-KIT, C-ABL, bcr-ABL and PDGFRA).
SS Role of neoadjuvant and adjuvant imatinib therapy is still under trial.
SS GIST harboring mutation in exon 11 of KIT shows higher objective response and disease control than harboring
mutation in exon 9 of KIT or no KIT mutation.
SS In Imatinib resistant GIST, sunitinib shows improved progression-free survival.
[GIST is resistant to chemotherapy and radiotherapy.]
Gastric Lymphoma
SS Stomach is the most common site of primary GI lymphoma (lymphoma arising in the gut without any evidence of
systemic involvement at the time of presentation).
SS The most common gastric lymphoma is diffuse large B-cell lymphoma thought to arise in mucosa associated
lymphoid tissue (MALT). Low-grade MALT lymphoma arises in the setting of chronic gastritis associated with
H. pylori. These low-grade lymphomas then transformed into high-grade lymphoma [t (11:18) translocation is a risk
factor for high-grade lymphoma]
SS Occur in older patients with the peak incidence of sixth and seventh decades.
SS More common in men (2 : 1).
SS Most commonly involves the gastric antrum.
SS Usually present with vague symptoms like epigastric pain, early satiety and fatigue. Systemic B symptoms (fever,
weight loss, night sweat) may present in about 50% of patients.
SS Endoscopy generally reveals nonspecific gastritis or gastric ulcerations.
SS EUS with EUS guided biopsy is diagnostic and can determine the depth of gastric wall invasion and nature of tumor.
SS CT chest and abdomen, bone marrow biopsy should be done to exclude distant disease.
SS H.pylori testing should be performed.
SS Low-grade MALT lymphoma often disappears after H. pylori eradication therapy. If low-grade lymphoma persists
after H. pylori eradication therapy, radiation therapy is the treatment for stage I disease. For advanced lesions,
chemotherapy with or without radiation therapy is the treatment.
SS Primary treatment is chemotherapy: CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).
SS Subtotal gastrectomy is only indicated when there is bleeding or obstructive symptoms.

Other Gastric Lesions
Hypertrophic Gastritis (Menetrier’s Disease)
SS Characterized by excess mucus production, protein loss and hypochlorhydria.

SS Exact cause of the disease not known, but associated with cytomegalovirus infection in children and H.pylori
infection in adults. Recently, it is suggested that local overexpression of transforming growth factor alpha results in
stimulation of epidermal growth factor receptor. This causes diffuse hyperplasia of secreting mucus cells.
SS Patient presents with epigastric pain, vomiting, weight loss, anorexia and peripheral edema.
SS Endoscopy reveals typical mucosal changes and biopsy should be performed to rule out carcinoma or lymphoma.
SS Medical management with anticholinergic drugs, acid suppression, octreotide, H.pylori eradication.
SS Total gastrectomy should be considered in patients who is suffering from massive protein loss or dysplasia/
carcinoma develops.
SS Treatment with epidermal growth factor receptor blocking monoclonal antibody, cetuximab is effecti in some
patients.
Mallory-Weiss Tear Other Treatment Options
SS Balloon tamponade
SS Angiographic embolization
SS Vasopressin infusion (selec-
tive/ systemic).
Stomach 285
Dieulafoy’s Gastric Lesion
SS Congenital arteriovenous malformation.

SS Commonly develops in middle aged or elderly men.
SS Upper GI endoscopy is the diagnostic and therapeutic modality of choice (multipolar electrocoagulation, laser
photocoagulation, sclerotherapy and band ligation). Other treatment option is angiographic embolization.
SS Repeat endoscopy may be necessary (because bleeding is intermittent).
SS If surgery is needed, wide wedge resection of stomach include the offending vessel is all that needed.
Gastric Volvulus
Organoaxial volvulus Mesenteroaxial volvulus

SS Gastric volvulus may be asymptomatic.

SS Patients may present with acute onset of abdominal pain, distention, vomiting and hematemesis. Dyspnea (due to
pressure on lungs), dysphagia may be present.
SS Sudden onset of constant upper abdominal pain, recurrent retching with production of little vomitus, inability to
pass nasogastric tube—Borchardt’s triad.
SS Diagnosis is confirmed by barium study or upper GI endoscopy.
SS Gastric infarction following acute volvulus is a surgical emergency.
SS Volvulus with diaphragmatic defect is treated with detorsion of stomach with repair of the hiatal hernia.
SS Volvulus without diaphragmatic defect is treated with detorsion and fixation of stomach by gastropexy.
SS In asymptomatic patient, expectant nonoperative management is advised.
Bezoars
Phytobezoars
Concretions of undigestable materials of vegetable origin.

SS Most commonly found in persons with impaired gastric emptying.
SS Diabetics with autonomic neuropathy are at risk.
SS Most commonly presented with obstructive symptoms.
SS Diagnosis is by either endoscopy or barium meal.
SS Treatment:
zz Enzyme therapy (papain, cellulose and acetylcysteine)
zz Endoscopic disruption
zz Surgical removal.
Most common type of phytobezoars occurs following ingestion of persimmons

(Diospyros virginiana). Unripe persimmons contains large amounts of phlobatannin
which form a tenacious glue that entraps fibers.
Trichobezoars
Concretions of hair in stomach

SS Usually found in trichophagics.
SS Patients present with gastric ulceration and obstructive symptoms.
SS Small trichobezoars may respond to endoscopic disruption.
SS Large trichobezoars need surgical removal —A cast of stomach and duodenum is

usually found.
SS Trichophagic patients need psychiatric care.
Stomach 287
Gastric Varices
SS Isolated gastric varices commonly develop secondary to portal hypertension or secondary to splenic vein
thrombosis.
SS Patient may present with acute upper GI bleeding.
SS Upper GI endoscopy can detect the location of varices. USG abdomen is necessary to exclude splenic vein thrombosis.
SS Treatment:
zz Temporary control of exsanguinating hemorrhage with the use of Sengstaken–Blakemore tube.
zz Endoscopic treatment with sclerotherapy.
zz TIPS (transjugular intrahepatic portosystemic shunt) is not so much effective (in most of the patient, a
spontaneous gastrorenal shunt develops that decreases the effectiveness of TIPS).
zz In patients with splenic vein thrombosis, splenectomy is effective in control of bleeding.
zz Balloon-occluded retrograde transvenous obliteration is a highly effective method for management of gastric
varices.
Postvagotomy Syndromes
Postvagotomy Diarrhea
SS The incidence of diarrhea is highest after truncal vagotomy and almost negligible after selective or highly selective
vagotomy.
SS Vagotomy disrupts the integrity of gastric and duodenal pacemakers→Altered gut motility with bacterial
overgrowth and impaired absorption of bile salts and bile acids—This is the probable pathogenesis.
SS In most patients, diarrhea resolve within 3–4 months after vagotomy.
SS Treatment is cholestyramine (anionic exchange resin).
SS If not responding to cholestyramine, surgery is indicated.

Postvagotomy Gastric Atony
SS After truncal or selective vagotomy, gastric emptying of solid is delayed.

SS In contrast, emptying of liquids is accelerated, because of loss of receptive relaxation in the proximal stomach.
[Mechanical causes such as postoperative adhesions, afferent or efferent loop obstruction, internal hernia, anastomotic
have to be ruled out.]
SS Patients with functional gastric outlet obstruction and documented gastroparesis, pharmacotherapy with
metoclopramide or erythromycin is effective.
Incomplete Vagal Transection
SS Sometimes truncal vagotomy procedure may be incomplete.

SS Right vagus is more related with this problem than the left because of difficulty in identification during surgery.
SS Patient may present with recurrent ulcer formation.
SS Histologic confirmation of the transected specimen of nerve trunk is necessary.

Stomach 289
Early Dumping Syndrome
SS More common after partial gastrectomy with Bilroth II reconstruction.
Medical therapy
SS Modification of diet—
zz Avoidance of liquid during meals.
zz Hyperosmolar liquid (e.g. milk shake) have to be

avoided.
zz Addition of dietary fiber may be helpful.
SS Long acting somatostatin analogue—Octreotide.

Late Dumping Syndrome
Afferent Loop Syndrome
SS Due to partial obstruction of the afferent limb resulting in partial emptying of its contents
SS Pathology behind the syndrome:
zz Kinking and angulation of the afferent limb
zz Internal herniation behind the efferent limb
zz Stenosis of GJ anastomosis
zz Twisting of the afferent limb resulting volvulus
zz Adhesion.
SS If afferent limb is > 30–40 cm and antecolic anastomosis: Chance of syndrome is more
SS In both acute and chronic afferent loop syndrome, surgery is indicated.

Stomach 291
Efferent Loop Obstruction
SS Lesscommon than afferent loop syndrome
SS Pathology behind the syndrome:
zz Herniation of the limb behind the anastomosis in a right to left fashion.
SS Surgical intervention is almost always necessary.
Alkaline Reflux Gastritis
SS Patientspresent with severe epigastric abdominal pain with bilious vomiting and weight loss.
SS HIDA scan is diagnostic, endoscopy may be performed.
SS In most of the patients, medical therapy is not beneficial. Surgery is indicated in these group.
Retained Antrum Syndrome
SS It develops if residual antrum is left in the duodenal stump after Bilroth II reconstruction.
SS Retained antrum is exposed to alkaline secretions (duodenal, pancreatic and biliary)
⇓
↑↑Gastrin release
⇓
↑↑HCl secretion
⇓
Recurrent ulcer formation
SS If medical therapy fails, surgery is indicated.
Malignancy
SS Gastrectomy or vagotomy (Truncal/selective) and drainage are risk factors for development of cancer (4 times risk
than normal population).
SS The time interval between the operation and development of malignancy is at least 10 years.
CHAPTER 10
Intestine
Important Topics
z Intestinal Obstruction
zCrohn’s Disease
zTyphoid Enteritis
zIntestinal Tuberculosis
zJejunal and Ileal Diverticula
zMeckel’s Diverticulum
zNeoplasms of Small Intestine
zShort Bowel Syndrome
zDiverticular Disease of Colon
zVolvulus
zLarge Bowel Obstruction

zUlcerative Colitis
zColorectal Polyp
zCancer of Colon
‘Medicine rests upon four pillars — philosophy, astronomy, alchemy, and ethics ……………….. , the fourth shows
the physician those virtues which must stay with him up until his death, and it should support and complete the three other
pillars.’
Paracelsus (C. 1493–1541)
Swiss Doctor and Chemist
Diseases of the Intestine
Intestinal Obstruction
Small Intestinal Obstruction
Which Factors are Responsible?

Intestine 295
Adhesion causing small intestinal obstruction Band causing small intestinal obstruction
Mechanical obstruction is the most common surgical disease of the small intestine.
Adhesions
S Adhesions secondary to surgery is the most common cause of small bowel obstruction.
S Adhesions are more likely develop after pelvic operations (gynecologic operations, appendectomy and colorectal
resection).
Hernia
S External hernia
z Inguinal
z Femoral
z Umbilical
z Epigastric
z Incisional.
S Internal hernia
z Paraduodenal
z Herniation into foramen of winslow
z Obturator.
S Internal hernia due to surgical defects
z Lateral to an ileostomy
z Mesenteric defects after intestinal resection.
Neoplasm
S Mostly metastatic lesions secondary to peritoneal implant from ovarian, pancreatic, gastric or colonic carcinoma.
S Large intraabdominal tumors can cause obstruction by extrinsic compression.
Intraabdominal abscess
S Abscess may occur from ruptured appendix, diverticulum or dehiscence of an intestinal anastomosis.
S Obstruction occurs due to local ileus adjacent to the abscess or the bowel can form a part of the wall of the abscess
resulting in kinking of the bowel.
What happens when obstruction develops?

S Intestinal motility and contractile activity increases
in an effort to propel the obstruction as well as
luminal contents.
S Intestine becomes fatigued, contractions becoming
less frequent and less intense.
S Intestinal proximal to the obstruction gradually
dilates.
S Fluid accumulates both intraluminally and in the
bowel wall.
S pmucosal absorption (absorptive flux).
S nintestinal secretion (secretory flux).
S Microvascular perfusions of the intestine impaired.
Ischemic changes in bowel.

S Strangulation develops.
What is Strangulation Obstruction?

It is a consequence of intestinal obstruction where
viability of the bowel in threatened due to compromised
blood supply.
Strangulation develops in:

Intestine 297
Pathophysiology
What is Closed Loop Obstruction?
When bowel is obstructed at both the proximal and

distal point.
S No distension of proximal bowel in early stage.
S If obstruction unrelieved, it leads to strangulation

Clinical Features of Intestinal Obstruction
and bowel necrosis.
4 cardinal features of obstruction:

• Abdominal pain
• Vomiting
• Abdominal distension
• Constipation.
Abdominal pain
S Pain coincided with increased peristaltic activity.
S Pain colicky in nature.
S Usually centered around umbilicus.
Lately
S Colicky pain replaced by mild diffuse constant pain.
S Severe pain is suggestive of strangulation/peritonitis.

S Visibleperistalsis may be observed particularly in thin
patients.
S On auscultation, high pitched metallic ‘rushes’ and
‘groans’ followed by the metallic tinkling sounds.
S Later,minimal or no bowel sound.

S Localized tenderness, rebound tenderness, guarding
suggestive of strangulation/peritonitis.
Vomiting
S The more distal the obstruction, the longer the interval between onset of symptoms and the appearance of vomiting.
Distension
S The more distal the obstruction, the more is the abdominal distension.
Constipation
S Either absolute (neither flatus nor feces) or relative (flatus is only passed).
Constipation is not present in certain conditions:

z Richter’s hernia
z Gallstone obturation
z Mesenteric vascular occlusion
z Partial obstruction.
How symptoms vary according to the level of obstruction!
Other manifestations
S Dehydration — due to repeated vomiting and third-space loss.
S Oliguria — due to dehydration
S Tachycardia
S Hypotension } Patient is in hypovolemic shock
S Fever — think of strangulation, peritonitis

S Respiratory distress — due to abdominal distension.
Intestine 299
These should be noted during clinical examination
S Hernial orifices (inguinal, femoral)
— Think of obstructed hernia.
S If any surgical scar
— Think of obstruction due to adhesion.
S Rectum (by digital examination)
— Look for rectal mass (causing large gut obstruction)
— Look for gross blood (presence suggests strangulation).
S Features of strangulation — Severe constant pain, generalized tenderness, rigidity and septic shock.
Diagnostic Evaluation
Goals of diagnostic evaluation will be—
S Distinguishing mechanical obstruction from ileus
S Etiology of obstruction
S Partial or complete obstruction?
S Simple or strangulating obstruction?
Investigations to confirm diagnosis

1. Usually by X-ray abdomen: Diagnostic [in most cases]
S X-ray abdomen in supine position
S X-ray abdomen in upright position
S When fluid levels are pronounced, the obstruction is advanced
S More the fluid levels, more the obstruction
S More the fluid levels, more distal the obstruction.
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Look for: Any clues about the cause of obstruction—

S Impacted foreign body
S Gas in the biliary tree associated with radiopaque shadow in right iliac fossa — Gallstone ileus.
Exclude: Other possibilities
}
S Paralytic
ileus
S Pseudoobstruction
Air-fluid levels may be seen in all these conditions.
S Acute pancreatitis
S Intraabdominal sepsis
2. CT scan abdomen: When the diagnosis is inconclusive even after X-ray abdomen, CT is beneficial.
S CT can determine the location and cause of obstruction
S Can detect strangulation.
S CT findings in simple obstruction:
z Discrete transition zone with proximal bowel dilated
z Distal bowel decompressed
z Contrast not passing beyond transition zone
z Colon containing little gas or fluid.
S Findings in strangulation:
z Thickening of bowel wall
z Pneumatosis intestinalis (air in bowel wall)
z Mesenteric naziness
z Poor uptake of IV contrast into the wall of necrosed bowel.
3. Barium study:
S Barium study is only recommended in patients with recurrent obstruction or low grade mechanical obstruction
S Barium study can precisely locate the level of obstruction and the cause of obstruction.
[In pregnant patients, ultrasound is useful because radiation exposure from X-ray should be avoided.]
Treatment
Fluid resuscitation
S Isotonic fluid in IV route.
S Central venous catheter or pulmonary artery catheter

monitoring is necessary in patients with underlying
cardiac disease.
Gastric decompression – by nasogastric tube
S Effective gastric decompression decreases nausea,
abdominal distension, risk of aspiration.
Monitoring urine output
S Urine output should be monitored for assessing
adequate fluid resuscitation.
Intestine 301
Broad spectrum antibiotics (Coverage against gram negative aerobes and anaerobes)
S Commonly administered in any setting of intestinal obstruction concerning that bacterial translocation may occur.
S Mandatory for patients planning for resectional surgery.
Correction of electrolyte imbalance

S Hypokalemia must be corrected with IV potassium supplement after satisfactory urine output is achieved.
Surgery or nonoperative trial?

S Patient with uncomplicated small bowel obstruction should ideally be considered for nonoperative trial.
S No question of nonoperative trial if:
z Suspected ischemia
z Large bowel obstruction
z Strangulated hernia
z Suspected peritonitis.
S Think twice before surgery in:

z Partial small bowel obstruction
z Obstruction in early postoperative period
z Obstruction due to Crohn’s disease
z Carcinomatosis.
[Patient not improving with nonoperative management should

undergo surgical intervention, but how long the trial should be
continued is still remains controversial.]
Nonoperative to operative, but when? If conservative management not responding/abso-

S Patient is developing symptoms and signs of lute indication of surgery–then
complication—continuous abdominal pain, S Prepare the patient for surgery.
localized tenderness, rebound tenderness, fever, S Check whether patient is properly resuscitated or
tachycardia and leukocytosis. not.
S In X-ray abdomen, free gas or signs of closed-loop
S Check IV broad spectrum antibiotics is administered
obstruction. or not.
S In CT abdomen, signs of ischemia and strangulation.
Principles of Surgery in Intestinal Obstruction
S Ifthe site of obstruction

is not known, midline S Assess:
incision is best for z Site of obstruction
exposure.
z Nature of obstruction
z Viability of gut
S Ifcecum is collapsed, obstruction is in the

small bowel. A dilated cecum indicates
large bowel obstruction.
S Regardless of aetiology, affected intestine should be examined for viability.

S Viability is checked by inspecting the color of intestine, peristalsis and marginal arterial pulsations.
Note the changes in color of intestine
S If a segment of intestine with questionable viability, then

Intestine 303
S Type of operative procedure will be according to the cause of obstruction:
Intestinal segment is prepared for resection Anastomosis is performed
Different Types of Mechanical Small Bowel Obstruction
Obstruction due to adhesions and bands
[Adhesiolysis invites further adhesions, so aggressive adhesiolysis should be avoided.]

Obstruction due to internal hernia
Internal herniation also occurs through parduodenal fossa, intersigmoid fossa:
Treatment
Constriction ring released

Reduction of hernia
+
Resection of involved gut
S Release of constriction ring should be avoided in herniation through the foramen of Winslow, mesenteric defects,
paraduodenal fossa.
Intestine 305
Obstruction from enteric structures
S Small intestinal structures are usually due to

tuberculosis or Crohn’s disease.
S Strictures due to lymphoma is more common than
carcinomatous structure.
S Surgical management is resection + anastomosis.
S Management of stricture due to Crohn’s disease is

somehow different.
Bolus obstruction
Due to—
S Worms
S Gallstone Stricture in the terminal ileum

S Food
S Trichobezoars
S Phytobezoars.
Obstruction due to food bolus
S In the setting of partial or total gastrectomy, unchewed apple, coconut, brussel sprouts, dried fruit, orange pips
causes obstruction.
S Intraluminal crushing of the food bolus is the treatment.
Obstruction due to worm bolus
S Occurs particularly in children

S Attacks of obstruction usually follows after antihelminthic therapy.
Intussusception
Part of bowel invaginated within an adjacent segment.
How It Develops
S Ininfants, it occurs most commonly after weaning. (Peak incidence 3–9 months)
S Hyperplasia of the Peyer’s patches in terminal ileum may be the initiating event
S Adults patients is always associated with a lead point: Polyp, submucosal lipoma or tumor.
Are of Different Types
Ileocolic Ileoileocolic Ileoileal

Most common Second most common
[Retrograde intussusception—In some patients with Roux-en-Y gastric bypass, the proximal bowel is drown into the lumen
of distal bowel.]
Intestine 307
Presentation in an infant is classical.

S Sudden onset of screaming associated with drawing up the legs.
S Persists for few minutes and recur every 15 minutes.
S During attack, facial pallor develops.
S Initially stool may be normal, but latter ‘recurrent jelly stool’.
S Abdomen not distended.
S Lump may be palpable with concavity towards umbilicus.
S Feeling of emptiness in RIF (the sign of dance).
S Perrectal examination:
z Blood-stained mucus.
z Rarely, apex of the intussusception may be palpable in extensive

ileocolic or colocolic intussusception.
S Adult patients present with features of intestinal obstruction.
S X-rayabdomen: Features of small or large bowel obstruction.

S USG abdomen: USG shows ‘target sign’ (gut in the gut) in transverse section.
S Barium enema:
S CT abdomen— It is useful if previous investigations are inconclusive. (‘target sign’ is seen)
CT scan showing gut-in the gut appearance

Treatment
S Resuscitation S Squeezing the most distal part of the mass

S Nasogastric decompression. proximally–is the ideal technique.
S Do not pull.
S Viability of the bowel should be checked.

Intestine 309
Crohn’s Disease
S Chronic idiopathic transmural granulomatous inflammatory disease of the gastrointestinal tract.
Bimodal age distribution: First

peak of incidence (15–30 years),
second peak (55–60 years)
S Distal ileum is the most commonly involved site.

[In ulcerative colitis, terminal ileum is not commonly involved]
How the Disease Develops?
Macroscopic and Microscopic Features
S Skip lesion is characteristic of Crohn’s

disease
[In ulcerative colitis, the lesion is continuous.]
Intestine 311
On Opening the Affected Bowel

Under Microscope
[In ulcerative colitis, inflammation is limited to the mucosa and submucosa.]
Typical presentation
S Abdominal pain
z Intermittent and colicky
z Centered in the lower abdomen
z Initiated by meals
z Relieved by defecation.
S Diarrhea
z Stools are liquid or semisolid
z Stools rarely contain mucus, pus or blood.
S Weight loss
S Onset of symptoms is insidious
S Severity follows a waxing and waning course.
Other presentations
Intestinal Obstruction Perforation

Intestine 313
Anorectal lesions
S Anorectal lesions may appear separately as a manifestation of Crohn’s disease

S Anorectal lesions may appear many years before the intestinal disease
S Crohn’s disease should be suspected in any patient with multiple, chronic perianal fistulas
S Search for intestinal disease when histopathology of perianal lesions show features of Crohn’s disease.
S Keep in mind:
Risk of adenocarcinoma in small intestine and colon in longstanding Crohn’s disease is high.
Extraintestinal manifestations
Investigations
S Contrast study of small intestine and colon:

z Cobblestone appearance
z Long lengths of narrowed terminal ileum. — Kantor string sign.
z Fistulas between adjacent bowel loops.
S CT abdomen
z To detect intraabdominal abscesses
z To exclude other intraabdominal disorders.
S Sigmoidoscopy or colonoscopy
z Characteristic aphthous ulcers with surrounding mucosa.
S Serologic markers
z Perinuclear antineutrophil cytoplasmic antibody (pANCA) and antisaccharomyces cerevisiae (ASCA) are
associated with inflammatory bowel disease.
Treatment
S Goal of treatment is to palliate symptoms, not to achieve cure.
Medical therapy
Medical therapy is directed towards relieving acute exacerbations.

S Sulfasalazine
z Most commonly used drug for Crohn’s disease.
S Corticosteroids
z Mostly prednisone.
S Antibiotics
z Metronidazole (mostly used)
z Ciprofloxacin
z Tetracycline.
S Immunosuppressive agents:
z Azathioprine
z 6-mercaptopurine
z Methotrexate
z Cyclosporine
z Tacrolimus.
S Anticytokine and cytokine therapy
z Infliximab (monoclonal antibody to TNF-D)
z Newer anti-TNF D agents e.g. adalimumab, certolizumab pegol show promising results
z IL-10.
Intestine 315
Nutritional therapy
S Elemental feeding
S Liquid polymeric diet
S Total parenteral nutrition.
Surgery
Indications
S Intestinalobstruction
S Perforation with fistula formation or intraabdominal abscess
S Free perforation
S GI bleeding
S Urologic complications
S Cancer
S Perianal disease.
Principles of surgery
S Surgery should be directed to the complication.

S Abdomen is opened through midline incision.
S Only the segment of bowel with complication should be resected ignoring other parts of the diseased bowel.
Length of intestine resected should be minimized.
S Frozen section is not recommended.
S Creation of stoma rather than primary anastomosis after resection of diseased segment of bowel should be
considered in patients with sepsis, gross contamination of peritoneal cavity or patient taking immunosuppressive
therapy.
Specimen of right hemicolectomy [for stricture (?Crohn’s disease) in terminal ileum]

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Acute ileitis: Self-limited disease
Intestinal obstruction: Management

Intestine 317
Fistula: Management
Anti TNF-v DJHQWV ,QÀL[LPDE

adalimumab) show promising
results in healing chronic
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disease
Free perforation: Management

Intestine 319
Gl bleeding management:
S If bleeding is significant, then resection of the involved segment is indicated.
Duodenal disease management:

S Gastrojejunostomy is indicated rather than duodenal resection if duodenal obstruction is not responding to medical
therapy.
Perianal disease management:

S Pelvic MRI and endoanal USG are indicated to delineate complex fistulas
S Fistulotomy is indicated in superficial, low trans-sphincteric and low intersphincteric fistulas
S High trans-sphincteric, suprasphincteric fistulas are treated with noncutting setons
S Conservative management is sufficient in anal fissure
S Perianal abscess should be drained but liberal excision of tissue must be avoided
S Skin tags and hemorrhoids should not be excised unless they cause symptoms.
Typhoid Enteritis
S Acute systemic infection caused by Salmonella typhi.
S Treatment of uncomplicated typhoid fever with enteritis – Antibiotics.
S Surgery is indicated for hemorrhage and perforation.
S Classically, a single perforation occurs through the Peyer’s patch and simple closure is sufficient.
Intestine 321
Intestinal Tuberculosis
S History of pulmonary tuberculosis may be present.

S History of vague abdominal pain for few months, generalized ill health, loss of weight, changes in bowel habit.
S Perforation of the tuberculous ulcer is rare.

Diagnosis
S Diagnosis of ileocecal tuberculosis is difficult.

S If these findings are found in barium meal follow through, ileocecal tuberculosis is very much suggestive:
Barium meal follow through
Chest X-ray
S High lymphocyte count and raised ESR are suggestive of tuberculous infection.
S ADA estimation.
Treatment
S Uncomplicated—
zATD therapy.
S Complicated—
z Present with intestinal obstruction.

Intestine 323
Patient stable
Patient unstable
S Think of resection of diseased part if patient’s condition improve.

Jejunal and Ileal Diverticula
S Meckel’s diverticula is a congenital

diverticula.
S Usually asymptomatic.
S Complication in the form
of intestinal obstruction,
diverticulitis, hemorrhage,
perforation, malabsorption
may develop.
S Enteroclysis is the mot sensitive
test for jejunoileal diverticula.
Meckel’s diverticulum is a true diverticulum.
Treatment S Asymptomatic jejunoileal diverticula—No treatment required.

S Complicated diverticular diseases are managed with resection of involved segment followed
by anastomosis.
S Malabsorption secondary to bacterial overgrowth is treated with antibiotics.

Intestine 325
Duodenal Diverticula
S Duodenum is the second most common site for diverticula after the colon.
S Duodenal diverticula is the most common acquired diverticula of the small
intestine.
S Most of the duodenal diverticula arise in the periampullary region and project
from the medial wall of the duodenum.
Diverticula of the duodenal cap arises due to sequelae of long-standing duode-
nal ulcer.
S Most of them are asymptomatic.

S If diverticula is closely associated with ampulla of vater, patient may present with features of cholangitis and/or
pancreatitis (diverticula causes distortion of the CBD resulting in obstruction).
S Hemorrhage (due to erosion of superior mesenteric artery), perforation rarely develops.
S Blind loop syndrome —Stasis of intestinal contents in blind poucho overgrowth of bacteriaomalabsorption, leads
to development of steatorrhea, vitamin B12 deficiency anemia.
Diagnosis
S Most of the diverticulas are discovered incidentally during endoscopy, imaging or peroperatively
S USG and CT can detect diverticula (d/d– pancreatic pseudocyst, biliary cyst)
S Barium study of upper GI tract is the best diagnostic modality.
Treatment
S Asymptomaticdiverticula does not warrant treatment.

z Symptomatic (bleeding, obstruction) diverticula is treated by diverticulectomy.
[Careful detection of the ampulla is important during

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Meckel’s Diverticulum
S Most common congenital anomaly of the GI tract.
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Rule of ‘2’ (Two)
S Most of the Meckel’s diverticulum are asymptomatic.

Intestine 327
GI bleeding
S This diverticulum is the most frequent cause of painless

significant lower GI bleeding in a previously healthy
infant–presenting as melena or brickred colored rectal
bleeding.
S GI bleeding is the most common presentation in
children with Meckel’s diverticula.
Obstruction
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S Intestinal obstruction is the most common

presentation in adults with Meckel’s diverticula.
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Diverticulitis
Neoplasm
Rarely, benign or malignant neoplasm develops from the diverticulum.
Diagnosis
S In the absence of bleeding, Meckel’s diverticula are

rarely diagnosed prior to surgical intervention for
other causes.
S The most accurate diagnostic test for the diverticula
in children is scintigraphy with sodium 99mTc-
pertechnetate [The 99mTc-pertechnetate is selectively
taken up by mucous secreting cells of gastric mucosa
and ectopic gastric mucosa in the diverticulum].
S In adults, it is less sensitive.

S In adults, barium study may be helpful.
Intestine 329
Treatment
Management of symptomatic diverticulum

Management of incidental diverticulum
S Asymptomatic diverticula in children

during laparotomy should be resected.
S In adults, this issue is controversial.
S In selected asymptomatic patients,

diverticulectomy may be beneficial.
Neoplasm of Small Intestine
S Neoplasm in small intestine is very rare.
Benign Neoplasm
S Common benign neoplasms are:

z Benign GIST
z Adenoma
z Lipoma.
S Usually presented with nonspecific symptoms, e.g. dyspepsia,

anorexia, malaise and vague abdominal pain.
S Segmental resection and anastomosis is the treatment of choice.
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of intussusception
Malignant Neoplasm
S Common malignant neoplasms are:

z Adenocarcinoma
z Carcinoid tumor
z Malignant GIST
z Lymphoma.
S Presented with abdominal pain, weight loss, obstruction and lower GI bleeding
S Treatment of adenocarcinoma and lymphoma is wide resection with regional lymphadenectomy
S For GIST, wide resection is sufficient, lymph node dissection not necessary
S Adjuvant radiotherapy or chemotherapy have very little role.

Intestine 331
Metastatic Tumor
S Metastatictumors are much more common than primary tumors

S Stomach, colon, pancreas, cervix, ovaries, kidneys are usual intraabdominal primary sites
S Cutaneous melanoma is the most common extraabdominal primary site
S Presented with anorexia, weight loss, anemia and partial bowel obstruction
S Treatment is palliative resection or bypass procedure.
Short Bowel Syndrome

Causes
The ability of a patient to adapt after massive small bowel resection depends on—
S Diarrhea
S Fluidand electrolyte deficiency

S Malnutrition
S Increased chance of gallstone formation
S Increased chance of nephrolithiasis (due to hyperoxaluria).
Treatment
Prevention
S InCrohn’s disease, limited resection should only be performed.
S Inintestinal ischemia, only infarcted bowel should be resected. Second-look operation may be indicated for further
assessment of ischemic bowel.
Intestine 333
Management in acute phase
S Control of diarrhea by:
z H blockers/proton pump inhibitors–by p acid secretion due to hypergastrinemia
2
z Cholestyramine–by binding excessive bile salts
z Antimotility agent (codeine, diphenoxylate)
z Octreotide
S Replacement of fluid and electrolytes
S Total parenteral nutrition.
Management in late phase

S Enteralnutrition:
z High carbohydrate, high protein diet in its simplest form
z Reduction of dietary fat
z Fat-soluble vitamins, calcium, magnesium, zinc supplementation.
S Surgical intervention:
z Longitudinal intestinal lengthening and tailoring (LILT) procedure–first described by Bianchi
z Serial transverse enteroplasty procedure (STEP)
z Intestinal transplantation.
Diverticular Disease of Colon

Diverticulas are outpouchings from the lumen of a viscus.
S Diverticulosis is colonic diverticula with

no associated inflammation.
S Diverticulitis is inflammation of the
diverticula.
S Diverticular disease covers the spectrum
from diverticulosis to diverticulitis.
S Diverticulosis is characterized by false

diverticula, muscular thickening and
redundant folds of mucosa.
S The thickening of colonic smooth
muscle develops before the appearance
of diverticula is known as myochosis.
How they Develops
S Normal segmentation during transport of feces
S Relaxation of contraction ring allows passage of feces
Clinical Presentation of Diverticulosis
S Most of the patients are asymptomatic

S Diverticula may be detected as incidental finding in investigations done for other reasons.
Management of Diverticulosis
S If is not certain that diet modifications can decrease the chance of complications of diverticulosis.
S Surgery is not advised for uncomplicated diverticular disease.
Intestine 335
(Diverticulitis is the inflammation of one or more diverticulum, usually associated with pericolitis.)
Uncomplicated diverticulitis
CT scan of abdomen
z Sigmoid diverticulas are present

z Thickening of colonic wall > 4 mm
z Inflammation within the pericolic

fat
S CT scan is considered to the most reliable investigation to confirm the suspected diagnosis of diverticulitis.
S Accurately reveals the location of the infection, extent of inflammatory process, location of an abscess, involvement
of other organs.
[Barium enema or colonoscopy should not be performed in the acute setting because of higher risk of colonic perfora-
tion.
Barium enema or colonoscopy should be performed about 6 weeks after an attack of diverticulitis.]
Treatment
S Antibiotics(Oral/IV)–depending on severity
[Antibiotics coverage against gram-ve and anaerobic organisms].
S Uncomplicated disease usually respond to antibiotics within 48 hrs
S Surgery (elective sigmoidectomy) should be considered if patient suffers from recurrent attacks of diverticulitis.
What is Hinchey Staging System
For staging the severity of complicated diverticulitis

Intestine 337
Management of abscess
Hinchey type 1 and 2

Hinchey type 3 and 4
*=J=CAIAJPKBłOPQH=
S Investigations should be done to determine the

site and complexity of tracts.
S Other couses of fistula are–Crohn’s disease,
malignancy should be ruled out.
S The basic principle of surgical management is to
excise the diverticular segment of the bowel and
repair the defect of involved organ.
S Primary anastomosis of bowel following
resection is the preferred method.
Intestine 339
Management of obstruction
S Resection with primary anastomosis

S Hartmann’s procedure
S Stenting (if patient inoperable).
Volvulus of the Colon
Volvulus is torsion or twist of an organ on a pedicle.
X-ray abdomen showing typical appearance of

VLJPRLGYROYXOXV
Sigmoid Volvulus
S Commonest colonic volvulus (about 65%)
S An elongated mesentery is essential for the development of colonic volvulus.
How it develops
Predisposing Factors
S High residue diet
S Intake of large amount of food after fasting
S Phychotropic drugs (by affecting intestinal motility)
S Chronic constipation.
Intestine 341
Management
Principles of management of nonstrangulated volvulus—

S Relief of dorsion
S Prevention of recurrence.
Resective procedure Nonresective procedure
Resective Procedure
1. S Resection
of sigmoid followed by primary 2.
anastomosis.
S Resection followed by Hartmann’s procedure

Resection—anastomosis
3. S Mikulicz’s procedure
Nonresective Procedure
S Colopexy
z Mesosigmoidplasty
Intestine 343
Management of strangulated volvulus
S Resuscitation followed by resective procedure.
Cecal Volvulus
&HFDOEDVFXOHW\SHRIYROYXOXV
S More common in females.

S Usually presents with features of obstruction
S Straight X-ray of abdomen reveals a large dilated cecum assumes gas filled comma shape–concavity which faces
inferiorly and to the right.
Management
S No role of colonoscopic decompression

S Open reduction
p
Cecopexy
S In strangulated cecum–Right hemicolectomy.
Ileosigmoid Knotting
S Patient presents with features of intestinal obstruction, but the abdominal distension is mild.
S Straight X-ray of abdomen reveals distended ileal loops with a distended sigmoid colon.
S After decompression of the bowel, the gangrenous bowel (small bowel/colon) is resected with or without
anastomosis depending on the patients general condition.
Large Bowel Obstruction
Mechanical obstruction caused by:

S Carcinoma
S Diverticulitis
S Volvulus
S Most patients require surgical intervention.

S Differentsurgical options are
z Resection
z Bypass
z Loop ileostomy as decompressive procedure.

Intestine 345
Pseudoobstruction of Colon [Ogilvie’s Syndrome]
S Acute colonic pseudoobstruction should be suspected when a medically ill patient suddenly develops abdominal
distension.
S The most useful investigation is water-soluble contrast enema.
S Initial treatment includes nasogastric decompression, correction of fluid-electrolyte imbalance. Medications inhibit
bowel motility (e.g. opioids) must be avoided.
S Neostigmine in IV route resolves the condition in less than 10 minutes. Significant side effect is bradycardia and
atropine must make available.
Ulcerative Colitis
It is a chronic inflammatory bowel disease of unknown etiology.

How it Develops
Macroscopic Appearance and

Under Microscope
Intestine 347
S The cardinal symptoms are rectal bleeding and diarrhea.

S Commonly presents with frequent passage of watery stool mixed with blood, pus and mucus.
S Tenesmus, rectal urgency and even anal incontinence are present.
S On clinical examination, tenderness in abdomen with tympanicity.
S On rectal examination, tenderness and spasticity are found. Examining finger may be covered with blood, mucus
or pus.
S The disease severity can be assessed based on Truelove and Witt classification—It is based on six parameters:
z Frequency of stool/day
z Hematochezia
z Temperature
z Pulse rate
z Hb%
z ESR.
Extraintestinal Manifestations
What is Toxic Megacolon?
S Acute colonic dilatation—Rare life-threatening complication of ulcerative colitis

S Patient is severely ill (toxic).
Intestine 349
S Medical therapy consists of fluid and
electrolyte resuscitation, nasogastric
suction, broad spectrum antibiotics and
TPN.
S If no significant clinical improvement after
24–36 hrs of aggressive medical therapy,
or any signs of perforation, emergency
surgery is indicated.
S Total abdominal colectomy with ileostomy
and preservation of rectum is the preferred
surgical option.
Investigations for Diagnosis of Ulcerative Colitis

Endoscopy
S After acute disease has

subsided, complete colon-
oscopy with biopsy should
be performed to exclude
any malignant lesion.
Plain X-ray abdomen
S Plain X-ray abdomen may

identify toxic megacolon
and/ or perforation.
Barium enema
S Should not be performed in severely ill

patients because it may precipitate acute
colonic dilation.
S Upper GI contrast study with small bowel
follow through is necessary to rule out
Crohn’s disease.
Serology
S Perinuclear antineutrophil cytoplasmic antibodies (pANCA) are seen in about 86% of patients with ulcerative colitis
and is also used as a diagnostic test to differentiate it from Crohn’s disease.
Treatment
Medical therapy
S Goals of medical therapy are to treat the acute attack and to prevent relapse.
For mild to moderate disease
S Patient can be treated in outpatient basis

S Diet should be free of bovine milk
S Oral mesalamine/olsalazine/balsalazide is the drug of choice
S Mesalamine/steroid enema is also helpful
S High dose oral corticosteroids (40–60 mg/d prednisone) is effective
S No role of antibiotic therapy.
For severe disease
S Patient must be treated in hospital

S Nasogastric suction is required if there is colonic dilation or any risk of developing this complication
S Nutrition in the form of polymeric total enteral nutrition/total parenteral nutrition–according to the patient’s status
S Broad spectrum antibiotics are often used to prevent septicemia from bacterial translocation
S Corticosteroids are administered in IV route
S Electrolyte imbalance particularly hypokalemia if present, should be corrected promptly.
[Anticholinergics and opioids are better avoided as they may precipitate acute dilation of the colon.]
Intestine 351
Maintenance therapy
S Oral mesalamine or 5-aminosalicylic acid reduces relapse rates.
Surgical management
Surgical emergencies
S Emergency complications are though rare, may be life-threatening and need urgent surgical intervention.
S Emergency indications are:
S Fulminant colitis unresponsive to IV corticosteroids
S Toxic megacolon with impending perforation
S Colonic perforation
S Obstruction from stricture
S Intractable colitis.
[The primary goal of emergency surgery is to remove most part of the diseased colon, but not to compromise a
subsequent restorative procedure.]
Other surgical options (in emergency setting):

S Proctocolectomy with end ileostomy
S Blowhole colostomy with end ileostomy.

Indications of elective surgery
S Intractibility
S Mucosal dysplasia
S Intolerable side effects of medication
S Stricture formation without obstruction
S Malignancy of colon or rectum
S Extraintestinal manifestation.
Surgical options
S Total colectomy with kock pouch (continent ileostomy)—Rarely used due to significant morbidity.
Intestine 353
Colorectal Polyp
Hyperplastic Polyp
Peutz-Jeghers Polyps and Peutz-Jeghers Syndrome
S A type of hamartomatous polyp

S Autosomal dominant condition.
S Large, multiple and pedunculated polyps.
S Most common location of the polyp is in the upper

GI tract specifically the upper jejunum.
S Characteristic feature is tree-like branching of mus-

cularis mucosae.
S This syndrome is associated with hamartomatous polyps of the GI tract

and cutaneous melanin deposition.
S Melanin deposition is seen most frequently in perioral region, buccal
mucosa, genital region and on the hands and feet.
S Most of the patients are asymptomatic.
S Some patients present with obstruction or GI bleeding.
[Patients with Peutz-Jeghers syndrome are more prone to develop GI ma-

lignancies and extraintestinal malignancies (e.g. pancreas, lung, breast,
ovary and uterus).]
Juvenile Polyp and Polyposis
S A type of hamartomatous polyp

S Solitaryjuvenile polyp occur more often in rectum
S Juvenile polyps have no malignant patential
S Occures more commonly in children below 5 years of

age.
Intestine 355
S Spherical
S Smooth
S Slightly
surfaced
lobulated
S Stalk as long as 2 cm
S Large (1–3 cm)

} [4] 'S"
S Patientsmay present with rectal bleeding

S Polyp with long pedicle may prolapse through the anus
S Treatment is polypectomy.
Familial Juvenile Polyposis
S Itis a autosomal dominant disorder.

S May be present anywhere in the large bowel.
S Polyps may transformed into adenoma and eventually carcinoma.
S Annual screening of the family members should begin from 10 years.
S Treatment is either total abdominal colectomy with ileorectal anastomosis (if rectum is not involved) or total
proctocolectomy.
&JŃ=II=PKNU-KHULĠ-OAQ@KLKHUL
S Develops due to reepithelialization on the undermined ulcers in inflammatory bowel disease, mostly in ulcerative
colitis and rarely in Crohn’s disease.
S This type of polyp may also develop after amebic colitis, ischemic colitis.
S These polyps have no malignant potential.
S On gross appearance, these polyps are almost similar to adenomatous polyps.
S Polypectomy is the treatment of choice.

Tubular Adenoma (Adenomatous Polyp)
S Most common neoplastic polyp (about 75%).
S Most often found in distal colon and rectum

S Polyps may be single or multiple, sessile or pedunculated
S Males and females are equally affected.
S Most often pedunculated

S Vary in size (from < 1 cm to large spherical mass).
S The malignant potential of an adenoma depends

on size (> 4 cm), growth pattern and degree of
epithelial atypia.
Intestine 357
Villous Adenoma
z Most commonly found in the rectosigmoid

region, but may be located elsewhere in the
colon.
z Round to oval exophytic masses, usually

sessile
z Varying in size from 1–10 cm in diameter
z Less common than tublar adenoma.
z Severe atypia, CIS, invasive carcinoma are

seen more frequently.
S Males and females are equally affected.

S Smaller adenomas are usually asymptomatic. Larger ones usually present with rectal bleeding.
S Villous adenomas may secrete excessive mucoid material rich in protein and potassium resulting in hypoproteinemia
and hypokalemia.
Treatment
For pedunculated polyp
For sessile polyp

Intestine 359
Familial Adenomatous Polyposis (FAP)
S FAP is an autosomal dominant syndrome with nearly 100% penetrance

S Hundreds to thousands (>100) polyps in the colon and rectum
S Polyps may also present in the stomach, duodenum and small intestine (in about 50% of patients)
S The genetic abnormality is a mutation in the APC gene, located on chromosome 5q21
S Males and females are equally affected
S The lifetime incidence of colorectal cancer in untreated FAP is virtually 100%
S About 30% patients have de novo mutations and therefore no family history is present.
Screening
APC gene testing of family members
4
Annual flexible sigmoidos- Annual screening from age

copy from 10–15 years 50 years
S *Congenital hypertrophy of retinal pigment

epithelium is present as early as at 3 months of age
in affected persons (with APC gene mutation). This
abnormality predicts FAP with 97% sensitivity. This
can be detected in about two-third of patients of FAP
by indirect ophthalmoscopy.
Extracolonic Manifestations
Benign
S Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
S Mandibular osteoma
S Super numerary teeth
S Epidermal cyst
S Adrenal cortical adenoma
S Desmoid tumor.
Malignant
S Brain tumors (glioblastoma multiforme and medulloblastoma)
S Thyroid tumors
S Gastric and small intestinal polyp with risk of adenocarcinoma
S Ampullary carcinoma.
Intestine 361
Variants
Treatment
S *Sulindac and celecoxib—both reported to induce regression of polyps and used for chemoprevention
S *Sulindac, tamoxifen, low dose methotrexate can regress the desmoid tumors.
Cancer of Colon
S Most common malignancy of the GI tract.
Various Forms
Risk Factors
S Upto 100 colonic polyps

S [‘Nonpolyposis’ in comparison to FAP where thousands of polyps are present]
S Mostly in the right colon
S Flat polyps
S Onset of colorectal cancer at the mean age of 43 years.

Intestine 363
S In Lynch II syndrome, besides colonic polyps, extracolonic tumors are present in—
z Stomach
z Bile duct
z Pancreas
z Small bowel
z Renal pelvis
z Ureter
z Urinary bladder
z Uterus
z Ovary
z Skin.
S A variant of HNPCC is Muir-Torre syndrome (colonic polyps + skin tumor).
S HNPCC is classically defined by modified Amsterdam criteria.
S Genetic testing is absolutely not necessary in HNPCC.
S MSI (microsatellite instability) testing and hMLH1/hMSH2 immunohistochemistry can be performed on tumor
specimens.
S Surveillance colonoscopy should begin at the age of 20.
S In women, periodic vaccum curettage should begin at the age of 25 years, also pelvic USG screening and CA125
estimation. Prophylactic hysterectomy with bilateral salpingo-oophorectomy should be considered if family is
completed.
S Annual test for occult blood in the urine in both sexes should begin at the age of 30–35 years.
S If colon cancer is diagnosed in patient with HNPCC, abdominal colectomy with ileorectal anastomosis is the ideal
treatment. Annual proctoscopy is mandatory after this procedure.
Adenoma-Carcinoma Sequence
Intestine 365
Which Part of Colon Most Affected
S Classically, colon cancer is a disease of left colon

S Now, the trend is changing from left to right.
Under Microscope
S Regardless of their macroscopic morphology, almost all colonic carcinomas are adenocarcinoma from histologic
grading of well-differentiated to anaplastic variety.
S Other histologic types—
z Mucinous adenocarcinoma
z Signet ring cell carcinoma
z Small cell carcinoma.

Spread of Colon Cancer
Local spread
Lymphatic spread
Hematogenous spread
S Usually spread in the late phase of the disease

S Liver, lungs, brain, bones and ovaries are the usual site of metastasis.
Intestine 367
S Digital rectal examination is must in all patients present with any of these symptoms.
[In a middle aged or older patient who recently presents with alteration of bowel habit, the diagnosis is colon cancer
until proved otherwise.]
&JRAOPEC=PEKJOPK KJłNI!E=CJKOEO=J@0P=CEJC
Colonoscopy
Contrast enema
S Is always necessary?
S The major disadvantage is tissue biopsy not possible.
CT scan of abdomen
S To exclude liver metastasis, hydronephrosis or gross paraaortic lymph node involvement.
Chest X-ray in two planes/CT chest
S To rule out lung metastasis.

Intestine 369
How CEA Estimation Helpful
Surgery
S Preoperatively,elevated CEA CEA normal
z Indicates complete tumor removal
Surgery
S Preoperatively,elevated CEA CEA still elevated
z Indicates residual disease or disease recurrence.
Treatment
S Surgery is the treatment of choice in any colorectal carcinoma without widespread distant metastasis.
Principles of treatment
S Resection of the tumor with adequate margin

[extent of resection is determined by location of
the tumor, its blood supply and lymphatic drainage,
involvement of adjacent organs].
S Regional lymphadenectomy.
S Resection of metastasis (limited in number) in liver

or lungs (if technically possible).
S Restoration of the continuity of the GI tract.

Tumor in cecum or ascending colon
Vessels ligated Anatomical structures at risk

S Right branch of middle colic artery (MCA)
S Right colic artery (RCA) S Right
ureter
S Ileocolic artery (ICA). S Duodenum.
1QIKNEJDAL=PE?ŃATQNAKNPN=JORANOA?KHKJ
Vessels ligated Anatomical structures at risk
S Middle colic artery S Duodenum
S Right colic artery S Right ureter

S Ileocolic artery. S SMA/SMV, gastroepiploic vessels
S Spleen
S Left kidney.
Intestine 371
1QIKNEJOLHAJE?ŃATQNA
Anatomical structures of risk
Vessels ligated
S Duodenum
S Middle colic artery S SMA/SMV and gastroepiploic vessels

S Left colic artery S Spleen, left kidney
S Inferior mesenteric artery. S Left ureter, gonadal vessels, hypogastric nerve.
Tumor in descending colon
Vessels ligated Structures at risk
S Left branch of middle colic artery S SMA/SMV and gastroepiploic vessels

S Inferior mesenteric artery. S Spleen and left kidney
S Left ureter, gonadal vessels and hypogastric nerve.
Tumor in sigmoid colon
Vessels ligated Structures at risk
S Inferior
mesenteric artery S Spleen and left kidney
S Superior hemorrhoidal artery. S Left ureter, gonadal vessels and hypogastric nerve.
Management of complications
Bleeding from tumor

Blood transfusion + endoscopic fulguration, followed by surgery/radiotherapy.
Intestine 373
Obstruction from tumor
Dukes classification system (original) Modified dukes classification system

Stage A
Same
Stage B
Same
Stage C
Stage C1
Stage C2
Stage D
Intestine 375
TNM Staging
S T–Denotes the invasiveness of tumor [not the size]

S N–Denotes the number of lymph nodes [not the size or location]
S M–Denotes presence or absence of distant metastasis
S T –Tumor invades into but not through submucosa

1
S T –Tumor invades into but not through muscularis propria
2
S T –Tumor invades subserosa
3
S T –Tumor breaches serosa or directly involving adjacent organ
4
S N –1–2 lymph nodes involved
1
S N –3 or more nodes involved.
2
Chapter 11
Appendix
Important Topics
zzAcute Appendicitis
zzAppendicular Lump
zzNeoplasm of the Appendix
‘An organism is a molecular society, and biological order is a kind of social order. Social order is opposed to revolution, which
is an abrupt change of order and to anarchy, which is the absence of order.’
André Lwoff (1902–1994)
French Microbiologist
Acute Appendicitis
How it Develops?
SS Obstruction of the appendicular lumen is the major causative factor of acute appendicitis.
Cause of Obstruction
Gangrenous appendix and fecalith

Appendix 379
What Happens after
Obstruction?
How Appendix Looks in Acute Appendicitis
� Tenderness at McBurney’s point

� Rebound tenderness
� Direct percussion tenderness
� Muscle guarding
� Discomfort on moving, walking or coughing.

� Loss of appetite (an important symptom,
particularly in children).
� Uncommon symptoms:
— Frequency of micturition
— Diarrhea
— Microscopic hematuria
SS Any movement including coughing (Dunphy’s sign) causes increased pain.

SS Pain in the right lower quadrant during palpation of the left lower quadrant [Rovsing’s sign]
SS Pain on internal rotation of the hip (obturator sign)—typically found in pelvic appendix
SS Pain on extension of the right hip (iliopsoas sign)—typically found in retrocecal appendix
Appendix 381
Tenderness at McBurney’s point is minimal or absent in:
SS Appendicitis in retrocecal, pelvic or postileal appendix
SS Extremely obese people
SS Appendicitis in 2nd or 3rd trimester of pregnancy
SS In high up cecum with appendicitis or normally placed cecum with a long appendix.
In perforated appendicitis:
SS Patient looks seriously ill
SS Fever
SS Tachycardia
SS Rebound tendernes.
Risk Factors for Perforation
SS Extremes of age (Pediatric and geriatric population)

SS immunosuppression
SS Diabetes mellitus
SS Previous abdominal surgery (due to restricted spread of greater omentum).
Investigations to Confirm Diagnosis
SS High WBC count (>20,000/ml) suggests gangrenous or perforated appendicitis

SS No other blood tests are helpful. [Think twice before reaching the diagnosis of acute appendicitis if WBC count,
percentage of neutrophil and CRP level are normal.
USG
SS Useful imaging for diagnosis of acute appendicitis.
SSAppendix of 7 mm or more in anteroposte-

rior diameter.
SSThick-walled blind ending, nonperistaltic
noncompressible luminal structure.
SSPeriappendiceal fluid.
CECT
CECT is more sensitive and specific than USG in diagno-

sis of acute appendicitis.
SS CECT has high diagnostic accuracy for appendicitis.
SS Dilated (> 6 mm), thick-walled appendix—Not filled

with oral contrast or air.
SS Periappendiceal fat stranding.
Helical CT with IV contrast is the imaging of choice

if imaging is necessary—As per recommendation
of Surgical Infection Society and Infectious Disease
Society of America.
SS Diagnosis of appendicitis is highly unlikely if oral contrast fills the lumen of the appendix and no evidence of
surrounding inflammation.
SS In a young patient, in the setting of typical right lower abdominal pain and tenderness with signs of inflammation,
routine CT scan is unnecessary.
SS CT is useful where clinical findings are confusing and surgical intervention may carry increased risk.
How Diagnostic Laparoscopy Helpful
SS Inthe setting of pain in right lower abdomen in women of childbearing age where USG or CT scan is inconclusive,
diagnostic laparoscopy is very much helpful.
Think Other Possibilities Also
In Preschoolaged Children
SS Intussusception
SS Meckel’s diverticulitis
SS Gastroenteritis.
In Schoolaged Children
SS Mesenteric lymphadenitis
SS Gastroenteritis.
In Adults
SS Colitis
SS Diverticulitis
SS Pyelonephritis.
Appendix 383
In Women of Childbearing Age
SS Ectopic pregnancy
SS PID
SS Tuboovarian mass
SS Ruptured ovarian cyst
SS Twisted ovarian cyst.
Special Consideration in
SS Children
SS Elderage group
SS Pregnancy.
In Children
SS Perforation is common because patient often present later

SS Acute mesenteric lymphadenitis is the most common differential diagnosis
SS In children with equivocal history and physical examination, CT abdomen is indicated.
In Elder Age Group
SS Elderly patient may present with less specific symptoms and signs
SS Perforation is more common
SS Early CT is indicated to reach the proper diagnosis and delay in decision making can be avoided
SS Associated comorbidities aggravate postoperative morbidity and mortality in the setting of perforated appendicitis
SS Diverticulitis or perforation in the cecal growth should be in the differential diagnosis.
In Pregnancy
SS In the 1st and 2nd trimester, the presentation is similar in comparison to non-
pregnant women.
SS In the 3rd trimester, appendix is shifted superiorly above the iliac crest and the
appendiceal tip is rotated medially into the right upper quadrant.
SS Abdominal wall is lifted by the gravid uterus and due to decreased muscle tone,
signs of peritoneal irritation are not significant.
SS Ultrasound is the appropriate imaging modality. If USG is equivocal, MRI rather
than CT is indicated to avoid ionizing radiation exposure to the fetus.
SS If appendicitis is suspected, better proceed to appendectomy rather than
observation, because risk of fetal loss is directly related with the severity of
appendicitis.
SS There is controversy regarding safety of lap appendectomy.
What is Alvarado Scoring?
SS A scoring system for predicting appendicitis.

Findings Point
Migratory right iliac fossa pain 1
Anorexia 1
Nausea or vomiting 1
Tenderness 2
Rebound tenderness 1
Elevated temperature 1
Leukocytosis ≥ 10 × 109/L 2
Shift to the left 1
10
Score < 3 : Low possibility of appendicitis
Score 4–6 : Consider further imaging
Score ≥ 7 : High possibility of appendicitis
Another scoring system is developed— Appendicitis Inflammatory Response Score, which better predicts acute
appendicitis. This scoring system besides most of the parameters of Alvarado score, also includes C- reactive protein
concentration.
Pediatric Appendicitis Score (PAS)—
Migration of pain 1
Anorexia 1 Pediatric Appendicitis
Nausea/vomiting 1 Score 1–3: Negative for appendictis
Right lower quadrant tenderness 2 Score 4–7: Requires further diagnostic testing
Cough/hopping/percussion
tenderness in right lower quadrant 2
Increase in temperature 1 Score 8–10: Positive
Leukocytes > 10,000/μl 1
Polymorphonuclear neutrophilia > 75% 1
10
Appendix 385
Treatment
Open Appendectomy
SS Preoperative antibiotics significantly reduces the chance of postoperative wound infection and intraabdominal
abscess.
SS Choice of anesthesia – SA/GA.
SS After anesthesia and prior to giving incision, abdomen should be reexamined to rule out lump formation.
SS Which incision? McBurney’s Gridiron/Lanz incision
Contd...
Appendix 387
Contd...
Appendicular artery is visualized in

mesoappendix
Laparoscopic Appendectomy
Contd...
Appendix 389
Contd...
Other Approaches of Appendectomy
SS Laparoscopic Single-incision Appendectomy—The incision is made in the periumbilical site

SS Natural orifice transluminal endoscopic surgery (NOTES)— Transvaginal/Transgastric.
Appendiceal Mass (Appendicular Lump)

Appendix 391
During Appendectomy if these Things Happen
1.
So, it is better to
remove the appendix
2.
3.
It is dangerous to separate appendix in this situation, over

enthusiasm makes the situation more complicated.
Neoplasm of the Appendix
Carcinoid Tumor (Argentaffinoma)
Carcinoid tumors are neuroeudocrine tumors that arise from Kulchitsky cells of the crypts of Lieberkühn.
SS Most common neoplasm of the appendix.
SS Most of the appendiceal carcinoids are located at the tip of appendix.
SS Most of the carcinoids present as recurrent appendicitis.
SS Unlike carcinoids of other sites, appendiceal carcinoid rarely gives rise to metastases.
SS Only appendicectomy is indicated for tumor <2 cm.
SS For tumor > 2 cm, involving the base of appendix or mesoappendix, right hemicolectomy is recommended.
SS Patient with appendiceal carcinoids may present with second primary tumors (specially tumors in GI and
genitourinary tract), screening investigations (e.g. colonoscopy) are necessary to detect the second malignancy.
Chapter 12
Rectum and Anal Canal

Important Topics
zzProlapse of the Rectum

zzSolitary Rectal Ulcer Syndrome
zzFissure-in-ano
zzAnorectal Abscess
zzFistula-in-ano
zzHemorrhoids
zzPilonidal Sinus
zzRectal Cancer
zzCancer of the Anus
‘[F]rom the simplicity Nature employs in all her works. We may conclude …... From these considerations it is highly probable
that the question about the mutual union and anastomosis of the vessels can be solved; for if Nature once circulates the blood
within vessels and combines their ends in a network, it is probable that they are joined by anastomosis at other times too.’
Marcello Malpighi (1628–1694)
Italian Physician, Physiologist and Microscopist.
Rectum and Anal Canal 395
Prolapse of the Rectum
How It Develops?
SS Exact etiology unknown

SS It is the result of intussusception or infolding of the rectum, usually beginning 6–8 cm from the anal verge
SS It is still unknown what causes the intussusception.

Associated With Some Anatomical Changes
SS Rectovesical pouch (in male).

How Will You Differentiate Complete Rectal Prolapse From Mucosal Prolapse?
Mucosal Prolapse Complete Rectal Prolapse
Complete rectal prolapse
In children
SS Prolapse often evident after a diarrheal episode or illness causing acute loss of body weight
SS Usually apparent during defecation. Otherwise becoming well and continent
SS Usually it is a mucosal prolapse.
Keep in mind other possibilities:

zz Prolapsed rectal polyp
zz Apex of intussusception.
In adult
SS Rectal prolopse is more common in women (6 : 1)
SS Incidence maximum in seventh decade in women. In men, incidence is unrelated to age
SS Initially apparent during evacuation and other straining
SS Later, soiling of underclothes with blood and mucus
SS Incontinence of feces and flatus may present
SS Anal sphincter is very weak
SS Ulceration may develop over the prolapsed mucosa due to repeated friction injury
SS Palpation reveals double thickness of tissue (in complete rectal prolapse).

Investigation
Sigmoidoscopy is Essential
All patients with rectal prolapse should be examined with flexible sigmoidoscope to rule out polyps, cancer or inflam-
matory bowel disease.
SS Defecation proctography is indicated if there is suspicion of internal prolapse.
SS Patient of rectal prolapse probably due to damage of pudendal nerve should be evaluated with electromyography
and pudendal nerve. Terminal motor latency test.
Treatment
SS Rectal prolapse in children usually responds to

conservative measures. Correction of bowel habit and
use of laxatives are sufficient to treat the disease.
SS Complete rectal prolapse in adults need surgery.
Abdominal Procedures
Thiersch procedure—Anal encirclement with nylon or polypropylene suture. Now, abandoned due to complications,
e.g. perianal sepsis and stenosis.
Sutured rectopexy—Suturing the mobilized rectum to the sacrum with 4–6 interrupted nonabsorbable suture.
Perineal Procedure
SS Recommended for high-risk patients

SS Also recommended in young men in whom impotence is concerned as complication of abdominal approach.
Altemeier procedure—Perineal proctosigmoidectomy + Anterior levatoroplasty.
Delorme’s operation—It is the preferred perineal procedure. Circumferential stripping of the mucosa from the
prolapsed rectum, plication of the underlying muscle with a series of sutures, suturing of the anal canal mucosa with
the remaining rectal mucosa at the tip of the prolapse.
Solitary Rectal Ulcer Syndrome
SS Solitary rectal ulcer syndrome (SRUS) is commonly associated with internal intussusception.
SS This lesion is always present on the anterior wall of rectum, 4–12 cm from the anal verge.
SS The lesion ranges from crater-like ulcer to polypoidal growth.
SS This syndrome commonly affect young females.
SS Patient commonly presents with history of chronic constipation, digital disimpaction of stool, rectal bleeding,
mucus discharge.
SS Diagnosis of the underlying pathology (internal prolapse, full thicknes prolapse) is done by defecography.
Colonoscopy and biopsy of the ulcer or polypoidal mass is essential to exclude Crohn’s disease, malignancy or CMV
infection.
SS Most of the patients response to conservative therapy (high fiber diet, pelvic floor retraining, topical anti-
inflammatory preparation containing mesalamine).
Surgical intervention (rectopexy by abdominal or perineal approach) is indicated in symptomatic patients who
failed to respond in conservative therapy.
Fissure-in-Ano
SS Women are more commonly affected than men

SS Fissure can occur in any age group.
Location of Fissure
Posterior midline location—Most common location

Why posterior midline is so common?
SS In the posterior part of anal canal, the external sphincter fibers are in elliptical arrangement
SS This arrangement of sphincter causes lack of anatomical support to this area favors early tearing
SS Vascular watershed in the posterior midline—A site of decreased blood supply.

How Fissure Develops?
More pain, less bleeding

SS The history is typical.
SS Pain is the predominant symptom—Sharp and agonizing pain

starts during defecation and lasts for hours.
SS Patient tends to become constipated due to pain.
SS Bleeding is slight and usually streaks on the stool or toilet paper.
SS Mile discharge may present.
Typical history, tightly closed puckered anus and inspection of the lower end of fissure is sufficient to diagnose an acute
anal fissure. In chronic fissure, classic findings of fissure-in-ano are evident.
Digital and proctoscopic examination

should be delayed for 4–6 weeks when
acute pain resolves.
Avoid proctoscopy in acute fissure Avoid digital rectal examination in acute fissure
Treatment
Medical Management
Particularly effective in management of acute fissure. Medical management focuses on the cycle of pain, spasm and
ischemia.
SS Symptomatic therapy with warm sitz bath and SS Nifedipine (0.3%) ointment
bulking agent zz A calcium channel blocker.
zz Decrease muscle spasm. zz Heals fissure by lowering the resting anal pressure
zz Make the stool more soften thereby decrease the and vasodilatation.
trauma. zz Side effects (e.g. headache) may present.
Reversible chemical sphincterotomy with SS Arginine—It acts as a nitric oxide donor, relaxes the
SS Glyceryl trinitrate [nitroglycerine 0.2% ointment] internal anal sphincter.
zz It is nitric oxide donor—
Relaxes the internal sphincter
Improves blood flow to the anoderm
Major side effect is headache.
SS Diltiazem (2%) ointment SS Bethanecol—As a muscarinic agonist, provides

zz It is a calcium channel blocker nitric oxide synthesis in nonadrenegic, noncholinegic
zz Similar efficacy to nitroglycerine
neurons.
zz Heals fissure by lowering the resting anal pressure.
zz Side effects (headache, flushing of face and limb)

may present.
SS Botulinum injection
zz Botulinum prevents release of acetylcholine from
presynaptic nerve teminals, thereby paresis of
the injected muscle develops. The vicious cycle of
spasm-pain-ischemia breaks.
Surgical Treatment
SS Anal stretching (Lord procedure)

zz No longer performed.
SS Lateral anal sphincterotomy—Most commonly performed procedure.
zz Closed technique
zz Open technique.
Closed technique Open technique
Anorectal Abscess
Infection of the glandular secretion of the anal crypts results in suppuration and abscess formation.
SS Infection primarily originates in the intersphincteric plane, and then extends
Vertical Extension
SS Upward
SS Downward.
Horizontal Extension
Circumferential Extension
Circumferential spread may occur in supralevator, ischiorectal and intersphincteric abscess.
Sites of Anorectal Abscess Clinical Presentation
SS Perianal (most common) SS Dull perianal discomfort aggravated by local pressure, pruritus.
SS Ischiorectal (second common) SS Erythematous, defined, fluctuant subcutaneous mass near the
SS Intersphincteric anal orifice (perianal abscess).
SS Supralevator SS Large swelling over the buttock (ischiorectal abscess).
SS Submucosal. SS Clinical examination alone cannot diagnose intersphincteric

abscess and particularly supralevator abscess.
Investigations
SS Required only to diagnose some type of abscesses

SS To exclude primary causes of sepsis (e.g. pelvic sepsis, IBD and malignancy)
SS Anal ultrasonography
SS MRI–investigation of choice for complex anorectal sepsis—
SS Proctosigmoidoscopy—To find out primary cause of sepsis.
Treatment
Don’t wait for fluctuation.

Don’t depend on conservative treatment, because—
SS Antibiotic therapy delays surgical drainage
SS Delay in drainage results in chronic infection and destruction of tissue
SS Drainage should be done ↓ anesthesia. Pus must be sent for culture and
sensitivity.
Drainage of Perianal Abscess Drainage of Ischiorectal Abscess
Drainage of Intersphincteric Abscess
Drainage of Submucous Abscess
Intersphincteric abscess is difficult to diagnose because of absence

of external signs of inflammation.
Drainage of Supralevator Abscess
SS This type of abscess is least common and most difficult to diagnose.

SS Develops in one of the 3 ways:
zz Upward extension of intersphincteric abscess
zz Upward extension of ischiorectal abscess
zz From perforated diverticulitis or appendicitis.
SS It is important to identify the origin of supralevator abscess before treatment.
SS If it is due to upward extension of intersphincteric abscess, it is drained through rectal route.
SS If it is due to upward extension of ischiorectal abscess, it should be drained through ischiorectal fossa.
SS If it is secondary to abdominal pathology, it may be drained either transabdominally, or rectal route or through
ischiorectal fossa based on the location of abscess and general condition of the patient.
What is Horseshoe Abscess?
SS Circumferential spread of anorectal abscess may occcur in intersphincteric plane, the ischiorectal fossa, or in the
supralevator plane, causing horseshoe abscess.
SS Horseshoe abscess in the ischiorectal fossa is drained by posterior drainage and counterincision in both ischiorectal
fossa.
SS Abscess in the intersphincteric plane can be drained by dividing the internal sphincter for the height of the abscess
cavity.
SS Abscess in the supralevator plane can be drained by incising both ischiorectal fossa upto the level of abscess.
Fistula-in-ano
SS Most fistulas arise from sepsis originating in the anal glands at the
dentate line.
SS Anorectal abscesses are either treated by drainage or spontaneously
discharged. Once the anorectal abscess has drained, there is potential
communication pathway along the line of extension of abscess.
Classification of Fistula
Intersphincteric Fistula [Most Common]
Transsphincteric Fistula [Second Common] Suprasphincteric Fistula
Extrasphincteric Fistula
SS Purulent discharge around the anus and/or from within the anal canal.
SS Pain in perianal region, gradually increasing in intensity, and then discharge starts with immediate relief of pain.
This history often repeats with few months interval.
SS History of one or more operations for abscess or fistula.
How To Examine A Fistula?
Note:
1. Visual examination SS External fistulous opening is
of perianal region solitary/multiple.
and perineum SS Anteriorly/posteriorly placed.
SS Distance from anal margin.
SS Any scar present or not.
External opening of fistula (solitary anterior)
2. Palpation of the perianal

region and anal canal.
[It is important to find out the in-
ternal opening of the fistula be-
cause chance of recurrence after
surgery is high if internal opening
is not located.]
3. Proctoscopy
4. Probing of fistula track

Beware of not to create false passage.
SS Ifinternal opening cannot be identified by probing, then methylene blue is injected into the external opening with
pediatric feeding tube.
[Proctosigmoidoscopy—To exclude primary colorectal disorders, particularly Crohn’s disease. It is mandatory in all
patients with fistula.]
There is limitations of preoperative clinical evaluation particularly in complex and recurrent fistula.
So, investigations are essential for defining the fistula track against the three-dimensional anatomy of the perineum
and anorectum along with sphincter complex.
Investigation
Fistulogram? MRI? CT? Endoanal USG?

SS Not so helpful for de- SS MRI is regarded as SS Not helpful SS Provides high quality images of fistula
lineation of the track the investigation for fistula but tract and anorectal abscesses.
and its relation to the of choice in for anorectal SS Can be used in the operating room at
normal anatomic struc- complex fistula. abscess. the time of surgery.
tures.
What is Goodsall’s Rule?
Exception to the Rule

SS Anterior openings that are more than 3 cm from the anal margin
SS Multiple fistulous openings.
Treatment
SS Asymptomatic fistula requires no treatment

SS Symptomatic fistula requires surgery (because spontaneous healing is very rare)
SS Different surgical options are present but which one is preferable, depends on type of fistula.
Principles of Surgery
SS Drainage of intersphincteric primary focus of infection in all fistulas

SS Management of primary track across the external sphincter and secondary tracks within the anorectal fossa
SS In superficial fistulas involving minimal sphincter muscle, fistulotomy is preferred
SS In anterior fistulas in women and fistulas involving most of the sphincters, seton placement is preferred.
Fistulotomy
SS Principle of fistuloto-
my is identification of
the fistula tract and
lay open the tract.
SS Intersphincteric and
low transsphincteric
fistulas are effective-
ly treated by fistul-
otomy.
SS Any secondary tract should be drained

SS Granulation tissue from the tract should be sent for biopsy.
[Fistula involving more than one-third of the sphincter complex, anterior fistula particularly
in women and fistula with impaired continence are not ideal candidates for fistulotomy.]
Seton
Seton is a drain through a fistula to maintain drainage or induce fibrosis.
SS Draining seton
SS Cutting seton.
Draining seton Cutting seton
SS The seton (usually, vessel loop) is placed in the tract SS The seton [suture (e.g. nylon, prolene)/rubber
to prevent it from closing. band] slowly cuts through the sphincter, allowing
SS It is indicated in— the tract to become more superficial with minimal
zz Anterior fistula in female
separation of sphincter muscle.
SS It is indicated in—
zz Elderly patient with poor sphincter function
zz High transsphincteric fistula
zz Multiple fistulas.
zz Complex fistula.
Cutting seton placement

Mucosal Advancement Flap
SS Particularly useful in extrasphincteric and suprasphincteric fistula.

SS Principle of the technique—
zz Covering the internal opening by internal sphincter and anal mucosa advanced from above
zz Opening the external component of the fistula.
Fistulectomy Fibrin Glue
SS Useful when histology of the tract is necessary SS Useful for treatment of complex, recurrent fistulas.
SS It is the excision of principle tract and side tracts also. SS Fibringlue is injected into the fistula track. The
glue hardens and fills the track.
Recent Techniques
SS SISplug—This cone-shaped plug is made of porcine small intestinal submucosa. It is inserted into the fistula track
SS LIFT (ligation of the intersphincteric fistula tract).
Hemorrhoids or Piles
SS ‘Hemorrhoid’ is derived from the Greek word ‘haimorrhoides’—Meaning bleeding (haima = blood, rhoos = flowing).
SS ‘Pile’ is derived from the Latin word ‘pila’—Meaning a ball’.
What is Hemorrhoids?
SS Hemorrhoids are nothing but downward sliding of one or more anal cushions causing symptoms.
What is Anal Cushion?

How Prolapse of Anal Cushions Develops?
Anchoring muscular extensions from longitudinal muscle of rectum to the internal sphincter and anal cushions keep
the cushions in position.
Types
SS Painless, bright red bleeding per rectum during defecation—Dripping of blood or even squirting of blood
SS Something coming out per rectum during defecation
SS Mucoid discharge is frequently associated with prolapsed hemorrhoids
SS Pain is not a usual symptom except thrombosed external hemorrhoids
SS Internal hemorrhoids are classified according to the extent of prolapse
zz First degree
zz Second degree
zz Third degree
zz Fourth degree.
4th degree hemorrhoids
How to Examine a Patient with Hemorrhoids?
SS Inspection—
zz Large third-degree and all fourth-degree hemorrhoids are readily recognized

zz After straining, second-degree hemorrhoids become apparent
zz In first degree hemorrhoids, no abnormality can be seen.
[Other associated pathologies (e.g. fissure and fistula) may be present.]

SS Palpation
zz Assessment of sphincter tone
zz Exclusion of any anal canal or low rectal neoplasm.
SS Proctoscopy—To confirm the finding during inspection and

palpation.
SS Sigmoidoscopy—To exclude proximal inflammation or neoplasia.
SS Colonoscopy—It is essential if:
zz Symptoms not corroborating with clinical findings
zz Patient is older than 40 years Proctoscopy is essential for diagnosis of

hemorrhoids
zz Patient with risk factors for colonic carcinoma.
Treatment
First-Degree Hemorrhoids Second-Degree Hemorrhoids

SS Dietary modifications—Fiber supplementa-
tion, adequate fluid intake.
SS Avoidance of excessive straining.
SS Stool softeners.
Rubber band ligation
[Care is to be taken during banding, so that bands are

not placed at or distal to the dentate line (severe pain
develops due to presence of sensory nerves distal to
the dentate line]
This method is the most successful nonsurgical treatment method of hemorrhoids.

Sclerotherapy
[Other sclerosants—Sodium morrhuate, quinine urea]
[Be cautious that sclerosant is not injected too deeply.]
Infrared photocoagulation
SS An effective treatment for small second-degree hemorrhoids.

SS Infrared radiation coagulates tissue protein and evaporates water in the cell, thereby small hemorrhoids are
managed.
Third-Degree and Fourth-Degree Hemorrhoids
SS Treatment of choice is hemorrhoidectomy

zz Open method
zz Closed method.
SS Hemorrhoidectomy should also be considered if:
zz Repeated attempts at conservative measures failed
zz Associated with other pathologies, e.g. strangulated external hemorrhoids, fissure and fistula.
Open technique
SS Milligan and Morgan hemorrhoidec-

tomy.
Closed submucosal hemorrhoidectomy
SS Parks or Ferguson hemorrhoidectomy
Principles of Hemorrhoidectomy
SS Surgeon should treat each hemorrhoid case individually—Excise one hemorrhoid in a case and three in other cases.
SS Adequate bridges of healthy tissue must be left between excision sites.

Postoperative Complications
Newer Methods
1. Stapled hemorrhoidectomy or stapled hemorrhoi- SS Treatment of external hemorrhoids: Hemor-
dopexy: This method excises the lower rectal and rhoidectomy is indicated for symptomatic patients.
upper anal canal mucosa and submucosa circumfer- SS Treatment of mixed (both internal and external)
entially and then a reanastomosis by a circular stapler. hemorrhoids: Hemorrhoidectomy is indicated for
2. Doppler-guided hemorrhoidal artery ligation. large, symptomatic hemorrhoids.
Thrombosed External Hemorrhoids
SS Patients present with painful mass in perianal area with throbbing pain
SS The condition is self-limiting (within 4–5 days)
SS Treatment is aimed to relief severe pain, prevention of recurrent thromboses and management of residual skin tag
SS Histopathology of thrombosed external hemorrhoids reveal thrombus in the capillaries
SS The clot is removed after giving an elliptical incision over the mass.
Pilonidal Sinus
SS Pilonidal sinus is also found in finger web, axilla,
perineum, umbilicus, breast.
[L.pilus - hair; nidus = nest] SS Women engaged in sheep shearing, dog
SS Sinus in the natal cleft containing hairs. beauticians, hairdressers— Pilonidal sinus in breast.
SS So commonly found in jeep riders in the 1935–45 war, SS Barber’s pilonidal sinus—In the finger web.
it is also known as ‘jeep disease’.

SS Exact pathogenesis is still controversial and whether
it is congenital or acquired in origin is still debatable.
How it Develops?
Bascom’s Theory
Karydakis’s Explanation
SS Shaft of loose hair inserts into the depth of the natal

cleft
SS Foreign body reaction occurs leading to infection
SS Secondary opening develops due to self-propelling

ability of hair or spontaneous rupture of abscess
SS Most of the patients are hirsute and obese.

SS Hirsute people with dark hairs have an increased
tendency.
SS Males and females—Both affected, but males are
more commonly affected.
SS Typical location of the midline pits is approx 5 cm
posterior to the anus overlying the sacrum and
coccyx—In the intergluteal cleft.
SS Secondary openings are marked by elevations of
granulation tissue and discharge of seroprulent
material.
Hairs seen protruding from the pits.
Treatment
Conservative Surgery
SS Removing all hairs from the area SS Bascom’s technique
SS Cleaning out the track SS Karydakis method
SS Frequent washing of the area with soap and water SS Z-plasty.
SS Long sitting, e.g. driving a car should be avoided.

Bascom’s technique
Karydakis technique
Z-plasty
Rectal Cancer
SS Rectalcancer shares many of the genetic, morphologic characteristics of colon cancer.
SS Butalso, rectum is different from colon in many aspects—
zz Retroperitoneally located in the narrow pelvis
zz Close proximity to the urogenital organs, autonomic nerves and anal sphincters makes surgical access difficult
zz Dissection in proper plane is needed and it needs expertise
zz Due to its pelvic location, radiation therapy without collateral radiation damage of small intestine is possible.
Spread of Rectal Carcinoma
SS Retrograde lymphatic drainage occurs if only proximal lymphnodes or lymphatics are blocked
SS Involvement of inguinal lymph nodes occurs if the lesion invades the dentate line.
SS Rectal bleeding (most common symptom)—[Rectal carcinoma must be ruled out in any adult patient presents
with rectal bleeding].
SS Alteration of bowel habit.
SS Passage of mucus with stool.
SS Sense of incomplete evacuation.
SS Sense of rectal ‘fullness’.
SS Subacute intestinal obstruction (complete obstruction rarely develops in carcinoma rectum).
SS Weight loss, anorexia.
SS Rectal pain or low back pain (if there is extensive local invasion).
SS Family history of rectal cancer, FAP, HNPCC and IBD may be present.
Assessment of Tumor
Also assess—
SS Vaginal involvement (by pelvic examination).
SS Barium enema or virtual colonoscopy is indicated if colonoscope cannot be negotiated due to circumferential
involvement or in uncooperative patient.
Preoperative Staging
SS Preoperative staging can determine whether radical resection or neoadjuvant chemoradiation is appropiate.
SS CT scan of abdomen and pelvis can demonstrate local tumor extension, lymphatic and distant metastases, tumor
related complications (e.g. perforation, fistula, etc.).
In CECT, function of the kidneys and ureteral involvement by the tumor can be assessed.
SS Endorectal ultrasound (EUS) is now the most effective preoperative staging technique for T and N stage.
EUS defines five interface layers— Mucosa, muscularis mucosa, submucosa, muscularis propria and perirectal fat.
SS Endorectal coil MRI is similar in accuracy compared to endorectal USG.
SS Chest X-ray/CT chest—To rule out pulmonary metastases.
Preoperative Estimation of CEA (Carcinoembryonic antigen)

SS Preoperative CEA > 5 ng/ml signifies a worse prognosis.
SS Elevated preoperative CEA that do not normalize after surgical resection implies presence of persistent disease.
SS Elevated preoperative CEA that normalize after resection, and then elevation after a period of time implies
recurrence.
Treatment
Goals of Resection of Rectal Tumors

SS Removal of tumor with an adequate margin
SS Removal of draining lymph nodes and lymphatics.
Local Excision
SS T lesions (low probability of microscopic nodal
1
disease) are best candidates for local excision.
SS Patients with extensive metastatic disease and poor
prognosis, who require local control.
[T1— Tumor invades submucosa]
Transanal excision
Transcoccygeal excision
SS Particularly useful in lesion in posterior wall of

rectum.
Transanal endoscopic microsurgery (tem)
SS Particularly
useful for T1 lesion in middle and lower third of rectum.
SS Instruments required are—
zz Operating proctoscope
zz Binocular microscope and video scope
zz CO insufflator
2
zz Long surgical instruments.
Anterior Resection with TME
SS It is particularly applicable in carcinoma of upper third

of rectum.
SS ‘Anterior’ term is used to differentiate abdominal
(anterior) approach from posterior approach.
[Anterior resection should not be attempted if anal
sphincter is destroyed or involved by disease.]
SS It is basically—
Wide resection of sigmoid colon and proximal rectum

with distal clearance margin of 2 cm
+
Resection of lymphatic field
⇓
End to end colorectal anastomosis
[As distal intramural spread is no more than 1 cm, it is safe
to keep the distal clearance margin to 2 cm.]
What is mesorectum and TME?
SS Mesorectum is the structure covered by visceral layer of endopelvic fascia (fascia propria of rectum) that contains
the blood supply and lymphatics of upper, middle and lower rectum.
SS TME is sharp dissection under direct vision in an avascular plane.
SS This avascular plane is between the fascia propria of rectum (visceral layer of endopelvic fascia) and parietal layer of
endopelvic fascia overlying the pelvic wall structures. This avascular plane is called the ‘Holy Plane’.
[After a proper TME, the specimen is typically shiny and lobed.]

SS TME allows adequate clearance of lymph nodes as well as radial margins of the tumor (radial margin is more related
to local recurrence).
Abdominoperineal Resection
SS Usually
indicated for distal rectal cancer.
SS Alsoappropriate where cancer involves the sphincter
complex or patient is already incontinent.
Abdominal dissection Perineal dissection

APR + Posterior Vaginectomy Total Pelvic Exenteration
SS Indicated for locally advanced low rectal cancers SS Indicated for patients with locally advanced rectal
involving the vagina. cancer involving prostate and bladder.
Cancer of the Anus

Cancer in the anal canal [from top of the anorectal ring to
the anal verge]
+
Cancer in anal margin [beyond anal verge]
Anal cancers are not so common as rectal cancer.

Anal canal cancers are 3–4 times more common than
cancer in anal margin.
Risk Factors
SS Human papilloma virus [HPV]—HPV type 16—Very high risk for anal squamous cancer.
Other types with moderate risk are type 18, 31, 33, 35.
[Sexual contact is the mode of transmission of HPV. (increased risk in receptive anal intercourse in women and homo-
sexsual activity in men).]
SS HIV– All HIV exposure categories including male homosexual anal intercourse (highest risk of anal cancer), injection
drug use, transfusion and heterosexual contact for women are associated with increased risk of anal cancer.
SS Tobacco smoking is associated with five fold increased risk.
[Benign anal pathologies, e.g. fistula, fissure, hemorrhoids do not increase the risk of cancer.]
Pathology
Anal intraepithelial neoplasia (AIN) is an important entity.

SS Epithelial tumors are the most common type of cancer in the anal canal.
SS Squamous cell carcinoma accounts for about 70% of the tumors. Other varities are adenocarcinoma, mucinous
adenocarcinoma, small cell CA, undifferentiated CA.
SS Basaloid, cloacogenic or transitional types are considered as a variant of squamous cell carcinoma.
SS Melanoma, sarcoma and lymphomas are unusual in this region.
SS Histologically, most of the anal margin tumors are squamous cell carcinoma. Other varieties are basal cell CA, Paget
disease.
Bowen disease (intraepidermal squamous cell CA) and verrucous carcinoma (variant of squamous cell CA) are rarely
encountered.
SS Most of the patients presents with bleeding per rectum

SS Pain,tenesmus and pruritus may be present
SS Patient can feel a mass in the anus
SS Patients may present with a mass in the inguinal region due to metastatic lymph nodes.
Assessment of the Tumor and investigations to confirm Diagnosis
SS Digital rectal examination (DRE)—Size, location, fixity to adjacent structures are assessed
SS Proctoscopy
SS Examination of inguinal lymph nodes

SS Pelvic examination is indicated to rule out presence of other HPV associated concers
SS Biopsy from the tumor mass
SS FNAC from the inguinal lymph nodes
Staging is completed by CT or MRI of abdomen and pelvis, transanal USG and CT chest
[MRI can better delineate the soft tissue planes.]
Treatment
Treatment of AIN
SS Local surgery
SS Photodynamic therapy
SS Topical immunomodulators (e.g. imiquimod).
Treatment of Invasive Cancer
Combination of chemotherapy + radiotherapy [Nigro regime].

Chapter 13
Breast
Important Topics
zzInflammations and Infections of Breast

zzBreast Lump
zzNipple Discharge
zzMastalgia
zzANDI
zzBreast Carcinoma
‘Surgical knowledge depends on long practice, not from speculations.’

M. Malpighi
Italian Physician, Physiologist and Microscopist
Diseases of the Breast
Inflammations and Infections of Breast
SS Acute mastitis
SS Lactationalbreast abscess
SS Periductal mastitis
{
SS Nonlactational breast abscess
SS Tuberculosis of the breast

SS Hidradenitis suppurativa
Uncommon entity
SS Pilonidal abscess
Lactational Breast Abscess
Develops during breastfeeding.
Usually occurs at the commence-

ment of breastfeeding (inexperi-
enced mother develops cracked
nipples) and at weaning (incom-
plete drainage of milk leads to
engorgement and about 6 months
of age child’s first teeth develops).
SS Discomfort in the breast followed by painful swelling.

SS The affected breast or a segment shows the signs
of acute inflammation in early phase, and later the
features of an abscess.
SS If not treated, abscess spontaneously discharge on to
the skin surface.
Breast 435
Confirmation of the diagnosis
? Acute mastitis
? Abscess
? Inflammatory carcinoma.
Or
to confirm
abscess
Any suspicion of inflammatory carcinoma, then—

SS Full thickness skin biopsy
SS Cytology of aspirated material.
If antibiotic is used in the presence of undrained abscess,

‘antibioma’ develops. It is a sterile edematous swelling. It
takes many weeks to resolve.
Inflammatory carcinoma is a high grade malignancy. So if
you treat an ‘inflammatory carcinoma’ like a mastitis, you
may loose your patient.
Treatment
Treatment of mastitis
SS Appropriate antibiotics (coverage against penicillinase producing Staph.aureus)
zz Second generation penicillin
zz Cephalosporin.
SS Feeding on the opposite breast
SS Infected breast should be emptied of milk either mannually/or by breast pump
SS Gentle washing of the cracked nipple
SS Support of the breast, analgesia—To relieve pain.

Treatment of breast abscess
Or
SS If incision and drainage is planned, then the site of incision is planned according to the site of abscess:
Choice of incision
Technique of abscess drainage

Breast 437
Nonlactational Breast Abscess
Fistula in periareolar skin with slit retraction of nipple
SS It is one of the manifestations of periductal

mastitis/duct ectasia.
SS Systemic manifestations are less prominent.
SS Periductal mastitis is associated with smoking.
Treatment
SS Inflammatory mass/abscess should be aspirated,

then; pus should be sent for—
zz Aerobic culture
zz Anaerobic culture.
SS If indicated, repeated aspiration.
SS Antibiotics (coverage against Staph.aureus and

anaerobes).
[Open drainage is better avoided.]
SS In refractory cases, duct excision—under antibiotic
prophylaxis.
Duct Ectasia and Periductal Mastitis
SS Duct ectasia is a involutionary and age-related Is smoking related with periductal mastitis?
condition not associated with significant clinical SS Smoking is important in the natural history of non-
problems. lactational breast abscess and may predispose
SS Periductal mastitis is a pathological, inflammatory to anaerobic infections and the development of
disease leading to abscess and fistula. mammary fistula.
Recurrent periductal mastitis is also known as ‘Zuska’s disease’.

What happens in periductal mastitis?

Breast 439
USG of breast Mammography
SS Galactography (ductography) — Injection of contrast into a discharging duct to identify filling defect or other
irregularities.
It is useful only for patients with single duct discharge.
Ductogram showing dilated duct
SS FNAC: If patient presents with a mass, FNAC should be done to rule out carcinoma.
Treatment
SS Patient is advised to stop smoking.

SS In duct ectasia, surgery is rarely needed except; discharge is persisting and blood-stained.
SS Antibiotics are needed in periductal mastitis—Coverage against gram (+ve), (–ve) and anaerobes.
SS Clinically detected/USG detected abscess ⇒ Recurrent abscess

| |
Needs needle aspiration Needs incision
+ +
Antibiotics Drainage
SS Surgery is needed, but when? and which one?
Breast 441
Other Uncommon Infections of the Breast
Tuberculosis of the Breast
SS The possibility of tuberculosis should always be considered in endemic regions when a woman presents with
thickening of the skin and the underlying breast parenchyma with or without lump.
SS It may also present with sinus and skin tethering.
SS USG, mammography and FNAC are usual diagnostic methods for diagnosis.
If mammography and cytology are inconclusive, open biopsy for H/P or for identification of AFB is necessary for
diagnosis.
SS Treatment is by ATD, and if breast deformity, then mastectomy followed by reconstruction is indicated.
Hidradenitis Suppurativa
SS Mostly found in axilla, but may present in the inframammary fold and nipple areola complex.
SS Conservative management rather than excision is the preferred treatment option.
Pilonidal Abscess
SS Seen in the periareolar area of the breast of women engaged in sheep shearing (roustabouts’ breast).
SS Also seen in dog beauticians and hair dressers.
Mondor’s Disease
SS Thrombophlebitis involving the superficial veins of anterior chest wall and breast.
SS Veins commonly involved are—lateral thoracic vein, thoracoepigastric vein.
SS Patient presents with acute pain in anterior chest wall or lateral part of the breast. On examination, tender cord like
structure is palpable along the course of the superficial vein.
SS Treatment is avoidance of strenuous wark on diseased side, application of warm compress and topical
antiinflammatory agents.
If symptoms persist even after weeks, excision of the involved segment may be considered.
Breast Lump
First, judge whether the lump is a true abnormality or within the spectrum of normality.
Second, if it is a true abnormality, then assess whether it is benign or malignant.
‘Triple assessment’: Standard approach to all breast lumps
SS Clinical breast examination
SS Breast imaging (mammography or USG)
SS Pathology (FNAC/wide-bore needle biopsy). Wide bore needle biopsy is more preferable because—
zz Histological diagnosis possible
zz Immunohistochemical examination (ER, PR and HER-2 neu) can be done.

Fibroadenoma
Most common benign tumor (?) of breast
Diagnosis
SS In younger age groups, a clinical diagnosis of fibroadenoma is highly accurate due to its characteristic findings.
SS However, a tissue diagnosis is required to rule out malignancy (incidence of malignancy in newly discovered
fibroadenoma is exceedingly rare).
[If neoplasia develops in the epithelial component, they are mostly lobular carcinoma.]
Treatment
SS In women under 25 years of age, after tissue diagnosis, reassurance (no cancer, chance of malignant transformation
is rare) is the recommended treatment because:
zz A small number increase in size
zz Most of them become smaller and some disappear.
SS In older age group and if patient wishes, excision biopsy is considered.
SS Excision biopsy is also considered if FNAC report is inconclusive or there is family history of breast carcinoma.
Breast 443
Giant Fibroadenoma
SS Bimodal age of presentation at the extremes of reproductive life—In 14–18 years and in 45–50 years.
SS Histologically almost similar to simple fibroadenoma; histologically different from phyllodes tumor (phyllodes
exhibit more cellularity, pleomorphism and mitotic activity).
SS Patients present with pain in the breast with rapid increase in size. On examination, breast enlarged, overlying skin
is characteristically shiny, venous prominences may be present.
SS Treatment is enucleation through an appropriately placed cosmetic incision.
Phyllodes Tumor
Phyllodes tumor—Large bosselated tumor
Operated specimen of phyllodes tumor
Malignant phyllodes
SS Behave like sarcoma

SS About 23–50% are histologically malignant
SS Axillary lymph node may present
SS Metastasis may present (lungs is the most common site).
Treatment
SS Metastatic phyllodes behave like sarcoma. So when systemic therapy is

planned for metastatic malignant phyllodes, treatment is based on the
guidelines of sarcoma management.
Breast Cyst
SS True breast cysts are very common.
SS They occur most commonly in the

last decade of reproductive life
due to nonintegrated involution
of stroma and epithelium.
SS Specific cause of this aberration is
unknown.
Types
SS Two types:
zz Simple cyst
zz Apocrine cyst.
Breast 445
Galactocele
SS Presents as a cyst in a woman who has recently

stopped breastfeeding.
SS Pathogenesis unknown.
Sclerosing Adenosis
Fat Necrosis
SS Benign proliferation of small ductules or acini,
and intralobular fibrosis. SS It may follow an episode of trauma (direct/indirect).
SS It simulate carcinoma in gross appearance and Frequently, there is no history of trauma.
histologically. SS It is a painless lump, that may mimic carcinoma. Even
SS On mammography, microcalcifications is seen skin tethering and nipple retraction are sometimes
indistinguishable from intraductal carcinoma. present.
SS It is the most common pathologic diagnosis un- SS FNAC is diagnostic.
dergoing needle-directed biopsy of microcalcifi- SS Excision biopsy may be considered if the lump is not
cations. subsided after 6 weeks follow up.
SS No malignant potential. SS No malignant potential.
Gynecomastia [Hypertrophy of Male Breast]
SS Enlargement of ductal and periductal stromal tissues of the male breast.

SS Due to increase in estrogen/androgen ratio: Either ↑↑ estrogen or ↓↓
androgen.
SS Types:
zz Physiological (primary)
zz Pathological (secondary).
Physiological gynecomastia—
zz Neonatal (due to maternal estrogen)
zz Pubertal (due to ↑ estrogen relative to testosterone)
zz Senescent ↓ (androgen/estrogen ratio).
[At least 2 cm of subareolar breast tissue must be present to make the

diagnosis of gynecomastia.]
Bilateral gynecomostia
Clinical classification of gynecomastia

Grade I: Mild breast enlargement without skin redundancy
Grade IIa: Moderate breast enlargement without skin redundancy
Grade IIb: Moderate breast enlargement with skin redundancy
Grade III: Marked breast enlargement with skin redundancy and ptosis.
Treatment required or not? Workup Includes

SS Pubertal gynecomastia requires no treatment— SS Liver function test
Only reassurance is all that needed. SS Thyroid function test
SS Gynecomastia in adult age group warrants proper SS Chest X-ray
workup and detailed drug history. SS Testicular ultrasound

SS Hormonal profile (hCG, LH, testosterone and
estrogen).
Proper workup also needed in elderly patient to differ-
entiate between physiological gynecomastia and patho-
logical one.
Treatment
SS Surgery is needed for symptomatic patients and for cosmetic reasons.
Breast 447
Nipple Discharge
SS Nipple discharge is important when it

occurs spontaneously and it is a dominant
symptom.
Investigation
Which investigation is necessary and which

not?
SS High resolution USG is the first line of
investigation.
SS Galactography (ductography) is only
indicated if there is spontaneous blood/
serous discharge from single duct.
SS Cytology of nipple discharge has little
value in diagnosis.
SS MRI may be considered if USG and/
galactography findings are inconclusive.
SS Mammography must be considered to
exclude occult carcinoma.
Patient with colored opalescent discharge
How to manage?
SS Clinical examination
SS Mammography if patient > 35 years
SS Mild discharge: Reassurance
SS Profuse discharge:
zz From single duct: Microdochectomy
zz From multiple ducts: Radical duct excision.
Patient with bloody discharge
How to manage?
SS If patient < 30 years, wait and watch policy can be taken after
triple assessment.
SS If persisting discharge, then
zz Microdochectomy (in < 30 years)
zz Major duct excision (in > 45 years).
SS Major duct excision should be considered if there is strong family

history of breast carcinoma/patient is significantly worried.
Bloody nipple discharge
Mastalgia
SS Mastalgia may interfere with daily activities, disturb her sleep and sexual life.
Factors responsible Types
SS Exact etiology still unknown. SS Cyclicalmastalgia

SS Relative hyperestrogenism–previously believed concept SS Noncyclical mastalgia
SS Abnormal prolactin secretion due to impaired hypothalamic zz True mastalgia
control of release of prolactin
zz Musculoskeletal pain.
SS Inadequate essential fatty acid (EFA) intake
⇓
↓↓ production of prostaglandin E1
⇓
↑ prolactin effect on breast cells.
Cyclical mastalgia
SS Commoner than noncyclical mastalgia.
SS Pain and nodularity in one or both breast for more than one week per cycle is considered as significant.
SS Thorough history taking, proper clinical examination, appropriate radiological evaluation – are necessary to exclude
cancer.
SS Reassurance is the most important role in treatment: ‘She does not have breast cancer’ – is sufficient for most of the
patients.
SS Remaining patients warrant therapy for pain.
SS Well fitting bra (sports bra), ↓ dietary fat intake, topical application of NSAIDs
⇓ No response
zz Evening primrose oil—(72% linoleic acid, 7% linolenic acid) [Richest natural source of EFA]:
Should be continued for 3 months

⇓ No response
zz Danazol—Used as second line agent 50 mg daily response 50 mg twice daily
[Higher incidence of side effects: Amenorrhea, weight gain, acne, hirsutism]
or
zz Bromocriptine: Prolactin lowering agent, and blocks the release of prolactin from pituitary by dopaminergic
receptor stimulation.
⇓ No response/↓response
zz Tamoxifen/LH-RH analog (goserelin): 10 mg daily on 15–25 days of cycle for 3 months.
[Patients who are taking danazol/bromocriptine should take precaution against pregnancy because both are
potentially teratogenic and interfere the efficacy of OCP.]
Breast 449
Noncyclical mastalgia
SS True noncyclical mastalgia is well-localized and most frequently in the upper outer quadrant.
SS Tietze’ssyndrome is the most common differential diagnosis.
SS In Tietze’s syndrome, the pain is felt within the medial quadrants of the breast and tenderness is over the affected
costochondral junction.
SS Response of drug therapies are not so satisfactory.
SS Danazol is considered as first line drug.
ANDI
Aberrations of Normal Development and Involution

A concept: First suggested at Cardiff breast clinic
SS Most benign breast conditions follow a spectrum:
Normal ⇒ Aberration ⇒ Disease

SS Different phases of activity (in lobules, stroma and ductal structures of breast):
zz Developmental phase
zz Cyclical phase
zz Involutional phase.
Normal Aberration Disease

Developmental phase Lobular development Fibroadenoma Giant fibroadenoma
Cyclical phase Cyclical changes of menstruation Cyclical mastalgia Incapacitating mastalgia
Involutional phase Duct involution Duct ectasia Periductal mastitis
This concept encompasses all aspects:

SS Pathogenesis
SS Symptoms and signs
SS Histology
SS General principles of management.

Breast Carcinoma
Risk factors
Other cancers associated with BRCA1

and BRCA2—Male breast cancer,
fallopian tube cancer, prostate cancer.
Pathology
Breast 451
Cancer arising in BRCA1 mutations have increased incidence of medullary type of histology.
Breast 453
Spread of breast carcinoma
History is very important in this setting:

SS Age at menarche
SS Age at menopause
SS History of breastfeeding
SS Drug history
zz HRT
zz OCP.
SS Family history of carcinoma breast and ovary
SS Diagnosis of atypical hyperplasia/lobular carcinoma in situ.

Symptoms due to distant metastasis
SS Cough, respiratory distress (in lung metastasis) Unilateral retraction of nipple develops within a short
SS Bonepain, pathological fracture (in bone metastasis) period—Think of carcinoma first
SS Drowsiness, convulsion (in brain metastasis). Bilateral retraction of nipple persisting for years—
Think of periductal mastitis first.
Confirmation of diagnosis with proper workup
SS Confirmation of diagnosis of carcinoma in a clinically or mammographically suspicious lesion can only be determined
by tissue sampling. For this, biopsy is the standard technique.
Biopsy techniques for palpable breast lesion:
SS Fine needle aspiration (FNA)
SS Core cut needle biopsy
SS Excision biopsy.
Biopsy techniques for nonpalpable breast lesion:

SS USG guided core needle biopsy
SS Stereotactic core biopsy (under mammographic guidance)
SS Wire guided biopsy (USG/mammographic guidance)
SS MRI guided biopsy
SS Vacuum assisted biopsy (USG/mammographic guidance).

Breast 455
Metastatic workup
SS USG abdomen—to detect distant metastasis (e.g. liver)

SS Chest X-ray/CT chest—to detect lung metastasis.
SS Bone scan
SS CT brain
} are only indicated if clinical features are suggestive or metastases (e.g. bone pain, pathological
fracture/drowsiness, convulsion)
FNAC (fine needle aspiration cytology)
To obtain cytologic diagnosis.

FNA diagnosis of malignant cells is sufficient
to proceed to the definitive management.
[FNA cannot distinguish in situ and invasive
disease. So FNA may leads to overtreatment
of DCIS.]
For correct interpretation, needs expertise.
Core cut needle biopsy
SS Applicablefor both palpable and nonpalpable breast

lesions.
SS Provides histologic specimen for interpretation by
any pathologist.
SS ER, PR status and HER-2 overexpression can be
determined. So, it is the diagnostic technique of
choice who is a candidate of neoadjuvant therapy.
Excision biopsy
SS Excision biopsy is less cost-effective than needle biopsy for differentiating between benign and malignant lesion.
Biopsy techniques for nonpalpable breast lesion
USG-guided biopsy MRI-guided biopsy

SS Particularly useful in USG-detected lesions. SS Indicated only for those lesions that are only
SS Technically easier than stereotactic-guided biopsy. detectable with MRI.

As in USG, real time imaging allows surgeon or
radiologist to visualize the biopsy procedure.
Stereotactic breast biopsy: Method of sampling

breast lesions that are detected mammographi-
cally.
Breast 457
Multiple tissue samples are taken.
A clip is placed in the biopsy site to mark
the site of lesion.
Needle localization biopsy: Aim of this method is to facilitate complete removal of the nonpalpable lesion under
mammographic/USG guidance.
Vacuum-assisted biopsy: New technique of breast bi-

opsy using a vacuum assisted instrument.
SS Can be used under USG/stereotactic guidance.
SS The instrument does not have to be withdrawn

each time.
SS The suction aspect of the device ensures minimal
hematoma formation.
Imaging
Breast 459
Mammography remains the most useful imaging
tool for detecting breast cancer.
Mammogram is important because it allows assess-
ment of the contralateral breast as well as multifocal
disease.
Mammography delivers a radiation dose of 0.1 cen-
tigray (cGy)-a chest X-ray delivers 25% of this dose.
Screening mammography zz False-positive results warrants further workup and

SS Is performed in asymptomatic women with the goal of causes increased patient anxiety.
detecting breast carcinoma which is not yet clinically SS Screening protocol:
evident.
zz Annually to women 50 years and older.
SS Clinically not detected but mammographically
detected cancers have a better prognosis and require zz Biennially to women 40–49 years.
less aggressive treatment. zz Annually to younger women with significant family
SS Disadvantages: history, histologic risk factors, history of previous
zz Cost of screening breast cancer.
Different views of screening mammography:

SS Craniocaudal view (CC) SS Mediolateral oblique view (MLO)
zz Better visualization of medial aspect of the breast zz Covers the greatest volume of breast tissue.
zz Better visualization of upper outer quadrant

and axillary tail of Spence.
Mammogram (CC view) Mammogram (MLO view)

Diagnostic mammography–is used Additional views:

SS To evaluate the breasts of patients with breast SS 90-degree lateral view
symptoms such as nipple discharge or a palpable SS Spot compression view.
mass. Additional uses of mammography:
SS In patients with abnormal screening mammography.
SS Is used to guide interventional procedures, e.g.
SS In case of diagnosed breast carcinoma for assessment stereotactic core needle biopsy, wire localization
of contralateral breast as well as multifocal disease. biopsy.
SS In patients who have had breast carcinoma treated
with breast conservative therapy.
What is BIRADS?
B I R A D S
Breast Imaging Reporting And Data System
zz Developed by the American College of Radiology to standardize mammographic reporting
Assessment Category Recommendation
BIRADS 0 Needs additional imaging Add views or USG
1 Negative Annual mammography
2 Benign finding Annual mammography
3 Probably benign 6 months mammography for a period of 2 years
4 Suspicious abnormality Biopsy should be considered
5 Highly suggestive of malignancy Biopsy
6 Known carcinoma
Role of MRI
As a diagnostic tool
As a screening tool
SS Technique of choice in the differentiation between
SS Annual MRI in—
the postoperative scarring and the local recurrence.
zz BRCA mutation
SS It is also the investigation of choice for evaluation
zz Untested first degree relative of BRCA carrier of implant integrity and detection of cancer in the
zz Lifetime risk of breast carcinoma 20–25% augmented breast.
SS It is helpful in the differentiation of axillary recurrence
and postradiotherapy, brachial plexopathy.
Plan of management
The type of therapy is determined by the stage of the disease.
? Surgery ? Neoadjuvant therapy

Staging is also important, because—
SS Gives some indication of prognosis.
SS Evaluation of the results of treatment.
SS For exchange of information between treatment centers.

Breast 461
AJCC (American Joint Committee on Cancer) Staging (2002) is based on—
TX—Primary tumor cannot be NX – Regional lymph nodes can

assessed not be assessed (e.g. previously
TO—No evidence of primary tu- removed)
mor N0 – No regional lymph node
Tis—(DCIS) metastasis
Tis—(LCIS) N1 – Ipsilateral mobile axillary
Tis—(Paget’s) lymph nodes palpable
N2 – Ipsilateral fixed axillary
lymph nodes palpable
N3 – Ipsilateral infraclavicular
lymph node palpable (a)
SS Ipsilateral internal mammary
lymph node palpable (b)
SS Ipsilateral supraclavicular
lymph node palpable (c)
MX—Metastasis cannot be assessed

MO—No metastasis
M1—Distant metastasis present.
According to gene expression pattern, carcinoma breast is divided into:

(1) Luminal A (2) Luminal B (3) Normal breast-like (4) HER 2 amplified (5) Basal
1. Luminal A — ER and/ or PR positive
HER-2/neu negative
2. Luminal B — ER and/or PR positive
HER-2/neu positive
3. HER 2 amplified— ER negative/PR negative
HER-2/neu positive
4. Basal — ER negative, PR negative
HER-2/neu negative
Treatment
Dcis is considered as a precursor of invasive ductal carcinoma, so the goal of treatment is to remove the DCIS.
Breast conserving therapy (BCT) with radiation is for localized DCIS, to reduce the chance of local recurrence
Mastectomy is considered when—
SS It is multicentric DCIS
SS Negative margins cannot be obtained
SS Patient not willing to preserve her breast
SS Radiotherapy is contraindicated.
Breast 463
Advantages of bct
SS Preservation of cosmesis.
SS Less anxiety, depression.
SS Improved body image, sexuality and self-esteem than

mastectomy.
SS Provide survival and recurrence almost equivalent to
mastectomy.
Pathologist must be made aware of the anterior, poste-

rior, superior, inferior, medial and lateral margins.
Orientation of the specimen is essential for appropriate
pathological evaluation. If margin/margins are not free of
tumor, the pathologist must inform the surgeon which
margin or margins are involved.
Breast 465
Simple mastectomy
SS Isthe treatment of choice for early breast carcinoma.

SS Mastectomy with or without breast reconstruction is the surgical approach for
the patients who has contraindications to BCT or who prefer treatment with
mastectomy.
Latissimus dorsi flap—This myocutaneous flap is supplied by thoracodorsal artery

Breast 467
Management of axilla
Axillary dissection provides prognostic information.

Axillary dissection plays a therapeutic role by removing posi-
tive axillary nodes.
But, axillary dissection is not considered in all patients of ear-
ly breast carcinoma, with no palpable axillary lymph nodes.
Because, axillary dissection is the primary cause of post-
treatment morbidity (e.g. lymphedema).
Then, the concept of sentinel node biopsy developed.
Morbidity is much lower than axillary dissection.
Techniques of sentinel lymph node biopsy
Two mapping agents are used Timing of injection

SS Vital blue dye SS Blue dye must be injected intraoperatively,
SS Technetium-labeled sulfur colloid because it passes through the sentinel lymph

node after about half an hour.
SS Radiocolloid can be injected anytime from 1 hour
to 24 hours before surgery.
How the procedure is done—

Breast 469
Adjuvant systemic therapy
SS Goal of this therapy is to prevent the recurrence by eradicating micrometastases.

SS Indicated in—
zz All node-positive cancers.
zz Node negative cancers with adverse prognostic features (vascular invasion, high nuclear grade, high histologic
grade, HER-2/neu over expression, negative hormone receptor status).
zz Tumor > 1 cm.
SS 3 types of systemic therapy—
A. Endocrine therapy—Hormone-receptor positive (ER, PR or both) patients are candidates for this therapy—
1. Tamoxifen—Tamoxifen, a selective estrogen receptor modulator (SERM) acts as a competitive antagonist
in breast tissue and acts like estrogen in skeletal and cardiovascular tissues. Other SERMS are Raloxifene,
Toremifine.
Tamoxifen is recommended for 5 years in all ER positive patients irrespective of age, menopausal status,
size of the tumor or nodal status.
Tamoxifen when used for 5 years, decreases the chance of recurrence and mortality.
2. Aromatase inhibitors—These agents inhibit the conversion of androstenedione to estrone.
Anastrozole is preferred for ER positive postmenopausal patients, because it suppresses the estrogen
production in peripheral sites (e.g. adipose tissue).
3. Ovarian suppression—By using leuteinizing hormone-releasing hormone (LHRH) agonist, e.g. goserelin,
leuprolide.
Nonpulsatile administration of LHRH agonist inhibits the release of gonodotropins (FSH and LH) from
pituitary, thereby decreasing estrogen synthesis.
B. Chemotherapy is indicated irrespective of hormone-receptor status or HER-2 status, based mainly on tumor
size, nodal status and other several prognostic factor (e.g. > 1 cm node positive) lymph vessel invasion, high
histologic grade, high mitotic rate, negative hormone receptor status, HER-2/neu overexpression.
C. Anti-HER-2 therapy– Tumors with HER-2 overexpression are candidates for trastuzumab.
Adjuvant radiotherapy
Breast 471
Fluorouracil, Epirubicin, Cyclophosphamide

(FEC) or Doxorubicin, Cyclophosphamide,
Docetaxel
or
FEC + transtuzumab (if tumor overexpress

HER 2-neu)
Tumors that overexpress HER 2/neu are

most likely respond to higher doses of
Doxorubicin-containing chemotherapy
regimes
Neoadjuvant therapy — can downstage inoperable tumor to operable one.

— can downstage the tumor to a size eligible for BCT.
Management of metastatic breast disease
Stage IV— Any T, any N, M1

Treatment is palliative, not curative one.
SS Goals of treatment —
zz Reduction of cancer-related symptoms or complications.
zz Maintenance of quality of life.
SS Endocrine therapy is the main treatment modality for hormone-receptor positive metastatic breast carcinoma.
SS Chemotherapy is also a treatment modality irrespective of hormone-receptor status. (Taxane based/anthracycline

based).
SS Taxane based chemotherapeutic agent— Paclitaxel, Docetaxel.
Anthracycline based agent—Doxorubicin, Epirubicin.

SS Capecitabine, an oral chemotherapeutic agent (metabolized into the body to 5-FU) improves survival in anthracycline
and taxane resistant tumors.
SS In HER-2/neu positive tumors, transtuzumab along with chemotherapy is indicated (concurrent administration of
anthracycline based chemotherapy should be avoided because both have cardiac side effects.)
Prognostic factors
SS Size of the tumor.

SS Involvement of axillary lymph nodes (percentage of positive lymph nodes is more accurate determinant than the
absolute number of positive lymph nodes).
SS Histologic grading—
zz Can be measured by Notingham combined histologic grading system.
zz Tumor with poor nuclear grade has higher risk of recurrence.
SS ER, PR status—
zz Tumors lacking ER and PR are not responsive to endocrine treatment.
zz Patient with ER/PR positive tumors have increased disease free survival.
SS HER-2/neu expression— Tumors with HER-2/neu overexpression is associated with poor prognosis.
SS Lymphovascular invasion—Tumors with lymphovascular invasion have poorer prognosis.
SS Patient’s age—Younger patients (<35 years) have poorer prognosis.
SS S-phaseanalysis—Tumor with cells more in S-phase have more chance of recurrence, but highly responsive to
chemotherapy.
SS Tumor angiogenesis.
Prognostic signatures
SS Mammaprint—A 70-gene signature.
Recurrence scoring system
SS Oncotype DX recurrence score.

Chapter 14
Thyroid
Important Topics
zzHypothyroidism
zzThyrotoxicosis
zzThyroiditis
zzNeoplasms of Thyroid
zzSurgical Approaches to Thyroid
‘Scientific reasoning is a kind of dialogue between the possible and the actual, between what might be and what is in fact
the case.’
Peter Brian Medawar (1915–1987)
Brazilian-born British immunologist
Thyroid 475
Diseases of the Thyroid Gland
Different Thyroid Pathologies
Hypothyroidism
SS Deficiencyin the circulating levels of thyroid hormone (T3, T4)

SS Iodine deficiency is the most common cause of hypothyroidism worldwide
SS Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the areas of iodine sufficiency.
Cretinism
Hypothyroidism in infancy or early childhood.
Causes
Thyroid 477
Clinical presentation Management
Untreated congenital hypothyroidism has severe neuro-

logical consequences.
SS Neonatal screening is done by estimation of TSH/T in
4
heel-prick specimen.
SS Ifhypothyroidism is confirmed, treatment to be done

with T4.
SS Early treatment results in normal IQ levels.
Adult hypothyroidism
Investigation for confirmation of diagnosis Treatment
SS ↓ T and T4 + ↑ TSH – Primary thyroid failure SS Thyroxine is the treatment of choice.

3
SS ↓ T and T + ↓ TSH – Secondary hypothyroidism SS 50–200 µg/day—according to patient’s weight and
3 4
SS Other biochemical findings— condition.
↑ CPK, ↑ cholesterol and triglycerides, ↓ Hb% SS Dosage of thyroxine is titrated according to clinical
When clinical or subclinical hypothyroidism is con- response and TSH levels.

firmed, the etiology is established by presence of TPO
antibodies or by FNAC.
[TPO antibodies are present in > 90% of patients
with autoimmune hypothyroidism]
Thyrotoxicosis
SS It is a hypermetabolic state
caused by ↑ circulating levels
of free T3 and T4.
How thyrotoxicosis develops?
Major etiologies of thyrotoxicosis:

Thyroid 479
Graves’ disease
How it develops?
Autoantibodies to the TSH re-

ceptor have crucial role to dis-
ease pathogenesis.
About 80% of patients with
Graves’ disease have high titer
of TPO antibodies.
Different types of autoantibodies

Under microscope
Clinical manifestation
Thyroid 481
Contd...
Contd...
SS Due to deposition of glycosaminoglycans and

lymphocyte infiltration in the dermis leads to
thickening of dermis.
Thyroid 483
Other clinical manifestations
SS Features of hypermetabolic state—

zz Sweating
zz Weight loss but increased appetite
zz Heat intolerance
zz Increased thirst.
SS Cardiovascular features—
zz High cardiac output
Bounding pulse
Widened pulse pressure
Aortic systolic murmur
Heart failure.
zz ↑ sleeping pulse rate
zz Cardiac arrhythmia—
Sinus tachycardia
↓
Multiple extrasystoles
↓
Paroxysmal atrial tachycardia
↓
Paroxysmal atrial fibrillation
↓
Persistent atrial fibrillation, not responding to digoxin
SS Neurologic features—
zz Fine tremor
zz Hyperreflexia
zz Muscle wasting
zz Proximal myopathy without fasciculation.
SS Gastrointestinal features—
zz Increased stool frequency.
SS Oligomenorrhea or amenorrhea, impaired sexual function in men.
Patients are extremely excitable, restless, emotionally unstable.

SS Thyrotoxicosis is sometimes associated with a from of hypokalemic periodic paralysis—particularly in Asian males.
SS Thyroid acropachy—A form of clubbing found in <1% of patients with Graves’ disease.
Eye signs
Thyroid 485
Upper sclera is visible in this patient
SS ↑ free T3 and ↑ free T4 + ↓↓ or undetectable level of TSH – confirm the thyrotoxicosis.

SS If eye signs are present, 123I scan is not indicated.
SS If eye signs are absent, I scan should be performed to exclude other cause of hyperthyroidism.
123
SS TSI or TBII is specific for Graves’ disease.
SS Anti-Tg and Anti TPO antibodies are elevated but not specific.
SS MRI of the orbit is useful in evaluating Graves’ ophthalmopathy.

Treatment
Antithyroid drugs SS Patients should be monitored for the side effects

SS All antithyroid drugs inhibit the function of TPO — (granulocytopenia, skin rashes, fever, peripheral
thereby ↓ oxidation and organification of iodide. Also neuritis) and asked to stop the drug if they develop
they reduce thyroid autoantibody level. sore throat or fever.
SS Propylthiouracil also inhibits deiodination of T → T . SS Dose of antithyroid medication is titrated according
4 3
SS Methimazole, carbimazole can cross the placenta and
the TSH and T4 level.
also excreted in breast milk. SS Propranolol or longer acting beta blockers, such as
Propylthiouracil has a lower risk of transplacental atenolol, is helpful to control adrenergic symptoms,
transfer. So PTU is preferred in pregnant and breast- particularly in the early phases of treatment before
feeding women. antithyroid drug take effect.
Radioactive iodine (131I)

Thyroid 487
Surgery
It causes complete and permanent control of disease with minimal morbidity (RLN injury and hypoparathyroid).
Preparation of the patient before surgery—

SS Patient should be euthyroid before the date of operation; antithyroid drugs should be continued till the day of
surgery.
SS Lugol’s iodide solution (3 drops twice daily) or supersaturated potassium iodide should be started 10 days before
the operation to reduce vascularity of the gland and decrease the risk of thyroid storm.
Total thyroidectomy is indicated in—

SS Patient with coexistent carcinoma.
SS Patient with severe ophthalmopathy.
SS Patient who have life threatening complications to antithyroid

medications (vasculitis and agranulocytosis).
Treatment of ophthalmopathy
SS Protecting the eyes from light and dust by dark
glasses.
SS Elevation of the head of the bed.
SS Diuretics (to decrease periorbital and retroorbital

edema).
SS High dose glucocorticoids–efficacy unpredictable.
SS If medical treatment fails—
zz Lateral tarsorrhaphy
zz Retrobulbar irradiation
zz Surgical decompression of the orbit.
Toxic multinodular goiter
SS How they become autonomous, still not known. SS Thyroid scan–Heterogenous uptake with multiple
SS Recent exposure to iodine (from contrast media/other regions of increased and decreased uptake.
sources) may precipitate thyrotoxicosis. Treatment—
SS Patient may present with palpitation, tremor, weight SS Antithyroid drugs.
loss, nervousness, tachycardia and atrial fibrillation. SS Subtotal thyroidectomy is the treatment of choice.
SS T normal or minimally elevated, T more elevated, TSH SS RAI therapy is indicated in elderly patients who are in
4 3
level is low. poor operative risk.
Thyroid 489
Toxic adenoma (Plummer’s disease)
SS Clinical examination reveals a solitary thyroid nodule without palpable thyroid tissue on the contralateral side
(no eye changes, no skin changes).
SS RAI scanning – ‘Hot’ nodule with suppression of the rest of thyroid gland.
SS Treatment—
Or
Radioiodine ablation (131 I) is the treatment of choice. [Lobectomy + Isthmusectomy] is recommended

for young patients and for large nodule.
Nontoxic goiter
Nontoxic diffuse (simple goiter)
SS Alsocalled colloid goiter because of presence of colloid distended follicles

SS Most commonly caused by iodine deficiency.
SS Endemic goiter is also caused by exposure to environmental goitrogens
}
zz Vegetables of the cruciferae family (e.g. cabbage, cauliflowers, brussels sprouts)
zz Cassava root (contains thiocyanate)

goitrogens
zz Milk from regions where goitrogen are present in the grass.
SS Normal T and TSH, but ↓ T

3 4
SS Thyroid scan and USG are not generally indicated.
Surgery (subtotal thyroidectomy) is indicated for pressure

symptoms or obstruction of thoracic inlet or for cosmetic
reasons.
Thyroid hormone replacement is the primary therapy.
Nontoxic multinodular goiter
SS More common in iodine-deficient regions but also

occurs in regions of iodine sufficiency.
SS More common in women.
SS Most of the patients are asymptomatic.

Thyroid 491
SS The goiter may become large causing pressure symptoms.
SS Tracheal deviation is common, but airway compromise is not so
common, (because compression must exceed at least 70% of the
tracheal diameter for airway compromise).
SS Serum TSH is estimated to excluded subclinical hypo or hyperthyroidism.
SS USG of the swelling should be done to identify which nodule is

to be biopsied and if any sonographic features of malignancy
(microcalcification, hypoechogenicity, hypervascularity) are present.
SS CT or MRI may be indicated to evaluate the anatomy of the swelling and
to assess any substernal extension.
SS T suppression may be started at low dose (50 µg) with titration of the
3
dose according to TSH level.
SS Radioioddine ( I) treatment is very much effective by selectively
131
ablating the autonomous nodule.

SS Surgery (subtotal thyroidectomy) is also a effective treatment option,
particularly if patient not responds to T3 suppression or 131I treatment.
Thyroiditis
Thyroid gland is resistant to infection because–

SS Extensive blood supply and lymphatic supply
SS High iodide content
SS Fibrous capsule.
Acute (Suppurative) Thyroiditis
SS Rare type of thyroiditis.

SS More common in children, mostly due to presence of
a pyriform sinus (a remnant of the fourth branchial
pouch that connects the oropharynx with the thyroid.
SS Presented with severe neck pain radiating to the jaws
or ear, fever, odynophagia and dysphonia.
SS White cell count and ESR are raised, but thyroid profile
is normal.
SS FNA biopsy shows neutrophilic infiltration.
SS CT scan is helpful to delineate the extent of infection.

Piriform sinus fistula (begins at the apex
SS Treatment is parenteral antibiotics and drainage of
of piriform sinus, coursed anteroinferiorly
abscess. through the thyroid gland into the
SS If piriform sinus fistula is detected, the fistula tract perithyroid space)
must be resected including the area of thyroid
attachment.
Subacute Thyroiditis
Subacute granulomatous (de Quervain’s)

thyroiditis
SS Itis believed to be cause by viral infection (mumps.

coxsackie, influenza, adenovirus and echovirus) or
postviral inflammatory process.
Inflammatory destruction of follicular cells
↓
Formation of granuloma
↓
Fibroblast proliferation
SS Clinically manifested by sudden onset or chronic

onset neck pain radiating towards mandible or ear.
History of a preceding URTI is often present.
SS The thyroid gland is tender and become enlarged.
SS The disease is self-limited, so symptomatic treatment

is all that needed.
SS Aspirin or NSAIDs are usually used to control pain.
SS If patient has marked local or systemic symptoms,

steroid should be given.
SS Levothyroxine replacement (in low dose) may be
necessary if hypothyroid phase is prolonged.
[Antithyroid drugs have no role in treatment of thyrotoxic
phase.]
Thyroid 493
Subacute lymphocytic thyroiditis (Silent thyroiditis)
SS This disease is most likely autoimmune in etiology.

SS It may occur sporadically or in the postpartum period (3–6 months after pregnancy) postpartum thyroiditis.
SS It also progresses through 3 stages:
Thyrotoxic phase → hypothyroid phase → resolution phase.

SS Clinical examination reveals a normal or minimally enlarged nontender thyroid gland.
SS Silent thyroiditis can be distinguished from de Quervain’s thyroiditis by—
zz Painless goiter
zz Normal ESR
zz Presence of TPO antibodies.
SS Thyroxine replacement is indicated in hypothyroid phase and propranolol, it severe thyrotoxic symptoms.
[Steroid treatment is not indicated].

Chronic Lymphocytic (Hashimoto) Thyroiditis
SS Hashimoto thyroiditis is the most common cause of hypothyroidism in world where iodine levels are
sufficient.
SS It is a autoimmune thyroiditis characterized by ‘3’ cardinal features:
zz Diffuse enlargement of thyroid
zz Lymphocytic infiltration of thyroid
zz Presence of thyroid autoantibodies.
How it develops
Thyroid 495
SS More common in women (10 : 1) between 30 and 50 years of age.
SS Most commonly presented as painless diffuse enlargement of thyroid, usually associated with hypothyroidism in
a middle-aged women.
In some cases, it may be preceded by transient thyrotoxicosis due to disruption of thyroid follicles (hashitoxicosis).
SS Features of other autoimmune diseases, if present, must be investigated—
zz Type I diabetes mellitus
zz Addison’s disease
zz Pernicious anemia
zz Vitiligo.
SS Increased risk of developing B-cell non Hodgkin lymphoma.
Investigations to Confirm Diagnosis Treatment
SS ↑ TSH, ↓ T3, ↓T4, presence of thyroid autoantibodies SS Thyroxine replacement therapy–to maintain normal
confirm the diagnosis. TSH.
SS FNA biopsy is indicated in patient presents with SS Replacement therapy is particularly indicated when
solitary suspicious nodule or rapidly enlarging goiter. TSH > 10 mu/l or in euthyroid patients with large
goiter.
SS Surgery is indicated for suspicion of malignancy, for
pressure symptoms and cosmetic reason.
Riedel’s Thyroiditis
SS Rare disease of thyroid

SS Also known as Riedel’s struma or invasive fibrous thyroiditis.
Fibrosis involving the thyroid and

continuous neck structure
SS Etiology is unknown, but most likely this disease is a

part of multifocal idiopathic fibrosclerosis.
SS Usually FNA biopsy is inadequate, the diagnosis is

confirmed by open biopsy.
SS Surgery is the treatment. The goal of surgical
intervention is to decompress the trachea by
excision of isthmus. More extensive resections are
not attempted because extensive fibrosis obscures
anatomical landmarks and structures.
Neoplasm of Thyroid
Follicular Adenoma
Most common benign thyroid neoplasm.

SS This neoplasm is derived from follicular
epithelium
SS The TSH receptor signalling pathway
plays an important role in the
pathogenesis of adenoma.
SS A typical thyroid adenoma is a solitary,
spherical lesion that compresses adjacent normal tissue.
Thyroid 497
Tumor cells show various growth patterns and according to these:

zz Microfollicular adenoma
zz Macrofollicular adenoma
zz Normofollicular adenoma
zz Trabecular adenoma
} ↓↓risk of malignancy
zz Hurthle cell adenoma
zz Atypical adenoma.
SS Clinically, most adenomas present as painless nodules
SS Treatment is lobectomy. Long-term follow up is unnecessary.
Malignant Tumors of the Thyroid Gland
SS Primary
SS Secondary.
SS Malignant tumor of thyroid gland is the common malignancy of the endocrine system.
SS About 95% of all primary thyroid malignancies are carcinomas.
SS Primary lymphoma constitutes < 5% of malignancies. Most of them evolve from autoimmune thyroiditis.
SS Sarcoma is extremely rare.
SS Secondary thyroid malignancies are also rare.

Types of primary thyroid malignancy
Follicular cell—
SS Line the colloid
follicles.
SS Concentrate iodine.
SS Produce thyroid
hormones.
C or parafollicular
cell—
SS Produce calcitonin.
Primary thyroid malignancies can also be classified according to aggressiveness:

1. Well-differentiated (e.g. papillary carcinoma, follicular carcinoma)
2. Intermediate (e.g. medullary carcinoma, Hürthle cell carcinoma)
3. undifferentiated (e.g. anaplastic carcinoma).
Pathogenesis of primary thyroid malignancy

SS Radiation – High dose external radiation.
Differentiated thyroid carcinoma, particularly papillary carcinoma follows radiation exposure of neck in childhood.
Radiation derived from 131I therapy may contribute minimal increased risk of carcinoma.
SS TSH and growth factor – Many differentiated thyroid cancers express TSH receptors.
The incidence of follicular carcinoma is high in endemic goitrous areas, particularly due to TSH stimulation.
SS Oncogenes and tumor-suppressor genes — Distinct mutations are seen in different histologic types, but no
evidence of adenoma-carcinoma sequence (like colon cancer).
zz Papillary carcinoma—
Mutation in RET protooncogene (located on chromosome 10)
Gene rearrangement in NTRK1 gene.
zz Follicular carcinoma—
Mutation in RAS oncogenes (HRAS, NRAS, KRAS).
zz Medullary carcinoma—
Point mutation in RET-protooncogene.
zz Anaplastic carcinoma—
Inactivation of point mutaiton in p53 tumor suppressor gene
Mutation in gene coding for b-catenin pathway.

Thyroid 499
Staging system
Low risk High risk

< 40 years > 40 years
Tumor size < 2 cm Tumor size > 4 cm
Female Male
No local extension, intrathyroidal, no capsular invasion Extrathyroidal extension, capsular invasion
No metastasis Regional/distant metastases
Well-differentiated Poorly differentiated
Papillary thyroid carcinoma (PTC)
SS Most common type of thyroid cancer 70–90% of well-differentiated thyroid malignancies.

SS Predominant thyroid cancer in individuals exposed to external radiation in neck during childhood.
SS More common in females (2:1), mean age at presentation is 30–40 years.
SS Slow growing malignant tumor, tends to be multifocal.
SS Propensity to spread by lymphatics, leads to involvement of regional lymph nodes.
SS Most of the patients are euthyroid.
SS Hematogenous spread is not so common, Lungs> Bone> Liver> Brain.
SS Most often present as a painless mass in the neck, either in the thyroid or as metastasis in cervical lymph node.
Investigations
SS FNAB can confirm the diagnosis of papillary carcinoma as well as metastasis in cervical lymph node.
[FNAB can confirm the diagnosis of most primary thyroid cancer—Papillary, medullary, anaplastic, lymphoma,
meta-statics to the thyroid gland.]
SS High resolution USG is helpful for:
zz Size assessment of tumor mass
zz Evidence of microcalcification, irregular margin, hypervascularity (suggestive of malignancy)
zz Assessment of nodal status in neck.

Thyroid 501
SS Distant metastatic status is evaluated by:
zz Chest X-ray
zz Radionuclide scanning
zz CT scan.
}according to clinical suspicion
SS Serum thyroglobulin estimation – valuable investigation for follow up and detection of recurrence after total
thyroidectomy.
Treatment
Primary treatment is surgery.
Lobectomy + Isthmusectomy
{
? Tumor may be multifocal
Disadvantages ? Adjuvant radioiodine treatment not possible.
? Follow up with serum thyroglobulin not possible.
Total thyroidectomy + Modified radical neck dissection (Level II-VI)
{
Any occult tumor, if present can be resected
Advantages Adjuvant radioiodine treatment possible
Follow up with serum thyroglobulin possible
Total thyroidectomy
No survival benefit of prophylactic neck dissection for nonpalpable nodes.
Patient with extrathyroidal extension:
Postoperative Measures after Total Thyroidectomy

Thyroid 503
SS Postablation whole body iodine scanning is usually performed after 1 week of ablation therapy.
SS Allpatients need lifelong thyroxine replacement.

SS After total thyroidectomy, Tg level should be undetectable (<2 ng/ml).
SS Delectable Tg level after total thyroidectomy suggests persistence of functioning thyroid tissue or recurrence of
carcinoma.
Follicular carcinoma (FTC)
SS Account for about 10% of thyroid cancers and more commonly in iodine-deficient areas.
SS Most of the follicular pattern thyroid malignancies represent the follicular variant of papillary carcinoma and share
the natural history and many features of papillary carcinoma.
SS Older population (50 years or more) are commonly affected.
SS More common in females (3 : 1).

Treatment protocol
Hürthle cell carcinoma
SS A subtype of follicular carcinoma closely resembles follicular thyroid carcinoma on gross and microscopic
appearance.
SS The tumor contains abundance of oxyphilic cells or oncocytes and characterized by vascular or capsular invasion.
SS More often multifocal, bilateral and more likely metastasize to regional nodes and distant sites.
SS Work up and management are similar to follicular carcinoma.

Thyroid 505
Medullary carcinoma of thyroid (MTC)
SS MTC usually found in upper and middle thirds of

thyroid lobe.
SS Also found particularly in the posterior part of lobe.
3 Distinctive Features
MTC arise as
Familial MTC is more

agressive than spo-
radic MTC.
Genetic event in
MTC is point muta-
tion in RET protoonco-
gene.
Patient with famil-
ial MTC are identified
by screening are pre-
sented with micro-
scopic disease only.
Workup
It is very important to rule out coexisting pheochromocytoma to avoid hypertensive crisis and death.
131
I scan have no utility because MTC does not concentrate iodine.
Treatment
SS In sporadic cases
Thyroid 507
SS IfMTC is associated with
pheochromocytoma:
SS Near total thyroidectomy is better avoided.
Chemotherapy and EBRT have no role as curative therapy. They may have some role as palliative measures in advanced
disease.
Prophylactic total thyroidectomy is indicated in RET mutation carriers.
SS In MEN 2A – before 6 years
SS In MEN 2B – before 1 year
Prognosis is better in Non-Men familial MTC > MEN 2A > sporadic > MEN 2B.
Anaplastic thyroid carcinoma
SS Poorly differentiated, aggressive cancer.

[It is one of the most aggressive and difficult human malignancies to treat.]
SS Predominantly found in 7th–8th decades.
It is commonly related to a prior or concurrent diagnosis of well-differentiated thyroid cancer or benign nodular
thyroid disease.
SS Older patients with long standing thyroid swelling which rapidly enlarged and become painful—think of anaplastic
thyroid carcinoma.
SS Dysphagia, dyspnea, dysphonia are common.
SS Tumors are usually large (8–9 cm).
SS Lymph nodes are usually palpable.
SS Distant metastasis to lung, bone and liver may also present.
SS Diagnosis is confirmed by FNA biopsy revealing characteristic giant cell and multinucleated cells.
SS Prognosis is very poor, most patients die within 6 months of diagnosis.
SS Majority of patients die from aggressive locoregional disease. So, aggressive local therapy is indicated in all
patients.
Thyroid 509
I therapy has no role

131
Surgical Approaches to Thyroid

Preoperative Preparation
SS Patientshould undergo vocal cord assessment by IDL when—
zz History of recent change in voice
zz Malignancy is suspected
zz History of previous thyroid surgery
SS Thyrotoxic patients need to be euthyroid before surgery.
SS Prophylactic antibiotic is not indicated.
Preoperative Investigations
SS Hb, Tc, Dc, ESR

SS Blood sugar, urea, creatinine
SS T , T , TSH.
3 4
SS Chest X-ray
SS X-ray of neck
SS ECG
SS CT scan of neck (if only suspicion of invasion of adjacent structures by thyroid mass).
X-ray of neck in thyroid swelling CT neck in a large thyroid swelling

Thyroid 511
Basic Steps of Thyroidectomy
Positioning of patient
Preoperative positioning of the patient
Incision
Raising the flaps
Superior flap is raised

Dissection of middle thyroid vein
Dissection of superior thyroid vessels
Superior thyroid vessels are ligated
Dissection of inferior thyroid vessels
Skin is closed, closed suction drain is placed
Skin is closed after placing closed suction drain.

Thyroid 513
Neck dissection
Secondary thyroid malignancies

Chapter 15
Parathyroid, Adrenal,
Endocrine Pancreas and MEN
Important Topics
zzHyperparathyroidism
zzHypoparathyroidism
zzAnatomy of Adrenal Gland

zzDiseases of Adrenal Cortex
zzDiseases of Adrenal Medulla
zzPrinciples of Adrenal Surgery
zzPancreatic Endocrine Neoplasms
zzMEN Syndromes
‘Let people who have to observe sickness and death look back and try to register in their observation the appearances which
have preceded relapse, attack or death, and not assert that there were none, or that there were not the right ones. A want of
the habit of observing conditions and an inveterate habit of taking averages are each of them often equally misleading.’
Florence Nightingale (1820–1910)
British Nurse and Reformer
Parathyroid
Sites of Ectopic Parathyroid

Parathyroid, Adrenal, Endocrine Pancreas and MEN 517
Under Microscope
SS Most numerous is chief cell.

SS Oxyphil and clear cells derived from chief cell.
SS Chief cell is the major source of PTH.
How Ca2+ Level Maintains?

Diseases of Parathyroid
Primary Hyperparathyroidism
SS 3rd most common endocrine disorder after diabetes mellitus and thyroid disease.
SS A generalized disorder of calcium, phosphate and bone metabolism.
SS Most cases of primary hyperparathyroidism (PHPT) are sporadic.
SS PHPT may present as inherited disorder—
zz As part of MEN1, MEN 2A
zz Isolated familial HPT
zz Familial HPT with jaw-tumor syndrome } inherited as autosomal dominant disorder

Causes
SS Halfor more patients are asymptomatic.
}
SS Classic pentad of symptoms:
zz Kidney stones
zz Painful bones
zz Abdominal groans This presentation is rare nowadays because. The disease is now early diagnosed
zz Psychic moans
zz Fatigue overtones
SS Because of serum calcium is routinely assessed nowadays for unrelated clinical conditions, clinically silent
hyperparathyroidism is early detected.
SS Many of the classic manifestations particularly bone and renal diseases are now seen less frequently.
Renal disease
Hyperparathyroidism must be considered in every

patient presenting with renal stone or nephrocalcinosis.
Bone disease
SS Osteopenia
SS Osteoporosis
SS Bone cysts
SS Osteitis fibrosa cystica—
zz It is due to osteoclastic resorption of bone and its
replacement by connective tissue.
SS Skullmay also affected, X-ray shows mottled (salt and pepper) appearance with loss of definition of the inner and
outer cortex.
Gastrointestinal manifestations
SS Increased incidence of cholelithiasis, pancreatitis

and peptic ulcer disease.
SS Nonspecific symptoms like nausea, vomiting,
anorexia are more common.
Neuropsychiatric manifestations
Neuromuscular manifestations
SS Proximal muscle weakness

SS Easy fatigueability
SS Atrophy of muscles.
Metastatic calcifications in various organs
SS A parathyroid adenoma is very rarely palpable in the

neck.
SS A palpable neck mass in a patient with PHPT is more
likely to be thyroid in origin or parathyroid cancer.
SS ↑ PTH and ↑ serum Ca2+ Diagnostic findings of primary hyperparathyroidism.

SS 24 hour urinary calcium— increased
SS ↑ Alkaline phosphatase in presence of bone involvement.
zz Hand X-ray is recommended when ↑ alkaline phosphatase [to rule out osteitis fibrosa cystica]
zz Bone mineral density study can be used to assess the severity of bone changes.
Treatment
SS National Institute of Health (NIH)

consensus conference guidelines,
2002, surgery is recommended in:
[For Asymptomatic PHPT].
SS Serum calcium 1.0 mg/dl (0.3
mmol/l) above upper limit of
normal.
SS 24 hour urinary calcium > 400 mg.
SS Creatinine clearance reduced by

30%.
SS Bone mineral density T-score
< – 2.5 at any site.
SS Age < 50 years.
SS Asymptomatic patients not meeting these criterias may be monitored regularly and surgical intervention must
always be undertaken when indicated.
SS The goals of strict monitoring are early detection of worsening hypercalcemia deteriorating bone or renal status or
development of other complications of hyperparathyroidism.
If surgery is indicated
SS Parathyroid surgery is technically demanding procedure and must be done by an experienced surgeon.
SS Experienced surgeon with thorough knowledge of parathyroid anatomy and meticulous technique is crucial for a
desirable surgical outcome.
SS Which Approach?
?Bilateral neck exploration ?Unilateral neck exploration [Minimally invasive ap-

SS [Classic and Traditional surgical approach for proach]
primary HPT]. SS Can be planned if localization study (Sestamibi scan)
This approach is indicated in— is available as well as intraoperative PTH assay.
SS Localization study (Sestamibi scan) or intraoperative
PTH estimation facility not available.
SS Localization studies fail to identify any abnormal
parathyroid gland or identify multiple abnormal
glands.
SS Patients with family history of PHPT, MEN 1 or MEN
2A.
SS Patient with concomitant thyroid disorder that
requires bilateral exploration.
What is sestamibi scan?

SS
99m
Tc sestamibi scan is the most widely used localization study method for detection of parathyroid adenoma
(sensitivity > 80%).
SS It is also known as cardiolite (initially introduced for cardiac imaging)
SS It is concentrated in mitochondria rich tissues.

Unilateral neck exploration (Minimally invasive approach)
Contd...
Contd...
Bilateral neck exploration

99m
Tc sestamibi scan—Not available
Intraoperative PTH estimation facility—Not available
Facilities available but,
zz Sestamibi scan identify multiple abnormal glands
zz Patients with family history of PHPT, MEN1 or MEN2A
zz Patients with concomitant thyroid disorders
General anesthesia with endotracheal intubation
Patient’s positioning, incision and initial dissection and exposure similar to thyroidectomy
SS In most cases, parathyroid tumor is found attached to the posterior capsule of the thyroid gland
Superior parathyroid glands lie posterior to the RLN, where it enters the cricothyroid muscle. Inferior parathyroid glands
lie anterior to the RLN.
SS Care must be taken to avoid bleeding and not to traumatize the parathyroid gland, because the color of the gland
is useful in distinguishing it from surrounding thyroid, thymus, lymph node and fat.
SS Care must be taken to avoid rupture of the gland (rupture results in parathyromatosis and recurrent
hyperparathyroidism).
In patients with familial HPT and MEN1 and MEN2Al
Secondary Hyperparathyroidism
↑ Secretion of PTH due to disease other than parathyroid.
Treatment
Conservative management—
SS Low-phosphate diet
SS Phosphate binders
SS Calcium and Vit D supplementation.

3
Surgery is indicated when—
SS Renal osteodystrophy (osteitis fibrosa cystica, osteomalacia, adynamic bone disease).
SS Ca > 11 mg/dl with markedly elevated PTH

2+
SS Soft tissue calcification and tumoral calcinosis
SS Calciphylaxis (rare, severe complication characterized by calcification of the media of small to medium sized arteries).
Surgical approach
Preoperative locali-
zation is not indicated
because there is com-
pensatory hyperplasia
of all parathyroids.
Bilateral neck ex-
ploration is required
for identification of all
glands.
?Subtotal parathy-
roidectomy or ? Total
parathyroidectomy with
autotransplantation.
Tertiary Hyperparathyroidism
SS Surgical intervention is indicated for symptomatic disease (renal stones, pathologic fractures, bone pain, mental
status changes) or ↑ PTH secretion persisting for more than 1 year after successful transplant.
SS Subtotal parathyroidectomy is the preferred surgical approach, if all of the glands become autonomous.
Hypoparathyroidism
An endocrine disorder characterized by decreased PTH secretion or action.
Types of hypoparathyroidism
Causes of primary hypoparathyroidism
SS After thyroid surgery, particularly after total thyroidectomy with neck dissection—Most common cause
SS After parathyroid exploration
SS Hereditary polyglandular deficiency syndrome (beside parathyroid, thyroid, adrenal, pancreas also affected)
SS Infiltrative disease (hemochromatosis, Wilson’s disease, sarcoidosis and tuberculosis)
SS Congenital absence of parathyroids and thymus – DiGeorge syndrome.
SS Characterized by hypocalcemia, hyperphosphetamia, hypocalciuria.
Pseudohypoparathyroidism
SS Characterized by signs and symptoms of hypoparathyroidism.

SS Shortstature, short metacarpals and metatarsals, flat nose, round face, multiple exostoses (Albright’s hereditary
osteodystrophy).
Pseudopseudohypoparathyroidism
SS Rare familial disorder with clinical features of pseudohypoparathyroidism

SS Tissues normally respond to PTH
SS No hypocalcemia or hyperphosphatemia.
Clinical presentation of hypoparathyroidism
Signs and symptoms of hypocalcemia are due to neuromuscular excitability from reduced ionized calcium in plasma.
SS Early symptoms are tingling and numbness in fingertip and circumoral region.
SS Late symptoms are anxiety, confusion, depression and tetany.
SS Inextreme cases, carpopedal spams

and tetany.
What is tetany
Tonic-clonic seizures
+
carpopedal spasm
+
Laryngeal stridor
[Tetany may become fatal and should be avoided.]
SS Latent tetany may be elicited by:
Chvostek’s sign
Trousseau’s sign
Treatment of hypoparathyroidism
SS Inacute cases, slow IV Ca gluconate (10%) 10–20 ml

SS For long-term management, 1,25 (OH)2 D3 combined with high oral calcium
SS Thiazide diuretics help to lower urinary calcium and thereby decreasing the chance of kidney stone formation.
Diseases of Adrenal Gland

Anatomy and Anatomical Variations
SS Right adrenal gland is pyramidal shaped

SS Each gland is drained by ‘single’ vein
SS Right adrenal vein drains into IVC (80% cases)
SS Left adrenal vein drains into left renal vein.
Each gland is supplied by ‘3’ arteries:

SS Superior adrenal artery
—— Branch of inferior phrenic artery.
SS Middle adrenal artery
—— Branch of abdominal aorta.
SS Inferior adrenal artery
—— Branch of renal artery.
[Inferior adrenal artery is the most prominent artery and can be

distinctly identified during operation.]
Arteries supply to the adrenals branch into numerous arterioles

to form a arterial plexus beneath the glandular capsule.
Therefore, careful dissection, ligation and division is neces-
sary during adrenalectomy.
Variant Drainage of Right Adrenal Vein
Adrenal Vein Drains into Renal Vein-IVC Confluence
Adrenal Vein Drains into Right Hepatic Vein-IVC Confluence

Adrenal Vein Drains into Right Hepatic Adrenal Vein Drains into Right Renal Vein
Vein
Surgeon must keep in mind the variations of right adrenal vein to avoid unnecessary intraoperative hemorrhagic com-
plications.
Microscopic Features of Adrenal Gland
Cortex and medulla differ in their development, structure and function.
Sympathetic fibers synapse directly with

the chromaffin cell. These cells are called
‘chromaffin cells’ because the secretory
granules yield a brown colored reaction
when treated with chromium salts.
Hyperaldosteronism
Characteristic Microscopic Features of Adenoma
Classic findings in primary hyperaldosteronism are:

zz Hypertension and hypokalemia
How Hypertension and Hypokalemia Develops?
SS Disease is most frequently found in middle adult life, more common in females
SS Malaise, muscle weakness, polyuria, polydipsia, muscle cramps, paresthesias are usual presentations
SS Hypertension is moderate to severe – Refractory to medical therapy.
Primary hyperaldosteronism is associated with significantly increased risk for stroke, AMI and atrial fibrillation.
[Primary hyperaldosteronism is the most common cause of secondary hypertension.]
SS Hypertension at an early age!

SS Hypertension refractory to medical management!
SS K level is normal or low

+
}
Think of primary hyperaldosteronism?
Then biochemical screening [screening based on the fact that primary hyperaldosteronism suppresses renin secre-
tion:
SS Plasma aldosterone conc (ng/dl): Plasma renin activity (ng/ml/h) > 20
SS Setting of absolute plasma aldosterone conc. > 15 ng/dl
Suggest primary hyperaldosteronism?

SS Warrants confirmatory biochemical studies.
Then, confirmatory test:

SS Failure to suppress aldosterone secretion with sodium loading (oral salt/IV Nacl infusion) confirm the diagnosis of
primary hyperaldosteronism.
Then, localization of the pathology:
SS Unilateral? or Bilateral?
SS This is important because in unilateral pathology—
Surgery is the best management.

In bilateral pathology—
SS Medical therapy is the best management.
Localization
SS Localization is performed by thin-cut (3 mm) adrenal CT.

[Finding of a solitary adrenal mass (> 1 cm) and a normal contralateral adrenal in CT is sufficient to proceed to adre-
nalectomy without further testing.]
If, CT scan is equivocal or negative—
Then, adrenal vein sampling — Most certain way to localize an aldosteronoma.
Adrenal vein sampling
1.
2.
Aldosterone: Cortisol > 4 Aldosterone: Cortisol < 4

Then, it can be interpretated that, pathology is on right side.
Treatment
SS Goal of treatment is to prevent the complications of hypertension and hypokalemia.

Surgery
SS Indicated for aldosteronoma, unilateral adrenal hyperplasia, cortical carcinoma
SS Usually aldosteronomas are small and benign, so laparoscopic adrenalectomy is the surgery of choice
SS In open approach, lateral transabdominal approach is the preferred approach
SS Bilateral adrenalectomy is not indicated.
Preoperative preparation:
zz Blood pressure and hypokalemia should be corrected before surgery
zz Spironolactone is the drug of choice for treating the manifestations.
Medical therapy?
SS Indicated for idiopathic hyperaldosteronism and for patients not fit for surgery.
SS Goal of therapy is to control hypertension and hypokalemia.
SS Spironolactone is the preferred agent.
SS Amiloride, ACE inhibitors, calcium-channel blockers are also used.
Hypercortisolism [Cushing Syndrome]
SS Excessive serum level of cortisol, regardles of etiology.
Types
SS PituitaryCushing’s syndrome
SS Adrenal Cushing’s syndrome (10–20%)
SS Ectopic ACTH syndrome (<10%)
SS Iatrogenic Cushing’s syndrome.

1. Pituitary Cushing’s syndrome
SS Also
known as Cushing disease
SS Females are more affected (5:1)
SS ACTH dependent.
2. Adrenal Cushing’s syndrome
SS ACTH-independant
3. Ectopic ACTH syndrome (< 10%)
4. Iatrogenic Cushing’s syndrome
Most common cause of Cushing’s syndrome.

Progressive truncal obesity is the most common symptom.
zz Osteoporosis — leads to collapse of vertebral bodies and pathologic fractures of bones

zz Hypertension
zz Hyperglycemia, glucosuria, polydipsia (due to ↑ hepatic gluconeogenesis and insulin resistance).
zz Hyperpigmentation of the skin (think of ectopic ACTH syndrome)
(due to melanocyte stimulating activity of ACTH precursor molecule).

[Typical striae, myopathy, easy bruising, virilizing signs are suggestive findings of Cushing’s syndrome.]
Clinical suspicion of Cushing’s syndrome

⇓
1. Over night dexamethasone suppression test [based on the fact that in Cushing’s syndrome, ↑ glucocorticoid level is
not suppressed by exogenous cortisol administration]
1 mg dexamethasone IV at 11 pm
⇓
Estimation of plasma cortisol at 8 am
[In normal adults, cortisol level will be < 3 mg/dl
In Cushing’s syndrome, it will not happen.]
Then, if overnight dexamethasone suppression test is positive, the diagnosis of Cushing’s syndrome is established.
But, test is negative
Then
2. Classic low dose dexamethasone suppression test.
Dexamethasone 0.5 mg every 6 hours for 8 time 2 mg over 48 hours
⇓
In Cushing’s syndrome, plasma cortisol level will not be lowered.
So, positive overnight dexamethasone suppression test or positive classic low dose dexamethasone suppression test
along with 24 hours elevated urinary cortisol—
Diagnostic of Cushing’s syndrome,
SS Once the diagnosis of Cushing’s syndrome is established, then determine—

[Patients suspected of having ectopic ACTH syndrome should also undergo estimation of serum calcitonin (to rule of
medullary thyroid carcinoma) and urinary catecholamines (to rule out pheochromocytoma)].
Treatment
Primary treatment is surgery
Surgery for adrenal Cushing syndrome
Surgery for pituitary Cushing syndrome

Surgery for ectopic ACTH syndrome
In patients undergoing adrenalectomy, perioperative 'stress dose' steroid (hydrocortisone, 100 mg every 8 hours for
24 hours) is recommended.
After total adrenalectomy, lifelong corticosteroid maintenance therapy is necessary.
Adrenogenital Syndrome
Diagnosis
SS Diagnosis is established by ↑ level of plasma or urinary 17-ketosteroids.
Treatment
SS Feminizing adrenal tumors are all malignant, so radiographic and intraoperative assessment for evidence of
metastasis are necessary.
SS For benign tumor—Lap adrenalectomy
SS For malignant tumor—Open adrenalectomy.

Adrenal Insufficiency
Clinical Presentations
SS Both in primary and secondary adrenocortical insufficiency, most of the symptoms and signs are similar except
hyperpigmentation, which is absent in secondary adrenocortical insufficiency.
SS Insidious onset of fatigueability, weakness, anorexia, nausea, vomiting, weight loss, cutaneous and mucosal
pigmentation and hypotension.
SS Characteristic lab. findings—
zz Hyponatremia
zz Hyperkalemia
zz Fasting or reactive hypoglycemia
zz Eosinophilia
SS ACTH stimulation test—
ACTH (20 mg) IV infusion

↓
Peak cortisol < 20 mg/dl after 1 hour
—— Suggest adrenal insufficiency
? Primary ? Secondary
| |
ACTH ↑ ↑ ACTH ↓ ↓
Cortisol ↓ ↓ Cortisol ↓
Treatment
SS Hormone replacement therapy:
Glucocorticoid replacement
Cortisol (hydrocortisone) – (20–30 mg/d)
2/3rd of dose in the morning
1/3rd of dose in the late afternoon.
Mineralocorticoid replacement
SS Fludrocortisole
SS Ample intake of sodium (3 – 4 g/d).
[Mineralocorticoid therapy is not necessary in secondary insufficiency]

SS Patients must know about his/her disease
SS He/she should carry medical identification and must know the method of parenteral self administration of steroids.
Adrenal Crisis
Acute adrenal insufficiency may cause life-threatining condition.
SS Due to—
zz Stress, infection or trauma in patients of Addison’s disease
zz Waterhouse— Friderichsen syndrome
zz Anticoagulant therapy or coagulation disorders causing bilateral adrenal hemorrhage.
zz Rapid withdrawal of steroids from patient with adrenal atrophy.
SS Patients present with—
zz Nausea, vomiting and abdominal pain
zz Hypovolemic shock.
SS Treatment—
zz Replacement of sodium and water deficit (> 2l)
zz Replacement of glucorticoids (hydrocortisone/dexamethasone).
[Initially mineralocorticoid replacement is not necessary.]

Diseases of Adrenal Medulla
Tumors are the most significant

lesions of adrenal medulla
Tumors arising from embryonic Tumors arising from chromaffin

nerve cells cells
• Neuroblastoma • Pheochromocytoma
• Ganglioneuroma
Pheochromocytoma
SS Catecholamine-producing tumor arising from chromaffin cells

SS Surgically correctable cause of hypertension
SS Its removal can prevent death from hypertensive crisis.
It is often called ‘10% tumor‘ because—

zz 10% bilateral
zz 10% malignant
zz 10% in pediatric patients
zz 10% are extraadrenal
zz 10% familial.
Other extraadrenal sites are—

SS Urinary bladder
SS Renal hilum
SS Chest
SS Neck.
{
Familial pheochromocytomas are associated with—
SS MEN 2A (MTC, HPT, pheochromocytoma)
SS MEN 2B (MTC, mucosal neuroma, marfanoid habitus, ganglioneuromatosis and pheochromocytoma)

Likely
SS Von Recklinghausen’s disease (café au lait spots, neurofibromatosis and pheochromocytoma)
bilateral
SS Von Hippel-Lindau disease (Retinan hemangioma, hemangioblastoma of CNS, renal cyst and
carcinoma, pancreatic cyst, epididymal cystadenoma and pheochromocytoma).
Etiology
SS Etiology
of sporadic pheochromocytoma is unknown, but in familial cases, various germline mutations are
detected—
RET, VHL, NFI, SDHB, SDHC, SDHD
SS Grossly,pheochromocytoma appears as circumscribed lesion

SS On cut section, areas of hemorrhage and necrosis are seen.
SS Microscopically, it looks—
zz Tumor cells arranged as well-defined nests
(Zell-Ballen pattern).
zz Tumor cells are large, polyhedral, pleomor-
phic with abundant granular cytoplasm.
SS Presentation is so variable, from a incidentaloma to hypertensive crisis with CVS and cardiac complications.
termed as ‘the great masquerader’.
SS Classic triad
1. Palpitation 2. Headache 3. Profuse sweating

– Episodic presentation
+
Hypertension — Almost confirms the diagnosis
|
Most common clinical sign is hypertension
SS Hypertension may be
zz Paroxysmal with intervening normotension
zz Sustained hypertension with paroxysms
zz Sustained hypertension alone

SS Paroxysms (episodes of hormone release) usually lasts for less than an hour.
During paroxysms, patients become anxious and pale, suffering from palpitation and profuse sweating.
SS Paroxysms precipitated by positional changes, exercise, pregnancy, surgery, urination and medications (tricyclic
antidepressants, opiods, metoclopramide).
SS Anxiety, tremulousness, flushing, chestpain, shortness of breath, abdominal pain, nausea, vomiting are nonspecific
symptoms.
[Catecholamine crises can lead to heart failure, arrhythmia, intracranial hemorrhage.]
By documentation of catecholamine excess
Plasma metanephrine measurement is the most sensitive assay.
If biochemical studies confirm the presence of catecholamine secreting tumor—
SS CT is the imaging of choice (accuracy of 90–95%).

If showing normal adrenals, then
�
131
I or 123I labelled metaiodobenzylguanidine (MIBG) scanning is valuable, because
Only ectopic areas of adrenergic tissue show uptake of MIBG.
SS T2-weighted MRI with godolinium contrast is also helpful to detect extradrenal pheochromocytomas and
paragangliomas.
[If you are suspecting multiple, malignant, metastatic, extraadrenal pheochromocytoma – MIBG is the choice.]
[Be cautious – Arteriography and FNAC can precipitate hypertensive crisis.]
Treatment
Complete tumor removal is the therapeutic goal

Preoperative patient preparation — Essential for safe surgery
SS Nonselective a-adrenergic blocker, phenoxy benzamine (20–40 mg/d) – Dose is gradually increased until
hypertension is controlled and mild orthostatic hypotension is induced.
SS Nonselective a-adrenergic blocker takes some time to act, during this period – oral prazosin or IV phentolamine to
manage paroxysms.
SS b-blocker, propranolol is added 3–7 days before surgical intervention-for treating persistent tachycardia and
arrhythmia.
SS Volume replacement preoperatively to avoid postoperative hypotension.
During surgery
SS Arterial
and venous line are necessary
SS Sodium nitroprusside infusion to treat hypertensive crisis
SS b-blockers – to treat cardiac dysrhythmia
SS Volume infusion to treat hypotension.
Be cautious during—
zz Induction of anesthesia
zz Manipulation of tumor
zz Immediately after removal of tumor.

Which approach—
SS Lap or open? Total or cortical sparing?
In patients of MEN2 and bilateral pheochromocytoma—

SS Total adrenalectomy on the side of larger tumor
SS Cortical sparing subtotal adrenalectomy on the side of smaller tumor.
Incidentaloma
Nonadrenal related workup Incidentally discovered adrenal mass.

Assessment of functionality
FNAC should be reserved for patient who are not candidates for surgical resection
Pheochromocytoma must be excluded before attempting FNAC.
adrenal mass with history of malignancy in other site— Think of metastatic disease in adrenals
SS Bilateral
[Primary tumors those can metastasize to adrenals: lung cancer, breast carcinoma, renal cell carcinoma, melanoma]
Management of incidentaloma
SS All functional masses should be removed regardless of size

SS Nonfunctional lesion, size > 6 cm, suspicious features in imaging

Adrenalectomy
SS Nonfunctional lesion, size < 4 cm, benign features in imaging

Periodic follow-up with 6 monthly interval CT
SS Nonfunctional lesion, size 4–6 cm, benign features in imaging
? Periodic follow-up ? Surgery

SS Choice depends on case-specific factors—
zz Age
zz Surgical risk factors
zz Tumor growth rate during periodic follow-up
zz Patient preference.
Principles of Adrenal Surgery
1. Proper Preoperative Preparation
2. Approach
Endocrine Pancreas
SS The islets of Langerhans form 1–2%

of the pancreatic tissue.
SS The islets are interspersed within the

structure of exocrine pancreas.
Pancreatic Endocrine Neoplasms
SS Also known as 'islet cell tumor'

SS Rare in comparison to exocrine pancreatic tumors.
SS Feedback mechanism does not exist.
SS Types:
zz Insulinoma (most common)
zz Gastrinoma (most common malignant endocrine tumor)
zz Glucagonoma
zz Somatostatinoma
zz VIPoma.
Insulinoma
Most common pancreatic endocrine neoplasm

SS Small < 1.5 cm.
SS Encapsulated, pale to red brown nodules anywhere in the

pancreas.
SS Single (10% multiple).
SS Benign (5–10% malignant).
SS Almost always in the pancreas.
Diagnostic laboratory findings
SS Serum insulin > 5 mU/ml during symptomatic hypoglycemia

SS Serum insulin: serum glucose > 0.4
(mU/ml) (mg/dl)
SS C peptide > 2 nmol.
Localization of tumor
SS Imaging—
}
zz Enhanced CT
zz Enhanced MRI Based on the fact that islet tumors have rich blood supply compared to normal parenchyma.
zz Arteriography
SS Selective intra arterial injection of calcium in—
zz Gastroduodenal, superior mesenteric, right hepatic, splenic arteries (Based on the fact that calcium releases
insulin).
SS Insulin assay from right hepatic vein.
Management
SS Treatment is surgical
zz Open approach
zz Laparoscopic approach.
SS Surgeon operating on insulinomas must be familiar with

intraoperative ultrasonography
SS Enucleation of the tumor from normal pancreatic parenchyma.
Gastrinoma [Zollinger-Ellison Syndrome]
SS Second most common islet cell tumor.

SS Most common symptomatic malignant
endocrine tumor of pancreas.
SS 60–90% of gastrinomas are found in the
'gastrinoma triangle'.
Sporadic (75%) Associated with MEN-1 (25%)
SS Most gastrinomas are found (50–70%) in the

duodenum (1st part > 2nd part> 3rd part; never in
4th part).
SS 20–40% are found in pancreas, rest in other intra-
abdominal sites.
SS Usually single lesion.
SS Gastrinomas are usually in the duodenum (50–90%)

or in the pancreas (10 – 30%).
SS Always multiple lesion.
SS 60–90% of gastrinomas are malignant with metastatic spread to lymph nodes and liver.
Think of gastrinoma if
Diagnosis is confirmed by
hypergastrinemia (> 1000 ng/l) in the setting of gastric pH ≤ 2, the diagnosis of gastrinoma is established
SS Fasting
SS Diagnosis is in doubt, then secretin provocation test.
Fasting gastrin level estimation

IV secretin (2 CU/kg)

Gastrin level estimation at 2, 5, 10, 20 minutes later
Increase of gastrin level more than 200 pg/ml

highly suggestive of gastrinoma
SS If, Secretin test is equivocal, then calcium infusion test to be done.
Increase in serum gastrin level > 395 pg/ml
Confirms the diagnosis
Localization tests
Accurate localization of the site of tumor is important for definite therapy and assessment of prognosis.
SS CECT abdomen and pelvis
zz Endoscopic USG
zz MRI
zz Arteriography
zz Selective portovenous sampling
zz Selective intraarterial secretin infusion with hepatic vein sampling
SS Somatostatin receptor scintigraphy (SRS)—
zz 90% of gastrinomas have receptors for somatostatin
zz Sensitive for both primary and metastatic gastrinomas.

Treatment
Glucagonoma
SS Secretes excess glucagon
SS Characterized by—
zz Characteristic dermatitis (migratory necrolytic erythema)—Annular erythema at intertriginous and periorificial
sites.
zz Glucose intolerance.
zz Weight loss.
SS Diagnosis is confirmed by
zz Plasma glucagon > 1000 ng/dl.
SS Treatment is surgical excision of the tumor. Almost all glucagonomas are malignant, an agressive approach to
remove the primary and metastatic tumor is warranted.
SS Symptomatic relief – is achieved by octreotide.
Somatostatinoma
SS Exceedingly rare tumor

SS Secretes ↑↑ somatostatin
SS Primarily located in the head of pancreas
SS Syndrome complex characterized by diabetes mellitus, gallbladder disease, diarrhea, steatorrhea
SS In most cases, it is diagnosed incidentally at the time of cholecystectomy or during endoscopy
SS Treatment is surgical resection, rather than enucleation.
VIPoma [Verner-Morrison Syndrome]
SS Secretes VIP (Vasoactive intestinal polypeptide)

SS Diagnostic triad—
1. Secretory diarrhea (persists despite nasogastric aspiration)
2. ↑↑ circulating VIP
3. Pancreatic tumor.
SS Symptoms—
zz Large volume secretory diarrhea — severe enough to cause hypokalemia, dehydration
zz Hypochlorhydria
zz Flushing.
SS Localization is done by SRS or endoscopic USG
SS Octreotide is helpful in control of diarrhea
SS Most VIPoma can be excised by distal pancreatectomy.

Multiple Endocrine Neoplasia (MEN) Syndromes

Multiple Endocrine Neoplasia Type I
SS Alsocalled Wermer’s syndrome

SS Everyone into inherits MEN1 gene develops at least one clinical manifestation during his/her lifetime.
SS Most common type of MEN.
SS Inherited as autosomal dominant trait.
SS MEN1 gene is a tumor-suppressor gene, located at chromosome 11q13.
SS Primary hyperparathyroidism is the SS Enteropancreatic tumor is the second most SS Hyperprolactinemia

most common manifestation. common manifestation. (due to prolac-
SS Earliest manifestation. SS Gastrinoma is the most common tinoma) is the most
SS Manifested like sporadic HPT. enteropancreatic tumor. common manifesta-
SS Insulinoma is the second most common
tion due to pituitary
SS Management is difficult because:
enteropancreatic tumor. tumor.
zz Early onset.
SS Acromegaly (due to
SS Tumor producing insulin, glucagon, VIP
zz Significant chance of
should be resected. ↑↑GH) and Cushing’s
recurrence. disease may present.
zz Multiplicity of parathyroid
SS Dopamine agonists
involvement. (bromocriptine,
SS Observation policy for cabergoline,
asymptomatic HPT. quinagolide) are
SS Parathyroid exploration when: effective for control
zz Serum Ca >12 mg/dl
2+ of prolactin level and
for prevention of
zz Complications of HPT
tumor growth.
zz Age < 50 years.
SS Surgical resection is
SS Surgical approaches are:
indicated for mass
zz Total parathyroidectomy effects.
zz Subtotal parathyroidectomy.
Other tumors in MEN1

SS Bronchial and thymic carcinoids
SS Benign thyroid tumor
SS Benign and malignant adrenocortical tumors
SS Lipoma
SS Ependymomas of CNS
SS Facial cutaneous angiofibroma.

Multiple Endocrine Neoplasia Type II
SS Inherited as autosomal dominant trait.

SS Caused by germline mutations in the RET gene on
chromosome 10.
SS The hallmark of these syndrome is MTC, which is
bilateral and multifocal.
SS All persons who carry the disease allele develops MTC.
MEN 2A
SS Most common manifesta- SS Multifocal, bilateral with adrenal medullary hyper- SS Manifestations are same
tion. plasia. like primary HPT
SS Multifocal, bilateral lesion SS ↑↑ epinephrine secretion in comparison to SS Multiple glands
with C-cell hyperplasia. norepinephrine. are involved with
SS Total thyroidectomy with SS Rarely malignant. hyperplasia.
central lymph node dis- SS Almost never extraadrenal. SS Total parathyroidectomy
section should be per- SS Partial or complete adrenalectomy is the treatment.
with autotransplantation
formed in children carry- at the time of total
SS In unilateral tumor, ? Unilateral or ? Bilateral
ing the mutant gene. thyroidectomy.
adrenalectomy.
MEN 2B
SS All MEN2B patients develop MTC.

SS MTC presents at very young age (in infancy); most aggressive form of MTC.
SS All MEN2B patients develop mucosal neuromas.
SS Mucosal neuromas (in tip of tongue, lip, under the eyelid, gingiva, buccal mucosa, nasal mucosa) and marfanoid
habitus are the most distinctive features and easily identifiable in childhood.
SS 40–50% patients develop pheochromocytomas.
SS All patients have megacolon, chronic bowel problems (intermittent colic, pseudoobstruction and diarrhea).
Chapter 16
Trauma
Important Topics
zzTypes of Injury
zzHospital Care of Trauma
zzHead Injury
zzMaxillofacial Injuries
zzNeck Injury
zzSpinal Injury
zzThoracic Trauma
zzAbdominal Injuries
zzGenitourinary Injuries
zzDamage Control Injuries
‘That man can interrogate as well as observe nature, was a lesson slowly learned in his evolution.’
William Osler (1849–1919)
Canadian Physician
Trauma 565
Introduction
SS Trauma is characterized by a structural alteration and/or physiologic imbalance that results when energy is imported
or vital functions compromised during interaction with physical or chemical agents.
SS Trauma is the leading cause of death and disability and is the third most common cause of death.
Types of Injury
Different types of injury
Blunt Penetrating Blast Thermal Chemical
Blunt Trauma
Motor-vehicle accident Fall from height Assault by blunt object
Different types
of blunt trauma
Stampede Injury by wild animal

Different types of motor vehicle accidents
Head-on car collision Car fall from height
Collision with heavy objects Car hitting pedestrians
Different types of injuries

of which some have distinct patterns!
Front end car collision causes specific injuries in drivers
• Head strike the windshield causing facial fracture Impact between driver’s knee
and cervical spine fracture and dashboard
Causing
• Chest and upper abdomen strike the steering

wheel causing laceration of thoracic aorta,
myocardial contusion, injury of liver and spleen > Patellar fracture
> Posterior dislocation of knee
with popliteal artery injury
> Femoral shaft fracture
> Fracture of posterior rim of the
acetabulum
More energy is transferred over a wider area during blunt trauma than a penetrating trauma.
Determinants of impact force:
SS Area of application
SS Duration of application
SS Direction of application.
Trauma 567
Adult pedestrian (static)
Vehicle (moving)
Head injury from striking

the windshield
Injury of tibia and fibula from striking

by the bumper
Victim sweft from the ground
Injury to the upper

extremity
due to fall on the ground
Young pedestrians have a distinct pattern of injuries:
SS Fracture femur from striking the bumper.

SS Abdominal solid organ injury from striking the fender. Waddell triad
SS Opposite-side head injury from landing on the
pavement.
Trauma deaths have

trimodal distribution
Time of injury Time of injury Time of injury
Days
Few minutes Few hours
to weeks
Immediate Early Late
death (50%) death (30%) deaths (20%)
• These first few hours are

• Due to– called the ‘golden hours • Due to–
of trauma’
• Due to– sepsis or
multiple
organ failure
> airway obstruction

> disruption of breathing
• These type of injuries
are not treatable,
rather preventable
Massive blood loss
Preventive measures :
Wearing seat belts
Road safety
measures
Wearing helmets
Trauma 569
Prehospital Retrieval and Care
SS Assess:
zz ? Patient need an emergency treatment at the site of incident

zz Distance between the site of incident and a well-equipped hospital.
SS Then, choose any one:
zz ‘Scoop and run’ policy (immediate evacuation)
zz ‘Stay and play’ policy (scene resuscitation).
SS If, ‘stay and play’ policy: Field professionals perform 3 major functions:
zz Assessment of the injury scene
zz Stabilization and monitoring of injured patient
zz Safe and rapid transportation of critically ill patients to the appropriate trauma center.
Field professionals must be properly trained (PHTLS course): Prehospital trauma life support course.
SS Then, ‘Triage’ – if major civil disaster or war.
‘Triage’ came from the french word ‘trier’, means to shift or to sort.
Triage is a dynamic process of sorting casualities to identify the priority of treatment and evacuation of the wounded.
Triage – It need to be repeated at each level of

care from point of injury to hospital
Point of injury Triage is for

evacuation to hospital
Triage is for
Hospital access to resuscitation
and to operating rooms
Triage sieve A method of quick survey
Triage sort
Dead Injured
Immediate
Minimal
Delayed
Green
tagging
Red
tagging
Yellow
tagging
Minor injuries
(minor laceration
– Requires life saving surgery
– patient with respiratory obstruction, abrasion, fracture
of small bone)
unstable chest and abdominal
injuries, emergency amputation Expectant
Needs surgery but general

condition permits delay in treatment
Large muscle wound, fracture
of long bones, stable abdominal and Black
thoracic wound tagging
Penetrating head injury,

high spinal cord injury mutilating
wounds involving multiple organs.
Survival would be unlikely
Prehospital Management
1. Neck, spine immobilization
All patients with major blunt trauma should be suspected of having
spinal injury. Cervical spine is immobilized by Philadelphia collar.
2. Airway management
Grasping the mandible
SS Cleaning of solid debris from mouth and pharynx in the midline and drawing
it forward until the lower
SS Chin lift/jaw thrust maneuvers: for relief of airway obstruction teeth are leading
Trauma 571
SS Suctioning of mouth and pharynx to clear blood,
mucus and vomitus.
SS Insertion of an airway device: if field professional is
expert enough
[Nasopharyngeal intubation is better avoided.]
Oropharyngeal intubation is
preferred
SS Upper airway is occluded and endotracheal intubation
cannot be done, then:
Through
14 gauge cricothyroid 6 mm pediatric
needle tracheostomy tube Through
membrane
cricothyroid
O2 O2 membrane
Open cricothyroidotomy
Needle cricothyroidotomy (Particularly indicated Open cricothyroidotomy is contraindicated below 12 years

below 12 years) because of the risk of damage to the cricoid cartilage and
subsequent risk of subglottic stenosis.
3. Intravenous access 4. Fracture immobilization
2 liter Ringer
lactate
Recognition and splinting of all major

fractures before transportation
Large bore IV catheter

(14/16 gauge)
5. Cardiac arrest management

[Prehospital management period should not ex-
ceed 30 minutes.]
6. Prehospital transport
SS Ideally by ground or air ambulance.
SS Ideally transport time should not exceed 15 minutes.
SS Resuscitation should be continued during transporta-

tion.
SS If no ambulance is available, station wagon or truck is
preferable to a passenger car.
SS Should be transported in the supine position.
Primary survey
Hospital Care
Resuscitation
SS Trauma victims require a precise, rapid and systematic
Evaluation system
approach. consists of: Secondary survey
SS The advanced trauma life support (ATLS) system is the
best approach to the severely injured patient.
Definitive
management
Primary survey
A B C D E
SS Itis a systematic, rapid evaluation of the injured

patient following the mnemonic: Airway Breathing Disability Exposure
Circulation
1. Airway
SS Establishing a patent airway is the highest priority, because irreversible brain damage from hypoxia can occur
within minutes.
SS A patient who is able to respond verbally has a patent airway: Therefore early attention to the airway is not required.
Exceptions are:
}
zz Penetrating injuries in neck with expanding hematoma.
zz Chemical or thermal injuries to the mouth and nose.

these patients need elective intu-
zz Extensive subcutaneous emphysema in neck.
bation prior to airway compromise
zz Complex maxillofacial trauma.
Trauma 573
SS Oxygen is administered via nasal cannula or bag valve facemask at the rate of 10–12 l/minute and oxygen saturation
is measured using pulse oximeter.
SS If basic maneuvers like suctioning, jaw-thrust maneuvers are not done as prehospital care, these must be done.
SS Then orotracheal intubation using Rapid-sequence induction (RSI).
Preoxygenation
with 100% O2
Short-acting sedative
(e.g. midazolam)
Paralytic agent
(succinylcholine is
the choice)
After onset of
paralysis, ET tube
is inserted under
direct vision
SS Cricothyroidotomy is the method when orotracheal intubation is not possible (unsuccessful intubation attempts or
massive facial injuries).
zz Open cricothyroidotomy is indicated for adults
zz Needle cricothyroidotomy is indicated below 12 years.
2. Breathing
SS Once an airway is established, it is necessary to make certain that ventilation is adequate.
Patent airway
Ventilation
adequate
Ventilation
impaired
SS Chest is examined to detect life-threatening conditions:

zz Tension pneumothorax
zz Massive hemothorax
zz Open pneumothorax
zz Flail chest with pulmonary contusion
zz Tracheobronchial disruption.
SS All these conditions can be diagnosed with a combination of clinical examination (inspection, palpation, percussion
and auscultation) and chest X-ray.
Suspect tension pneumothorax if respiratory distress is present along with any of the following signs:
Distended Tracheal deviation

neck away from the side
veins of pathology
Systemic
hypotension
Tear in the visceral
pleura acts as a valve
allowing air entry into

the pleural cavity during
inspiration but preventing
escape
Absent or
diminished
breath sound
Don’t wait for chest X-ray confirmation

Immediately, needle thoracocentesis.
• Insertion of large
bore needle
in the second
intercostal
space along
midclavicular line
This maneuver
convert the tension
pneumothorax to a
simple pneumothorax
SS Prepare the patient for tube thoracostomy

SS Needle should be left in place.
• Chest drain tube is inserted at the

midaxillary line at the fifth intercostal
space
• Direction of the tube will be
posteriorly and superiorly
• Tube is attached with waterseal bag
• Column of water moves with inspiration and expiration

(if tube is placed in pleural space)
• Bubbling suggest air drainage is present
Trauma 575
Open pneumothorax
• Chest wound
communicating
with pleural space
• Wound size
2/3rd diameter
of trachea
• During breathing • Sealing the wound • This dressing like Untaped side
air moves in and with occlusive sterile an flutter valve only
out of the chest dressing (taped on allows accumulated air
wall opening instead three sides) to escape – prevents
of trachea tension pneumothorax
• Closure of the wound

• Tube thoracostomy
Flail chest
• Three or more contiguous

ribs with two or more
fractures per rib
• The segment produce

paradoxical movement
SS Endotracheal intubation Anterior flail

Lateral flail
and mechanical ventila- segment segment
tion may be required to
maintain adequate venti-
lation.
SS Underlying pulmonary
contusion must be seri-
ously considered. During inspiration flail
segment moves inwards
Massive hemothorax
> 1500 ml of blood in

a hemithorax
• Treatment is tube thoracostomy
+
Treatment of hypovolemic shock
• Three or more contiguous

3. Circulation ribs with two or more
fractures per rib
SS Primary goal is identification and control of hemorrhage.
SS Control of hemorrhage by:
– Direct – Elevation of the

pressure bleeding point and
splint application
If these measures fail, tourniquet is helpful
Periodical release of tourniquet is must–otherwise irrep-

airable vascular and neurological damage will occur.
Blind clamping should be avoided-damage of adjacent

structures particularly nerve, may occur.
Trauma 577
SS Vascular access: For fluid resuscitation
by—
zz Large bore peripheral venous catheterization 16 gauge
or more
zz Saphenous vein cut down/femoral vein catheteri-
zation [if vigorous fluid resuscitation is required].
In patients less than 6 years of age, percutaneous
femoral vein cannulation is contraindicated because of
the risk of venous thrombosis.
If two attempts of peripheral access are unsuccessful,
then interosseous cannulation.
Proximal
tibia
SS Nature of fluid: Ringer lactate or normal saline

zz Blood transfusion (packed RBC) must be started
whenever available.
[Flow of liquid through a tubular structure is propor-
tional to the diameter and inversely proportional to
the length.]
4. Disability
The goal of this phase is to identify and treat life-threatening neurologic injuries.
(a) Level of consciousness is quickly assessed by –
A V P U
Patient Awake Open eyes Open eyes to Unarousable

to Voice Painful stimulus
(b) Examination of pupil
Size Symmetry Response

to light
(c) Focal neurologic deficits

5. Exposure
SS The purpose of this phase is complete visual inspection of the injured patient along with measures taken to avoid
excessive heat loss.
zz Patient is completely disrobed (clothes cut away)
zz Visual inspection including logrolling to examine the back.
zz Splaying of the legs to examine the perineum.

� Elevation of the arms to inspect the axilla
Warm resuscitation
fluid
Warm
resuscitation These measures
room prevent hypothermia
Warm blanket
Secondary survey
SS Itis the phase of ‘fingers and tubes’ in every orifice.

SS Complete, systematic head to toe examination of the patient along with complete history.
SS Aims of secondary survey-detection of:
zz Progressive changes in clinical findings
zz Missed injuries
zz Response to resuscitation.
SS Radiographic evaluation (USG, CT and even MRI) may be performed in this phase.
Trauma 579
Secondary survey of ‘Head’
SS Patient’s conscious level is evaluated by GCS (Glasgow

Coma Scale)—It measures
zz Eye opening
zz Best verbal response
zz Best motor response.
I am
in hospital
Patient with GCS < 8 should be considered to have severe Open your
neurologic deficit. tongue
Scalp
SS Explore deep lacerations in scalp with a gloved finger–
to rule out depressed fracture.
Skull bone
SS Search for signs of basal skull Light halo of CSF

fracture
Darker center spot
(containing blood components)
CSF mixed with

blood through nose - produces Think of anterior
double ring if dropped on fossa fracture
pillow or hospital sheet
Bilateral
periorbital
hematoma
(raccoon eyes)
CSF otorrhea/ Mastoid

bleeding from external hematoma
auditory meatus (battle sign)
Bilateral periorbital hematoma

Secondary survey of ‘Face’
• Eyes are checked for

– Foreign bodies
– Perforating injuries
– Subconjunctival hemorrhage
– Visual acuity Abnormal dental occlusion if
– Pupillary and corneal reflex present, is highly suggestive
of mandibular or maxillary fracture
• ? Septal hematoma
• Maxillary fracture should

be excluded
Mouth is checked for – Midfacial fracture may
broken teeth, loose endanger airway
dentures, any foreign bodies
Secondary survey of ‘Neck’
SS Neckis inspected and

palpated to exclude:
zz Cervical spine injury.
zz Aerodigestive tract
injury (larynx, trachea,
esophagus).
zz Vascular injury (carotid
arteries, subclavian
artery, jugular vein
and subclavian vein).
? Midline cervical spine tenderness, vertebral step-off-suspect spinal cord injury.

In unconscious or intoxicated patient, cervical spine should be considered unstable unless excluded by CT or MRI
of spine.
Subcutaneous emphysema in neck: Suspect aerodigestive tract injury.
Secondary survey of ‘Thorax’
Position of the trachea

Penetrating or blunt trauma below the nipple (in
male patient)—
Suspect intraabdominal injuries (particularly Quality and
symmetry of
liver, spleen, stomach and transverse colon). breath sound
Symmetric
excursion
of chest
Subcutaneous emphysema
Trauma 581
Secondary survey of ‘Abdomen’: Diaphragm to pelvic floor
Nipple
Abdominal injury
Abdomen
Blunt Penetrating
Inguinal trauma trauma
crease
Unstable patient with Stable patient with

multiple injuries multiple injuries
Do FAST DPL
CT abdomen
(if CT facility
and pelvis
unavailable)
CT abdomen and
pelvis (when patient
become stable)
? Stab wound ? Missile wound
Local wound * High probability of

exploration significant intra-
abdominal injury
Peritoneum not
breached
Peritoneum is
breached
? Significant intraabdominal
injury
Wound can be Must be excluded by
treated as deep – Laparoscopy vs Celiotomy
laceration – FAST
– CT
– DPL
– Close observation
SS Bowel eviscerated?
zz Eviscerated bowel should be covered in warm wet packs and must not be returned to the peritoneum.
Eviscerated
bowel
Warm wet
pack
Secondary survey of ‘Pelvis’ Secondary survey of ‘Extremities’

SS Assess for stability by palpating the iliac wings and SS To exclude—
gentle compression of pelvis. zz Soft tissue injury
SS Search for signs of pelvis fracture— zz Bony injury
zz Scrotal hematoma zz Vascular injury
zz Unequal leg length zz Neurologic injury.
zz Iliac wing hematoma. SS Search for—
SS Suspect urethral injury, if pelvic fracture is present. zz Gross deformity of limb
Secondary survey of ‘Genitalia’ and ‘Perineum’ zz Active bleeding
SS Inspection for hematoma and lacerations zz Open wounds
SS Rectal examination is mandatory. zz Expanding hematoma
zz Evidence of ischemia.
Head Injury
Scalp injury
Fracture
cranial vault
Fracture
skull bone Fracture base
of the skull
Different types
Epidural
Intracranial hemorrhage
hemorrhage
Subdural
hemorrhage
Diffuse axonal injury Subarachnoid
hemorrhage
Intracerebral
hemorrhage
Trauma 583
Traumatic brain injury (TBI)
is classified into
Acceleration/deceleration injury
Primary injury Secondary injury
(occurs at the time (occurs as a result of events
of impact) after the initial injury)
• Cerebral concussion • Intracranial hematomas Mechanisms Impact injury
• Cerebral contusion • Cerebral swelling of injury
and laceration • Cerebral ischemia
• Diffuse axonal injury • Infection
• Skull bone fracture • Epilepsy Penetrating injury
Acceleration/Deceleration Injury
SS Classically seen in high speed motor vehicle accidents.
Contrecoup injury
(extensive contusion
opposite the point of impact)
Coup injury
(minor
contusion)
• Abrupt deceleration of moving head
• As the skull and brain accelerate

and decelerate differentially,
brain moves within
the skull and this brain impacts against
intracranial bony irregularites
(floor of frontal sinus, sphenoid wing,
petrous ridge)
Bridging Dural
vein sinus
SS Kinetic force causes

shear injury to neurons
and blood vessels
Differential acceleration
and deceleration of skull Diffuse axonal injury
and brain causes stretching (DAI) and hematoma
of veins leads to rupture
Impact Injury
SS Classicallyseen following injury by blunt objects (e.g. Impact force

bat, wooden or iron rod).
SS Severity of brain injury is less. Skull absorbs most of the
kinetic force of impact injury
Commonly, Epidural
Penetrating Injury skull fracture hematoma
Penetrating injury
Low velocity High velocity

injuries injuries
SS Most low velocity injuries (by

pen, pencil, branches, dart) occur
through relatively thin skull bone–
particularly orbitocranial window
Structures Missile’s kinetic

Causing damage to the structures along the path injury is absorbed by
along the path of entry. are injured the skull and brain, causing
diffuse injury in brain
Trauma 585
Different Types of Head Injuries and Their Specific Management
1. Scalp injury
SS Scalp has a rich blood supply–So significant blood loss may occur after injury.
SS Skull fracture must be excluded in deep lacerations–by a gloved finger.
Simple laceration
• Copious irrigation
with normal saline
Separate galeal apposition

is recommended for long wounds
Primary closure with mattress suture
Laceration with tissue loss
Debridement followed by advancement flap.
2. Skull fracture
SS Fracture of cranial vault
SS Fracture of base of the skull
Skull fracture in general indicate that a significant force is transmitted to the head.
SS Closed undisplaced fracture usually do not SS Open undisplaced fracture require repair of
require treatment. scalp and broad spectrum antibiotics.
zz Patient should be admitted for observation.
Communited fracture
(multiple fracture fragments)
Stellate fracture
(multiple fracture
radiating from
a point)
Linear
3D reconstruction of CT brain showing commu-

nited skull bone fracture
Fractures that cross the middle meningeal groove may

cause tearing of artery leads to epidural hematoma.
SS Inminor depressed fracture, there is less chance of

dural tear or underlying brain injury.
zz Elevation of this depressed fracture is indicated
mainly for cosmetic reasons, when they are in the
frontal region.
CT brain showing depresed skull bone fracture with underlying

intracranial hemorrhage
SS In severe depressed fracture, the bone fragments

with multiple sharp edges may lacerate dura, brain
and vessels.
SS Venous sinus involved in the depressed fracture,

Surgery is better avoided for risk of excessive bleeding.
Antibiotic treatment alone is given.
Surgery is usually undertaken to prevent the risk of infec-
tion, to alleviate mass effect.
Treatment of depressed fracture
SS Fragments to be elevated
SS If dural tear, then duraplasty
SS Postoperative antibiotics.
Depression of the outer table of the depressed frag-

ment below the level of inner table of surrounding
Burr hole at the skull is indication for operative elevation.
edge of depression
Trauma 587
Ping-pong fracture (‘Pond’ fracture)
No fracture
of inner table
Bone is
No tearing of elevated
dura
Smooth depression of
cranial vault CT scan showing ‘pond fracture’ of skull bone
Surgery is advocated to prevent the formation of a leptomeningeal cyst.

SS Through a burr hole adjacent to depressed fracture, the bone is ‘popped’ back into normal shape by Adson’s
periosteal elevator or surgeon’s finger.
SS Fractures through the paranasal sinuses with associated pneumocephalus and dural tears require repair.
Fracture anterior skull base

Fracture of base
of the skull
Fracture middle cranial fossa
Anosmia (due to damage

of olfactory nerve)
Periorbital ecchymoses
(’raccoon eyes’)
[‘raccoon eyes’ also found in subgaleal hemorrhage]
CSF rhinorrhea
CSF mixed with blood form

a double ring – ‘halo test’
[If still in doubt, the fluid can

Fracture of anterior be sent for beta-transferrin
skull bone (CSF is beta-transferrin positive)]
Vertigo, ipsilateral deafness,

facial paralysis (due to damage
of facial or vestibulocochlear nerve)
Otorrhea
Ecchymoses behind the ear

Fracture of middle (Battle’s sign)
cranial fossa
SS Most of the CSF leaks will heal with elevation of head of the bed for several days.
SS No proven role of prophylactic antibiotics to prevent meningitis.
SS Dura is repaired with autologous, vascularized graft.
SS Facial nerve palsy may benefit with steroid. If not responding within 72 hours, surgical decompression of the petrous
part of the nerve is indicated.
3. Epidural (extradural hematoma)
SS Epidural hematoma is accumulation of blood between the skull bone

and the dura.
SS Usually results from arterial disruption (specially the middle
meningeal artery)
SS Mostly underlie a skull fracture.
SS Most common location is the temporal fossa– Temporal squamosa is

the thinnest part of the cranial vault.
SS Rarely, a skull fracture may cross a venous sinus (superior sagittal sinus
or transverse sinus).
• Dura is closely adhered

to the inside of the skull
• Spread of hematoma is
limited by dural adhesion
to skull
Hematoma
Dura
Trauma 589
EDH has classic 3 stage clinical presentation: (seen in about 20% of patients)
SS Stage of concussion–transient loss of consciousness
SS Lucid interval–Patient awakens
SS Patient becomes lethargic and proceeds to coma stage
Herniation of the
medial temporal
lobe through
tentorial hiatus
Causes ipsilateral III nerve palsy
Dilated pupil on the side of expanding lesion – an important localizing sign.
• Dilated pupil and impaired

or absent reaction to light –
on the side of lesion
• Contralateral hemiparesis
CT scan of brain shows
Biconvex hyperdense lesion

with well-defined border that
usually respects cranial
suture lines
CT brain showing extradural hematoma Midline shift with compression

of ipsilateral ventricle
Management
Urgent evacuation of hematoma? Close observation? with serial CT
Most of the EDH needs urgent evacuation. SS GCS 14/15 or 15/15

By CT scan, the site of burr hole/craniotomy is accurately SS On CT thickness of hematoma < 5 mm
delineated. zz Volume < 25 ml
zz No midline shift, adjacent edema, ventricular

compression.
Hematoma
Burr hole is evacuated
Bleeding vassels
are secured
Bone flap
Scalp flap
Scalp flap
Trauma 591
4. Acute subdural hematoma
Hematoma formation due
to tearing of bridging veins
Dural venous sinus
After head
Normal injury
anatomy
In most cases of acute subdural

hematoma, associated contusions
Bridging veins (running from and cerebral edema results
cerebral cortex to dural sinus) in mass effect
Clinical presentation CT scan of brain shows
SS Altered consciousness
SS Seizure
SS Contralateral hemiparesis.
The longer the interval of development of hematoma • Subdural hematoma
and surgical intervention, more the deterioration of the follows the subdural
patient’s condition due to secondary effects. space over the convexity
of the brain
SS So, quick decision making and opening the dura is • Appears as biconcave
necessary for better outcome. hyperdense lession
Skin flap
SS A large craniotomy flap is planned because besides

evacuation of subdural hematoma, underlying Bone flap
cerebral hemorrhagic contusions and intracerebral
hematomas have to be evacuated.
SS Frontotemporoparietal flap is mostly needed [for
better exposure]
Bulging dura is
opened through
cruciate incision
SS Evacuation of clot.
SS Gently lavage and suction allows visualization of
bleeding bridging veins.
SS Bleeding vessels coagulated.
SS Underlying intracerebral hematoma along with

necrotic brain is also evacuated.
5. Chronic subdural hematoma
Initial trauma
SS Predominantly found in infants and elderly. (sometimes patient
have forgotten the
history of injury)
Predisposing factors
No increase in
intracranial pressure
SS Cerebral atrophy due to cortical shrinkage
SS Low CSF pressure (after shunt/fistula)

SS Alcoholism
SS Coagulation disorders.
Membrane grows out from

the dura to encapsulate the
Clinical presentation hematoma (clotted for
2–3 weeks)
SS Alteredconsciousness
SS Headache
SS Neurological deficit (seizure, contralateral

hemiparesis).
Hematorma liquefies
and expands significantly
CT scan of brain shows
Acute subdural hematoma

appears hyperdense
No midline shift
After 2–3 weeks
Chronic component
Acute component
Midline shift
Trauma 593
Chronic SDH thicker than 1 cm and all symptomatic chronic SDH must be surgically drained.
Burr hole – one or two

burr holes over the center
of the clot is the universally
accepted method
Dark altered blood

comes out spontaneously
after dural incision
Saline wash followed

by placement of drain
in subdural space
Follow up CT scan in immediate postoperative period and after 1 month is essential to document resolution.
6. Intracerebral hematoma
Frontal pole
These areas suffer major

shear strains –
During acceleration
Temporal pole deceleration injury
Midline CT brain showing intracerebral hematoma
Rupture of midline
Frontal contusion Temporal contusion
bridging veins
Areas of contusions coalesces

to form contusional hematoma
Appears on CT as hyperdense lesion
Surrounding cerebral edema
Midline shift
Surgery is indicated if—

SS Midline shift (> 0.3 cm)
SS Progressive deterioration of sensorium
SS Progressive focal neurological deficit
SS Herniation with brainstem compression
SS Increased intracranial pressure.
[Scalp incision and burr hole placement are same for a standard trauma craniotomy.]
Trauma 595
7. Concussion 8. Contusion
SS Temporary neuronal dysfunction after blunt trauma SS Itis a bruise of the brain.
in brain. SS Frontal, temporal and occipital poles are most often
SS Amnesia of the event is very common. Confusion, involved.
loss of consciousness may also present. These SS Contusions may coalesce to form contusional
deficits resolve over minutes to hours. hematoma or edema may develop around
SS CT scan is normal. contusion, causing mass effect.
SS Brain is much more susceptible to injury from minor SS Contusions may seen opposite the site of impact,
trauma in the first 1–2 weeks after concussion. then it is called ‘contrecoup injury’.
9. Diffuse axonal injury (DAI)

SS As a result of shearing following deceleration, disruption of axons specially at the gray-white matter interface,
develops.
SS Macroscopically, punctate hemorrhages may seen in corpus callosum and superior cerebellar peduncle.
SS Microscopically, retraction balls and microglial clusters are seen diffusely in the white matter.
Retraction balls
Microglial clusters
SS Patient may present with mild coma to death.
Assessment of Severity of Brain Injury
Assessment done by
1. Level of consciousness 2. Localizing signs [signs of CNS 3. Imaging
dysfunction]
SS Assessed by GCS scoring CT brain X-ray skull
SS GCS scoring consists of CT is indicated [where CT scan fa-
zz Eye opening SS GCS < 13/15 at any cility not available]
zz Best motor response point since injury. SS Standard view
zz Best verbal response SS GCS 13-14/15 at 02 are

SS GCS score is summation of hrs postinjury. zz Antero-
point in each category. SS Suspected open/ posterior

SS Pupil is assessed by—
SS GCS ranges from 3–15. depressed skull zz Lateral
zz Size
fracture. zz Towne’s
SS Mild head injury GCS>13;
zz Equality
moderate head injury SS Any sign of basal SS Useful to
zz Reaction to light skull fracture.
9<GCS<12; severe head identify skull
injury GCS<8. SS Dilated pupil and asymmetry SS Posttraumatic fracture, but
SS GCS score is an indicator
> 1mm are important seizure. not useful for
of prognosis and have localizing signs. SS Focal neurological intracranial
predictive value regarding SS Asymmetric movement in deficit. lesion.
neurosurgical intervention. response to painful stimulus SS >1 episode of
– suggestive of focal lesion. vomiting (in adult).
Why resuscitative measures are necessary in TBI?

SS In TBI, the total trauma effect is the combination of primary injury and subsequent secondary injuries.
SS Primary injury is the anatomic and physiologic disruption of brain itself.
Secondary injury is the sequela of primary injury and resulting from cerebral edema, increased ICP, hypoperfusion,
hypoxemia.
SS Hypoperfusion and hypoxemia are the most significant factors lead to poor neurologic outcome.
SS Systolic BP > 90 mmHg, adequate oxygenation and ventilation, PaO > 60 mmHg, prevention of elevated PaCO ,
2 2
maintaining ↓ICP are the basic goals of resuscitation.
Measures taken in TBI—

SS Management of hemodynamic instability
SS Management of neurologic instability (this instability is mostly due to intracranial hypertension).
Treatment of Intracranial Hypertension
SS Decreasing brain volume

zz IV mannitol-establishes a osmotic gradient across blood-brain barrier, thereby draws interstitial water out of the
brain.
zz Hypernatremia–controls cerebral edema by normalizing the Na gradient across cellular membranes.
+
SS Decreasing CSF volume
zz Ventriculostomy (intermittent drainage of CSF according to ICP).
SS Decreasing intracranial blood volume
zz Surgical evacuation of blood clot.
SS Others
zz Elevation of the head of the bed.
zz Preventing rising of intrathoracic pressure (seizure, coughing, vomiting, straining)
zz Decreasing cerebral metabolism–by barbiturates, propofol.
[Steroid has no beneficial role.]
Control of Seizure
SS Patient with seizure attack is treated with phenytoin (15–20 mg/kg IV loading dose), followed by maintenance dose
of 300–400 mg/day for 7 days.
SS Status epilepticus are treated with benzodiazepines.
SS Prophylactic anticonvulsants should be given in patients with epidural hematoma, subdural hematoma,
intraparenchymal contusion to prevent early posttraumatic seizures.
In the absence of seizures, anticonvulsant can be discontinued after 7 days.
Trauma 597
Maxillofacial Injuries
Different types of injuries
Soft tissue injury Bony injury Others
Fracture of Fracture of Fracture of Fracture of

mandible maxilla zygoma nasal bone
Facial nerve injury Parotid duct injury Injury of lacrimal

apparatus
Principles of Treatment
SS Proper cleansing of wound [to

avoid pigmented scars]
SS Accurate apposition of tissues in layers with

fine sutures.
SS Suturesideally should be removed after 3 days to prevent additional scarring, but wound must be supported with
adhesive skin tape for another 5–10 days.
Maxillofacial injuries (particularly bony injuries) are usually not life-threatening injuries except midfacial injuries
which have a potential to develop airway obstruction.
Orotracheal intubation is difficult or impossible and nasotracheal intubation is contraindicated in midfacial in-
juries.
SS Therefore surgical airway is indicated during initial resuscitation.
Examination of the Injuries
SS Face must be examined from

front.
Look for—
SS Gentle palpation, using both
SS Asymmetry, as a whole.
hands, then
SS Flattening of check (depressed
Examination of soft tissue
zygomatic fracture).
⇓
SS Nasal deviation.
Bony structures
SS Intercanthal distance > 3.5 cm –
⇓
nasoethmoidal fracture.
Intraoral examination
SS Uneven pupillary level (orbital floor
fracture).
SS Subconjunctival hemorrhage
without a posterior border (orbital
wall fracture).
SS Dental malocclusion (mandibular/
maxillary fracture).
Examination of bony structures (above downwards)
Supraorbital ridge
Infraorbital ridge
Zygoma including zygomatic arch
Nasal bridge
Maxilla
Condyle of mandible
Posterior and lower border of mandible
Then, intraoral examination with good illumination

SS Cheek
SS Tongue
SS Floor of mouth.
Then, sensory function of the face: Anesthesia suggests fracture proximally along the path of the nerve.
SS CT of face is more accurate than radiographs in determining fractures of facial bones.
Trauma 599
Fracture of Mandible
Coronoid process
Condyle (Most
SS Fracture can present in any anatomical common site)
region of mandible.
SS Different imaging techniques— Neck of condyle
zz Plain X-ray: Orthopantomogram is

Ramus
the radiograph of choice.
zz Panoramic tomography.
zz Helical CT.
SS Treatment is reduction and fixation.

Angle of mandible
Symphysis Parasymphysis
Different types of fixation
1. Interdental Eyelet Wiring 2. Transosseous wiring 3. Plating

Fracture Maxilla
Le Fort I Le Fort II Le Fort III

Complete craniofacial
dysjunction
Different types of fixation
SS Treatment is reduction and fixation.

Plating
SS Treatment is not indicated as lifesaving procedure.
If airway is clear and antibiotic therapy is
instituted, the procedure can be awaited for 24-48 Frontal suspension
hours. During this period, patient’s condition can
be improved and facial edema is subsided.
Arch bar
Intermaxillay wiring
Fracture Nasal Bone
SS Most common fracture of face.

SS Without proper reduction of fracture, asymmetry and loss of normal
contour may develop and also deviated nasal septum.
SS Reduction is usually indicated 7-10 days of injury (facial edema
is mostly subsided) and before 3 weeks (manipulation is almost
impossible).
Trauma 601
Other Injuries
Facial nerve injury Parotid duct/gland injury Lacrimal apparatus injury

SS It may happen in Le Fort
II and III type of injuries.
SS It is unwise to repair
this type of injury.
Management is better
done by an opthalmic
surgeon.
SS Clinical signs suggest that main

SS Injury of parotid gland tissue will lead to
division is involved
parotid fistula if left untreated.
SS Treatment is suturing the tissue in layers
and a compressive dressing for 48 hours.
SS If parotid duct is transected, sialogram have

SS Primary repair (microsurgical
to performed to reveal the ductal system.
nerve repair)
Then severed ends is approximated over a
fine tube using microscope.
Gland end
of duct
SS If expertise or proper instrument is not

available, then an internal fistula can be
created by suturing the gland end of the
severed duct in buccal mucosa.
Neck Injury
SS Neck contains multiple vital structures with little anatomic protection.
Penetrating injury
Evaluation of penetrating neck injuries—
Different neck injuries
Penetrating neck injuries can be analyzed based on
Blunt injury 1. Craniocaudally [neck is divided into 3 horizontal zones]
2. Anteroposteriorly.
Base of skull
Zone III
Angle of mandible
Zone II
Cricoid cartilage
Zone I
Sternal notch
Major vascular (carotid arteries, subclavian arteries, jug- Anterior triangle

ular vein, subclavian vein), major aerodigestive (larynx,
trachea, esophagus) structures, thyroid, thoracic duct – Posterior triangle
All located in the anterior triangle.
Cervical spine, spinal cord, neck musculature are all that
located in the posterior triangle.
Trauma 603
Management of Penetrating Neck Injuries
Penetrating neck wounds that have not penetrated platysma, are treated by only repair of the wound.
Zone I injury
SS Injury in this zone carries highest mortality due to presence of major vessels (proximal carotid arteries, subclavian
vessels, major vessels of chest).
SS Management of injuries in this zone
is complicated by overlying ribs,
sternum and clavicle.
In hemodynamically stable patients—
SS Angiography of great vessels
SS Contrast esophagogram
SS Esophagoscopy
SS Bronchoscopy Zone I injury

SS Thin slice CT scan of neck.
In unstable patients—
Patient should be taken directly to the Supraclavicular
incision
operation theater.
SS Exploration of such a wound will
require simultaneous access to both Median sternotomy
neck and mediastinum. So, a median incision
sternotomy is also needed.
[Surgery should be performed by an experienced vascular surgeon.]
Zone II injury
SS Injuries in this zone are clinically apparent with
significant hematoma or frank external hemorrhage. Approaches
SS Vascular control is relatively easy.
SS Stab and gunshot wounds are most commonly

situated in this zone.
SS 2 school of thoughts regarding treatment approach
Selective approach Mandatory exploration
where no suspicious clinical findings.
Selective approach
Suspicious clinical findings:
Exploration after extensive evaluation—
SS Significant external hemorrhage
SS Angiography [color flow Doppler imaging is an reliable
SS Large or expanding hematoma
and safer alternative to angiography].
SS Voice changes
SS Esophagoscopy.
SS Dysphagia
SS Esophagography.
SS Crepitus in neck.
SS Helical CT with IV contrast.
Zone III injury

SS Exposure is much more difficult.
SS Radiographic vascular imaging (carotid and vertebral angiography) is essential before surgical exploration in stable
patients.
SS Patient with evidence of vascular injury or injury to the aerodigestive tract must require surgical repair.
Neck exploration
SS Goal of neck exploration is to explore the structures of the neck.

SS In case of unilateral injury, oblique incision along the anterior border of sternocleidomastoid.
SS If bilateral exploration is necessary, modified coller-type incision along the sternocleidomastoid of both sides is
required.
[Intraoperative endoscopy is a very useful modality during surgical exploration.]
SS Management of vascular injuries—

zz Vascular injuries are common in penetrating wounds, not in blunt injuries.
zz Hemostasis is primarily maintained by digital occlusion and then proximal and distal control by vascular clamps.
zz Arterial injuries should be debrided and repaired primarily, if possible.

SS Temporary intraluminal shunt may be considered to preserve cerebral perfusion during repair.
SS Simple closure of a linear defect in common carotid or internal carotid can be simply sutured but a vein patch is
preferable to prevent stenosis.
Maintaining distal
perfusion
Simple closure
or
Temporary shunt
Double ligature Vein patch

sling with snub
Trauma 605
SS If primary repair is not possible due to loss of length, a
interposition graft should be used.
SS Injuries of the proximal internal carotid can be treated
Autologous vein
by transposition procedure. graft
or
Synthetic graft
(PTFE/Dacron)
SS Major injuries to the external carotid can be safely ligated, but the surgeon must be sure that this is not the
internal carotid artery.
In this area, external carotid has branches, internal carotid has not.
SS Subclavian artery injuries are preferably managed by primary repair, but ligation is also safe.
SS Venous injuries are best managed by ligation.
[Chance of air embolism must be kept in mind and can be prevented by lowering the patient’s head.]
SS An injured internal jugular vein can be ligated if contralateral vein is patent.
SS Major nerve injuries: Primary repair

SS Thoracic duct injury: Best managed by ligation.
Management of Airway Injuries

SS It is better to perform a formal tracheostomy below
the injury site rather than insertion of a tracheostomy
tube through the injury opening.
SS Laryngeal injuries are treated by repair of mucosal
Injury site
lacerations and repair of cartilagineous structures
through the perichondrium using synthetic absorb-
able suture.
SS Simple lacerations of trachea can be repaired by
primary repair. Trachea can be mobilized for a
sufficient length (about the breadth of two tracheal
rings).
SS Loss of large area of trachea need complex
reconstructive procedures.
Management of Esophageal Injuries

SS If injury is diagnosed within 12 hours, primary repair with drain placement is the ideal treatment
SS If injury is more than 12 hours old, cervical esophagostomy followed by complex reconstruction later.
Spinal Injury
SS Most of the spinal injuries are due to road traffic accidents and fall from height
SS A few percentage are due to gunshot injuries.
Mechanisms of injury
SS Vertical compression: Object falling on head or jumping from a height.
Burst
fracture Ligaments
intact
Stable fracture MRI of spine showing vertebral fracture
SS Hinge injury: Object falling on back or blow to the forehead.
Ligaments
Wedge disrupted
fracture Ligaments
intact
Stable fracture Unstable fracture
SS Hyperextension Injury SS Shearing injury: Fall from height or road traffic

accident.
Disrupted anterior often associated

longitudinal ligament with a rotational force
Ligaments
disrupted
Unstable fracture Unstable fracture

Trauma 607
Mechanisms of cord injury
Cord compression by Rotational injury causing Intervertebral fragments compressing

bony fragments stretch injury of cord spinal cord or anterior spinal artery
Suspect spinal injury in every injured patient.

High index of suspicion when:
SS Major trauma
SS Minor trauma with neurological symptoms
SS Injury in RTA, fall from height or diving injuries
SS If preexisting spinal diseases like rheumatoid arthritis, osteoporosis, ankylosing spondylitis are present.
Initial management of spinal injury
SS Spinal immobilization: Initially manual

immobilization by keeping the head and neck of
the patient in neutral position and then:
SS Airway: Fiberoptic intubation is preferred because

less manipulation is required.
Patient with injuries above C3 are often completely
apneic: Early intubation at the site of injury is
necessary.
Forearms preventing Both hands around the neck
High cervical spine injuries can cause ventilatory decom- head movement interlocking them behind
pensation due to loss of phrenic nerve function (C3–C5)
and intercostal muscle function (thoracic root).
SS Circulation: No significant blood loss/perfusion is not Suspect cervical spinal injury, if:
improving after adequate fluid infusion SS Flaccid areflexia
⇓ SS Ability to flex but not to extend the elbow
Think of, spinal shock SS Hypotension with bradycardia
⇓ SS Diaphragmatic breathing
Vasopressor (e.g. dopamine) + Controlled fluid infusion SS Painless urinary retention
Excessive fluid administration can compromise respira- SS Priapism
tory function and increases spinal cord edema. SS ↓ anal tone
Examination of the patient
SS Examination of spine
SS Neurological examination.
1. Examination of the spine:

SS Tenderness.
SS Step-deformity.
SS Widening of interspinous
spaces.
SS Prominence of spinous
processes.
Log roll the patient
Neck is manually
stabilized
2. Neurological examination:
Motor function of all Sensory function of all Assessment of low spinal cord reflexes
major nerve roots major nerve roots
SS Muscle strength is SS Sensation is assessed SS Anal sphincter tone.
measured using 0–5 by pin prick and light SS Anal cutaneous reflex (anal sphincter contraction in
grading system. touch. response to scratching the perianal skin)
SS Bulbocavernosus reflex (contraction of bulbocavernosus
muscle in response to squeezing the glans penis).
The most caudal location which has intact (normal) motor and sensory function must be recorded.
Bulbocavernosus reflex is absent—Patient is in spinal shock.
Once the reflexes have returned (after few days or weeks), then the neurological examination can elicit the true extent
of cord injury.
2 Patterns of spinal cord injury
Complete injury Incomplete injury

SS No motor or sensory function below the level of injury. SS Some motor or sensory function below the level of
SS Very little hope of recovery. injury.

SS Restoration of spinal canal anatomy and SS Most of the patients will improve with time.
decompression of spinal cord do not improve the SS Restoration of spinal canal anatomy and decompres-
outcome. sion of spinal cord may lead to improved outcome.
Trauma 609
Different patterns of incomplete spinal cord injury
Anterior cord Brown-Séquard Central cord Cauda equina

syndrome syndrome syndrome syndrome
Anterior cord syndrome
SS Often related to injury of anterior spinal artery.

SS Damage of spinothalamic tract and corticospinal Corticospinal
tract
tract.
SS Dorsal column is intact.
SS Preservation of touch and position sense.
Lateral Anterior
spinothalamic tract spinal artery
Brown-Séquard syndrome
One side of Ipsilateral motor

the midline weakness and loss
is involved of proprioception
Contralateral loss
of pain perception
Motor tracts cross over at the level of the brainstem,
whereas sensory tracts cross near the level of the spinal
root.
Central cord syndrome
SS Typically seen in elderly patients following extension

injuries to neck.
⇓
SS Blood flow in spinal arteries is interfered.
SS Proximal muscles of the upper extremity and function

of lower extremity are preserved.
SS In most cases, no radiologically identifiable fracture of Hypoperfusion of the
cord at watershed line
spine. (central part of the cord)
Cauda equina syndrome
SS Lossof motor and sensory control of bladder

SS Impotence and fecal incontinence may develop
SS Sensory deficits develop over the ‘saddle’ area.
Bony dislocation causing compression

of lumbosacral roots below the
conus medullaris
Evaluation
SS X-ray
SS CT scan
SS MRI.
Standard views for cervical spine

SS Anteroposterior view SS Lateral view—Most informative SS Open-mouth view (odontoid)
? Widening of
? Soft tissue swelling spinous process
in pre and para
vertebral region
? Any malalignment of
posterior or anterior
margins of vertebra
Other views for cervical spine

SS Swimmer’s view: To visualize C7 and C7–T1 junction
SS Oblique view: To demonstrate facet fractures or dislocations.
Flexion/Extension view: To assess neck stability (should be done under expert supervision).
Trauma 611
Standard views for thoracolumbar spine: When CT scan is indicated?
SS Anteroposterior view SS Cervical fracture is identified/X-ray findings are
SS Lateral view. equivocal.

If vertebral fracture is found in any region, the entire zz CT provides superior visualization of the bone
spine should be imaged. spine and paraspinal soft tissues.

zz 3D reconstruction is also possible from helical
CT image.
SS MRI is sensitive for ligamentous injuries, intraspinal
hemorrhage, disk prolapse.
Management of spinal cord injury

1. Supportive management
SS Patient with upper cervical cord injuries depends primarily on diaphragmatic activity for breathing, so ultimately
patient becomes fatigued and require mechanical ventilation.
Because of loss of sympathetic tone, BP is usually low causing secondary injury. A mean BP of 85–90 mmHg should be
maintained for first 7 days after injury to ensure adequate perfusion of the injured cord.
2. Medical management
}
SS Intravenousmethylprednisolone—
zz 30 mg/kg – Bolus dose (for 1 hour)
If cord injury is recognized within 8 hours,
⇓
better if within 3 hours
zz 5.4 mg/kg/hr – Maintenance dose (for next 23 hours)
zz Same dose — Should be continued for total 48 hours

(5.4 mg/kg/hr)
} If more than 3 hours but less than 8
hours.
3. Surgical management
SS Ifneurological function in incomplete cord injury is progressively deteriorating, operative decompression is

indicated.
SS Surgery is indicated for—
zz Decompression
zz Stability—
Initial immobilization by — Halo brace, Gardner-Wells tongs for cervical spine
Moulded jacket for thoracic and lumbar spine
Definite stability by spinal fusion with metal plates, rods or bone fusion.
4. Rehabilitation
SS Skin care
zz Two hourly turning prevent bedsores
zz Use of air or water bed.
SS Patient should be trained for intermittent self-catheterization
SS Physiotherapy (to prevent flexion contracture)
SS Patient with high risk of DVT require prophylaxis with LMW heparin and/or pneumatic compression stockings
SS Patient education of daily living and job retraining
SS Emotional support.
Prognosis
SS Injury above C3 require immediate ventilatory support. [at the place of injury]
SS Injury above C7 usually dependant on others
SS Sparing of C7 segment provides a degree of independence
SS Injury in thoraco-lumbar region regains full degree of independence overtime.
Thoracic Trauma
Rib Fracture
SS Most common injury following blunt chest trauma

SS Ribs (4 – 10) are more prone to fracture.
Types of rib fracture:

zz Isolated rib fracture
zz Multiple rib fracture
zz Rib fracture with flail segment
zz First rib fracture.

Trauma 613
First rib fracture

• Think of underlying significant chest injury
(associated injuries to brain, heart great
vessels, upper abdominal viscera may
be present)
• Contrast enhanced thoracic
CT – to rule out injuries
• Rule out pneumothorax
Fracture ribs (8th to 12th)

• Think of injury to liver, spleen
and kidneys
SS Uncomplicated fractures need adequate analgesia to prevent complications like atelectasis and pneumonia
SS Epidural analgesia may be indicated for multiple or bilateral fractures.
[Strapping the chest wall with adhesive tape or use of elastic bandage — is contraindicated, because it interferes with
adequate ventilation].
SS Flail chest—Previously described.
Sternal Fracture
SS Due to deceleration — impact with steering wheel or seat belt.

SS Patient complains of chest pain particularly over the sternum and crepitus
is often found.
SS CXR and lateral sternal X-ray are necessary for confirmation of fracture.
[Usually transverse fracture is found in sternum].
[Suspect underlying myocardial contusion, myocardial rupture, esopha-
geal perforation, tracheobronchial injuries.]
SS Constant ECG monitoring, serial cardiac enzyme estimation is indicated.
SS Other underlying injuries need to be excluded with proper investigations.
SS For stable fracture, analgesia is the treatment.
SS For unstable chest wall and debilitating chest pain, open reduction and
internal fixation is indicated.
Pneumothorax
Pneumothorax (air in the pleural cavity)
Simple pneumothorax Tension pneumothorax Open pneumothorax
Simple pneumothorax
Air from an injured lung or airway is

trapped within the pleural cavity and
increases the intrapleural pressure
Lung parenchymal injury due to

Rib fractures penetrating lung parenchyma sudden pressure change
On Examination
Chest X-ray is indicated to confirm the diagnosis.
SS Diminished breath sound on affected side Typical chest X-ray features:
SS Visible lung edge with absent lung markings
SS Percussion note is hyperresonant
beyond.
SS Decreased chest expansion of affected side.
SS Deep sulcus sign (hemidiaphragm on the affected
side is deeper in the midline than expected).
Treatment
All traumatic pneumothorax must be drained through tube thoracostomy because of the possibility of conversion to
tension pneumothorax, a life-threatening condition.
Trauma 615
Tension pneumothorax
Previously discussed.
Open pneumothorax
Previously discussed.
Hemothorax
Blood in the pleural cavity.
On Examination
SS Diminished breath sound on the affected side
SS Percussion note is dull.
Blood in the pleural cavity
Chest X-ray (in erect posture) is diagnostic. Obliteration of costophrenic angle or blurring of the hemidiaphragm
contour is the characteristics chest X-ray finding.
Chest X-ray (in supine posture) Diffuse haziness or none at all. [It is also difficult to differentiate between hemothorax
and pulmonary contusion in supine film.]
SS Massive hemothorax (more than 1500 ml of blood in single pleural space).
zz Resulting hypovolemic shock and hypoxia
zz In most of the cases, tube thoracostomy is the treatment. (Wide bore tube > 28 Fr)
zz Additional basal drain is sometimes necessary.
zz Urgent thoracotomy is indicated if—
After tube insertion, > 1.5 liter of blood is drained
> 200 ml/hr drainage for 6 hours.

Chest Drain
SS Important anatomical landmarks
Level of 2nd rib

(rib counting from
this landmark)
Lateral border of pectoralis major
Anterior border of
latissimus dorsi
Midaxillary 5th 5th intercostal 6th

line rib space rib
SS How chest drain helps—

zz Prevents development of tension pneumothorax from simple pneumothorax
zz Allows reexpansion of the lung-expanded lung compresses the injured vessels and reduces further blood loss
zz Allows the mediastinal structures to return to the midline and relieve compression of contralateral lung
zz Prevents further development empyema thoracis.
SS Technique of chest drain insertion—
zz Skin is cleaned with bactericidal solution (povidoneiodine) solution and covered with sterile drapes.
zz Skin, soft tissue and intercostal muscle at the site of insertion is infiltrated with local anesthetic (about 10 ml of
1% lignocaine).
zz A 2–3 cm transverse incision is made in the 5th intercostal space, along the midaxillary line, close to upper
border of the lower rib.
6th rib
Incision over the 5th

5th rib intercostal space
Trauma 617
5th rib This approach prevents chance of damage of neurovas-

cular bundle.
Neurovascular
bundle
6th rib
Using a large curved hemostat, the soft tissue is dissect-

ed, parietal pleura is punctured.
Finger is introduced into the pleural space to ensure

that pleural cavity has been entered and no viscera is
adhered to the chest wall.
Chest drain tube of > 28 Fr is inserted

using the hemostat and is directed su-
periorly and posteriorly.
Ensure that all the drainage

holes are within the pleural
cavity
Chest drain is secured

with a silk suture with the skin
Tube is connected with
Water-deal drainage bag
Ensure that
the drainage bag Check that the fluid meniscus
is below the level is swinging in the tube with
of the patient inspiration and expiration
Chest X-ray is done to confirm proper placement of chest drain tube.
Pulmonary Parenchymal Injury
SS Associated with both blunt and penetrating thoracic trauma.

SS In patient with flail chest, pulmonary parenchymal injury must be ruled out because about 2/3rd of patients have
parenchymal injury.
SS Many of these patients are associated with pneumothorax and hemothorax.
SS These patients have adequate perfusion but ↓ ventilation. This ventilation-perfusion mismatch results in severe
hypoxemia.
Trauma 619
On examination
zz Copious thin, blood tinged secretions
zz Chest pain
zz Labored respiration
zz Restlessness
zz Dyspnea, tachypnea, cyanosis and

Entry wound Exit wound
tachycardia.
SS Chest X-ray in initial stage appears as
patchy opacifications. It becomes more
prominent with time
zz Progress to diffuse opacification Tractotomy
[suggestive of acute respiratory
distress syndrome].
SS Tube thoracostomy is indicated for drainage of air and blood and for monitoring of continuous air leakage.
SS Severe contusions often require intubation and mechanical ventilatory support.
SS Laceration with persistent air leak may require exploration by thoracotomy, followed by:
zz Over sewing or stapling of wound
zz Wedge/lobar resection
zz Tractotomy—Opening up the missile trajectomy.
Tracheobronchial Injuries
SS Blunt injuries of the airway are due to compression of the airway between the sternum and the vertebral column in
high velocity RTA. About 80% of injuries are located within 2–5 cm from the carina.
SS Penetrating injuries may occur at any location.
SS Patient present with pneumothorax, pneumomediastinum, hemoptysis, massive subcutaneous emphysema.
[Suspect major airway injury when continuing bubbling of gas through the water-seal chest drain or lung fails to re-
expand after chest drain insertion.]
SS Upper tracheal injuries require median sternotomy.
SS Distal tracheal or right bronchial injuries are approached through right thoracotomy. Left bronchial injuries are
approached via left thoracotomy.
SS In most of the cases, debridement followed by primary repair is indicated. Complex reconstructive procedures are
rarely needed.
Tracheal
injury
Right Left
bronchial bronchial
injury injury
Cardiac Injury
Injuries to pericardium
and heart
Due to blunt trauma Due to penetrating trauma
Blunt cardiac injury (BCI)
Blunt cardiac injury should be suspected in all patients of high velocity RTA with chest trauma.
SS Injuries vary from myocardial contusion to rupture of cardiac chamber or valves.
SS Right ventricle is most frequently involved chamber due to its close proximity to the sternum.
SS Patients may present with varying presentations from unexplained sinus tachycardia to cardiogenic shock.
SS ECG is the primary investigation (a normal ECG excludes significant BCI.)
SS ECG abnormality (sinus tachycardia, ST changes, T wave changes, supraventricular and ventricular arrhythmias,
RBBB) warrants for continuous ECG monitoring for 24 hours.
SS In unstable patient, transthoracic echocardiogram should be performed to rule out valvular or myocardial rupture.
[Cardiae enzymes have no specific role in diagnosis.]

SS Arrhythmias are treated according to the protocol.
SS Patient with frank myocardial or valvular rupture require immediate operative repair.
Penetrating cardiac injury
Level of clavicle
Midclavicular line
Penetrating injuries in this area
Suspect cardiac injury unless

proved otherwise
Level of costal margins

Trauma 621
SS Suspect pericardial tamponade if present with
(1) muffled heart sound (2) distended neck vein
(3) shock – Beck’s triad.
SS Tension pneumothorax must be excluded.
SS Stable patient must undergo echocardiography

(transesophageal).
SS Hemodynamically unstable patients should be taken
to operating room for emergency thoracotomy.
SS The operative approach is via median sternotomy.
SS Atrial and ventricular wounds are repaired with Closure of wound

monofilament sutures. using buttressed
sutures and avoiding
SS Care must be taken to avoid injury to coronary coronary vessels
arteries.
Pericardial tamponade
SS Blood from injured great vessel, cardiac chamber,

coronary or pericardial vesel accumulated in the
pericardial sac and restricts diastolic filling.
SS Patient present with Beck’s triad, pulsus paradoxus,
Kussmaul’s sign.
Normal atrial filling and

normal right ventricular
preload
Normal heart
Right atrial filling

is impaired
Pressure in pericardial sac

>Right atrial pressure
Reduced right ventricular preload
Pericardial tamponade
SS FAST using the subxiphoid or parasternal view is helpful for diagnosis.

SS Emergency pericardiocentesis improves the pa-

tient’s hemodynamic status immediately.
SS Then,emergency thoracotomy via left anterolateral

approach
Pigtail catheter in
pericardial sac
45º
Evacuation of pericar- Temporary control of

dial sac cardiac injury Repeated aspiration of blood
Definite repair
Great Vessel Injury

Great vessel injury
In blunt trauma
SS The descending thoracic aorta just below the origin of the

left subclavian artery is the vulnerable area of the aorta
for rupture in deceleration injury, as it is tethered by the
ligamentum arteriosum.
SS Complete transection causes immediate death, only patient
with partial disruption may arrive trauma center.
SS In erect chest X-ray, findings like widened mediastinum,
obscured aortic knob, opacification of aortopulmonary
window, warrants further investigation.
SS Helical CT is the investigation of choice. If interpretation is
inconclusive, then four vessel arteriography is indicated.
SS The injury is repaired (primary anastomosis or prosthetic
interposition graft) via left anterolateral thoracotomy.
Shunt is maintaining the distal
perfusion during repair of
descending thoracic aorta
Trauma 623
In penetrating trauma
SS In stable patients, aortography, endoscopy, contrast swallow study, echocardiography and helical CT – for complete
evaluation.
SS In unstable patient, urgent thoracotomy is indicated.
SS Operative approach depends on the vessel injured (median sternotomy/left anterolateral thoracotomy).
SS Primary repair should be performed for aortic and vena caval injuries.
SS Brachiocephalic and innominate venous injuries can be ligated.
Esophageal Injuries
SS Most of the injuries are due to penetrating, rarely due to blunt trauma (esophagus is well-protected in the posterior
mediastinum).
[All transmediastinal gunshot wounds or stab wounds near the posterior midline should be evaluated to exclude es-
ophageal injury.]
SS These injuries warrant early recognition as delay in diagnosis increases the morbidity and mortality.
SS Esophagoscopy and gastrograffin swallow study can detect all injuries.
SS Operative approach is determined by the location of injury. Type of surgical approach is determined by the age of
injury.
SS Right thoracotomy is the best approach for thoracic esophagus. Left thoracotomy is a better option for distal
esophagus.
SS If injury is recognized within 24 hours, debridement, primary repair (buttressed with a vascularized flap, e.g.
pleural or pericardial or fundoplication) and drain placement (near the repair) is the treatment.
SS If after 24 hours, then cervical esophagostomy and distal feeding access.
Diaphragmatic Injuries
SS Often caused by penetrating injuries
[Think of diaphragmatic injury, if entry wound is below
the nipple and above the costal margins.]
SS In most of the time, diagnosis is made during
celiotomy. Chest X-ray or CT sometimes diagnose
this injury.
SS After blunt trauma, left-sided injuries are more
common. Patient presented with respiratory distress
after severe blow to the abdomen. Herniated stomach
SS Chest X-ray demonstrates visceral herniation (in right through diaphragmatic
injuries
liver and in left stomach and colon).
SS Injuries are repaired with synthetic monofilament
sutures (interrupted horizontal mattress).
SS Larger defects require the use of prosthetic material.
SS Care should be taken in the central tendon area

during repair to avoid inadvertent cardiac injury.
Repair (Interrupted
horizontal mattress)
Abdominal Injuries Abdominal Trauma
SS Noncompliant organs (liver spleen, pancreas, SS Smallbowel is in most risk because of its larger
kidneys are at greater risk). volume in abdomen.
SS Due to rapid deceleration.
SS Pancreas, mesentery, intestine are at greater risk.
SS Due to use of seat belt (compression against
vertebral column).
Approach to the patient
SS Is it penetrating trauma or blunt trauma? 4th intercostal

SS If penetrating trauma, is it gunshot (GSW) wound space
or stab wound?
SS If gunshot wound, is it anterior truncal GSW or
GSW to the back and flank?
zz Entry/exit wound in anterior truncal zone
suggests peritoneal penetration.
zz Should proceed for immediate exploratory
Anterior trunk
laparotomy.
zz Chance of injury > 90%.
Pubic symphysis
Trauma 625
Area between anterior and

posterior axillary line from 6th
intercostal space to iliac crest Level at the tip of scapula
Area posterior to posterior

Back axillary line from tip of scapula
Flank to iliac crest
Level at the iliac crest

Posterior axillary line
GSW in back of flank
SS ? Conservative
SS ? Laparotomy
SS If any doubt, laparotomy is desirable
SS If shock or peritonitis, then urgent laparotomy.
Stab wound (patient stable)
SS Inlower chest—
zz Wound is explored to find any diaphragmatic penetration
zz Any diaphragmatic penetration is an indication for laparotomy.
� In anterior and lateral

trunk—
� Wound exploration ↓ LA t o
determine whether perito-
neum is breached or not.
� If peritoneum breached
� Laparotomy.
� If Peritoneum not breached
� No further evaluation or intervention.
SS Inflank or back — evaluation is difficult.

zz Triple contrast CT is helpful to detect occult retroperitoneal injuries of colon, duodenum and urinary tract.
zz Soluble contrast X-ray of duodenum and colon is particularly helpful for enteric injuries.
Blunt trauma ? then assess –
Hemodynamically stable ? Hemodynamically unstable ?
FAST Evaluation by USG in the resuscitation

room without interfering resuscitation
No fluid in peritoneum Fluid in peritoneum CT not available
Repeat USG CECT abdomen Chest X-ray X-ray abdomen Contrast study of GI
and genitourinary tract
No fluid Search for –

• Air in peritoneal cavity or retroperitoneum
• Ruptured hemidiaphragm Proceed for laparotomy
• Grade IV and V injury of liver, spleen, kidney
No need of CT • Contrast extravasation
Trauma assessment
Assessment of trauma
FAST
Diagnostic peritoneal lavage Abdominal CT Plain radiograph
(Focused abdominal sonography for trauma)
FAST [Focused Abdominal Sonography for Trauma]
SS The ideal modality for immediate evaluation of blunt trauma

abdomen.
SS Goal of FAST examination is the detection of abnormal collections
of intraperitoneal fluid, not to identify or stage solid organ injury or
hollow viscus injury.
SS Primary focus is on the peritoneal cavity. Subxiphoid
SS Abdomen is examined through four sonographic windows–
RUQ LUQ
subxiphoid, RUQ, LUQ, pelvis.
SS FAST helps to detect which cavity have to be opened first in
(3.5–5 MHZ)
thoracoabdominal injuries. Pelvis
SS FAST can identify pericardial fluid also and helps to diagnose
hemopneumothorax.
SS Most surgeon recommend initial scan in RUQ as more than half of
the positive FAST examination will reveal fluid in this area.
SS Unstable patient + Positive FAST ⇒ Urgent exploratory laparotomy
Trauma 627
Diagnostic peritoneal lavage
SS Itis useful when USG or CT is not available

SS Two techniques—
zz Closed technique—using Seldinger method
zz Open technique.
Catheter is introduced
under direct vision
Direction is towards the pelvis
Infraumbilical
incision
1 liter of NS
< 10 ml is
aspirated If 10 ml free blood is aspirated
Proceed to laparotomy
≥ 100,000 RBC/µl
• Lavage fluid is allowed to drain by ≥ 500 WBC/µl Considered positive
gravity Amylase ≥ 175 unit/dl
• At least 200 ml of lavage fluid is sent for
Presence of bile
cell count (RBC and WBC), amylase,
Presence of food Proceed to laparotomy
particulate matter (bile and food particle) Particles (microscopic)
Abdominal CT
SS Itis indicated to evaluate a stable patient with blunt trauma abdomen.

SS Can detect solid organ injury and as well as grading of injury — which is useful for decision making regarding
nonoperative management.
SS Very much useful for detecting retroperitoneal injuries, but is not so reliable regarding diagnosis of hollow viscus
injury.
SS Presence of free fluid in abdomen without solid organ injury—
zz Think of mesenteric/intestinal/bladder injury ⇒ exploratory laparotomy is warranted.
SS Contrast extravasation in CT with even minor hepatic/splenic injuries ⇒ proceed for laparotomy
[Multislice spiral CT is helpful regarding nonoperative management of stab wound in anterior abdomen.]
Plain radiography
SS Chest X-ray is useful to reveal pneumoperitoneum, abdominal visceras in chest (ruptured hemidiaphragm), lower
rib fractures (increased chance of splenic/hepatic injury).
Management of specific injuries

1. Abdominal wall injuries
SS Often lacerated wound is present in blunt trauma. Early debridement is indicated to avoid complication like
necrotizing fasciitis.
SS Irrigation and debridement of entry and exit wound is necessary to remove foreign bodies, necrotic tissues.
SS Large abdominal wall defects require prosthetic material (e.g. polypropylene mesh) or myocutaneous flap.
2. Stomach injuries
SS More commonly due to penetrating trauma

SS Injuriesdue to blunt trauma is rare due to partial protection by rib cage.
SS Suspect gastric injury if—
zz Penetrating injury in upper abdomen
zz Ryle’s tube aspirate contains blood.
SS During intraoperative evaluation, through search for injury in following sites:
Esophagogastric junction
Posterior fundus – Chance of missed

injury is high
Lesser curvature
within the mesentery Posterior gastric wall
(Opening the gastrocolic ligament)
Chance of missed
injury is high
Trauma 629
Stomach must be clamped at the pylorus and inflated with air or methylene blue-colored saline. Any extravasation of
bluish fluid suggests injury.
Extravasation
of methylene blue
(Injury in posterior
fundus)
SS Penetrating wounds are managed by debridement of wound edges and primary closure in layers (2 layers)
SS Injuries in both nerve of Latarjet or both vagi must be treated with a drainage procedure
SS If distal antrum or pylorus is injured, then Billroth I/II procedure
SS If there is major tissue loss – Gastric resection followed by reconstruction.
3. Gallbladder and extrahepatic bile duct injury
Suturing with absorbable suture

(to prevent stone formation)
OR
Gallbladder injury
Cholecystectomy
T-tube insertion followed

by repair of wound with
4–0/5–0 absorbable suture
CBD injury with minimal loss

of tissue
Roux-en-Y
choledochojejunostomy
Complete craniofacial
dysjunction
CBD is transected or significant

tissue loss
Intubate the duct

for external drainage
Injury of hepatic duct
Injury of extrahepatic bile duct— management is challenging because—

SS Associated injury of adjacent structures (portal vein, hepatic artery and vena cava) are often present
SS Ducts are of normal size and normal wall thickness— So repair or anastomosis is difficult.
4. Duodenal injuries
SS Duodenal hematoma
SS Duodenal perforation
Why most often duodenal injuries are missed?
zz Often within the retroperitoneum
zz Duodenal contents are neutral pH, so clinical presentations are not obvious initially
zz Less bacterial load in duodenum, so in initial stage, peritonitis do not develop.
Duodenal hematoma
SS Intramural hematoma can be diagnosed with CT or upper GI gastrograffin study (coiled spring or stocked coin
sign).
SS Treatment is prolonged nasogastric decompression and nutritional support (either TPN or enteral nutrition distal
to the injury).
SS If patient not responding to conservative management (obstruction not resolving) or CT shows persisting
hematoma, even after 2 weeks; surgical intervention is indicated.
631 Illustrated Surgery—A Road Map Trauma 631
Duodenal perforation
SS Retroperitoneal air outlining the C-loop of the duodenum in right upper quadrant in X-ray abdomen
zz Diagnostic of duodenal perforation.
SS Other findings in X-ray abdomen—
zz Obliteration of right psoas shadow
zz Mild scoliosis
zz Absence of air in duodenal bulb.
SS CT with oral and IV contrast or gastrograffin study of upper GI series – For definitive diagnosis.
Suspect duodenal injury peroperatively, if

SS Retroperitoneal crepitus is present
SS Retroperitoneal bile staining
SS Retroperitoneal hematoma—think of associated pancreatic injury also.
Bile staining in the triangle formed

by colon and duodernum
SS Grading of duodenal injury – essential because it determines the type of surgical intervention needed.
SS Grade I—
zz Hematoma — In single part of duodenum
zz Laceration — Partial thickness, no perforation.
SS Grade II—
zz Hematoma — In more than one part of duodenum
zz Laceration — Disruption < 50% of the circumference.

Management of Grade I and II injuries are same, but consider, whether injury is diagnosed > or < 6 hours after
> 6 hrs
Primary repair
Duodenal decompression by tube jejunostomy

< 6 hrs (To decrease the chance of anastomotic leakage)
Primary
repair
only
SS Grade III—
zz Laceration – Disruption of 50–75% circumference of D2
zz Disruption of 50–100% circumferenc of D1, D3, D4.
Management is challenging!
If possible, debridement with primary repair must be performed. The repair should be protected by a diversion proce-
dure. Pyloric exclusion with gastrojejunostomy is the preferred method for diversion.
Pyloric exclusion
procedure
Gastrostomy is made on
the greater curvature as
close to pylorus as possible
Contd...
Trauma 633
Contd...
Pylorus is grasped through

the gastrostomy
Debridement followed by Pyloric muscle ring is closed with

primary repair of the injury continuous suture with 1 polypropylene
Other diversion methods

SS Duodenal diverticulization [truncal
vagotomy + antrectomy + gastroje-
junostomy]
SS Triple tube drainage [tube gastros-
tomy + retrograde tube duodenos-

tomy + antegrade jejunostomy]. Pyloric exclusion
Gastrojejunostomy
Feeding jejunostomy
Primary repair
SS Grade
IV Injuries – Laceration – Disruption > 75% of circumference of D2 and involving ampulla/CBD
Management is more challenging!
Repair of CBD over a
T-tube with long transpapillary limb
Primary repair
of duodenum
Or
Biliary enteric
anastomosis
Ligation of
injured CBD
Primary repair
of duodenum
If duodenal injuries with tissue loss is distal to the papilla of Vater and proximal to the superior mesenteric vessels—
It is best managed by Roux-en-Y duodenojejunostomy.
SS Grade V injuries – Pancreaticoduodenectomy

is the only option. In a trauma setting, the
morbidity and mortality of this procedure is
high.
SS In a trauma setting, the morbidity and
mortality of this procedure is high.
Distal jejunum is sutured Distal duodenum

to proximal duodenum
(Roux-en-Y duodenojejunostomy)
Proximal jejunum
Distal jejunum
5. Pancreatic injuries
SS Rare and accounts for about 10–20% of all abdominal injuries.

SS Most of the injuries are due to penetrating trauma.
SS Direct blow or seat belt injury may cause pancreatic disruption due to compression of pancreas against vertebral
column.
SS Major vascular injuries and/or solid organ injuries are usually associated with pancreatic injury. Concominant
duodenal-pancreatic injuries also common.
SS Because of its retropancreatic location, the symptoms and signs usually appear lately.
SS CT is the best imaging modality.
SS Persistent hyperamylasemia in trauma setting is highly suggestive of pancreatic injuries.
SS Upper GI gastrograffin study – ‘Widening of duodenal C loop’ finding is highly suggestive.

Trauma 635
SS Management is determined by—
zz Location of injury
zz Main pancreatic duct is injured or not.
SS So, assess—
zz Which part of pancreas is injured
zz Whether main pancreatic duct is injured or not.
SS For these assessments—
zz Intraoperative inspection is the best method
SS For intraoperative inspection—
zz Adequate exploration of the pancreas is necessary.
SS For adequate exploration—

zz Proper maneuvers are necessary:
Kocher maneuver
– To inspect the
head of pancreas
Division of retroperitoneal attachment
along the inferior border of pancreas
– To inspect the posterior aspect of
pancreas
Transection of gastrohepatic and gastrocolic ligament

– To inspect the body and tail of pancreas
SS Now, grade the injury – then, surgical option according to grade:

Grade I – Hematoma – Minor contusion without duct injury
Laceration – Superficial laceration without duct injury
Grade II – Hematoma – Major contusion without duct injury or tissue loss
Laceration – Major laceration without duct injury or tissue loss
For Grade I and II injuries, debridement with drain placement is (closed suction drain) sufficient.
Grade III Laceration— Distal (left of the superior mesenteric vessels) transection or parenchymal injury with duct in-
jury.
Transection with duct injury
Superior
mesenteric vessels
Treatment is distal
pancreatectomy
Grade IV – Laceration – Proximal (right of the superior mesenteric vessels) transection or parenchymal injury involving
the ampulla.
Closure of proximal pancreas
Roux-en-Y pancreaticojejunostomy
Trauma 637
Grade V — Laceration – Massive disruption of pancreatic head.
Pancreatico
duodenectomy
Very high morbidity
Drain and mortality
Damage control surgery should be

the ideal option
6. Small bowel injuries

Small bowel injuries
Due to penetrating trauma

Due to blunt trauma (small bowel is the most common
organ injured after penetrating trauma)
Deceleration injury
Crush injury Closed loop rupture
(deceleration shearing at the
(between vertebral bodies and (due to sudden increase of
fixed point, e.g. ligament of Treitz,
steering wheel) intraabdominal pressure)
ileocecal valve)
SS Presence of seat belt sign – suspect small intestinal and mesenteric injuries.
SS Blunt trauma patients with signs of peritoneal irritation must be explored.
SS All gunshot injuries must be explored.
SS Stab injuries with peritoneal breach must be explored.
SS Blunt trauma without clear indication of surgical exploration–
Small intestinal injuries is ruled out by—

zz Plain X-ray of abdomen — It may reveal free gas under diaphragm, but not in all injuries.
zz CT abdomen with oral and IV contrast (significant false-negativity should be kept in mind).
zz DPL— where CT facility is not available.
On exploration of abdomen
SS Carefulexamination of the entire small intestine (from ligament of Treitz to ileocecal junction).
SS All mesenteric hematomas (adjacent to mesentery-intestinal junction must be explored because of possibility of
small bowel injuries.
Wound of intestine must be debrided to get freshly bleeding tissues.
Mesenteric hematomas
(adjacent to mesentery-intestinal
junction) must be explored
Debridement of wound Trauma causing perforation

in small intestine
Small tears are managed by primary repair
If two adjacent perforated injuries are present,
Injuries can be connected Closure in transverse direction

Trauma 639
Extensive laceration, multiple laceration in a short segment, devascularized segment — if present.
Resection of injured segment End-to-end anastomosis
7. Colon injuries
SS Due to blunt trauma (rare)

SS Due to penetrating trauma
SS Gunshot injuries in anterior abdomen must be explored, so workup for detecting any colonic injuries is unnecessary
SS Stab wound in back and flank – DPL or triple contrast (oral, IV and rectal) CT scan is necessary.
3 methods of treating
colonic injuries
1. Primary repair 2. Colostomy 3. Exteriorized repair
Primary suturing of Resection of injured colon and

perforation then reconstruction [ileocolic/
colocolic anastomosis]
SS Primary Repair: Is the method of choice when—

zz Early diagnosis (4–6 hours)
zz Patient not in shock
zz Absence of gross contamination of peritoneal cavity
zz Absence of colonic vascular injury
zz Blood transfusion < 6 units.

Resection of injured colon
OR
Suturing of perforation
Reconstruction
(colocolic anastomosis)
SS Colostomy: Where primary repair is not considered as safe and effective.
Complete or almost
complete transection
of colon
OR
End colostomy
Mucous fistula
Injured colon can be Proximal colon is delivered as end

exteriorized as a loop colostomy colostomy and distal colon as mucous fistula
Trauma 641
SS Exteriorized repair: No longer performed nowadays.
Suspending a repaired If no leakage after 10 days,

perforation on the abdominal it can be returned to the
wall with an appliance abdominal cavity
SS Loop colostomy proximal to a repair (suturing/anastomosis) does not protect the suture line.
SS Systemic factors are more important than local factors in determining whether a suture line will heal or not.
8. Rectal injuries
SS Most of the rectal injuries are penetrating injuries, particularly from gunshot wounds.
SS Transpelvic gunshot wounds, penetrating injury to the lower abdomen and buttock—Suspect rectal injury.
SS Then,
zz Digital rectal examination [presence of blood is suggestive of rectal injury.]
zz Proctoscopy and rigid proctosigmoidoscopy [hematoma, contusion, gross blood is indicative of rectal injury].
SS If diagnosis in doubt, soluble contrast enema.

SS If still in doubt, then patient should be treated as they do have an injury.
SS Rectal injuries may be:

zz Intraperitoneal
zz Extraperitoneal.
Management of intraperitoneal rectal injury
Usually treated by primary closure and a diverting colostomy
Intraperitoneal injury
Diverting colostomy
(Properly constructed loop colostomy)
Primary closure
If intraperitoneal injuries are so extensive, that primary repair is not feasible, then–
Proximal end is
delivered as end
colostomy
Division of rectum at the level of injury Distal end is closed
Management of extraperitoneal rectal injury
Access to extraperitoneal injuries are very difficult.

SS Consider 3 'Ds‘ when treating extraperitoneal Diverting sigmoid
loop colostomy
injuries–
1. Diversion:
Properly constructed
loop colostomy can
Extraperitoneal provide total fecal
injury diversion
Trauma 643
2. Drainage: Presacral drain (Penrose/closed suction) prevents fecal contamination of perirectal space.
Presacral drain
Drain is placed through the perineum into the retrorectal space.
3. Distal washout: Washout of distal rectal stump decreases the incidence of pelvic abscess, rectal fistula and sepsis.
Anus should be mechanically dilated Irrigation fluid should be isotonic
9. Liver injuries
SS Due to blunt trauma

SS Due to penetrating trauma.
Management of blunt trauma liver
Assess
Patient stable? Patient unstable?
CT abdomen with IV and oral contrast (oral contrast

Operative exploration and control of hemorrhage
to rule out concomitant hollow visus injury)
Site of injury (liver/

and Grading of injury (I – V) Grade IV and V
spleen/ kidneys
Laparotomy
CT grade I – III in liver injuries warrant nonoperative

management
Should be admitted in ICU
Close monitoring is
essential for at least
48 hours
Serial hematocrit
Close hemodynamic monitoring
Patient unstable? Patient stable? +↓ Hematocrit decreasing

Stable hematocrit
Operative intervention Continue monitoring

Continue monitoring
Always keep in mind the possible complications (biliary
leak, abscess, pseudoaneurysm, delayed hemorrhage)
Nonoperative management is successful in most of Think of angiography and embolization of bleeding

the blunt hepatic trauma source
Trauma 645
Management of penetrating trauma of liver
SS Laparotomy is warranted in every penetrating injuries of liver.

SS In the setting of hepatic injuries, control of bleeding is a challenging job. So it needs a systematic approach—
1. Generous exposure
Coronary ligament Left triangular ligament
SS Division of triangular ligament, superior and inferior SS Extension of midline incision into the chest by
coronary ligament. median sternotomy.
2. Temporary control of bleeding
SS Basic maneuvers (3 ‘Ps’)— SS Special maneuvers (ABC)—

zz Pressure application [hepatic compression] zz Atriocaval shunt
zz Pringle maneuver zz Balloon [Moore-Pilcher balloon]
zz Perihepatic packing. zz Clamps [multiple clamps].
Hepatic compression
SS Manual compression is very much effective

for immediate control of hemorrhage.
SS Proper skill is required.
CT abdomen showing hematoma

in liver after blunt trauma
The Pringle maneuver
SS Vascular clamp is applied around the porta hepatis [Lower blade is

within the foramen of Winslow].
SS If bleeding stops after clamping, it can be interpretated that the injury
is in the portal vein or hepatic artery.
SS If bleeding continues after clamping, an injury to the hepatic veins or
retrohepatic vena cava is suspected.
SS Duration of clamping is important because liver cannot tolerate warm
ischaemia for more than 1 hour.
Vascular clamp
Perihepatic packing
SS Strategically placing of laparotomy pads over and around the bleeding

sites. Additional pads are placed between the liver, diaphragm and anterior
abdominal wall.
SS Effective method for control of hemorrhage from right lobe, not so effective
for left lobe.
SS Two complications must be keep in mind—
zz Compressed IVC results in decreased cardiac filling.
zz Cephalad displacement of diaphragm results in decreased tidal volume

and functional residual capacity.
Atriocaval shunt
Technically very difficult and mortality rate is very high.
Moore-Pilcher balloon
This is introduced through the femoral vein and placed it into the retrohepatic vena cava. When balloon is inflated, the
hepatic veins and vena cava are occluded.
Trauma 647
Clamps
Multiple clamps can be applied—

SS At porta hepatis
SS Aorta at the diaphragm
SS At suprarenal and suprahepatic vena cava.
3. Definitive control of bleeding
SS Raw surface oozing can be controlled by electrocautery, argon beam coagulation or topical hemostatic agents
(microcrystalline collagen, oxidized cellulose).
SS Persistentlybleeding lacerations can also be controlled by interrupted horizontal mattress sutures parallel to the
edge of laceration using No. O-chromic in large curved blunt needle.
SS Omentum can also be used to fill large defects over which sutures can be given.
[Omentum is a rich source of macrophage, thereby it fills dead space with viable tissue.]

SS Deep liver lacerations should not be simply closed due risk

of abscess formation and hemobilia.
SS By finger fracture technique, the lacerations are extended to
expose the bleeding vessels and ducts and then ligate them. Finger fracture
Ligation of
bledding vessels
and ducts
SS If multiple superficial lacerations are present, wrapping of each lobe

by the absorbable mesh is a useful technique.
SS Resectional debridement is indicated for nonviable hepatic parenchyma

in peripheral location.
SS Debrided liver parenchyma must not exceed 25% of the liver volume.
SS Formal hepatic resection is abandoned due to high morbidity and mortality.

SS Avoid coagulopathy, hypothermia and acidosis: Follow damage control surgery early if the vicious cycle
starts.
Trauma 649
10. Splenic injuries
Assess—
SS ? Blunt trauma
SS ? Penetrating trauma.
Management of blunt trauma
FAST
– Free fluid in peritoneum – Free fluid in peritoneum

– Patient stable – Patient unstable
CT with IV and oral Proceed for

contrast laparotomy
Source of bleeding Presence of hollow

Grading of injury (I – V) Contrast extravasation
(spleen/liver/both) viscus injuries
SS Then, assess which treatment option is ideal—
Treatment
Angiography and selective

Nonoperative approach? Surgery?
embolization?
• Injury grade (I – III) • Injury grade (IV and V)

• No contrast extravasation • Presence of hollow viscus
• No indication for laparoto- injuries
my for other injuries
Nonoperative mangement
SS Patient should be in ICU

SS Continuous monitoring of vital signs, serial abdominal examinations,
serial hematocrit estimation.
} For 48 – 72 hours
Assessment
Patient stable after 48 – 72 • Patient stable • Patient unstable

hours • ↓ hematocrit • Not responding to conservative
• Contrast extravasation management
Transfer the patient to • Requirement of blood transfu-
intermediate care unit sion > 4 units in 24 – 48 hours
Angiography and
• Patient will start eating and
selective embolization
walking
• Clinical monitoring Surgical intervention
On discharge, patients are

advised to avoid intense
physical activity and contact
sports for 3 months
Surgery ?
Indicated in—
SS Grade IV and V injuries
SS In unstable patient.
Then, think Operative picture of splenic injury
1. ? Splenic repair 2. ? Partial splenec-

3. ? Splenectomy
[splenorrhaphy ] tomy
SS OPSI – most often in young children and immunocompromised adults. So, attempts to salvage the spleen must be
more vigorous in these group of patients.
SS To safely repair or remove the spleen, mobilization must be done to such an extent so that the spleen can be
brought to the surface of abdominal wall without tension.
SS In the setting of splenic trauma, hematoma dissects most of the ligamentous attachments of spleen.
1. Small capsular laceration Controlled by

Topical hemostatic agent
Trauma 651
2. Deeper laceration
Repaired by absorbable hori-

zontal mattress sutures (2 – 0)
Wrapping the spleen in ab-
sorbable mesh (Vicryl mesh)
Omentum can be mobilized to
cover large defects
3. Major laceration involving superior May be managed

by partial
or inferior pole splenectomy
5. Injury involving the hilum or

4. Shattered spleen 6. Less extensive injury in spleen
central area of spleen
associated with other organ injury
Splenectomy
All patients undergo splenectomy require postoperative immunization against S. pneumoniae, H. influenzae, N. menin-
gitidis.
Vaccines should be given whenever patient becomes stable.
[Concept of implanting splenic fragments in an omental pouch (autotrasplantation) is still controversial).]
11. Retroperitoneal injuries
SS Retroperitoneal injuries present with frank intraabdominal hemorrhage or retroperitoneal hematoma due to injury
of major retroperitoneal vessels or their abdominal branches.
SS For control of such hemorrhage, a systematic approach is necessary:
1. Proximal control of aorta.
2. Adequate exposure of the vessels.
SS Mattox maneuver [a left medial visceral rotation].

zz For adequate exposure of aorta, celiac axis, SMA,
left renal artery, iliac arteries.
Celiccoris
SS Cattell maneuver [right + medial visceral SMA
rotation] + Kocher maneuver.
zz For adequate exposure of vena cava, right
renal vessels, iliac veins. Mattox
maneuver
Left renal artery
Right renal Iliac arteries

vessels
Vena cava
Iliac veins
Cattell-Braasch maneuver
+
Kocher maneuver
Trauma 653
3. Exploration of hematoma
Zone I Zone II Zone III

[central abdominal hematoma] [flank hematoma] [pelvic hematoma]
SS All zone I hematomas warrant operative exploration.

SS These hematomas are caused by injuries to supra or infrarenal aorta, celiac axis,
proximal SMA, proximal renal artery and IVC.
SS Proximal and distal control of the involved vessel should be obtained prior to
exploration of hematoma.
SS Zone III hematomas are usually due to pelvic fractures.
SS These hematomas should not be explored unless iliac vessel injury is suspected.
SS For temporary control of hemorrhage, pelvic binder around the pelvis is helpful. Zone I
Zone Zone
SS Pelvic angiography with selective embolization is the intervention of choice where
II II
pelvic fractures are the suspected source of ongoing hemorrhage.
SS Zone II hemotomas are suggestive of injury to renal artery, vein or renal
parenchyma.
SS Unless the hematoma is rapidly expanding, pulsatile or ruptured, it should not be Zone III
explored.
SS CT is necessary to assess the function of kidneys.
SS If exploration of the hematoma is required, nephrectomy (total or partial) is indicated for a shattered kidney.
4. Repair of Vascular Injuries

zz Venous injuries—
Vena cava, iliac veins, SMV, portal vein, renal veins should be repaired.
zz Arterial injuries—
Aorta, iliac arteries, common hepatic artery, SMA, renal artery – must be repaired.
Left gastric artery, splenic artery – may be ligated.
–– Ligation of splenic artery if needed, then splenectomy have to be done.
12. Genitourinary injuries
Genitourinary Injuries
Testes Penis Scrotum Kidneys Ureter Bladder Urethra

Think of urinary tract injuries, if–

SS Direct blow to flanks or back
SS Fall from height
SS Motor vehicle accidents
SS Penetrating injuries to lower chest, upper abdomen and flank.
Suspect
Upper urinary tract injuries, if

SS Fracture of lower ribs or spinous processes of vertebra
SS Gross or microscopic hematuria.
Lower urinary tract injuries, if

SS Blood in external urethral meatus
SS Distended bladder
SS Large perineal hematoma
SS Displaced prostate found in PR examination.
Renal injuries
SS Ofall injuries to the genitourinary tract, renal injuries are the most common
SS Microscopic or gross hematuria is present in more than 95% of patients with renal injury.
Assess
Hematuria due Hematuria due

to blunt trauma to penetrating trauma
All patients should be

Assess, 1 hematuria is gross Assess, 2 Patient is in shock imaged (CT with IV contrast)
or microscopic ? (SBP<90 mmHg)
or not?
SS Allpatients with gross hematuria should be imaged (CT with IV contrast)

SS Allpatients with microscopic hematuria and shock should be imaged.
SS Patients with microscopic hematuria without shock can be observed clinically without imaging.
SS Patient without hematuria but high suspicion of renal injury must be imaged.
SS Hematuria after trivial injury to the kidneys, then think of—
zz Preexisting pathology (e.g. calculus, tuberculosis, hydronephrosis).

Trauma 655
Grading of injuries (by CT with IV contrast)
I II
SS Contusion— SS Hematoma—
Microscopic or gross hema- Nonexpanding perirenal
turia. hematoma confined to re-
SS Hematoma— nal retroperitoneum.
Subcapsular, nonexpand- SS Laceration—
ing without parenchymal < 1 cm parenchymal depth
laceration. of renal cortex without
urinary extravasation.
III IV
SS Laceration— SS Laceration—
> 1 cm parenchyrnal depth Parenchymal laceration

of renal cortex without extending through cor-
collecting system rupture or tex, medulla and col-
urinary extravasation. lecting system.
� Vascular—
Main renal or venous

injury with contained
hemorrhage.
V
SS Laceration—
Completely shattered
kidney.
SS Vascular—
Avulsion of renal hilum,

kidney is devascularized.
SS Is
excretory urography has any role? Treatment
A significant role in a specific scenario.
zz
zz On abdominal exploration, surgeon encounters SS Operative approach—

an unexpected retroperitoneal hematoma
zz Persistent renal bleeding
surrounding a kidney
zz Expanding perirenal hematoma, pulsatile
↓ perirenal hematoma.
zz ‘Single-shot’ intraoperative IVP [single film is taken
SS Nonoperative approach—
10 minutes after contrast injection]
zz Upto grade III injuries in hemodynamically stable
↓ patients.
zz Any abnormal findings
zz Grade IV isolated renal injuries can be managed
↓ nonoperatively under close monitoring [vital
zz The kidney should be explored. signs, hematocrit, serial renal CT].
Operative principles
Early vascular control before opening Gerota’s fascia

can decrease renal tissue loss
Approach to the kidney must be transperitoneal so that

other intraabdominal organs can be examined SS Now, take decision—
zz Renorrhaphy?
zz Partial nephrectomy?
zz Nephrectomy?
1. Renorrhaphy
Debridement of non- SS Hemostasis Repair of margin with 3 – 0

viable tissue SS Closure of absorbable suture and use
collecting system of gelfoam bolster
2. Partial nephrectomy
If diagnosis within 8 hours of injury
SS Water tight closure of collecting

system
Sharp removal of non- SS Main renal artery/vein must be Coverage of open parenchyma
viable tissue repaired with vascular suture (5–0) with omental pedicle flap
Trauma 657
3. Nephrectomy
SS Isindicated in extensive renal injuries in a hemodynamically unstable patient [provided the contralateral kidney is
normal].
Injury to ureter
SS Penetrating injury with any degree of hematuria or any possibility of genitourinary injuries should be imaged.
SS Blunt trauma with any degree of hematuria with hypotension or history of significant deceleration should be
imaged.
SS Now, do the imaging—
zz CT with IV contrast—
Medial extravasation of contrast or nonopacification of ipsilateral ureter is – highly suggestive of ureteral

injury.
SS On exploration of abdomen, suspicious of ureter injury—
Do, one-shot pyelography.
1. Mobilization of ureter 1 cm away to avoid injury to delicate
vascular plexus.
2. Debridement of ureter – until the edges bleed.
3. Repair of ureter—
Spatulated, tension free, stented and watertight anastomosis.
Stent
Anastomosis
Technique of repair according to the site of injury—
1. Injuries of upper and middle thirds of ureter
Ureteroureterostomy
Omental wrap may be used to protect the repair

Drain is essential for all ureter repairs.
2. Injuries in distal ureter
Psoas muscle
Ureter
Bladder wall is
hitched up and
fixed to psoas
muscle
When minimal additional

length is needed
Trauma 659
Long flap is developed
from the bladder
When more additional Ureter is anastomosed Flap is tubularized and

length is needed to the flap donor defect is closed
SS Patient is too unstable to definite repair
Percutaneous
nephrostomy
Severed ends are ligated
Bladder injuries
Suspect bladder injury, if blunt is associated with pelvic fracture

Suspicion is high, if pelvic fracture is associated with hematuria.
Bladder
Sharp bony fragments

causing injury
SS Bladder rupture may be—

zz Intraperitoneal (about 20%)
zz Extraperitoneal (about 80%)—mostly associated with pelvic fracture.
Sudden elevation of
intravesical pressure
Direct impact
on full bladder It is better to travel with
an empty bladder !
Impact due to – • Blow or fall

• Rapid deceleration in
motor vehicle accident
How to detect the injury
SS Gross hematuria is the most reliable sign. Other clinical features are suprapubic tenderness.
zz Inability to void
zz Lower abdominal bruising
zz Muscle guarding and rigidity.
SS Cystography must be done—
zz If gross hematuria + pelvic fracture.
SS Cystography may be done – If
zz Gross hematuria, no pelvic fracture
zz Microscopic hematuria, + pelvic fracture
zz Microscopic hematuria, no pelvic fracture
SS Don’t miss a postvoid film—
zz It will help to identify lateral and posterior injuries.
SS CT facility available? Then, do CT cystography; no need of plain film cystography.

Trauma 661
Management
Manage the patient
Extraperitoneal Intraperitoneal bladder

rupture rupture
Uncomplicated Complicated Immediate surgical

rupture rupture repair
(fistula, persistent
leakage)
• Large bore Foley
catheter (22 fr) for
adequate drainage
• Catheter must be in situ
for atleast 2 weeks
• Cystography should be
done before catheter
removal
Bladder repair
Perivesical drain (in two layers with
absorbable suture)
Urethral catheter
(2–3 weeks)
Urethral injuries
SS Rareinjury in women.
SS Suspect urethral injury, if—
zz Blood is at the external meatus Full bladder
zz Bruise in the perineum Blood at external

zz Bladder full urethral meatus
zz Bogginess of pelvis
Bruise in perineum
Digital rectal
examination (DRE)
reveals –
• High riding prostate
• Pelvic bogginess
SS Urethral injury is suspected, then—
Retrograde urethrogram
Free extravasation
of contrast into No extravasation
preperitoneal space
Manage according Catheter can be

to site of injury advanced to the bladder
Cystogram
Catheterization should not be attempted. It converts a

incomplete tear to a complete one
Trauma 663
SS Urethral injuries may be—
zz Anterior urtheral injuries [distal to urogenital diaphragm] bulbous urethra + penile urethra
zz Posterior urethral injuries [proximal to urogenital diaphragm] membranous urethra + prostatic urethra.
Prostatic urethra Posterior

Membranous urethra urethra
Bulbous urethra
Urogenital diaphragm
Anterior
urethra Penile
urethra
Injury to anterior urethra
Injury to Penile Urethra
SS Uncommon injury.
SS Usually due to penetrating injury to penis.
SS Hematoma contained by Buck’s fascia and dissect along the penile shaft.
Injury to Bulbar Urethra
SS Most common urethral injury.

SS Most of these occur after straddle injury.
SS Patients present with blood at the meatus, perineal hematoma, urinary retention, gross hematuria.
SS Hematoma contained by Colles’ fascia and presents with perineal hematoma.

Accident in loose manhole cover Cycling accident
Gymnasium accident
Initial retrograde urethragram can classify

injuries into
Contusion Incomplete disruption Complete disruption

Trauma 665
SS Suprapubic cystostomy only for contusion and suprapubic cystostomy followed
by delayed reconstruction for incomplete and complete disruption.
SS Prior to reconstruction, retrograde urethrogram and voiding cystourethrogram
is necessary to define the site and extent of stricture.
SS Anastomotic urethroplasty (tension free, end to end anastomosis) is the
procedure of choice.
Injury to posterior urethra
SS Mostly occur in association with multisystem trauma from motor vehicle accidents, falls from height.
SS ‘Straddle fractures’ involving all four pubic rami, open fractures and fractures with vertical and rotational pelvic
instability are associated with higher risk of urethral injury.
Management
SS Ifurethral injury is suspected, retrograde urethrogram should be performed before catheterization.

SS Immediate suprapubic cystostomy is indicated for diversion.
SS In stable patients, primary endoscopic realignment and delayed repair is the treatment.
SS In unstable patients, endoscopic realignment is indicated when patient becomes stable.
SS Open posterior urethroplasty through a perineal approach is the procedure of choice for most urethral distraction
injuries.
SS Different types of trauma—

zz Degloving injuries
13. Genital injuries
zz Zipper injuries
Penile trauma zz Animal and human bites
zz Strangulation injuries
Keep in mind during management, penile skin has a zz Fracture of penis.

very good blood supply and very elastic.
1. Degloving injuries—
SS Mostly due to industrial accidents where clothing is caught in machinery.
SS Management — Copious irrigation of the wound to remove foreign bodies
⇓
Either, burying the denuded penile shaft in a scrotal tunnel
Denuded shaft Denuded shaft

buried in scrotal
tunnel
Or, split thickness skin grafting
Denuded shaft Thick,

nonmeshed
split thickness
skin graft
2. Zipper injuries
SS Impatient boys and intoxicated adults are susceptible groups.
SS Most commonly, the foreskin is trapped within the zipper.

Trauma 667
SS Firstly,
the patient have to be released from the clothing.
SS Then, freeing the entrapped skin by various mechanisms:
zz Zipper sliding piece and adjacent skin are lubricated and single attempt to
unzip.
zz Cloth material connected to the zipper is incised perpendicularly between
each tooth to release the lateral support of zipper.
Sliding piece
Median bar
SS Cutter can be used to cut the median bar of the sliding piece, thereby upper and lower shields of
the sliding device fall apart.
SS Circumcision may be indicated in extreme cases.
SS After freeing the skin, it is essential to assess the injury and then treated accordingly.
3. Animal and human bites

SS Dog bite is the most common type of bite injury.
SS Management includes—
zz Copius irrigation
zz Debridement
zz Primary closure after infiltrating rabies immunoglobulin.
4. Strangulation injuries
SS Accidentally placed thread, rubber band in penis of children — causes strangulation injuries.
SS String, metal constricting device in penis of adults – Most likely self-inflicted [for sexual gratification or to prolong
erection!]
SS String, thread, rubber band? — Can be incised without much difficulty.
SS Solid constricting device? — Technically challenging!
zz First, distal shaft is wrapped by latex tourniquet to decrease the edema
⇓ If method fails
Strangulating object
Thick silk or umbilical tape is passed

proximally under the strangulating
object and wrapped the penis distal Unwinding the tape from proximal
to the strangulating object end will displace the object distally
5. Fracture of penis
SS Disruption of the tunica albuginea with rupture of corpus cavernosum.
SS Fracture typically occurs during vigorous sexual intercourse, when the erect penis slips out the vagina and strikes
the perineum or public bone. This abnormal bending causes increase in intracavernosal pressure exceeds the
tensile strength of tunica, leading to laceration of shaft of penis.
Corpus cavernosum
Tunica albuginea Skin
SS Patient commonly describes a cracking or popping sound followed by pain, detumescence and swelling of shaft.
SS If Buck’s fascia is intact, the hematoma is contained between the skin and tunica, resulting in eggplant deformity.
SS If Buck’s fascia is disrupted, hematoma is extended to the scrotum, perineum and suprapubic regions. The penis is
often deviated to the side opposite the tunical tear.
SS Urethral evaluation is necessary in all penile fracture patients.
SS Imaging is not so helpful for diagnosis, typical history and clinical findings are sufficient for diagnosis.
SS MRI is helpful if there is clinical suspicion but absence of typical history and clinical findings.
Trauma 669
SS All suspected penile fractures should be promptly explored.
Circumferential
subcoronal
incison Tunical tear
with hematoma
Penile skin is
dissected
proximally in
sleeve fashion
Operative picture showing
tunical tear with hematoma
• Hematoma is evacuated
• Defect in tunica is repaired
with 2–0 / 3–0 absorbable
suture
SS Deep corporal ligation or excessive debridement of cavernosal tissue must be avoided.
Testicular injury
SS Mostly due to blunt trauma (assault, contact sports, motor vehicle accidents)
SS Rupture of testis must be suspected in every cases of blunt scrotal injury
SS Patients present with swelling and ecchymosis
SS USG is helpful to assess the integrity as well as vascularity of testis
SS Even small defects in the tunica must be repaired (with absorbable suture).
Repair of
testis with
absorbable
suture
[Salvaging the testis must be attempted, if possible]
Scrotal injury
SS Upto 50% scrotal skin loss can be managed by primary repair.

SS More extensive skin loss warrants placement of testis in thigh pouches or wrapping with wet dressing until
reconstruction.
SS Meshed split-thickness skin graft are useful for scrotal reconstruction.
Damage Control Surgery
SS The concept of ‘damage control surgery’ is evolved — to cut off Active hemorrhage
the vicious cycle of coagulopathy, hypothermia and metabolic
acidosis resulting from persistent bleeding.
SS Consider ‘damage control’, if—
zz pH < 7.2
Coagulopathy Hypothermia
zz Core temperature < 34°C
zz Shock
Metabolic acidosis
zz Coagulopathy.
SS Goal of ‘damage control surgery’ — Is to restore the normal physiology rather than normal anatomy.
SS Philosophy of ‘damage control surgery’ — A live patient above all else.
SS Divided into 3 phases:

Trauma 671
Phase I [Initial Exploration] — to Attain Rapid Control of Active Hemorrhage and
Contamination
In a setting of abdominal trauma
Midline incision
If exsanguinating hemorrhage
Four quadrant packing (resuscitative packing) and then,

sequential removal of packing and control of hemor-
rhage in particular quadrant.
[Primary goal is hemorrhage control, not
maintenance of blood flow.]
Contd...
Contd...
Attention then focused to find out any enteric spillage,

biliary leak.
No anastomosis
No stoma formation
Placement of drain.
SS Laparotomy pads are reinserted [therapeutic

packing].
SS No primary fascial closure.
SS Closure with alternate method [vaccum closure,

Bogota bag, prosthetic mesh placement, zipper
closure, skin closure with towel clips].
SS Vaccum closure is the most commonly used
method of closure of abdomen.
Phase II [Secondary Resuscitation]
SS Patient is shifted to ICU from operation theater and focus is given to correct hypothermia, coagulopathy and
acidosis.
SS Hypothermia can be prevented by elevating room temperature, using warm blankets, transfusion of prewarmed IV
fluids and blood.
SS Coagulopathy is managed by rapid infusion of FFP, cryoprecipitate and platelets. Recombinant factor VIIa is also
helpful.
SS Correction of hemodynamic instability corrects the metabolic acidosis.
SS Abdominal compartment syndrome, a lethal complication, may develop in this phase. It should be aggressively
treated.
Phase III [Definitive Operation]
SS Consists of planned reexploration and definite repair, usually after 48–72 hours following the initial operation and
successful secondary resuscitation.
SS Definite repair must be attempted.
SS Complex reconstructions and risky anastomoses are better avoided.
SS Abdomen should be closed primarily, if possible.
SS An abdominal X-ray should be arranged to ensure that all packs have been removed.
[Counting in the operation theater is unreliable in damage control scenario.]

Trauma 673
Abdominal Compartment Syndrome
SS Caused by acute increase of intraabdominal pressure due to accumulation of blood and bowel edema.
SS Sequelae of increased intraabdominal pressure–
zz Cardiac output and venous return are decreased.
zz Reduction in blood flow to liver, kidneys and intestines.
zz Diaphragms are displaced to thoracic side, leading to decreasing thoracic volume.
zz CVP, pulmonary capillary wedge pressure, right atrial pressure increases.
SS Measurement of intraabdominal pressure is done by measuring urinary bladder pressure (normal adult
intraabdominal pressure is 5–7 mmHg).
SS Management—
< 15 cm H2O Normal No need of decompression

15 – 25 cm H2O Mild May need decompression
26 – 35 cm H2O Moderate Need decompression
> 35 cm H2O Severe Urgent decompression
According to WSACS (World Society for the Abdominal Compartment syndrome), intraabdominal hypertension (IAH) is
defined as IAP ≥ 12 mmHg and abdominal compartment syndrome (ACS) as IAP> 20 mmHg with new organ dysfunc-
tion or failure.
Risk Factors (According to WSACS)
SS Related to abdominal collections of fluid, air or blood.

zz Abdominal infection (pancreatitis, peritonitis, abscess)
zz Hemoperitoneum
zz Major trauma
zz Liver dysfunction with ascites.
SS Related to increased intraabdominal contents—
zz Ileus
zz Intraperitoneal or retroperitoneal tumor
zz Damage control laparotomy
zz Colonic pseudoobstruction.
SS Related to diminished abdominal wall compliance—
zz Burns with abdominal eschars
zz Correction of large hernias, gastroschisis or omphalocele.
zz Abdominal wall bleeding or rectus-sheath hematoma.

Chapter 17
Burn
Important Topics
zzMechanisms of Burn Injury

zzManagament of Burn
zzSystemic Changes in Burn
zzElectric Burn
zzChemical Burn
zzComplication of Burn
‘Clinical science has as good a claim to the name and rights and self subsistence of a science as any other department of
biology.’
James Paget (1814–1899)
British Surgeon and Physiologist.
Introduction
SS Burn injury implies damage of skin and its contents by thermal, electrical, chemical energies or its combinations.
Different Mechanisms of Burn Injury

Burn 677
Flame:
SS Ignition of clothings during cooking
SS Improper use of stoves
SS Use of open fires at night of winter season
SS Smoking related (smoking in the mosquito net).
Scald:
SS Scald from hot water – most commonly
SS Thick soup, hot oil, sauces also cause scald.
SS Tar and Asphalt burn are a special kind of scald.
Contact:
SS Contact with hot metals, plastic, hot coals
SS In motor vehicle accidents, contact with hot engine parts
SS The exhaust pipe of motor cycle cause a characteristic burn in the medial aspect of lower leg.
SS Exposed areas of skin tend to be burned less deeply than clothed areas, because clothing retains the heat as well as
the hot liquid for longer period.
SS Immersion scald burns are usually deep burns, spill scald burns are not so deep.
When You Refer a Burn Patient to a Dedicated Burn Center?
SS First
assess,
zz Site of burn—
Burn involving face, hands, feet, genitalia, perineum major joints
zz Types of burn
Electrical burn including lighting injury
Chemical burn
Burn with inhalation injury.
SS Assess, age of the patient
zz Full thickness burn > 5 × TBSA in any age group
zz Partial or full thickness burn > 10% TBSA in < 10 or > 50 years
zz Partial or full thickness burn > 20% TBSA in ≥ 10 but ≤ 50 years
SS Assess, thickness of burn
SS Burn with preexisting medical disorders.
Management of Burn Injury
SS At the scene
SS In the emergency
SS In the burn center.
At the Scene
SS Burned patients must be removed from the source of injury.

SS All burned clothes are removed as soon as possible.
SS Rings, watches, jewellery must be removed as it retain heat and produce a tourniquet like effect when edema
develops.
SS Room temperature water can be poured in the wound to reduce the depth of burn.
SS Iced water should not be used–Causes systemic hypothermia and further thermal damage due to cutaneous
vasoconstriction.
SS Inhalation injury is always suspected and 100% oxygen should be given by facemask.
SS Emergency medical personnel should start IV fluid administration with lactated Ringer @ 1 liter/hour.
SS In high voltage electrical injuries or carbon monoxide poisoning, CPR may be warranted.
SS If patient is unconscious or in respiratory distress, endotracheal intubation should be performed (if facility and
expertise is available).
Burn 679
In the Emergency
SS In all burns, patients are assessed by primary survey and secondary survey.
SS Burned points should be evaluated and treated as patients of polytrauma because of associated injuries secondary
to explosion, fall or escape attempts.
Primary survey (A, B, C, E)—
1. Airway assessment is the first priority
SS Endotracheal intubation is indicated if
zz Patient is unconscious
zz Deep burns in face and neck
zz Inhalation injury—
Should be suspected if patient sustained burn in enclosed area or burn due to explosion
Suspicion is almost confirmed if hoarseness, stridor, expectoration of carbonaceous sputum.
SS The decision of intubation should be made early to avoid difficult intubation or intubation failure.
SS Emergency tracheostomy is indicated if there is intubation failure.
2. Breathing
SS Rhonchi or crepitation suggest inhalation injury or aspiration.
SS Severely burned patients may develop early respiratory failure.
3. Circulation
SS Burn causes both hypovolemic and distributive shock–due to release of inflammatory mediators.
zz Due to fluid shift from intravascular compartment to the interstitial spaces.
zz Due to evaporative fluid loss from the injury site.
4. Exposure
SS Remove all clothes to prevent further injury from the burnt clothes and to assess the BSA involved
SS Irrigate the burn with normal saline to remove burned residues.
Secondary survey
SS Estimation of percentage of BSA

SS Assessment of depth of burn.
Estimation of percentage of BSA

SS Why estimation of percentage is important?
zz To take decision whether patient will be transferred to specialized burn center or not.
zz To calculate the amount of fluid for resuscitation.
zz To calculate the calorie requirements.
SS Estimated by—
zz Wallace ‘Rule of nines’ —if large area of burn
zz Palm of patients hand equals to 1% of BSA— if small area of burn
zz Lund and Browder chart (age-related chart) – if pediatric burn.
SS ‘Rule of nines’ is accurate for adults, but not for pediatric patients. Infants and children have a proportionally greater
BSA in the head and neck and less in the lower extremities.
Assessment of depth of burn

SS Depth of burn is the primary determinant of patient’s functional and cosmetic outcome.
SS According to depth, burn injury is divided into—
First degree
zz Limited to epidermis
zz Painful burn
zz No blisters
zz Spontaneous healing after 3–4 days.
Second degree
zz Limited to dermis
zz Painful burn
zz Blister develops.
Third degree
zz All layers of skin and its appendages, sensory fibers for touch, pain, temperature and pressure and damaged
zz Painless burn.
Fourth degree
zz Also involve fascia, muscle and bone.
SS Is accurate assessment of depth is essential?

zz When nonoperative treatment is the main approach, accurate assessment of depth of burn is of little importance.
zz When operative treatment is the main approach, accurate assessment of depth is crucial.
SS How to assess the depth?
Clinical assessment by an experienced surgeon–Accurate in most of the cases.
}
SS Biopsy, ultrasound, vital dyes to detect dead cells or denatured collagen.
SS Laser Doppler, fluorometry, thermography–to assess the changes in blood flow. not so much accurate than
SS Light reflectance method to analyse the color of the wound an experienced surgeon’s
eyes.
SS Still now, clinical observation is mostly used to assess the depth of burn.
Prognosis
SS Baux score: Mortality risk = age + % TBSA

SS Other risk factors—inhalation injury, coexistent trauma, comorbidities (kidney/liver disease, HIV infection,
metastatic cancer).
Burn 681
Management
SS Oxygen—
zz 100% oxygen in face mask in all burn patients except very minor injuries.
zz 100% oxygen decreases the half life of carboxy Hb (from 2½ hours to 40 minutes)
SS Intravenous access – Burn of > 20% BSA requires IV fluids.
zz With two 16 gauge peripheral venous catheter.
zz Patient with associated medical problems, extremes of age should have additional central venous access for
invasive hemodynamic monitoring.

SS Types of fluid and amount of fluid: Crystalloid? or Colloid?

zz For the first 24 hours, crystalloid is the ideal type of fluid. Which crystalloid?
zz For the first 24 hours, Ringer lactate is the crystalloid of choice. What amount?
zz Amount of fluid is calculated by modified Park land formula.
The formula is:

Total calculated volume of RL for 24 hours = [4 × body wt (in kg) × % BSA] ml
Half of the calculated volume is given in the first 8 hours, rest half is given in the next 16 hours.
SS The time is calculated from the time of injury, not from when patient is attended.
SS Prehospital fluid resuscitation volume must be substracted from the total estimated volume.
SS Formula is for a near accurate estimation of fluid, SS Laboratory examination—

more or less fluid is further determined according to zz CBC, electrolytes, serum urea, creatinine,
urine output (30 – 50 ml/hr). grouping and cross matching, arterial blood gas
SS Other formulas are: and urinalysis.
zz Brooke formula SS Photographs and diagrams—
zz Galveston formula – for pediatric patients. zz Facilitates communication between members of
SS Is colloid essential?
the team.
zz This documentation is helpful for medicolegal
zz For first 24 hours postburn period, colloid infusion
increases mortality, rather than beneficial. purpose.
zz After 24 hours, colloid may be used to decrease
the total volume of crystalloids, thereby
minimizing the cardiopulmonary and electrolyte
related complications.
SS Monitoring urine output—
zz Catheterization (with Foley’s catheter) is used to

monitor urine output (reliable index of adequate
resuscitation).
zz Urine output 1 ml/kg/hour in children (≤ 30
kg) and 0.5 ml/kg/hour in adults is indicative of
adequate tissue perfusion.
SS Monitoring oxygen saturation—by pulse oximetry.
SS Tetanus prophylaxis — Is indicated because burn

is a tetanus-prone wound.
zz Immunization within 5 years– no prophylaxis.
zz Immunization within 10 years– booster dose of

tetanus toxoid.
zz Unknown immunization status-tetanus immuno-
globulin (250 IU) + Tetanus toxoid.
[Site of toxoid and immunoglobulin injection should
not be in same arm.]
SS Analgesia—
zz During shock phase, opioid analgesics should be

given intravenously.
zz IV opioid analgesics should be given in small
doses to avoid hypotension, respiratory
depression.
[Opioid analgesics in intramuscular route should not
be given in shock phase, because of variable absorp-
tion due to peripheral vasoconstriction. Injected opioid
analgesics form a pool at the site of injection. When re- SS Stressulcer prophylaxis—
suscitation becomes adequate, there is sudden pooling zz By H2 blockers or proton pump inhibitors.
of the drug in the circulation, leading to hypotension, SS DVT prophylaxis—
oversedation and particularly respiratory depression].
zz Routine heparin prophylaxis is cost-effective.
Burn 683
SS Irrigation and debridement of burn wound—
zz Using normal saline and sterile instruments, all
loose epidermal tissues should be removed.
zz Small blisters overlying superficial burns is
better to leave intact because the blisters offer
protection of the underlying dermis and permit
healing in a sterile environment.
zz Blisters overlying larger areas of burn is better
to debride because the blister fluid contains
inflammatory mediators that impairs local
microcirculation.
SS Escharotomy—
When to do?
zz In full thickness circumferential chest, neck and
extremity burn causing restriction of respiratory
effort and impairment of peripheral circulation.
How to assess, when?
zz – Skin color, capillary refilling and peripheral
pulses should be assessed on a frequent interval.
zz – If symptoms and signs of poor tissue perfusion
(cyanosis, progressive paresthesia, decrease or
absent pulse, cold extremities) arise.
zz – Laser Doppler flowmetry, if available may help
you to assess the timing.
What to do?
zz Full thickness incision through the eschar to
the subcutaneous fat by the help of scalpel or
electrocautery. Can be done at bedside.
SS No OT setup required
SS No need of anesthesia.
SS How and where?

zz Thoracic escharotomies are performed bilaterally
along the anterior axillary lines. If abdominal SS Wound care—
wall is also affected, then the incisions may be 1. Wound dressing
extended along the costal margins. 2. Application of topical antimicrobials
zz Longitudinal incision should be placed along 3. Excision and grafting.
the midmedial and midlateral aspect of
zz Wound dressing:
the extremities to avoid injury to the major
neurovascular and musculotendinous structures. Several advantages—
Protect the damaged epithelium
SS The incision should extend along the whole length
of the constricting burn and also across the involved Minimizes bacterial and fungal colonization
joints. Reduce evaporative heat loss
SS Escharotomy in the digits are of little benefit. Gives comfort in a painful wound.
Is Dressing Needed in All Burns? SS 0.5% silver nitrate solution

SS 5% mafenide acetate solution
zz Ist degree burn— SS 0.025% sodium hypochlorite (Dakin solution)
No need of dressing SS 0.25% acetic acid solution
Topical antimicrobials.
zz 2nd degree burn
zz Daily dressing with topical antimicrobials or

biologic/synthetic coverings.
zz Deep 2nd degree and 3rd degree
Synthetic/biologic coverings followed by

excision and grafting.
SS Choose any of the dressings—
Synthetic dressing—
zz Antimicrobial dressing
SS Biobrane
zz Synthetic dressing
zz Collagen-coated silicon in various form (e.g. in
zz Biologic dressings.
the shape of gloves).
SS Antimicrobial dressings
zz Adweres with the wound within 24-48 hours.
zz Antimicrobial salves
zz No antimicrobial properties.
zz Antimicrobial soaks.
zz When epithelialization becomes complete, it can
be peeled off the wound.
SS Transcyte
zz Biobrane + growth factor (from lysed fibroblasts)
zz In addition to advantages of biobrane, it also

stimulates wound healing.
SS Integra
zz Silicon sheet on outside (epidermal substitute

and collagen matrix on inside (dermal substitute).
zz After 2 weeks, the silicon layer is removed band
replaced by autograft.
SS Silversulfadiazine zz It can be used in full thickness burns.
SS Mafenide acetate zz Main advantage is limitation of scarring.
SS Bacitracin zz Disadvantage is no antimicrobial properties.
SS Neomycin Biologic dressing
SS Mupirocin SS Xenograft [from swine or porcine]
SS Polymyxin B SS Allograft [from cadaver donor]
zz Indicated for large partial thickness burn (> 50%

TBSA)
zz How it works?
Application of biologic dressing
↓ after several weeks

Rejection of dressing due to immune
mechanism
↓
Covering the wound with autograft skin
SS Disadvantage—Transmission of viral diseases with

allograft.
Burn 685
Topical antimicrobials— Fascial excision
SS Silver sulfadiazine SS Excision of the burned tissue including subcutaneous
zz Most commonly used topical antimicrobial. fat upto the level of investing fascia.
zz Broad spectrum coverage (gram-positive, gram- SS Particularly reserved for deep, large full thickness
negative, bacteria, fungus). burns.

zz Painless application. SS Excision is performed by electrocautery.
zz Transient leukopenia – after 3–5 days. It SS Assures a viable bed for grafting.
resolves spontaneously. No need of cessation of SS Leaves a permanent cosmetic defect.

application. SS More chance of injury to neuromuscular structures.
SS Mafenide acetate
zz Broad spectrum activity (due to sulfa moiety
zz Particularly effective against resistant pseu- Tangential excision

domonas, enterococcus species.
zz Can penetrate eschar, [Silver sulfadiazine can’t]
zz Carbonic anhydrase inhibitory property, so it

may cause metabolic acidosis.
SS Others
zz [Polymyxin B, neomycin, bacitracin, mupirocin]
zz Particularly used for facial burns, over the grafts,

donor sites, small partial thickness burns.
Excision and grafting?

Excision
SS Why indicated? Fascial excision
zz Dead burned tissue serves as a nidus for infection
and inflammation.
SS Where indicated?
zz In deep second and third degree burns.
SS When should be done?
zz Excision should be performed as early as possible

after the patient is stabilized. Usually within a
weeks of injury.
SS What should be done?
zz Excision > 10% TBSA must be done in a dedicated

burn center.
SS Different types of excision—
Tangential excision
SS Tangential removal of thin slices of burned tissue
until a viable bed appears (visible capillary bleeding). Grafting:
SS Excision is performed by humbly knife or power SS For covering of the excised burn wound.
driven (nitrogen) dermatome.
SS Autograft split thickness skin is an ideal one.
SS Each excision should be limited to <20% BSA or not
SS Burn area is small, donor area adequate:
more than 2 hours operating time.
zz Nonmeshed graft/meshed with a narrow ratio (< 2:1)
SS Be careful about blood loss and hypothermia.
Cosmetic outcome is good
SS Burnarea is large, donor area is limited

zz Widely expanded autograft (4 : 1)
SS Cadaver allograft may be used to cover the autograft and uncovered excised wound.
SS Burn
area is massive > 80% TBSA
zz Full thickness skin biopsy
↓
zz Keratinocytes are cultured in sheets [takes time of 2–3 weeks].
Nutritional support
SS Why nutritional support is needed?
zz Hypermetabolism and ↑ nitrogen loss start immediately

after burn injury [response to injury irrespective of
etiology].
Nutritional support is needed to prevent protein-calorie
malnutrition and maintain organ function.
SS How to calculate the calorie requirements?
zz By using Long’s modification of Harris-Benedict

equation (for burn >40% TBSA), in burn <40%– Curreri
formula.
SS Compositions of nutritional supplement
zz Protein—1–2 gm/kg/day
zz Carbohydrate—7gm/kg/day
zz Fat—additional fat has little support to prevent

malnutrition.
SS All vitamins (fat-soluble and water-soluble) must be
supplemented.
SS Vit C has particular role in wound healing by participating
in collagen synthesis (1000 mg of vit C daily is the recommended dose).
SS Mineral and trace element supplementation may be needed.
SS Zinc deficiency is documented in burn patients. So, emperic zinc supplementation is indicated following major
burn.
Burn 687
SS Idealnutritional regime:
zz High protein, high carbohydrate, low fat along with vitamins (particularly vit C), minerals (particularly zinc),
glutamine, trace element supplementation.
Routes of administration
SS Total Enteral Nutrition (TEN)
zz Early enteral nutrition through enteric tube is the preferred approach.
zz Enteral nutrition preserves the gut mucosal and integrity, leads to decrease the bacterial translocation.
zz Enteral nutrition enhances splanchnic perfusion and decrease Curling’s ulcer formation.
SS Total Parenteral Nutrition (TPN)—
zz TPN is indicated only when patient cannot tolerate enteral feeding.
Management of Sepsis
SS TBSA of burn is related with the incidence of infection. < 20% TBSA is rarely associated with life-threatening sepsis.
SS Prophylactic systemic antibiotics are not ideally indicated, as they only lead to increased bacterial resistance.
SS Children are more susceptible than adults for any given size of burn.
SS Hypotension, decreasing urine output, feeding intolerance, falling platelet count are all suggestive of sepsis.
Rehabilitation
SS Care of the skin of burn scar—

zz Prolonged exposure to sun should be aovided.
zz If exposure is inevitable (in face and hands), UV screening agents should be used.
zz Creams and lotions can be used to prevent drying and cracking.
SS Hypertrophic scar and keloid—
zz Can be minimized by the use of pressure garments for about 1 year (till the scar matures)
SS Both the surgeon and patient must be practical about the cosmetic outcome.
SS Patient should be informed that it may take years to achieve a acceptable outcome.
Systemic Changes in Burn
1. Increased vascular permeability
2. Effect on renal system
3. Effect on GI system
SS Mucosal atrophy
SS Decreased absorption of glucose, amino acid and fatty acid
SS Increased permeability to macromolecules.

Burn 689
4. Effect on immune system
SS Diminished macrophage production

SS Impairment of functions of neutrophils (e.g. diapedesis, chemotaxis and phagocytosis)
SS Function of helper T cell, cytotoxic T cell are decreased.
5. Effect on metabolism
Electric Burn
Severity depends on—

1. Voltage:
zz Low (< 1000 V) or
zz High (> 1000 V).

2. Tissue resistance: Tissues with higher resistance (bone > fat > tendon > skin) are more damaged than tissues with
less resistance (blood and nerve).
3. Types of current:
zz Alternating current causes repetitive, tetanic muscle contraction.
zz Direct current causes single muscle contraction, throwing the person away from the electricity.
zz Flexors are stronger than extensors, so the hand basically grips the electrical source, causing longer electrical
exposure.
4. Pathway through the body:

zz Current passing through the heart or brainstem causes ventricular fibrillation or apnea
zz Current passing through the muscle causes rhabdomyolysis, leads to myoglobinuria
zz Thrombosis frequently develops, leads to local tissue necrosis.
5. Duration of contact
Burn 691
Three types of electrical injury:
SS Injury from current flow
SS Arc or flash injury
SS Flame injury from the ignition of clothings.
Management of electric burn:

1. Care at the site of injury—
Start ABC evaluation and support accordingly
CPR should be started according to advanced cardiac life support protocol, (if pulses are not palpable)
Search for other life-threatening injuries (injuries due to fall from height, due to tetanic contractions)
2. Definite care—
Fingers, hands, forearms, feet, lower legs have more chance of damage than trunk, chest or abdomen
(smaller the area through which electricity passes, more intense heat production and less dissipation into
surrounding tissue).
zz High voltage electric injury may cause cardiac damage (myocardial contusion, infarction or conduction defect).
[If no dysrhythmia is found in ECG during initial evaluation, the likelihood of further development is rare].
zz Rhabdomyolysis may develop after electrical injury. Following rhabdomyolysis, myoglobin is released from
injured cells. Precipitation of myoglobin in the renal tubules can cause ARF.
Modern burn resuscitation protocol is adequate for management of myoglobinuria. If still chance of development
of ARF, mannitol infusion and infusion of sodium bicarbonate is indicated.
SS Every patient must have neurologic examination, because nervous system is very much sensitive to electrical energy.
Delayed transverse myelitis, anterior spinal artery syndrome may cause functional impairment.
SS Cataract may develop after high-voltage electrical injury, usually within 1–2 years.
3. Wound management—
zz Careful monitoring for compartment syndrome—if compartment pressure ≥ 30 mmHg or clinical features are
suggestive, then early escharotomy and fasciotomy is indicated.
zz Clinical findings suggestive of progressive median or ulnar nerve. deficit warrants decompression at the wrist.
zz Definite surgical procedures (excision and grafting) if indicated, can be done during the stipulated time.
Chemical Burn
SS Most chemical burns are accidental.

SS Strong acids and alkalis cause most of the chemical burns.
SS These burns are typically associated with industrial accidents, assaults, improper use of household cleaners.
SS Care of the burn—
zz All involved clothing should be removed.
zz Dry powders must be brushed before irrigation.
zz Irrigating the area for at least 15 minutes under a stream of tepid water dilutes the chemical.
zz If chemical composition is known (acid/alkali), surface pH is checked, continue the irrigation still pH is reached
the physiologic range (7 – 7.5).
zz Resuscitation is guided according to involved TBSA.
zz After resuscitation, operative debridement must be done.
zz After debridement, wound are dressed with antimicrobial agents or skin substitutes.
SS In acid injury, injuries may be more superficial than they appear; the reverse is true in case of alkali injury.
[Attempts to neutralize alkali with weak acids should not be attempted (heat released by neutralization reaction causes
further injury)]
SS Hydrofluoric acid burn—
zz Managed differently from other acid burns due to its chemical properties.
zz It produces dehydration and corrosion of tissues by free hydrogen ions. Fluoride ion complexes with calcium
and magnesium causing hypocalcemia, resulting in life-threatening arrhythmias.
zz Burned area is irrigated with clean water and 2.5% calcium gluconate gel. The gel is changed every 15 minutes.
If pain is not relieved after several applications of gel or symptoms recur, intradermal injection of 10% calcium
gluconate or intraarterial injection of calcium gluconate or both (in affected extremity).
zz All patients are admitted for cardiac monitoring, particularly for prolongation of QT interval.
zz Serum Mg , K are closely monitored.

2+ +
Late Complications of Burn
Keloid and hypertrophic scar

SS Can be limited by pressure garments
SS If keloid develops, intrakeloidal traimcinolone is helpful.
Hypertrophic scar following burn

Burn 693
Scar contracture Marjolin’s ulcer
SS In localized linear contracture, Y-V plasty. SS Chronic breakdown of a healed burn scar-suspect
SS In broad contracture, release of contracture followed Marjolin’s ulcer.

by skin grafting. SS Squamous cell carcinoma is the most common type
of malignancy that may develop.
SS Wide excision is the treatment.
Heterotopic ossification
SS Calcification in muscle and surrounding soft tissue
of the joint may occur in large full thickness burns.
SS Upper extremity is most commonly affected.
Marjolin’s ulcer
Chapter 18
Arterial Diseases, Venous

Diseases and Diseases of
Lymphatics
Important Topics
z Arterial Occlusive Diseases

zAneurysmal Vascular Disease
zDiseases of Thoracic Aorta
zVascular Trauma
zDeep Vein Thrombosis
z3AJKQO&JOQBł?EAJ?U
zAcute Lymphangitis
zLymphedema
zTumors of the Lymphatics
‘Where observation is concerned, chance favours only the prepared mind.’

Louis Pasteur (1822–1895)
French Microbiologist
Diseases of the Arteries
Arterial Occlusive Diseases
S Majority of arterial occlusive diseases are secondary to atherosclerotic changes of the intimal layer.
S Adverse events occur due to impaired circulation in the vital end organs (brain, heart, abdominal viscera) and
extremities.
Arterial Diseases, Venous Diseases and Diseases of Lymphatics 697
Peripheral Arterial Occlusive Disease
S Stenosis or occlusion of aorta or the arteries of the zEmbolism

limb. z Fibromuscular dysplasia.
S Atherosclerosis is the major cause of PAD in patients S Increased risk of PAD in—
of more than 40 years old. z Cigaret smokers
Other causes of occlusion: z Hypercholesterolemia
z Thrombosis
z Diabetes mellitus
z Vasculitis z Hypertension
z Trauma z Hyperhomocysteinemia.
What is atherosclerosis?
S A complex, chronic inflammatory process that primarily affects the intima, predilections for some locations and
sparing others, characterized by plaque (atheroma) formation.
S Lesions progress through a well-characterized stages before the development of clinical manifestations.
S Growth of plaque does not follow a smooth, linear fashion, rather intermittent periods of relative quiscence followed
by periods of rapid evolution.
Risk factors
S Hypercholesterolemia serum cholesterol > 200 mg/dl nn risk

z n LDL cholesterol (bad cholesterol ) nn risk
z [LDL has critical role in delivering cholesterol to peripheral tissues]
z HDL cholesterol (good cholesterol) n – p risk
z [HDL mobilizes cholesterol from developing and already existed atheromas and transports it to liver for excretion]
S Smoking
z n morbidity and mortality from coronary, cerebral and peripheral vascular diseases.
z Direct toxic effect of tobacco metabolites on the vascular endothelium.
S Diabetes mellitus
z Induces hypercholesterolemia
z Increases the risk of myocardial infarction, stroke and gangrene of lower extremities.
S Hypertension
z Independent risk factor for coronary atherosclerosis.
S Other risk factors:
z Advanced age
z Male gender
z Hypertriglyceridemia
z Hyperhomocysteinemia
z Sedentary lifestyle
z Family history.
How atheroma develops?
S Numerous hypotheses have been proposed, but the response to injury hypothesis is the most accepted.
S This ‘response to injury’ hypothesis views the atherosclerosis as a chronic inflammatory response of the arterial
wall to endothelial injury.
S Pathologic stages of atheroma development:
1. Endothelial injury is either mechanical injury or toxic injury

Due to shear stress, turbulence, flow separation, stasis
p
S Plaques tend to occur at the bifurcation or bends:
z Infrarenal abdominal aorta
z Carotid bifurcation
z Iliofemoral arteries (specially superficial femoral artery)
z Popliteal arteries.
Toxic injury
S Toxic metabolites (cigaret smoke and homocysteine)
S Hypoxia
S Infectious agents (cytomegalovirus, herpes virus and chlamydia).

2. Circulating monocytes attach to the damaged endothelium
3. Smooth muscle recruitment + Macrophage activation and recruitment
4. Macrophages and smooth muscle cells (SMCs) engulf lipid
S Theinitial lesion that can be seen is the ‘fatty streak’ consists of lipid-laden macrophages overlying lipid-laden
smooth muscle cells.
5. Some foam cells die as a result of apoptosis, forming the lipid rich center (necrotic core) and some foam cells release
cytokines and growth factors.
Further recruitment of SMCs and their elaboration of extracellular matrix finally converts a accumulation of foam cells
and SMCs to a atherosclerotic plaques.
Atherosclerotic plaque contains 3 types of compo- Atherosclerotic plaque made up of 3 areas:
nents: S Fibrous cap
S Cellular component – SMC, macrophage, T cells. S Shoulder
S Extracellular matrix collagen, elastic fibers, S Necrotic core.
proteoglycans.
S Lipid.
Atherosclerotic plaques: Complications with clinical significance—

Acute Arterial Occlusion of the Extremity
S Infarction develops after 4–8 minutes of ischemia S Infarction develops after 15–20 minutes of ischemia
S Infarction develops after 5–6 hours of ischemia

1. Emboli:
S Cardiac emboli: About 80% of arterial emboli are cardiac in origin.
S Arterial-arterial emboli: z Acute thrombosis also develops in the setting
z Emboli arising from ulcerated atheroma, of sepsis and hypercoagulable states (e.g.
unstable atheroma, disrupted plaque, from hyperhomocysteinemia, antithrombin III
aneurysm cause distal obstruction and ischemia. deficiency, antiphospholipid antibody, protein C
z Aortic aneurysms contain thrombi, but rarely
deficiency).
embolize.
3.
Trauma—
z Femoral and popliteal aneurysms frequently
z Stenosis or occlusion may develop after an initial
embolize.
flap or arterial wall hematoma.
S Symptoms of acute occlusion depend on the

location, duration, severity of the obstruction.
z What is ‘Blue toe’ syndrome?
S Presentation includes five Ps:
Diffuse microembolization causes painful,
bluish discoloration of toes with cutaneous 1. Pain
gangrene, livedo reticularis. Peripheral pulses S Most common symptom.
are present. S Sudden onset severe ischemic pain in extremity
It may also affect renal and mesenteric in a previously asymptomatic patient—Highly

circulations leads to progressive renal failure suggestive of embolic occlusion.
and intestinal infarction. 2. Pallor
S Venous-arterial emboli— S Cold, pale extremity with no sign of cutaneous
z Due to intracardiac shunt (e.g. patent foramen blood flow.

ovale). S Pallor and delayed capillary refilling on elevation
z Due to intrapulmonary AV malformations (in of extremity and rubor on dependency—Think of

Osler-Weber-Rendu syndrome). partial occlusion.
3. Pulse lessness
S Absence of distal pulses can indicate the site of
occlusion.
4. Paresthesia
S Light touch sensation is absent?—Beginning of
irreversible ischemia.
5. Paralysis
S Onset of motor paralysis indicates impending
gangrene—Warrants urgent revascularization.
S The 6th one is—Poikilothermy [inability to
thermoregulate].
Management
2.
Thrombosis—
S Acute embolic or acute thrombotic occlusion in
z Acute thrombosis usually develops over a pre- extremity can be diagnosed by history taking and
existing atherosclerosis. clinical examination in most of the cases.
Acute embolic occlusion? Acute thrombotic occlusion?

S Presence of risk factors (e.g. atrial fibrillation, recent S No risk factors for embolism.
AMI, prosthetic heart valve).
S Normal contralateral extremity.

S Contralateral extremity is also diseased.
S Once a diagnosis of acute arterial occlusion (due to emboli/thrombus) is made, immediate anticoagulation by IV
heparin should be started to slow the propagation of the thrombus and allows some time to assess the status of
collateral circulation and preparation for surgical intervention.
IV bolus [80 U/kg]
IV infusion [18 U/kg/hr]

[Partial thromboplastin time (PTT) should be maintained between 60–80 sec].
In embolic occlusion
1. Assess the viability and potential salvage of the affected limb:
S Viabilitypresent
z Time is precious!
z No need of preoperative angiography
z Minimal but expeditious evaluation [chest X-ray, 12 lead ECG, routine blood test]
z Procedure is rather not so complex.

Urgent intervention
Balloon Embolectomy
Contd...
Contd...
2. Search for source of embolus
S Transesophageal Echocardiography [to find source of cardiac emboli]

S Bubble Echocardiography: [when suspecting patent foramen ovale]
S CT of descending thoracic and abdominal aorta: [to find aortic thrombus].
In acute thrombotic occlusion
S First, do an arteriogram to know—

z Site of thrombotic occlusion
z Degree of occlusion
z Short or long segment involvement
z Status of inflow and outflow vessels.
Management is more complex, because—

S Diffuse atherosclerosis at multiple levels
S Various degree of collateral development.

About thrombolytic therapy
S Reteplase, alteplase are the thrombolytic agents.

S Fresher the thrombus, more the chance of successful thrombolysis.
S During thrombolysis, patient is monitored in ICU. Thrombin time, fibrinogen level, fibrinogen degradation product,
PTT and CBC must be evaluated to assess the risk of hemorrhage.
S Duration of therapy between 4–16 hours.
S Repeat arteriography is done after 6–18 hours to evaluate the result.
S Patient with high risk of major bleeding are not candidates:
z Patient with recent surgery
z Patient with trauma
z Gallbladder bleeding
z Intracranial tumors
z Recent stoke
z Pregnancy.
In traumatic occlusion
S Operative exploration should be done if limb is ischemic/arteriogram shows intimal flap/hematoma
S Proximal and distal control of the injured artery must be taken
S End-to-end anastomosis/graft placement (autologous vein graft)
S Completion angiogram is helpful to document the distal flow.

Chronic Occlusive Disease of the Extremity
S Lower extremities are more commonly affected by chronic occlusive disease of the arteries.
S Lower extremity chronic occlusive disease is subdivided into three anatomic sections—
z Aortoiliac [inflow disease]
Involves the infrarenal aorta, common iliac and external iliac arteries.
z Femoral-popliteal [outflow disease]
Involves the common femoral, superficial femoral and popliteal arteries.
z Tibial-peroneal [runoff disease]
Involves distal to popliteal artery.

1. Intermittent claudication
S Most common symptom
S Defined as pain, ache, cramp or sense of fatigue in the muscles, brought on by walking, gradually progresses until
the patient is compelled to stop walking.
S Site of claudication is distal to the site of occlusive lesion.
S In
femoropopliteal and tibial-peroneal occlusive disease, intermittent claudication develops in calf region.
S Claudication
less commonly occurs in the upper limb. If pain develops, is brought on by activities like writing or
manual work.
2. Rest pain S Systolic bruit is produced due to turbulence just
S Severe burning pain usually confined to the forefoot. proximal to the stenotic segment.
S Pain aggravated by elevation of the extremity or in S After total occlusion, usually bruit disappear.
horizontal position. 3. Disappearing pulse

S Patient can obtain same relief by hanging the leg S When peripheral pulses are apparently normal, after
over the side of the bed. [Gravity helps the delivery exercising the patient to the point of claudication,
of arterial blood]. the palpable pulses become disappear. After taking
S Rest pain usually preceded by claudication. a few minutes of rest, the pulse reappears.
3. Numbness and paresthesia 4. Skin temperature
S Common symptom is severe ischemia. S Decreased temperature is best detected by
4. Erectile dysfunction palpation of dorsum of patient’s foot with the back
of examiner’s hand.
S If arterial flow is obstructed in both hypogastric
arteries. 5. Color changes
S Blanching of limb on elevation and purple
On examination
discoloration on dependancy indicates advanced
1. Arterial pulsation
ischemia.
S Arterial pulsation is absent or diminished distal to
S The angle of elevation at which blanching appears
obstruction.
gives a rough estimations of degree of ischemia.
S The more it takes time to return of skin color on
dependancy, the more severe is the obstruction.
6. Integumentary changes
S Loss of hair in foot
S Thickening of toenails (onychomycosis)
S Atrophy of skin and subcutaneous tissue.
7. Atrophy: Gradual development of soft tissue and

muscle atrophy in the ischemic area.
8. Ulceration and gangrene
S Ischemic ulcers are very painful, develop on the
dorsum of feet, on the skin, around the malleoli.
Margin of ulcer is punched out, base is devoid of
granulation tissue.
S Usually, dry gangrene develops. The blackened,
mummified skin and tissues are characteristic–
unmistakable to a surgeon.
2. Bruit
Arterial Occlusive Disease of the Upper Extremity
S Rare disease.
S Most commonly affected vessel-Proximal subclavian artery > axillary artery > brachial artery.
S Typically present with arm claudication, ischemic or necrotic changes in fingers and hands.
S Most of the patients with subclavian artery occlusion are asymptomatic.
S If obstruction in subclavian artery develops proximal to the origin of vertebral artery, during exercise of the affected
upper limb
p
nn demand of blood flow
p
Retrograde flow from ipsilateral vertebral artery
p
p posterior cerebral circulation
Drop attacks
Ataxia
Sensory loss
Diplopia
} (Subclavian steal syndrome)
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S Noninvasive method
z Ankle-Brachial Index (ABI)
z Segmental limb pressure measurement
z Duplex scanning
z DSA
z MRA
z CTA.
S Invasive method
z Conventional angiography
S Noninvasive methods help—
z To identify hemodynamically significant stenosis
z To detect the sites of stenosis
z To assess the severity of hypoperfusion.
1. Ankle-Brachial Index (ABI): A quick screening test.

Ankle systolic pressure
ABI =
Highest brachial systolic pressure
ABI t 1.0 – in normal individuals
d 1.0 – in occlusive arterial disease
< 0.5 – in patient with severe ischemia
< 0.3 – in patient with imminent necrosis
S ABI > 1.2 or ABI value not proportionate to the patient’s clinical status — Think of vessel wall calcification (found in
diabetes, end state renal disease).
S Patient with history of claudication and normal resting waveform – Warrants postexercise ABI measurement.
2. Segmental limb pressure measurement: Delects and localizes hemodynamically significant vessel occlusion.
3. Duplex scanning is the combination of two forms of ultrasound.

B-mode ultrasound + Doppler ultrasound
| |
Creates gray-scale anatomic image of vessels Creates image of the moving structures in the
vessels (color map proportional to the flow velo-
city and an auditory signal)
S First line imaging tool for carotid arteries, lower extremity bypass grafts, abdominal aorta and for DVT.
[DSA (digital substraction angiography), MRA, CTA should not be used for routine diagnostic testing. It should be per-
formed if revascularization is planned.]
4. Computed tomographic angiography
S Noninvasive, contrast-dependent imaging method of arterial system.
S The images can be reconstructed in 3-D format. Thereby planning for vascular reconstruction is more accurate.
5. Magnetic resonance angiography (MRA)

S Noninvasive, contrast dependant (gadolinium) imaging method.
S Contraindicated in presence of metallic inplants.
6. Conventional angiography is indicated where besides diagnosis, PTA is also planned.

Treatment
1. Objectives—
S Relief of symptoms
S Prevention of limb loss
S To prevent further progression of disease process
S To reduce the risk of associated cardiovascular events (e.g. AMI).
[PAD is more a marker for early death than an indicator of imminent limb loss.]
2. Types of treatment—
S Conservative
S Endovascular
S Surgery.
Conservative treatment
Risk factor modification

a. Cessation of smoking: by counseling and adjunctive drug therapy
b. Control of hypertension
z Goal 130/85 mmHg
z ACE inhibitors and E-blockers help to reduce mortality associated with cardiovascular
events.
c. Cholesterol (LDL cholesterol) reduction
z Goal < 100 mg/dl—By treating with statins
d. Control of diabetes
z Aggressive control of diabetes is associated with slowing of progression of atherosclerotic disorder
z Goal—Glycosylated Hb 7%.
Exercise rehabilitation
S Unsupervised walking to supervised exercise on a treadmill, all significantly improves walking ability.
S Exercise for more than 30 minutes and more than 3 times a weeks are most effective.
Care of foot
Endovascular therapy
Indications
S For disabling, progressive, severe symptoms of

intermittent claudication despite medical therapy.
S In patient with critical limb ischemia.
S In Type A lesions.
S Different types of endovascular therapies:

S Feet should be inspected and washed daily.
z Percutaneous transluminal angioplasty—
S Well fitting and protective shoes are advised.
Dilation of a stenotic arterial segment using
S Toe nails should be trimmed carefully.
inflatable balloon catheter.
S Even minor foot infections and injuries should be
When balloon inflates, it stretches the media
treated aggressively.
and adventitia, fractures the plaque, thereby
S Avoid amateur chiropody.
widens the lumen.
S Avoid excessive drying by applying moisturizing
z Stenting—
creams.
Indications: Angioplasty failure, Eccentric
S Educating the point to understand the importance
stenotic lesions, recanalized iliac occlusion,
of foot care.
ulcerated emboligenic lesion.
Types:
Balloon-expandable (Palmaz type)

–
Pharmacotherapy
Self-expanding (Wallstent type).
–
In aortoiliac occlusive disease, balloon

angioplasty and stent placement produce
excellent long-term patency.
In infrainguinal occlusive disease, balloon
S Pentoxifylline— angio-plasty and stenting produce poorer
z A rheologic agent. Increases RBC flexibility and results than surgical bypass.
thereby improving capillary blood flow. z Atherectomy—
S Cilostazol A endovascular procedure where plaque is
z A type III phosphodiesterase inhibitor. removed by shaving with a cutting or rotating
z Inhibits platelet aggregation, increases vasodila- catheter.
tion, inhibits smooth muscle proliferation, lowers
HDL cholesterol and triglyceride.
z Significantly increase walking distance.
Surgery
z At least 3 months should be continued before
making decision about efficiency.
S All patients undergoing surgery warrants
z Contraindicated in CHF. preoperative cardiac risk assessment.
S Antiplatelet therapy with either aspirin or clopidog- S All patients undergoing surgery need angiographic
rel. evaluation of the symptomatic arterial segment.
z Clopidogrel is more effective but much more S Screening for carotid disease must be performed
expensive. (history of stroke, TA and carotid auscultation).
S Patient with angina, Prior AMI, ventricular ectopic, heart failure, diabetes are at increased risk.
S Several operative procedures available.
S Preferred procedure depends on:
z Location and extent of obstruction
z General medical condition of the patient.
In Aortoiliac Occlusive Disease
1. Aortobifemoral bypass
S Treatment of choice in low-risk point with diffuse aortoiliac occulsion and stenoses.
S Knitted dacron graft is used for bypass.
2. Axillobifemoral bypass
S Preferred procedure for high-risk point with short life expectancy (< 5 years).
3. Femorofemoral, Ilioiliac Iliofemoral bypass

S Choice for high-risk point with unilateral iliac disease.
4. Aortoiliac Endarterectomy
S May indicated in points with disease localized to distal aorta and common iliac vessels.
In Femoral, Popliteal and Tibial Occlusive Disease
1. Autogenous vein bypass graft

S Great saphenous vein is the vein of choice
S Short saphenous vein or arm vein are the suitable alternatives.
2. PTFE graft and cryopreserved vein graft

S When autogenous vein not available
S Cryopreserved vein graft is useful in a setting of infected field.
3. Endarterectomy
S May be indicated where autogenous vein unavailability or in the pressure of infected field.
Amputation—
S Indicated for patients with gangrene or persistent painful limb not amenable to vascular reconstruction
S Preserve as much length as safely possible
S Level of amputation is determined by clinical judgement.
Upper Extremity Occlusive Diseases

&J0Q>?H=RE=JNPANE=H,??HQOEKJ
Assess
Ipsilateral common carotid patent Ipsilateral common carotid occluded
Carotid-subclavian bypass (using Subclavian-subclavian bypass (using

prosthetic graft) prosthetic graft)
Thromboangiitis Obliterans
Also known as Buerger’s disease.
S Most frequently develop in men < 40

years with smoking
S Inflammatory occlusive
disease involving: Small
and medial sized arteries
and veins of extremities. Clinical examination reveals: Normal
brachial and popliteal pulses but
reduced or absent radial, ulnar, tibial
and arterial dorsalis pedis pulses.
S Clinicaltriad of:
1. Claudication of affected extremity
2. Raynaud’s phenomenon
3. Migratory superficial thrombophlebitis.
S Arteriography is helpful to make the diagnosis, but pathological examination is necessary for confirmation of
diagnosis.
S No specific treatment except abstinence from smoking.

Chronic Visceral Ischemia
Renovascular Occlusive Disease
Renovascular occlusive disease: Stenosis or occlusion of the renal arteries

Why occlusion develops?
1. Atherosclerosis (90%)
S Bilateral involvement (50%)

S Atherosclerotic process begins in the adjacent aorta with ‘spillover’ plaque encroaching into the proximal renal
artery (ostia and proximal 2 cm).
2. Fibromuscular dysplasia (second most common)
S Most commonly medial fibroplasia. S Lesions are multifocal.
S Found in young and middle-aged women. S ‘String-of-beads’ appearance on angiography.

3. Thromboembolism
4. Takayasu’s arteritis
5. Radiation vasculitis.
How hypertension develops in renovascular occlusive disease?
Contd...
Contd...
Suspect renovascular hypertension if:

S Severe hypertension in a child or young adult
S Sudden development or worsening of hypertension
S Hypertension refractory to multidrug antihypertensive therapy
S Hypertension associated with coronary disease, cerebrovascular disease, peripheral vascular disease.
Management
S Management of atherosclerotic occlusion and fibromuscular dysplasia.
[ Endovascular management (PTA) have high success rate

Failure to endovascular treatment warrants surgical therapy.]
Management of atherosclerotic renovascular occlusion
1. Medical therapy
S Combination of E-blocker and calcium channel blocker.
S Angiotensin II receptor inhibitor
S ACE inhibitor.
[ACE inhibitors are better avoided in bilateral disease or disease in solitary kidney.]
2. Surgery
S Indicated in uncontrollable hypertension refractory to maximal medical therapy.
S Also indicated in patient with concomitant aortic aneurysm or occlusive disease waiting for surgery.
S Different methods of surgical intervention:
z Aortorenal bypass
Classic open approach
z Renal endarterectomy
Used for bilateral orificial lesions
z Ex vivo renal artery reconstruction
z Nephrectomy
Indicated in renal infarction, severe nephrosclerosis, failed

revascularization.
3. Endovascular approach
S Indicated where failure of medical therapy and no clear indication for open
surgery.
S Balloon angioplasty is the procedure of choice.
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Acute mesenteric arterial occlusion
S Mostly due to cardiogenic embolus

S Embolus usually lodge at the segment of superior mesenteric artery from where middle colic and jejunal branches
arise.
S Sudden onset severe abdominal pain centered in the periumbilical region. The pain is out-of-proportion to the
degree of abdominal tenderness.
S In advanced stage, patient may present with features of peritonitis.
S Clinical evidences of cardiac disease (arrhythmia, recent MI, valvular disease) are present in most of the cases.
S Laboratory examination reveals elevated WBC count, metabolic acidosis.
S Plain radiograph shows fluid filled bowel loops with bowel wall edema.
S The mainstay of diagnosis is angiography of mesenteric vessels.
S Helical CT can detect the proximal mesenteric thrombosis.
S Early management is crucial for a acceptable outcome, but early management depends on high index of suspicion.
S Surgery should not be delayed if patient has enough clinical evidence.

Chronic mesenteric arterial occlusion
S Diffuse atherosclerosis involving the aorta and proximal superior mesenteric artery.
S Abundant collaterals develop in the period of chronic occlusion.
S Abdominal main begins within an hour after eating and abating within 4 hours—Intestinal angina.
S Patients also present with significant weight loss due to p absorption of nutrients and decreased food intake due
to pain.
S Diagnosis mainly depends on classical history and exclusion of other diagnosis (e.g. chronic pancreatitis, gastric
ulcer and malignancy).
S Abdominal bruit present in about 75% of cases.
S Duplex Doppler is most often successful to detect occlusion of proximal SMA and celiac artery.
S Definite diagnostic mode is arteriography.

S Treatment is:
Endovascular (balloon angioplasty or stenting)
or
Endarterectomy
or
Bypass grafting (autologous/prosthetic graft)
Balloon angioplasty Transaortic mesenteric Bypass grafting

endarterectomy
Mesenteric venous occlusion
S Venous occlusion develops in various clinical conditions:

z Cirrhosis with portal hypertension
z Inflammatory and infective conditions (peritonitis, IBD and intraabdominal abscess)
z Hypercoagulable states (DVT, neoplasm, antithrombin III and proteins deficiency)
z After splenectomy.
S Patients present with vague abdominal pain.
S Clinical findings are often equivocal.
S CT and arteriography reveals lack of prompt filling of the portal system.
S Treatment consists of hemodynamic support, anticoagulation and close observation.
S If peritonitis develops, then exploratory laparotomy is indicated.
S Surgical thrombectomy is not so beneficial.
S Prognosis is good because abundant collateral venous outflow develops.
+KJK??HQOERAIAOAJPANE?EJOQBł?EAJ?U
S Usually associated in patient with sepsis and cardiovascular compromised state resulting in vasoconstriction of
mesenteric vascular bed.
S Diffuse abdominal pain with out of proportional tenderness.
S Classic arteriographic findings–
z Absent large vessel occlusion
z Focal vasospasm with ‘beading’ of the major mesenteric branches.
z Pruned tree appearance to the distal vasculature.
S Fluid resuscitation, antibiotics, withdrawal of vasoconstrictors, infusion of papaverine into the SMA, angiographic
monitoring of vasospasm are the basic components of management.
S Surgery is indicated only when peritonitis develops.
S Prognosis is not good.

Aneurysmal Vascular Disease
Aneurysm – derived from the Greek Work ‘aneurysma’, means ‘widening’.

What is Aneurysm?
Permanent and irreversible localized dilation of arteries, at least 50% increase in diameter.
Different Types of Aneurysm
1. According to structure
S True aneurysm [involves all three layers of the arterial wall]
e.g.:
z Aortic aneurysm (most common)
z Iliac artery aneurysm
z Popliteal artery aneurysm.
S Pseudoaneurysm [lined by adventitia only or by a fibrous capsule]
e.g.:
z Iatrogenic injury during arterial catheterization
z Arterial graft anastomotic disruption.

2. According to shape
S Fusiform: [entire circumference of a segment of S Saccular: [part of circumference of vessel]

vessel]
3. According to etiology 4. According to location
S Degenerative: e.g. Atherosclerotic S Aortic
z In Marfan’s syndrome and Ehler-Danlos S Peripheral

syndrome type IV. S Splanchnic
S Inflammatory: e.g. Mycotic aneurysm. S Cerebral.
z In syphilis, tuberculosis.
S Congenital: e.g. Berry aneurysm.
S Dissecting
z Classically seen in arch of aorta in (Marfan’s

syndrome).
S Width of the aneurysm is the predicting factor of rupture.

Abdominal Aortic Aneurysms (AAAs)
S Most common type of aneurysm

S Five times more common in males.
Risk factors
S Age—Prevalence increases with age

S Atherosclerosis— nrisk
S Black race—Negative risk factor
S Cigaret smoking—8 : 1 preponderance of aneurysm in smokers
S Chlamydia pneumoniae infection—About 55% of AAAs show C. pneumoniae by immunohistochemistry
S COPD— nrisk
S Diabetes mellitus—Inverse relationship between DM and AAA
S Family history—1st degree relatives of patients have a 11 fold increase in relative risk to develop AAA.
How aneurysm develops?
About 90% of AAAs are degenerative in origin

Pathogenesis is multifactorial.
Genetic factor is also responsible—

z Familial clustering in about 15%–25%
z Inherited as either autosomal dominant or autosomal recessive or X chromosome linked.

Epidemiology
S About 90% of AAAs are degenerative in origin

S Aortic aneurysms are most commonly located in infrarenal aorta.
Most common
Other locations are
Natural history
1. 2.
Asymptomatic S Pressure symptoms—
S Detected on routine clinical examination as palpable, z Compression of ureter.
pulsatile, expansile, nontender mass, commonly z Compression of adjacent bowel—Causing
located just above and left side of umbilicus. chronic abdominal pain, early satiety.
z Compression of spine—Causing deep back pain.
Most common presentation
3.
Thrombosis and embolism
4.
Rupture
Rupture in the retroperitoneal space Rupture in the peritoneal cavity
Patient presents with severe abdominal pain with shock
5.
Fistula
Aortoiliac fistula Aortocaval fistula Aortoenteric fistula

S 4th part of duodenum mostly involved
S Patients present with— S Presented with shock and massive GI
z Unilateral or bilateral lower extremity edema

bleeding
z High output congestive heart failure
z Continuous abdominal bruit or palpable thrill.
AAA rupture may mimic— Pancreatitis

— Peritonitis
— Duodenal perforation
— Myocardial infarction.
2.
Abdominal ultrasound—
S Most widely used noninvasive test for AAAs
1. S Helpful to delineate structural details of
Plain radiograph of abdomen or lumbar the vessel wall, presence of atherosclerotic
spine— plaques.
‘eggshell’ pattern of calcification S Can accurately measure the size of aneurysm
[Negative findings does not exclude the diag- in both directions (longitudinal and cross-
nosis.] sectional).
3.
CT Scan—
S Most accurate test for AAAs
S Can identify proximal and distal extent of

the aneurysm
Diagnosis S Can identify occlusive or aneurysmal

disease in renal, visceral and iliac arteries
S Size of the aortic lumen, location of mural
thrombus, presence of calcific disease can
be well delineated
S Can also identify dissecting aneurysm, if
present
4.
Three-dimensional CT angiography—
S Optimal imaging modality when planning for
5.
AAA repair
Three-dimensional—
S Modality of choice when patient with AAA
having renal insufficiency is being planned
for AAA repair
Management
Elective management Management of ruptured aneurysm
Wait and watch Elective repair
Aneurysm size < 5.5 cm without risk fac- ,QGLFDWLRQVDUH²

tors— – Symptomatic aneurysm
Close surveillance using USG or CT scan – Size 5.5 cm in men
yearly or more frequently ] 4.5–5.4 cm in women
&HVVDWLRQRIVPRNLQJFRQWURORIK\SHUWHQ- – Saccular aneurysm (due to nchance of infec-
VLRQ&23'FRQWURO²,PSRUWDQWSDUWGXULQJ tion)
close surveillance policy ± 6PDOOHU LQ VL]H EXW DVVRFLDWHG VLJQL¿FDQW
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Promising result as medical therapy of ± 6L]HQRPDWWHUZKHQ
AAAs 3DWLHQWGHPDQGVUHSDLU
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pseudoaneurysm)
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H[SHFWDQF\ZDUUDQWHDUOLHUUHSDLU@
S Different options of repair

[In choosing option patient preference is of great importance.]
Repair
Open repair Endovascular aortic repair (EVAR)
[replacing the aneurysmal seg- 3UHIHUUHGLQ

ment with a synthetic graft] ± 2OGHUKLJKULVNSDWLHQWV
± 3DWLHQWZLWKµKRVWLOH¶DEGRPHQ
± 3DWLHQWZLWKVXFKFOLQLFDOFRQGL-
tions where open repair is risky
Transperitoneal approach Retroperitoneal approach
Transperitoneal approach for AAA repair —Gives maximum exposure of AA,

renal arteries, iliac arteries
Through long midline incision Through minilaparotomy incision
Retroperitoneal approach for AAA repair
S Indicated in—
z ‘Hostile’ abomen with multiple operations or exposure to
radiation treatment.
z Extension of aneurysm to suprarenal segment.
z Horseshoe kidney.
z Ascites.
Incision starts at 10th intercostal space at posterior axillary fold,

extends medially to lateral border of rectus toward a point midway
between umbilicus and symphysis pubis.
Basic steps of AAA repair
1. Mobilization
S Omentum and transverse colon are retracted superiorly.
S Posterior peritoneum between IMV and 4th part of duodenum is incised from the ligament of Treitz to aortic
bifurcation.
[Care is taken to avoid injury to IMA at its origin.]
2. Exposure
S Dissection is done proximally until the left renal vein is identified
z Renal arteries are identified and proximal infrarenal aneurysm neck is identified.
S Dissection is done distally upto the level of aortic bifurcation, exposing both common iliac arteries.
Excessive dissection of aortic bifurcation and proximal common iliac arteries should be avoided—To prevent the injury
of parasympathetic plexus [essential for ejaculatory function].
[Circumferential dissection of iliac arteries should be avoided—To minimize the injury of iliac veins.]
3. Heparinization
S IV heparin is administered.
4. Clamping
S Three minutes following heparin administration, the iliac arteries are clamped, followed by aorta.
[Ureters are passing near the iliac bifurcations and coursing along the anterior surface of iliac arteries—Be sure prior to
clamping.]
5. Opening the aneurysm

6. Repair
Endovascular aortic aneurysm repair
S An endovascular stent graft excludes the aneurysm

from blood flow.
Insertion of the stent is done through cannulation of
both femoral arteries.
S Criterias to be assessed before stent insertion:

z Length and diameter of nondilated infrarenal
aorta (neck of aneurysm).
z Angle between neck and aneurysm.
z Presence or absence of intraluminal thrombus.
z Shape of the aortic neck.

Management of ruptured AAA
Preoperative management
S Vigorous resuscitation with crystalloids, colloid, blood. Resuscitation is better done in the operating room
rather than emergency ward. Blood pressure needs to maintain at a minimum level to maintain end
organ and cerebral perfusion.
Operative management—
S Approach—Transperitoneal approach.
S First priority is to control the hemorrhage by gaining

proximal control of aorta at the supraceliac level
through the lesser omentum.
S After control of bleeding, rest of the maneuvers are
similar to electric repair.
Heparin should be avoided.
Aggressive use of blood, platelets and FFP are crucial for
survival.
Iliac Artery Aneurysm
S Isolated iliac artery aneurysm is rare, is usually associated with AAs

S Develops in association with
z Atherosclerosis
z Pregnancy
z Marfans syndrome
z Ehlers-Danlos syndrome
z Cystic medial necrosis.
S Most are palpable when they become large
S Symptoms are caused by compression of bladder and ureter, colon and rectum, lumbosacral nerves, pelvic veins
S Size>3.5 cm warrants elective repair
S Bilateral common iliac aneurysms require repair with bifurcated aortoiliac graft.
Femoral Artery Aneurysm
S Second most common peripheral artery aneurysm

S Mostly associated with aortoiliac aneurysm
S True aneurysms are always degenerative atherosclerotic aneurysms
S False aneurysms develop following catheterization, disruption of graft-artery anastomosis
S True aneurysms > 2 cm—Elective repair
S Surgical treatment includes resection and replacement with prosthetic graft.
Popliteal Artery Aneurysm
S Most common peripheral aneurysm.

S Patients are mostly male (about 97%).
S All symptomatic patients, size> 2 cm, thrombus in aneurysm, angiographic evidence of distal embolization—All are
indications for intervention.
S Reconstruction with a saphenous vein graft is the gold standard method of repair.
Recognition of popliteal artery aneurysm and its intervention is important because of the risk of limb loss.
Upper Extremity Aneurysms
S Rare phenomenon.
S Subclavian artery aneurysm is the most common type of upper extremity aneurysm.
S Usually caused by—
z Atherosclerosis
z Trauma
z Compression at thoracic outlet
z Infection.
Early diagnosis and intervention is important because of the risk of limb loss as well as life-threatening.
S Intervention includes—Resection of the aneurysm and reestablishment of arterial continuity with an interposition
graft.
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1. Splenic artery aneurysm

S Most common splanchnic aneurysm.
S Most are saccular type.
S Most are caused by degenerative atherosclerosis.
S Mostly females are affected.
S Percutaneous embolization of splenic artery is the

perfumed treatment.
2. Hepatic artery aneurysm

S Most extrahepatic aneurysms are true, most intrahepatic aneurysms are false
S Allhepatic aneurysms warrant intervention because risk of rupture is high
S Transcatheter embolization is the preferred treatment.
3. Renal artery aneurysm

S Most are saccular, mostly present at the bifurcation of primary or secondary
branches.
S Medial fibroplasia is the most common cause of true aneurysm.
S Spontaneous or traumatic dissection is the most common cause of false
aneurysm.
S If aneurysm ruptures in pregnant woman, fetal mortality 75%, maternal
mortality 50%, so aneurysm > 2 cm in women of childbearing age warrants
repair.
S Treatment includes reconstruction with a patch or bypass and treatment of
underlying renovascular hypertension.
Diseases of Thoracic Aorta
S Aorta consists of two major segments—

z Proximal aorta
Includes
– Ascending aorta
– Arch of aorta.
z Distal aorta
Includes
– Descending thoracic aorta

– Abdominal aorta.
S Common diseases of thoracic aorta—
z Aneurysm
z Aortic dissection.
[large volume of blood of high pressure flows through

the thoracic aorta; so, conditions that disrupt the inte-
grity of the aorta (e.g. dissection, aneurysm rupture)
have a catastrophic fate.]
Thoracic Aortic Aneurysm (TAA)
Different type of descending thoracic aortic aneurysm
Type A Type B
Type C
S Most of the aneurysms are asymptomatic.

S A few patients present with symptoms due to pressure over adjacent structures (left bronchus, esophagus, SVC,
RLN, porta hepatis), erosion into adjacent structures (esophagus, lungs, bronchus).
S Rupture of aneurysm.
S Distal embolization.
S Heart failure (if ascending aortic aneurysm involves the aortic root).
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S Chest X-ray—
z Widening of mediastinal shadow
z Displacement of trachea or left mainstem bronchus.
S Echocardiography—
z Both transthoracic and transesophageal echo provide excellent visualization of thoracic aorta.
S CT scan—
z Most useful imaging modality for evaluating thoracic aortic aneurysm.
S MRA
z Almost as useful as CT
z Additional advantages are no exposure to ionizing radiation and nephrotoxic contrast.
Treatment
Treat the Patient
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Marfan syndrome
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Patient with Marfan’s syndrome and patient predisposed to dissection and rupture (familial TAAD) with mutations in
transforming growth factor E-receptor type II-warrants surgical intervention at earlier stage due to rapid growth of
aneurysm and increased chance of rupture at smaller size.
Different methods of open repair
Modified Bentall procedure

[For proximal aneurysm causing aortic valve
insufficiency.]
Barts elephant trunk procedure

[For total aortic arch replacement.]
Endovascular repair
Criterias for graft placement—

S Adequate length and diameter of proximal and distal aneurysm neck
S Absence of mural thrombus.

Aortic Dissection
S Most common catastrophic event of the aorta.

S The initiating event is a primary intimal tear with secondary dissection into the media.
S The tear in the intima allows blood to flow from the true lumen to a newly formed channel (false lumen) by dissecting
the aortic wall.
S The initial tear after occurs along the right lateral wall of the ascending aorta or descending thoracic aorta just
below the ligamentum arteriosum.
Predisposing factors
S Systemic hypertension
S Cystic medial necrosis
S Marfan syndrome
S Ehler-Danlos syndrome
S Inflammatory aortitis (e.g. Takayasu’s arteritis, giant cell arteritis)
S Congential valve anomalies (e.g. bicuspid valve)
S Trauma (during cardiac catheterization)
S Pregnancy (n risk during 3rd trimester).
S Abrupt onset excruciating chest pain–classically described as ‘tearing’, associated with diaphoresis
S Location of pain depends on according to the aortic segment involved
S Site of dissection and acuteness of dissection have important clinical implications
Acute aortic dissection Chronic aortic dissection

(age of dissection < 14 days) (age of dissection > 14 days)
Suspect aortic dissection, if—

Male patient of sixth to seventh decades with acute chest pain, normal ECG finding and normal level of serum mark-
ers—Suspect aortic dissection.
S Once the diagnosis of aortic dissection is considered—
z Contrast CT is the investigation of choice
p
Double lumen aorta–is the classic finding
S If CT facility not available, then transthoracic or transesophageal echocardiography is indicated.
Treatment
Clinical suspicion of dissection (any type, any location)

p
Start pharmacologic therapy [to stabilize dissection and prevent rupture]
and
‘Antihypertensive therapy’ (E blockers, vasodilators, calcium channel blockers, ACE inhibitors)
Surgery for proximal aortic dissection
Surgery for distal aortic dissection
Surgical repair of this segment in the setting of

acute dissection is associated with high mortality.
S Limited graft repair is the approach to achieve the

goals (prevent fatal rupture, restore branch vessel
perfusion), but the risk is minimal.
Vascular Trauma
What Happens after Vascular Trauma?
1.
Exsanguinating hemorrhage leads to death
2.
Spasm of severed ends of artery and retraction
3. 4.
Pseudoaneurysm formation Formation of arteriovenous fistula
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artery)
Basic Principles of Management
1. Initial control of hemorrhage

S Digital or manual compression
S Catheter tamponade using Foley’s catheter
(in difficult access sites such as—high in neck, deep in pelvis).
2. Proper exposure
S In neck—By vascular exposure technique
S In chest—By choosing appropriate thoracotomy incision
S In abdomen—By appropriate operative maneuvers (e.g. Mattox maneuver, Cattell-Braasch maneuver).
3. Obtaining proximal control of injured vessel

4. Selection of appropriate repair technique
5. Damage control approach

Venous Diseases
Different Types
1. Superficial thrombophlebitis
S Appear spontaneously in patient with varicose veins,
in pregnancy, in Buerger’s disease, after IV therapy,
after localized trauma.
S Erythema, indurations, tenderness are usually pre-
sent.
S NSAIDs, elevation of the limb, local application of
heat are the primary treatment.
S Excision of the involved vein is considered if
symptoms persist after 2 wks treatment.
S If progressive proximal extension saphenofemoral
junction, then anticoagulant therapy/ligation and
resection of vein must be considered.
2. Thrombophlebitis migrans
S Specialvariety of superficial thrombophlebitis.
S Occurs in a migratory manner.
S Develops in presence of an abdominal cancer (e.g.

pancreatic cancer)— Known as Trousseau’s sign.
3. Venous insufficency 4. Deep vein thrombosis

Deep Vein Thrombosis (DVT)
S Most common location is in the lower limb (in the calf veins).
[With increased use of central venous catheter, permanent pacemakers, internal cardiac defibrillators, upper extremity
venous thrombosis is also now a common problem.]
[These thrombus rarely embolize and cause pulmonary embolism.]
How DVT Develops?
Stasis of blood flow

S Due to immobility, debilitating
conditions.
Virchow’s triad
Hypercoagulable state
S Factor V Leiden mutation.
S Protein C deficiency.
S Protein S deficiency.
S Antithrombin III deficiency.
S Surgery.
Endothelial damage
S Hyper homocysteinemia.
S Due to—
S Myeloproliferative disorders.
z Trauma.
S Malignancy (lung, colon, stomach,
z Venous cannulation.
breast).
z Transvenous pacing.
S Chemotherapy (cyclophosphamide
z Chemotherapy (bleomycin, vincristine, methotrexate, 5-FU).
doxorubicin).
Factors Associated with Increased Risk
S Immobilization—due to—
z Postoperative convalescence
z AMI
z CHF
z CVA.
S Hypercoagulable states
S Surgery—
z Orthopedic (particularly hip and knee surgery)
z Abdominal
z Genitourinary.
S Trauma—
z Fractures of spine, pelvis, femur and tibia.
S Malignancy (pancreas, stomach, lung and breast)
S Pregnancy
S Estrogen (as replacement or as contraceptive)
S Venulitis (Buerger’s desease, Behcet’s disease, homocysteinuria)
S History of DVT.
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For diagnosis, a high index of suspicion is needed

S Symptoms
First, do anand signs aretonot
arteriogram so helpful, as half of the patients are asymptomatic, porticularly patients with calf
know
thrombi.
z Site of thrombotic occlusion
Homan’s
z sign
Degree (calf pain on passive dorsiflexion of ankle) is not so reliable for clinical diagnosis.
of occlusion
Iliofemoral
S z venous thrombosis
Short or long segment results in massively swollen leg, pitting edema and blanching —
involvement
z
z Phegmasia alba and
Status of inflow dolens
outflow vessels.
Management is more complex, because
If disease further progress—Phlegmasia cerulea dolens (painful blue leg)
S Diffuse atherosclerosis at multiple levels
S Various degree of collated development
If still untreated—Venous gangrene
Diagnosis
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Lack of vein compressibility—Principal ful in these areas
criteria for diagnosis
Different Outcomes of DVT
Prophylaxis
S The goal is to prevent the morbidity and mortality of venous thromboembolism
S Potential candidates of prophylaxis
z elderly patient undergoing major abdominal (particularly cancer surgery) or major orthopaedic surgery (e.g. hip
surgery).
z Patient with major trauma.
z Prolonged immobility (> 3 days).

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Why LMWH is a preferable one?
S Longer half-life
S Higher bioavailability
S More predictable anticoagulant response
S No laboratory monitoring is necessary (PTT is unaffected)
S No contraindication in head injury and other traumas.
Treatment
Why treatment is necessary?

S To prevent morbidity and mortality associated with pulmonary embolism
S To prevent the postphlebitic syndrome
S To decrease the recurrence rate
S To limit further thrombosis.

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Risk Factors
S Occupation (prolonged standing)

S Heredity
S Gender (female sex)

S Obesity
S History of DVT
S Chronic constipation
S Tight clothing.
How Varicosity Develop?
S 3-factors maintain normal venous return, failure of any one factor or more cause varicose vein:
z Valvular competence
z Patency of veins
z Calf muscle pump.
S All varicose veins result from venous hypertension caused by flooding of venous blood in low pressure superficial
venous system.
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C = Clinical E = Etiological A = Anatomical P = Pathophysiological

z C0—No visible or tCongenital t Reflux
palpable veins tPrimary t Obstruction.
z C1—Telangiectasia tSecondary.
reticular vein
z C2—Varicose veins
z C3—Varicose vein with edema
z C4—Varicose vein with skin changes
z C5—Skin changes with healed ulceration
z C6—Skin changes with active ulceration.

S Venous prominences
S Heaviness of leg
S Swollen leg
S Aching leg.
S Ankle flare (corona phlebectatica).

S Pale area around ankle (atrophie blanche).
S Blackening and deformity around ankle (lipodermatoscle-
rosis/champagne bottle leg).
S Eczema.
S Ulceration.
Examination of the Patient
S Examination in the standing and lying down position

S Examination and assess—
z GSV territory, SSV territory or both involved?
z Saphenofemoral incompetence?
z Saphenopopliteal incompetence?
z Perforator incompetence?
S Look for complications—Eczema, blackening, ulceration, bleeding
S Feel the arterial pulses.

Clinical methods
1. Trendelenburg’s test
S The interpretation is saphenofemoral junction is incompetent.
S The interpretation is perforator incompetence.
2. Ochsner-Mahorner test (multiple tourniquet test)

3. Schwartz test 4. Fegan’s test
5. Modified perthe’s test
S The interpretation is deep vein is occluded by thrombus.
Assess
S Are the complaints (e.g. heaviness, swollen leg) are really due to venous insufficiency?
S Any complication present?
S Is your patient concerned about cosmesis?
Then, objective assessment
S Duplex scan of the venous system of lower limbs—It will give you the following informations:
z Status of GSV
z Status of SFJ (competent or incompetent)
z Status of SSV
z Status and location of SPJ (competent or incompetent)—SPJ is very much inconstant in location
z Status of deep veins
z Location and status (competent or incompetent) of leg and thigh perforators.
S Venography—Particularly indicated in recurrent varicose vein or if duplex scan is inconclusive.
Symptoms and signs suggestive of varicose vein but duplex scan is normal—Think of calf pump insufficency
Do, air plethysmography (give functional information on venous volume changes).
Treatment
S All symptomatic primary varicose veins should be intervened.

S All varicose veins with complications must be intervened.
S Patient treating for cosmesis purpose, patient should be counselled about the advantage and disadvantage of all
modalities of management.
1. Reassurance—Indicated in asymptomatic patients.

2. Compression therapy—Indicated in—

z Posthrombotic varicose veins
z Patient with minimal symptoms
z Not fit or unwilling to surgery
z After surgery, sclerotherapy and endovenous laser.
Elastic graduated compression stockings is the most

commonly used compression therapy method.
S Class I—Pressure 18–21 mmHg
S Class II—Pressure 26–34 mmHg
S Class III—Pressure > 34 mmHg.
Class II stockings is used for uncomplicated varicose vein.

Class III stockings is used for complicated varicose vein.
[Contraindicated in peripheral arterial disease and
cardiac failure.]
3. Pharmacological—Indicated in early stage of varicose veins, in association with compression therapy

S Commonly used phlebotropic drugs:
z Micronized purified flavonoid fraction—Acts by—
z Improving RBC rheology
z Antiinflammatory property
z Protective effect on venous valve
z Protective effect on venous wall.
Calcium dobesilate—Acts by—

S Increasing venous tone
S Antiedema and capillary protection effects.
Diosmin—Acts by—
S Profibrinolytic action
S Anti inflammatory property.
Rutin and troxerutin—Acts by—

S Improving RBC rheology
S Protective effect on venous wall.
4. Surgery—Indicated in
S Varicosities> 4 mm in diameter
S Varicosity with complication
S Refractory to medical therapy or compression therapy.

Trendelenburg’s surgery
Contd...
Contd...
S What is SEPS [subfascial endoscopic perforator

surgery?
z Endoscopic method of interrupting incompetent
medial calf perforators.
[In presence of lipodermatosclerosis, lack of space in
subfascial area leads to difficulty in introduction of endo-
scope and visualisation of perforators.]
5. Minimally invasive methods—

S Sclerotherapy—
z Indicated in telangiectasias, reticular varicosities and small varicose veins

z Sclerosing agents—
0.2% sodium tetradecyl sulfate
Polidocanol
Hypertonic saline.
25–30 gauge needle is used
No single injection dose exceeds 0.1 ml
Multiple injections may required
Pressure dressings must be kept for 72 hrs after sclerosant injecton.
S Endovenous laser—
z Using doppler USG, saphenous vein is mapped and marked

z The affected vein is cannulated under USG guidance and then laser fibre is introduced into the vein
z Then, the laser energy is fired.
S Radiofrequency ablation—
z Using doppler USG, saphenous vein is mapped and marked

z Under USG, guidance, special heater probe is inserted into the vein
z Collagen tissue of vein is denatured by heat.
S Foam sclerotherapy—
z Not more than 20 ml foam should be injected at one sitting. Multiple sitting may be required for maximum
success.
S Other methods—
z Catheter directed sclerotherapy

z Obliteration of varicose vein by hyperheated steam.
Venous Ulcer
S One of the common causes of leg ulceration is venous disease of the lower limb.
S Ulcer lying just proximal to the medial malleolus, associated with skin changes (lipodermatosclerosis)—Think of
venous ulcer.
S Examine the peripheral pulses—To rule out PAD.
S Examine the sensation, loss of sensation in foot with ulcer—Think of diabetic ulcer.
S Duplex USG of venous system and measurement of Doppler ankle blood pressure—Most appropriate investigation.
S Management—
z Venous ulceration due to—Superficial venous incompetence alone
Patient fit for surgery
Patient willing to undergo surgery
Varicose vein surgery

z Venous ulceration due to–Deep venous insufficency
Patient unfit for surgery
Patient unwilling to undergo surgery
Local ulcer management Compression therapy

+
Debridement of ulcer (by class III graduated compression stockings)
+
Irrigation with NS
+
Topical steroids (if eczematous reaction
around the ulcer)
[Topical antibiotics should be avoided.]
Disorders of Lymphatic System

Acute Lymphangitis
S Acute inflammation of the lymphatics when an area infected by pyogenic bacteria (specially, streptococci and
Staph.aureus), drained by the lymphatic system.
S Affected lymphatics are dilated and filled with exudate of neutrophils and monocytes.
S Clinically,
lymphangitis is manifestated by red painful subcutaneous streaks (inflammed lymphatics) with tender,
enlarged draining lymph nodes (acute lymphadenitis).
S Treatment—
z Rest of the affected part (to reduce lymphatic drainage)

z Elevation (to reduce swelling)
z Intravenous antibiotic (to treat the primary infection).
Lymphedema
Pathophysiology
S Lymphedema is the end result of improper lymphatic outflow due to aplasia, hypoplasia, hyperplasia, primary
decreased lymphatic contractility or inflammatory obliteration.
1.
2.
3.
S Secondary lymphedema is for more common than primary lymphedema

S Most common form of primary lymphedema is lymphedema praecox
S Most common form of secondary lymphedema worldwide is filarial lymphedema
S In developed countries, common causes of secondary lymphedema are—
z Tumor invasion
z Resection or ablation of regional lymph nodes by surgery, radiation therapy.
S Lymphedema characteristically involves the foot.

S Contour of the ankle is lost due to filling of submalleolar depression.
S ‘buffalo hump’ forms on the dorsum of the foot.
S Toes appear ‘square’.
S Skin over the edema cannot be pinched due to subcutaneous fibrosis (Stemmer’s sign).
S In early cases, pitting edema. In advanced stage, nonpitting edema due to fibrosis and dermal thickening.
S In advanced stage, chronic eczema, fungal infection of skin (dermatophytosis) and nail (onychomycosis), fissuring,
verrucae, papillae are seen.
S Ulcer may develop after a minor trauma.
S Chylous ascites, chylothorax, chyluria, chylorrhea (discharge of lymph from skin vesicles) suggest lymphangectasia
and chylous reflux.
S Ulceration, nonhealing bruise, purple-red nodules, if present—Think of lymphangiosarcoma.
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S Subclinical—
z Histological abnormalities in lymphatics and lymph nodes

z No clinically apparent lymphedema.
S Grade I—
z Edema pits on pressure
z Swelling mostly or completely disappears on elevation and bed rest.
S Grade II—
z Edema does not pit
z Swelling does not significantly reduce on elevation.
S Grade III—
z Edema is associated with irreversible skin changes—Fibrosis, papillae, fissuring, verrucae.
Lymphedema congenita (10%)

S Onset before 1st year of life
S More common in males
S More commonly bilateral and involving the whole leg
S The familial version is called the ‘Milroy’s disease’
S May be associated with disorders like yellow nail syndrome and Pierre-Robin syndrome.
Lymphedema praceox (80%)
S Onset from 1–35 years of age
S More common in females, peak incidence shortly after menarche
S More commonly unilateral
S Only extends upto the knee
S Familial version is called “Meige’s disease”.
Lymphedema tarda (10%)

S Onset after 35 years of age
S Patient must be investigated for malignancy of the pelvic organs, prostate and external genitalia.
KJłNI=PEKJKB!E=CJKOEO
S It is rather easy to clinically diagnose a case of lymphedema in second or third stage

S Diagnosis is difficult when the disease in a first stage
Primary? Secondary?
t Lymphoscintigraphy —Diagnostic test of choice t CT and MRI—Can exclude any mass
obstructing the lymphatic channels
– Almost 100% specific to differentiate t MRI can differentiate lymphedema from
lymphedema from other causes of limb swelling chronic venous edema and lipedema (excessive
subcutaneous fat and fluid)
– Cannot differentiate between primary and
secondary type
Lymphoscintigraphy
Lymphangiography
S Invasive study.
S This investigation is reserved for preoperative evaluation of a patient who is waiting for operations of the lymphatic
channels.
Management
Management
Conservative 2SHUDWLYH
Conservative measures
S Objectives are—
z Edema control
z Meticulous skin care
z Avoid injuries
z Avoid cellulitis and lymphangitis.
Different measures
S General measures—
z Patients must be educated about skin care and avoidance of injures
z Patients must be instructed to attend his/her physician whenever there is early signs of infection
z Infections must be aggressively treated with appropriate antibiotics
z Eczema requires treatment with steroid.
S Leg elevation—
z Avoid prolonged standing , foot end of the bed must be elevated.
S Compression garment—
z Graded compression stockings should be worn all time except at night
z Degree of compression required 20–60 mmHg
z Offer a protection against external trauma.
S Complex decongestive physical therapy (CDP)—
z Specialized technique to stimulate the remaining functional lymph vessels, evacuate stagnant protein rich fluid
and redirect lymph fluid to areas where lymph flow is normal.
S Compression pump therapy—
z Pneumatic compression pump therapy is a method—Similar principle to CDP.
S Pharmacotherapy—
z Benzopyrones, by stimulating proteolysis by tissue macrophages and also by stimulating the peristalsis and
pumping action of the collecting lymphatics may reduce lymphedema.
z Role is still doubtful.
Operative
S Only about 10% of the patients need surgical intervention.

S May be considered in patients with stage II and stage III lymphedema with severe functional impairment or recurrent
episodes of lymphangitis.
S 2 types of interventions
Reconstructive Excisional
t Indicated where lymphatic (a) Sistrunk operation
circulation is proximally obstructed
with normal distal lymphatic channels
t Different methods—
(a) Omental pedicle
(b) Anastomosis of lymph nodes (b) Homan’s operation
to veins
(c) Ileal mucosal patch (c) Charles operation
(d) Anastomosis of residual dilated
lymphatics to nearby veins
Chylothorax—
S Chylous pleural effusion.
S Due to thoracic duct trauma or advanced malignancy with lymphatic metastasis.
S Presence of chylomicron in pleural fluid and triglyceride > 110 mg/dl in pleural fluid—Diagnostic.
S Tube thoracostomy and medium-chain-triglyceride rich diet are the initial treatment.
S In patient with thoracic duct injury, if effusion persists for more than 1 week, ligation of the thoracic duct should be
done using video-assisted thoracoscopy.
S Pleurodesis is the last option.
Chylous ascites—
S Causes are—
z Congenital lymphatic abnormality
z Malignancy involving abdominal lymph nodes
S Presence of chylomicron and triglyceride level > 110 mg/dl in ascitic fluid is diagnostic
S Treatment is abdominal poracentesis and medium-chain triglyceride rich diet
S In duct injury, if chylous ascites not responds after 2 weeks duct must be ligated.
Chyluria—
S Filaria is the most common cause. Other causes are—
z Ascariasis
z Tumor
z Tuberculosis.
S Presents as painless passage of milky white urine, particularly after a fatty meal
S IVU/Lymphangiography demonstrate the presence of lymphourinary fistula
S Treatment is low fat diet, plenty of fluid to prevent clot, ligation of involved lymphatic channel.
Tumors of the lymphatics
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Chapter 19
Hernia
Important Topics
zzDifferent Types of Hernia

zzNyhus Classification of Groin Hernia
zzAnatomy of the Groin
zzInguinal Hernia
zzFemoral Hernia
zzUmbilical Hernia
zzEpigastric Hernia
zzIncisional Hernia
zzUnusual Hernia
‘The history of science, like the history of all human ideas, is a history of irresponsible dreams, of obstinacy and of error.
But science is one of the very few human activities—perhaps the only one— in which errors are systemically criticized and
fairly often, in time, corrected. This is why we can say that, in science, we often learn from our mistakes, ………..’
Karl Raimund Popper (1902–1994)
Austrian born British Philosopher of Science
Introduction
SS Theword ‘hernia’ derived from latin word meaning ‘a rupture’

SS Hernia is an abnormal protrusion of an organ or tissue through a defect in its surrounding wall
SS Hernia can occur in various sites, but it develops most commonly through the abdominal wall.
Other sites of hernia—

Hernia 777
There must be a weakness
Normal weakness Abnormal weakness
Present in all persons, due to anatomical

configurations Due to congenital Acquired
weakness
• In connective
tissue disorders, e.g.
– Osteogenesis imperfecta
– Ehler-Danlos syndrome
– Marfan syndrome
Composition of hernia
Different Types of Hernia

According to Presentation
zz External hernia—Protrusion through all layers of the abdominal wall
zz Internal hernia—Herniation of intestine or other abdominal viscera through a defect in peritoneal cavity.
According to Complication
SS Irreducible hernia—
Hernia 779
SS Obstructed hernia—
SS Strangulated hernia—
Femoral hernia is more likely to strangulate because of—

SS Narrow neck
SS Rigidity of surrounding structures.
According to Site
SS Inguinal hernia—
Neck of inguinal hernia is above and medial to pubic tubercle.

SS Femoral hernia—
SS Umbilical hernia—
SS Epigastric hernia—
Hernia 781
SS Incisional hernia—
SS Obturator hernia—
SS Spigelian hernia—
SS Lumbar hernia—
SS Sciatic hernia—
SS Perineal hernia—
Hernia 783
Nyhus Classification of Groin Hernia
SS Type I—Indirect inguinal hernia

zz Internal inguinal ring normal.
SS Type II—Indirect inguinal hernia
zz Internal inguinal ring dilated
zz Posterior wall intact.
SS Type III—Posterior wall defect
A. Direct inguinal hernia

B. Indirect inguinal hernia—Internal ring dilated and medially encroaching the transversalis fascia
C. Femoral hernia.
SS Type IV—Recurrent hernia
A. Direct
B. Indirect
C. Femoral
D. Combined.
Anatomy of the Groin
SS Anatomy is to be understood according to the surgeon’s approach to hernia repair.

SS When one is operating through a open approach, anatomy is to be considered from skin to the peritoneal cavity.
When one is operating through a laparoscopic approach, one should consider anatomy from abdominal cavity to
the skin.
SS Surgeon must know the anatomy to select the most suitable approach for repair, to lower the recurrence rate and
to avoid the complications.
What is Myopectineal Orifice of Fruchaud
SS According to Fruchaud, all groin hernias (indirect, direct and femoral) arise due to a common anatomic defect rather
than a isolated cause for each one.
SS His concept is that, all groin hernias are due to failure of the transversalis fascia over myopectineal orifice to retain
the peritoneum.
SS The myopectineal orifice is surrounded—
zz Superiorly, by internal oblique and transversus abdominis
zz Inferiorly, by Cooper’s ligament
zz Medially, by lateral border of rectus muscle and sheath
zz Laterally, by Iliopsoas muscle.
SS The inguinal ligament and iliopubic tract divide the myopectineal orifice of Fruchaud into superior and inferior
compartment.
The procedure ‘giant prosthetic reinforcement of visceral sac’ (GPRVS), developed by Stoppa, is basically reinforcing the
transversalis fascia over Fruchaud’s myopectineal orifice with the help of a prosthesis.
Basics of Anatomy of Groin

Hernia 785
Inguinal Hernia
SS About 75% of all hernias are inguinal hernias

SS In both male and female, inguinal hernias are the most common type of hernia
SS Men are 25 times more likely to develop groin hernia
SS Among inguinal hernias, about 75% are indirect and rest are direct hernias
SS Bilateral hernias are commonly direct hernias than indirect
SS Both indirect and femoral hernias commonly occur in right side
zz Due to delayed obliteration of processus vaginalis
zz Due to tamponading effect of sigmoid colon on the left femoral canal.
SS The prevalence of hernias as well as likelihood of strangulation increases with age
SS Among all strangulated hernias, most are indirect inguinal hernias.

SS History from the parents is more important than the physical examination—In the case of pediatric hernias
SS All patients with small-bowel obstruction must be searched for presence of obstructed hernia.
On Examination
SS Patientmust be examined both in lying and standing position.

SS Swelling appears in the groin on standing and after coughing, peristaltic
sound in the swelling, swelling is nontransilluminant—
Most likely inguinal hernia.
Hernia 787
SS A hernia that descends into the scrotum—Certainly an indirect inguinal hernia.

SS Bulge moving lateral to medial in the inguinal region after coughing—Most likely indirect inguinal hernia.
SS On straining, swelling (symmetric, circular) near the external ring appears from deep to superficial—Most likely
direct inguinal hernia.
SS When reducing the hernia, a gurgling sound is audible—Most likely an enterocele.
SS A patient who is used to reduce the swelling manually now cannot do it and surgeon cannot reduce the hernia by
‘Taxis’—It is an irreducible hernia.
[The distinction between indirect and direct inguinal hernia cannot be done accurately by clinical methods always and
it is not essential to differentiate because repair is approached in a same way regardless of type of hernia.]
Diagnosis
SS Appearance of swelling in groin after standing or coughing, presence of cough impulse, gurgling sound during
reduction—These clinical findings are highly suggestive of inguinal hernia, in most cases. No need of further
investigation for confirmation.
SS According to patient, swelling appears in the groin after straining, but not present on clinical examination—Makes
a dilemma both in pediatric and adult patients.
zz Standing or ambulatory for a period sometimes makes the undiagnosed hernia to become visible
zz Repeat examination at another time is also helpful.
SS USG has high degree of sensitivity and specificity in delection of occult direct and indirect hernias.
SS CT is also very much sensitive in doubtful situations.
SS Laparoscopy is the final approach to detect the exact nature of groin pathology.
Treatment
SS Temporary management is manual reduction.

Be aware of the possibility of reduction en masse.
SS Inguinal hernias should be electively repaired unless specific contraindications present.

SS Elderly patient can also well tolerated elective repair if associated medical problems can be controlled and local
anesthesia is perferred.
SS Patient with chronic bronchitis should not be denied repair, for these are the people having increased chance of
developing strangulated hernia.
SS Postoperative morbidity and mortality after a laparotomy for strangulated hernia are much more than elective
repair.
SS If patient has associated significant prostatic hyperplasia, chronic constipation, chronic cough—It should be treated
first.
SS Choice of anesthetic—LA, regional (spinal /epidural), GA.
zz In laparoscopic repair, GA is preferred to achieve complete muscle relaxation for insufflation.
SS Goals of hernia rapair
Elimination of peritoneal sac (herniotomy) Repair of fascial defect in inguinal floor

(herniorrhaphy/hernioplasty)
Only herniotomy is indicated in pediatric hernia and hernia in young adults.

Hernia 789
SS Surgicalmanagement includes—
zz Treatment of hernial sac
zz Reconstruction of inguinal floor.
Treatment of hernial sac
SS In indirect herina, the sac (pearly white structure lying on outer side
of cord) is dissected from the card structures (pampiniform plexus, vas
deferens) and cremasteric muscle.
SS During posterior dissection of sac, care must be taken to avoid injury to
vas and spermatic artery.
SS Large indirect sac extending upto the scrotum should not be dissected
beyond the pubic tubercle due to increased risk of ischemic orchitis.
Sac is identified by its pearly white color
SS Sac is opened, taking care not to injure any hernial

contents (intestine or omentum).
Sac is opened to look for any contents (intes-

tine or omentum)
SS Contents are reduced, sac is dissected upto the neck

(extraperitoneal fat is seen and inferior epigastric
vessels on the medial side).
Sac is ligated at the neck with absorbable suture.
Sac is ligated at the neck
SS Direct sacs should not be opened or ligated, but must be freed from transversalis fibers.
SS In preperitoneal approach, sac is reduced but not ligated.
SS In sliding hernia, sac is opened but no attempt should be made to dissect the contents from the sac, then the sac
is inverted.
SS Mobilizing the testis into the inguinal canal should be avoided to minimize the risk of testicular ischemic injury.
Reconstruction of inguinal floor

Primary tissue repair
SS Mostly abandoned due to high recurrence rates.

SS Particularlyindicated in strangulated inguinal hernia where mesh repair is contraindicated.
SS Different approaches—
1. Bassini repair
SS Conjointtendon is approximated to the inguinal ligament with the help of

nonabsorbable suture (polypropylene)
Hernia 791
2. Shouldice repair
SS A multilayer repair of the posterior wall of the inguinal canal by continuous running suture technique.
SS The 3rd layer brings together the conjoint tendon medially with the inguinal ligament laterally.
SS The 4th layer brings together the anterior rectus sheath medially with the posterior aspect of the external oblique
aponeurosis laterally.
3. McVay (Cooper’s ligament) repair
SS Isthe only technique that repairs both inguinal and femoral hernia
SS Edge of transversus abdominis is approximated to Cooper's ligament with nonabsorbable sutures.
4. Iliopubic tract repair
SS Transversus abdominis aponeurotic arch is approximat-

ed to the iliopubic tract with nonabsorbable interrupted
sutures.
Tension-free repair
SS Placement of a synthetic mesh prosthesis avoids any tension during repair—Therefore very few chances of
recurrence.
SS Different types of tension free repair—
1. Lichtenstein repair
A piece of polypropylene mesh is placed over the floor of inguinal canal.

SS Mesh is sutured to the
zz Fascia overlying the pubic tubercle, inferiorly.
zz Conjoint tendon, medially.
zz Inguinal ligament, laterally.
SS Mesh is slit at the level of internal ring, the two limbs are crossed around the spermatic cord, thus creating a new
internal ring.
Polypropylene mesh (6"×3")
Lichtenstein tension free repair (prolene

mesh is placed over the fascia transversalis)
Hernia 793
2. Plug-and-patch technique
SS First described by Gilbert.

SS Original Gilbert method—A mesh plug in the form of ‘upside down umbrella’ or ‘cone’ is snugly placed in the internal
ring.
SS Modified Gilbert method is—Original Gilbert method + Lichtenstein repair, also called ‘plugtenstein’.
3. Sandwich technique
SS Onlay patch is placed in the inguinal floor, underlay patch

is placed in the preperitoneal space. The two patches are
connected by a connector.
Open preperitoneal approach
SS Preperitoneal space is the space between the fascia transversalis

and the peritoneum.
SS This approach is based on the principle that the repair fixes the
hernia defect in the space between hernial contents and hernia
defect.
SS Indicated in recurrent inguinal hernia, sliding hernia, bilateral
hernia.
SS Large mesh is placed in the preperitoneal space to cover the
inguinal floor and myopectineal orifice.
Laparoscopic approach
SS This approach is based on the principle of preperitoneal approach.

SS Particularly indicated in bilateral and recurrent inguinal hernias.
SS 2 techniques :
zz TAPP
zz TEP }Final target is same (preperitoneal space), but initial access is different
In TAPP repair, the preperitoneal space is accessed after entering into the peritoneal caity
In TEP repair, the preperitoneal space is created using a balloon dissector.

Hernia 795
Special Types of Inguinal Hernia
Sliding Inguinal Hernia (Hernia-en-glissade)
SS A type of indirect inguinal hernia where the posterior wall of the sac
is formed by the sliding visceras.
SS On the right side, the cecum is most commonly involved; on the left
side, the sigmoid colon; and on either side, part of urinary bladder.
SS Exclusively found in males, most of them are present in the left side.
[It should be suspected in any large hernia that cannot be completely

reduced.]
[It is essential to identify the condition early in the operation otherwise
inadvertent entry into the bowel or bladder may occur.]
SS After dissecting the sac from the cord, the sliding hernial sac can be
reduced by series of inverting sutures (Bevan technique) and then
reconstruction of the posterior wall of the inguinal canal.
Very large sliding hernia can be treated by entering the peritone-
um through a separate incision, pulling the bowel back into the abdo-
men, fixing it to the posterior abdominal wall and then reconstruction
of floor of the canal.
[No attempt should be made to dissect the sliding viscera free
from pertoneum, it may cause fistula or peritonitis due to devascu-
larization.]
SS High recurrence rate in compare to simple hernia.
Strangulated Inguinal Hernia
SS Indirect inguinal hernias are more commonly strangulated

than direct hernias.
SS The risk of strangulation is highest in the first months to years
after the initial presentation.
SS Usually, the small intestine is involved in strangulation. Large
intestine rarely become involved.
SS Treatment is resuscitation (with IV fluids, Nasosgastric
suction, IV antibiotics) + surgical intervention (resection of
gangrenous gut and primary tissue repair).
[Mesh repair of hernia should be avoided due to increased
risk of bacterial translocation and wound infection.]
Some Unusual Types of Hernia
1. Richter’s hernia 3. Littre’s hernia
Strangulation without obstruction.
2. Maydl’s hernia 4. Pantaloon hernia
A cause of recurrence, if one of the sacs may be overlooked.

Hernia 797
Fermoral Hernia
SS Protrusion of extraperitoneal fat or abdominal contents through the femoral canal.

SS Femoral canal is surrounded by bone and ligaments on three sides. The narrowness of the sac and the rigidity of
femoral ring makes it most likely to be strangulated.
SS Most of the patients are 60–80 years old female patients.

SS More common in women than men.
SS May present with intermittent groin bulge or tender groin

lump.
[An elderly female patient presenting with small bowel
obstruction, but no history of abdominal surgery—Think of
occult femoral hernia.]
SS On clinical examination, rounded bulge appears in the
upper thigh just below the inguinal ligament, below and
lateral to the pubic tubercle.
Tender femoral hernia without features of intestinal obstruction—Think of Richter’s hernia.
SS Surgery is warranted once the diagnosis is made, because chance of strangulation is high.
SS Severalapproaches to the hernia, but all approaches follow the same principles—
zz Complete excision of hernial sac
zz Inspection of the contents
zz Closure of the defect in femoral canal.

SS Incision similar to inguinal hernia, but closer to the inguinal

ligament.
SS Fascia transversalis is incised along the line of incision.
SS Sac is identified and after opening it, is excised.
SS Femoral ring is obliterated by suturing the inguinal ligament

to the Cooper’s ligament.
SS Posterior wall of the inguinal canal must be reconstructed
as it has been weakened by exposure.
1. Inguinal (Lotheissen) 2. Low operation (Lockwood)
Different Approaches
SS Incision is 1 cm below and parallel to the inguinal ligament.
3. McEvedy
SS Vertical
incision over the swelling and
extended above the inguinal ligament.
Hernia 799
SS Femoral ring is obliterated either by suturing the inguinal ligament to the Cooper’s ligament or by placement of
mesh.
SS During repair, laterally femoral vein and medially bladder must be protected.
[Be aware about the presence of aberrant obturator artery (originates from inferior epigastric artery)
during placement of medial suture, aberrant obturator artery, if present, may be injured.]
Umbilical Hernia
Different types
1. Congenital umbilical 2. Acquired umbilical

3. Paraumbilical hernia
hernia hernia
SS Congenital umbilical hernia develops when umbilical scar fail to develop or weak.
SS Acquired umbilical hernia develops when umbilical scar is stretched by raised intraabdominal pressure.
SS Paraumbilical hernia develops just above or just below the umbilicus.
SS Umbilical hernia in infants and children are congenital umbilical hernia.

SS Usually, spontaneous closure of congenital umbilical hernia occurs by the age of 2 years. If defect persists even after
5 years, surgery is to be considered.

SS In adults, umbilical hernias are acquired.
SS Acquired umbilical hernias are more common in women, usually associated with pregnancy, obesity, ascites.
SS Strangulation is uncommon.
SS Small asymptomatic acquired hernia need no active intervention.
SS Large hernia, incarcerated hernia, thining of overlying skin, hernia due to uncontrolled ascites warrant repair.
SS Traditional ‘vest-over-pants’ technique by Mayo is not used nowadays due to increased recurrence rates.
SS Small defects (≤ 3 cm) can be repaired primarily with nonabsorbable sutures after dissecting the sac from the
umbilicus.
SS Larger defect > 3 cm need repair with prosthetic mesh.
Hernia 801
Epigastric Hernia
Also called 'fatty hernia of the linea alba'.
SS Thishernia occurs through a defect in the linea alba anywhere between the xiphoid process and the umbilicus.
SS Thisdefect develops due to weakened decussating fibers of linea alba associated with increased intraabdominal
pressure or chronic strain in abdominal wall.
SS In most cases, the hernia contains preperitoneal fat only and no sac. If sac presents, it usually contains omentum
and rarely intestine.
SS Middle aged male persons are mostly affected.
SS Multiple epigastric hernia is not so common, but not a rare finding.
[Failure to recognize the other hernial defects is the cause of ‘recurrence’.]

SS In most cases, epigastric hernias are asymptomatic. It is better felt than it can be seen.
In symptomatic cases, it is felt as a small, soft, reducible, mildly tender mass in the midline anywhere between xi-
phoid and umbilicus. This mass becomes more prominent with standing and Valsalva maneuver.
SS Rarely, imaging is needed for diagnosis. If needed, then CT scan is the preferred imaging method.
SS All symptomatic hernias must be repaired.
SS Small defects can be repaired by primary closure using nonabsorbable suture.
In larger defects (> 4 cm), the repair should be reinforced with prolene mesh.
Incisional Hernia
SS Develops at previous incision as a result of improper healing of fascial tissues.

SS Can occur at any type of abdominal wall incision, increased incidence in midline, standard paramedian, transverse
incisions, low incidence in appendicectomy and Pfannenstiel incisions. May also develop in tocar sites (10 mm).
Hernia 803
Factors responsible
Patient related factors Operative factors
• Advanced age
• Ascites
• Anemia
• Corticosteroid use
• Cancer (malignancy) 1. Types of surgery
• Cytotoxic drugs
• C vitamin deficiency
• Cigaret smoking
• Debilitated state (malnutri-
tion) Emergency
• Diabetes mellitus Elective
↑ risk of hernia
• Jaundice
• Uremia
• Obesity
• Surgical site infection
2. Types of incision
3. Technique of
closure
Mass closure/layered closure
}
Inadequate fascial bites Placement of drain or stoma in the primary operative
Tension of fascial edges ↑↑ risk wound— ↑ risk
Excessive tight closure
4. Suture material
Absorbable/nonabsorb- Length of suture material in

able respect to incision length
Hernia 805
SS Appearance of bulge over the operative scar

on straining.
SS In large hernias, skin may become pressure
necrosed leading to ulceration.
SS Sometimes present with intestinal obstruction
or strangulation.
SS On examination, the entire length of incision
must be inspected and palpated carefully, as
multiple defects may be present.
SS In obese patients with suspected hernia, CT abdomen is helpful to make the diagnosis.
Treatment
Surgical repair of hernia.
SS Three different types of repair—
Repair
3. Laparoscopic mesh
1. Primary suture repair 2. Open mesh repair
repair
Primary suture repair
SS If hernia defect <2–3 cm with strong, healthy surounding tissue.

Open mesh repair
SS Larger defects (>3 cm) must be repaired with mesh.
Various techniques of
placing mesh
Onlay technique Underlay technique
• Primary closure of the

fascial defect
⇓
• Placing of polypropylene Placement of mesh in retro- Placement of mesh in preperi-
mesh over the fascia rectus space toneal space
• Disadvantages—
– Increased chance of in-
fection
– Increased chance of
seroma formation
– More chance of recur-
rence
Hernia 807
SS Advantages of underlay technique—
zz Less chance of infection
zz Less chance of recurrence.
Mesh should be extended 5–6 cm beyond the superior and inferior borders
of the defect.
Mesh is placed in the retrorectal space
Laproscopic mesh repair
SS Intraperitoneal or preperitoneal mesh application is done in laparoscopic repair.
Polypropylene mesh in intraperitoneal position

should be avoided to prevent enterocutaneous fistula
formation
[Preperitoneal mesh repair is the commonly used

method for laparoscopic repair of incisional hernia.]
Components separation technique
Particularly useful in patients with large strangulated ventral hernia where mesh application is contraindicated.
Unusual Hernia
Obturator Hernia
SS One of the rarest hernias.

SS Female: male 6:1 — due to • broader pelvis
• wide obturator
canal
SS Most of the hernias present in the 7th and 8th
decades.
SS Weakening of the obturator membrane results
in enlargement of the canal and development of
hernial sac.
4 cardinal findings
3. Recurrent episodes of 4. Palpable mass in medial

1. Acute intestinal obstruction 2. Howship-Romberg sign
intestinal obstruction aspect of thigh
• Most common presentation • Second most common presenta- • Uncommon presentation

• Small bowel is most fre- tion
quently obstructed • Pain along the medial thigh due to
cornpression of the obturator nerve
between the canal and the sac
Another finding may be present — Hannington-kiff sign

↓
Loss of adductor reflex
An elderly female patient presents with small bowel obstruction —Think of obturator hernia.
Elderly female patient with history of pain in medial thigh or history of recurrent episodes of intestinal obstruction—
Think of obturator hernia.
SS Usually, patient with obturator hernia presents as acute small bowel obstruction. So, most of the time this hernia is
approached through a midline laparotomy approach (lower midline).
SS Three operative approaches 1. Lower midline transperitoneal
2. Lower midline extraperitoneal
3. Anterior thigh exposure
Hernia 809
Perineal Hernia
Also termed pelvic hernia, ischiorectal hernia

SS Heriniation through weakened pelvic floor.
SS Different types of perineal hernia—
Perineal hernia
According to etiology
According to location of
hernial defect
Primary
Secondary
• Atleast 5 times more • More common than prima-

common in women due to ry ones and develops after
– Broader pelvic floor APR, perineal prostatecto-
– Long-term effects of my or pelvic exenteration
pregnancy and child
birth
– Elongated pouch of Posterior
Douglas Anterior
SS Anterior perineal hernia emerges anterior to the transverse perinei muscle and presents as a swelling in posterior
part of labia majora.
Posterior perineal hernia presents as a bulge in perineum in men, and in women, as a bulge in the posterior vagina.
[Perineal hernias must be differentiated from more common cystocele or rectocele.]
SS Three approaches of repair 1. Transperitoneal—preferred method
2. Perineal
3. Combined
Spigelian Hernia
SS Spigelian hernia develops through the spigelian fascia along the semilunar line.
[Semilunar line traverses along the lateral rectus border from the ninth costal cartilage to pubic tubercle.]
[Spigelian fascia is an aponeurotic structure between the transversus abdominis laterally and posterior rectus sheath
medially.]
SS These hernias are often interparietal, most common type passed through the transversus abdominis and the
internal oblique aponeuroses.
SS Patients present with swelling in the lower abdomen just lateral to the rectus muscle.
SS USG is sometimes necessary when diagnosis is in doubt.
SS Treatment is repair of the defect.
Primary suture repair by apposing medial and lateral edges of the internal oblique and transversus abdominis
aponeuroses.
Large defects need mesh repair.
Hernia 811
Lumbar Hernia
Different types
Hernia through Hernia through inferior lumbar

Congenital Acquired superior lumbar triangle (Grynfeltt triangle (Petit's triangle)
triangle
SS Most commonly found in older males.

SS Acquired lumbar hernias are usually associated with—Back trauma, surgery in lumbar region, use of iliac crest as
donor site.
[Strangulation is rare, because three boundaries of the defect are soft and muscular.]
SS Patients usually present with a soft reducible swelling in the lumbar region, size increases after straining or valsalva
maneuver.
SS USG or CT is usually needed to confirm the diagnosis.
SS The defect is repaired by mesh repair.
Sciatic Hernia
Herniation through greater or lesser sciatic foramen.

SS Patientusually presents with pain in the buttock that radiates down the leg in sciatic nerve distribution or tender
lump in the buttock or infragluteal region.
SS Treatment is surgical (transperitoneal or transgluteal approach).
Interparietal Hernia
SS Hernia sac lies between the layers of the abdominal wall

SS Spigelian hernias are almost always interparietal
SS Clinically, it is difficult to diagnose. CT is useful to make correct diagnosis
SS Mesh repair or components separation technique is the surgical approach for repair.
Chapter 20
Diseases of the Testes,

Scrotum and Penis
Important Topics
zzUndescended Testis
zzVaricocele
zzHydrocele
zzHematocele
zzPyocele
zzChylocele
zzOther Scrotal Swellings
zzFournier's Gangrene
zzPhimosis
zzParaphimosis
‘Science can never be a closed book. It is like a tree, ever growing , ever reaching new heights. Occasionally the lower
branches, no longer giving nourishment to the tree, slough off. We should not be ashamed to change our methods; rather we
should be ashamed to do so.’
Charles Value Chapin (1856–1941)
American Physician and Public Health Officer
Diseases of the Testes, Scrotum and Penis 815
Diseases of the Testes
Undescended Testis
SS Present any where between the abdominal cavity and just outside the anatomic scrotum
SS Variations of incomplete descent
Right sided undescended testis

Imperfect descent Ectopic testis
Descent is arrested anywhere in the path of its Descent along the normal pathway upto external ring
descent ⇓
Then, it rests on an ectopic location (superficial inguinal pouch,
medial thigh, root of the penis, perineum)
Ectopic testis is fully developed.
SS Isit so common?
zz Found in 3% of full-term male newborns and 30% of preterm newborns
zz More prevalent in preterm, small for gestational age, low birth weight and twin neonates.
SS Don't become worry, wait for atleast 3 months—
zz About 70–77% of undescended testes will spontaneously descend, by 3 months of age
zz By the age of 1 year, incidence of spontaneous descent become 1%.
SS Brother is affected, chance is more—
zz Risk is 6.9 fold if brothers is affected, risk is 4.6 fold if father is affected.
SS When testis becomes nonpalpable?

zz Testis is intraabdominal
zz Absent (vanishing) testis
zz Atrophic testis
zz Missed on clinical examination.
Is 'Retractile Testis' Needs Attention?
Testis is retracted out of the scrotun toward the inguinal Retracted testis can be brought down into a dependant
canal due to overactive cremasteric reflex. position of the scrotum and remains there after traction
is released.
SS Itis not a true cryptorchid testis, not a perfectly descended testis
SS Patient with retractile testis should be monitored yearly, upto puberty or till the testis no longer retractible.
How Testis Descends and Why It Maldescends?
SS Testicular descent is divided into 3 phases:
SS After 23rd weeks of gestation:

Testis descends to just inside the internal ring
SS After 28th weeks of gestation:

Testis travels through the inguinal canal alongside and
posterior to processus vaginalis.
SS After28th weeks of gestation:

From external ring to the scrotum.
Factors Responsible for Testicular Descent

SS Decreased cells, degenerated cells in cryptorchid testis—

zz Changes started in between 1–2 years of age.
zz Changes—
Decreased no. of Leydig cells
Degenerated Sertoli cells
Delayed disappearance of gonocytes
Delayed appearance of adult dark (Ad) spermatogonia
Developmental failure of primary spermatocytes
Decreased number of total germ cell counts.
[Hypoplasia of the Leydig cells–earliest postnatal histological abnomality.]
Complications of Cryptorchidism
SS Infertility—Paternity is almost 90% in unilateral cryptorchidism, 35–65% in bilateral cryptorchidism.

SS Neoplasia—Men with persisting or treated cryptorchidism have a relative risk of 3.6 for developing testicular
cancer (seminoma); no increase in risk in men with history of spontaneous descent.
[Most common tumor in cryptorchid testis is seminoma.]
SS Hernia—Patent processus vaginalis is found in more than 90% of patients.
SS Torsion of testis— Increased susceptibility is due to developmental anatomic abnormality between the testis and
its mesentery.
Where is the Cryptorchid Testis?
SS Patient must be examined in supine, SS Less

accurate (44%) SS Accuracy >95%
sitting and also in squatting position SS Options USG SS With the existing ports,
SS Examiner's palpating fingers are to be
MRI the procedure can be
swept down from just above the internal converted to a therapeutic
ring along the inguinal canal into the procedure
scrotum
SS Examiner may feel the testis moving
back under the fingertips or a 'pop' as the
testis retracts back into its cryptorchid
position
SS Ectopic areas of descent must be
examined
Check that the following queries have answered:

SS Unilateral or bilateral?
SS Imperfect descended testis or ectopic testis?
SS Testis palpable or not?
SS Are other abnormalities present or not?
SS Are associated penile malformations present?

When to Treat, How to Treat and Why
SS Definitive
treatment should be started between 6 and 12 months of age, particularly in bilateral or unilateral
intraabdominal testis (to preserve most of the testicular tissues).
SS Child presenting after this time period also must be treated by orchiopexy to prevent further testicular impairment
(spermatogenic as well as endocrinal) and to attain the scrotal position for easy palpation (early detection is possible
if any malignant transformation). Orchiopexy does not reduce the risk of development of cancer.
SS Orchiectomy is indicated only for postpubescent patients with contratateral normally descended testis.
Standard Orchiopexy (Open Approach)
Operative picture showing complete mobilization of

spermatic cord and testis
Placement of testis in dartos pouch
Fowler–Stephens Orchiopexy (One Stage/Two Stage Procedure)
SS Indicated in high inguinal or intraabdominal testis.

SS In one stage procedure, ligation of the testicular vessels is done with a wide pedicle of peritoneum to preserve the
collateral circulation (deferential artery, a branch of inferior vesical artery; cremasteric artery, a branch of inferior
epigastric artery).
SS In two stage procedure, ligation of spermatic vessels is done as close to origin as possible. After 6 months or more
(allow to grow collaterals), the testis is mobilized and placed in the dartos pouch.
Torsion of the Testis (Syn. Torsion of the Spermatic Cord)
SS Torsion of the testis is a true surgical emergency.

Irreversible ischemic injury to the testis may develop as early as after 4 hours of torsion.
SS Predisposing factors:
1. High investment of tunica vaginalis—
2. Epididymis with a pedicle—
Torsion is confined to pedicle that connects the testis with epididymis

No torsion of the cord
SS How torsion develops?

zz When there is sudden contraction of cremasteric muscle (following trauma, athletic activity, lifting a heavy
weight, sexual intercourse)
⇓
Spiral attachment of cremaster onto the cord favors rotation around a vertical axis (as much as 360°)
zz Also develop spontaneously (in sleep). In many cases, adolescent boys are awakened from sleep after developing
torsion.
SS Patient presents with—Acute onset scrotal pain associated with nausea and vomiting. Many patients had history
of previous episodes of selflimited acute scrotal pain.
SS On examination, high lie of the testis and thickened, tender, twisted cord that can be palpated above the testis.
Absence of cremasteric reflex is a good clinical sign.

Torsion and acute epididymo-orchitis present almost similarly. So torsion must be differentiated as it is a true
surgical emergency.
Elevation of testis reduces pain in epididymo-orchitis but it is not a reliable clinical finding.
SS When torsion is suspected, Color Doppler study is to be done as early as possible (specificity 98.8%).
If there is any doubt about diagnosis, the scrotum should be explored urgently.
SS On exploration, testis with good or marginal viability must be preserved and after detorsion, it must be placed in
dartos pouch and fixed with fine, nonreactive, nonabsorbable suture.
If necrotic testis is found, orchidectomy should be done.
Contralateral hemiscrotum must be explored and the testis must be fixed to prevent subsequent torsion.
Varicocele
SS When veins of the pampiniform plexus becomes ectatic and tortuous, it is called varicocele.
SS How varicosity develops—
SS Left side is affected in 95% of cases.

SS Tall, thin men with pendulous scrotum are more frequently develop varicocele.
SS Most of the varicoceles are asymptomatic. Most of them discovered during routine physical examination for
preemployment check up.
SS Patient must be examined in both supine and standing position, with and without a valsalva maneuver.
SS On clinical examination, it is manifested as painless compressible mass (consistency of a "bag of worms") above or
surounding the testis, that decompresses when patient is in supine position.
SS Grading—
I. Small, palpable only after valsalva maneuver

II. Moderately sized, easily palpable without a valsalva maneuver
III. Large, visible through the scrotal skin.
SS Assessment of testicular consistency and volume is very much crucial

Subjective Can be assessed by Prader or disk orchidometer
SS Testis volume measurement is the mainstay of assessment of whether surgical intervention is needed or not.
SS If ipsilateral testis volume loss > 2 ml — Adolescent varicocele ablation is needed.
SS Treatment options —Different options, but same outcome.
Varicocele is approached through inguinal approach

Hydrocele
SS Abnormal collection of fluid in tunica or processus varginalis.

SS Different types:
SS Due to delayed closure of SS Persistence of processus SS Due to segmental closure of

processus vaginalis vaginalis allows peritoneal processus vaginalis.
⇓ fluid to communicate with SS Manifested as painless groin
Fluid trapped within the tunica the tunica vaginalis. swelling contiguous with the
vaginalis SS Classic description is that, cord structures.
SS Commonly seen at birth.
the swelling is smaller in the SS Can be palpated at any posi-
morning and becomes more tion just above the testis to
SS Tense, nontender swelling.
prominent as day progresses. superficial inguinal ring.
SS Transillumination positive.
SS Communication is too small SS Swelling moves downwards
SS Most of them resolve mithin 2
to allow herniation of in- and becomes less mobile
years of life. traabdominal contents. when testis is pulled down-
SS If surgical intervention is SS Most communicating hydro- wards.
indicated it must be intervened celes close spontaneously by SS Exploration must be done
through inguinal approach. 1 year of age. through inguinal approach.
SS All persistent communicating Ligation of the processus
hydroceles must be explored vaginalis at internal ring and
through inguinal incision. excision or unroofing of the
cyst is the treatment.
[Hydrocele of the canal of Nuck
is the counterpart in females.]
Primary Vaginal Hydrocele
SS Most common in middle and later life.

SS Develops due to defective absorption of fluid in tunica vaginalis.
(imbalance between secretion and absorption)
SS Nontender scrotal swelling, 'get above the swelling' present, transillumination positive.
Typical color of fluid in primary vaginal hydrocele

Operatic picture of Jaboulay's procedure

Secondary Hydrocele
SS Itis due to Epididymorchitis

Testicular tumor
Filaria
SS Clinically, lax hydrocele and underlying testis is palpable
SS Best treated by treating the cause of the hydrocele.
[A young patient with lax hydrocele—Always exclude testicular tumor before any surgical interventions.]
Hematocele
SS Bloody fluid in tunica vaginalis

SS Usually develops following trauma
SS Drainage is the treatment of choice.
Pyocele
SS Pus in tunica vaginalis

SS Drainage of pus after opening the tunica vaginalis is the treatment.
SS Sometimes, orchidectomy is needed.
Chylocele
SS Develops following rupture of lymphatic varix resulting in discharge of chyle into tunica vaginalis
SS Fluid is rich in cholesterol
SS Treatment is rest and aspiration.
Other Scrotal Swellings
SS Epididymal cyst
zz Cystic degeneration of epididymis
zz Usually both epididymis are involved
zz Contains crystal-clear fluid, therefore briliantly transilluminant
zz If cyst causing symptoms, then only it should be excised.

SS Cyst of a testicular appendage
zz Usually unilateral
zz Globular swelling at the superior pole.
zz Liable to torsion, so early intervention is indicated.
SS Spermatocele
zz Unilocular retention cyst contains spermatozoa

zz Always present in the head of epididymis
zz Clinically palpable as a soft, cystic lesion, above and behind the upper pole of testis
zz If it becomes larger, patient may feel it as a 'third testis'
zz Smaller ones need observation. Larger ones need to be aspirated or excised.
Other Scrotal Diseases
Idiopathic scrotal gangrene (Fournier's gangrene)

SS Sudden onset gangrene, resulting in sloughing out of scrotal skin.
SS It is basically a variety of necrotizing fascitis involving male genitalia and perineum. Testis is not involved.
SS Cause is unknown in most of the cases.
SS Precipitating factors—
zz Procedures in the perineal or periurethral area (e.g. urethral dilatation, sclerotherapy of hemorrhoids)
zz Diabetes mellitus
zz Immunocompromised state.
SS Organisms most commonly found— Staphylococcus, hemolytic

streptococcus, E. coli, C. welchil.
SS Parenteral broad-spectrum antibiotics and debridement are the
treatment. Reconstruction is indicated if extensive tissue loss develops.
Sebaceous cyst in scrotum
SS Scrotum is a common site for sebaceous cyst
SS Single cyst is excised
SS If small, multiple cysts involve a part of scrotal skin, that part of skin is
excised along with cysts. Multiple sebaceous cyst in scrotum
Carcinoma of Scrotum
SS Also called 'chimney sweeper's cancer' or 'mule-spinner's cancer'.
SS Workers using tar and shale oil are at more risk.
SS Carcinoma starts as a wart or ulcer.
SS Treatment is wide excision ± bilateral inguinal block dissection upto external iliac group of lymph nodes.
Phimosis
SS Inability to retract the foreskin over the glans penis.

SS Upto 3–4 years, a physiological phimosis present because of natural adhesion between prepuce and gland (preputial
glanular adhesion).
SS Accumulation of epithelial debris and intermittent penile erection gradually make the foreskin more retractable.
SS By the age of 3 years, 90% of the foreskin are retractable.
SS Phimosis after 4–5 years, phimosis with balanoposthitis, topical corticosteroids to the foreskin 3–4 times daily for 6
weeks loosens the phimotic ring in about 80% of cases.
SS Phimosis after age 7 years resistant to topical corticosteroid, phimosis with ballooning of foreskin or recurrent
balanitis— Circumcision is strongly indicated.
Circumcision should not be performed—
zz In neonates with hypospadias
zz Chordee without hypospadias
zz Dorsal hood deformity
zz Webbed penis
zz Micropenis
zz Neonate with large hydrocele or hernia.
SS Other indications of circumcision—
zz Religious reason—In muslims and jews
zz Prior to radiotherapy for carcinoma penis—To expose the glans
zz In suspected penile growth— To perform incisional biopsy from the lesion.
After circumcision
Paraphimosis
SS Develops when a tight prepuce is retracted beyond the corona that cannot be reduced to its normal position.
SS Arterial supply to glans may be compromised, so emergency reduction must be done.

SS Manual compression of edematous foreskin followed by forceful reduction of foreskin is sucessful in most of the
cases.
SS If reduction fails, then the constriction ring is incised or circumcision have to be done.
SS If manual reduction is successful, patient must be informed about the necessity of circumcision, but that procedure
is better to be deferred till swelling subsides.
Chapter 21
Diseases of the Esophagus

Important Topics
zzHiatus Hernia
zzGastroesophageal Reflux Disease
zzEsophageal Motility Disorder
zzEsophageal Diverticula
zzEsophageal Perforation
zzCancer of esophagus
‘Everything should be made as simple as possible, but not simpler.’

Hiatus Hernia
SS Hiatus hernia develops when a lax or defective phrenoesophageal membrane allows herniation of stomach through
the esophageal hiatus of the diaphragm.
SS Most commonly develop in women of 5th and 6th decades.
Different Types
Type I Type II
SS Phrenoesophageal liga- SS Focal defect in phreno-

ment is intact but lax. esophageal ligament
SS Gastroesophageal junc-
(defect in anterior and
tion is above the dia- lateral to esophagus).
phragm. SS Gastroesophageal junc-
Most common type of tion is anchored within

hiatal hernia. the abdomen.
Type III
SS More common than type II.

Diseases of the Esophagus 835
SS Patient with sliding hiatal hernia presents with symptoms related to gastroesophageal reflux (heartburn,
regurgitation, dysphagia).
SS Type I and III hernias present with postprandial pain or bloating, early satiety, difficulty in breathing during food
intake, dysphagia.
SS Herniated gastric part is susceptible to volvulus (organoaxial), obstruction, infarction.
SS About one third of patients with paraesophageal hernia become anemic, due to recurrent bleeding from ischemic
longitudinal ulcers in the mucosa of herniated stomach (Cameron ulcer).
Detect the Hernia— Presence and Type

1. Presence of air-fluid level in the posterior mediastinum in lateral view of chest X-ray— Think of hiatal hernia.
2. Contrast esophagogram— gives information about the extent of hernia, location of gastroesophageal junction and
type of hernia. It also gives functional information by assessing gastric emptying and evidence of gastroesophageal
reflux.
[Contrast study is more accurate in detecting paraesophageal hernia because it is a permanent herniation of
stomach into thoracic cavity.]
3. Endoscopy— Fiberoptic esophagoscopy is very much useful for diagnosis and classification of hiatal hernia.
Identification of pouch lined with gastric rugal folds at least 2

cm proximal to the crura—Sliding hiatal hernia.
Type I hiatal hernia.
On retroversion of the scope, a separate orifice adjacent to

gastroesophageal junction identified and where gastric rugal
folds ascend—
Type II hiatal hernia.
The scope is entering the pouch through a separate orifice

proximal to the crura—
Type III hiatal hernia.
4. Manometry is not mandatory for evaluation of paraesophageal hernia.
Management
1. Asymptomatic sliding hernia—No treatment required

2. Symptomatic sliding hernia warrants hiatal hernia repair
3. All patients of type II, III, IV require surgical intervention.
Approach
Abdominal Thoracic
Open Laparoscopy
SS As much as hernial sac is removed without injuring pleura, esophagus and inferior pulmonary veins.
SS Crura is reapproximated with nonabsorbable interrupted suture or defect is closed with prosthetic material.
SS As more than half of the patients of paraesophageal hernias have associated GERD and hypotensive LES, most of
the Surgeon perfer associated antireflux procedure.
Gastroesophageal Reflux Disease (GERD)
SS GERD is one of the common upper gastrointestinal disorders worldwide.
How it Develops?
SS Typical symptoms: Heartburn, regurgitation, dysphagia.

Substernal or epigastric burning pain that is aggravated in lying down position and promptly relieved after taking
antacids— Is the classic symptom.
SS Atypical symptoms: Cough, wheezing, chest pain, hoarseness.
SS On clinical examination, no specific findings found.

1. GERD can be reliably diagnosed if—

Patient having typical symptoms + Alleast one objective evidence of reflux (abnormal esophageal acid exposure on
24 hour pH monitoring/visible esophagitis on endoscopy).
Or, patient having atypical symptoms + two objective evidence of reflux.
2. Upper gastrointestinal endoscopy—To evaluate for esophagitis and presence of Barrett's esophagus.
New Savary–Miller classification of reflux esophagitis
Grade 1— Single or multiple erosions on a single fold
Grade 2— Multiple erosions affecting multiple folds
Grade 3— Multiple circumferential erosions.
Grade 4— Ulcer, stenosis or shortening of esophagus
Grade 5— Barrett's epithelium.
3. Esophageal pH testing—
zz Gold standard for diagnosing GERD.
zz Electrodes are placed in the esophagus and they are capable of sensing pH fluctuations.
zz Several informations are collected (e.g. total no. of reflux episodes, largest episode of reflux, extent of reflux in
upright and supine position).
zz With the help of Demeester scoring, GERD is diagnosed or excluded.
4. Esophageal manometry—
zz Is indicated when surgery is planned.
zz Can define the location and function of LES and helps to exclude other esophageal motility disorders.
zz Can also assess the status of esophageal contractility and peristatic wave progression, so that Surgeon can
choose the best antireflux procedure.
5. Contrast study—
zz Can detect the presence of haital hernia as well as any evidence of strictures and ulcers.
6. Esophageal impedance measurement—

zz Multiple intraluminal impedance (MII) is a technique to detect the flow of gas and liquid through a lumen
zz MII combined with pH monitoring is the most sensitive method for diagnosis of GERD.
Treatment
SS Avoid lying down after taking SS Avoid fatty foods, alcohol, SS H receptor antagonists
2
meals. caffeine, chocolate. SS Proton pump inhibitors
SS Avoid postural maneuvers SS Avoid smoking. SS Prokinetic agents.
(bending, straining) that ag- SS Eat smaller amount more
gravate reflux. frequent meals.
SS Head of the bed to be elevat-
ed to 6–8 inches.
SS Obese patients are advised to
lose weight.
Surgical management
SS Isindicated if—
zz Manometric evidence of defective LES
zz No relief after maximal medical management
zz Respiratory complications
zz Presence of Barrett's esophagus.

Esophageal Motility Disorder
1. Achalasia 1. Secondary to collagen vascular diseases

2. Vigorous achalasia 2. Secondary to neuromuscular diseases.
3. Diffuse and segmental esophageal spasm
4. Hypertensive lower esophageal sphincter.
Achalasia (Faliure to Relax)
SS Most common primary esophageal motility disorder.

SS Best understood and best known primary motility disorder of esophagus.
SS Etiology is unknown.
SS Characterized by loss of effective esophageal peristalsis and failure of LES to relax, resulting in impaired esophageal
emptying and gradual esophageal dilation.
[In Hirschsprung's disease, dilated colon contains normal ganglion cells, constricted part is aganglionic.]
SS Characteristic pathology is loss of ganglion cells in Aurbach plexus.
SS Increased risk of malignant transformation, particularly squamous cell carcinoma.
SS Patients usually present with classic triad of symptoms—
1. Dysphagia—Initially with liquids and then progress to solids. Stress and cold liquid exacerbate dysphagia.
2. Regurgitation—Regurgitation of undigested foods with foul odor tends to regurgitate after meals and in
supine position.
3. Weight loss
Other symptoms—Pneumonia, lung abscess, bronchiectasis may develop in longstanding achalasia due to recur-
rent aspiration.
[Rapid onset of symptoms with significant weight loss—Suspect pseudoachalasia (secondary to malignancy or extra-
luminal obstruction)]
SS Investigations to confirm diagnosis—
zz Esophagogram—
Dilated esophagus with a distal narrowing 'bird's beak' appearance.
Lack of peristaltic waves in the body and failure of relaxation of LES.
Lack of gastric air bubble.
In advanced stage, massive esophageal dilation, sigmoidal esophagus (megaesophagus) is seen.
['Birds beak' appearance is not specific for achalasia, but seen in other pathologies also (e.g. benign stricture, carci-
noma).]
zz Esophageal manometry—
Gold standard investigation.
Characteristic findings—
–– Elevated LES pressure
–– Incomplete relaxation of LES in response to swallowing
–– Absence of peristalsis in body of esophogus
–– Elevated intraesophageal pressure.
zz Endoscopy—
Must be performed to rule out strictures or malignancy.
Characteristic findings
Atonic, dilated esophagus with a tightly closed LES that fails to open with insufflation.
With gentle pressure, the scope can be admitted.
Treatment
SS Treatment is directed to relieve the symptoms, not to correct the pathology.

SS Goal of all treatments is to relieve the functional obstruction of distal esophagus.
Different treatment
options
1. Medical 2. Endoscopic 3. Surgical
• Nitrates and Ca2+ • Pneumatic graded balloon • Heller myotomy

channel blockers dilation. • Modified Heller myotomy.
• Botulinum injection.
SS Medical—
zz Nitrates and calcium channel blockers

Relax smooth muscle and thus decrease lower esophogeal sphincter pressure transiently.
zz Botulinum toxin type A injection into LES
Botulinum blocks acetylcholine release from nerve terminals.
[Medical therapy can be used for extended periods if patient is not suitable for definite treatment.]
SS Endoscopic—
zz Under fluoroscopic guidance, pneumatic polyethylene balloon (30 mm) are passed through LES and then
inflated, causing disruption of fibers of LES.
Single dilatation for each session. Multiple sessions of dilatation are required.
SS Surgical—
zz Heller myotomy (originally described by Ernest Heller)

Two myotomies along the GE junction (anterior and posterior)
zz Modified heller myotomy (only anterior myotomy).
SS Approaches—
Transthoracic
zz
Transabdominal
zz Open

Laparoscopic [preferred approach due to excellent visualization of distal esophagus and stomach]
SS Associated antireflux procedure is necessary or not?

zz Most surgeons prefer an associated antireflux procedure
zz Total (Nissen) or partial (Dor or Toupet) fundoplication?

SS A partial one, particularly Toupet (posterior)
fundoplication is preferred by most surgeons.
Vigorous Achalasia
SS A varlant of achalasia
SS Patients present with clinical and manometric features of classic achalasia and diffuse esophageal spasm
SS Patients also may present with spastic pain and more severe dysphagia
SS Treatment is a longer esophagomyotomy (proximal extension upto the aortic arch).
Diffuse Esophageal Spasm
SS Loss of normal peristaltic coordination resulting in simultaneous contraction of segments of the esophageal body.
SS Patients present with severe spastic pain, dysphagia, regurgitation and weight loss.
SS Diagnosis is confirmed by esophageal manometry
zz Characteristic finding – Spontaneous, repetitive, prolonged, high amplitude contractions.
SS Barium esophagogram may reveal classic ‘corkscrew’ esophagus.
SS Mainstay of treatment is nonsurgical:
zz Pharmacologic/endoscopic + treatment of associated psychiatric disorders (depression, anxiety, etc.) nitrates,

calcium channel blockers, anticholinergics are used as pharmacologic therapy.
SS Surgery is only indicated when patients not responding to medical treatment. Long esophagomyotomy [proximal
extension upto the aortic arch] along with Dor (anterior, partial) fundoplication is the surgery of choice.
Nutcracker Esophagus
SS Hypermotility disorder characterised by high amplitude (> 180 mmHg), prolonged (>6s) peristaltic contractions
SS Patients present with chest pain and dysphagia
SS Peristaltic contractions 2 standard deviations above the normal values in manometric study is diagnostic
SS Treatment is medical (Ca channel blocker, nitrates, antispasmodics)

2+
[Caffeine, hot foods, cold should be avoided as these factors trigger abnormal peristaltic contractions.]
Esophageal Diverticula
SS Diverticulaare focal pouches of esophageal wall consisting of mucosa, submucosa and sometimes muscular coat
SS Differenttypes—
zz According to location
Pharyngoesophageal diverticulum [Zenker’s]
Parabronchial [midesophageal]
Epiphrenic [supradiaphragmatic]
zz According to pathophysiology
Traction diverticula [resulting from an extrinsic process]— They are true diverticula (consists of mucosa,
submucosa and musculoris).
Pulsion diverticula [resulting from elevated intraluminal pressure]— They are false diverticula (consists of
mucosa and submucosa only)
Pharyngoesophageal (Zenker’s) Diverticulum
SS Itis a pulsion diverticulum.

SS Most common esophageal diverticulum.
SS This diverticulum herniates through the killian’s triangle—triangle
formed by oblique fibers of the thyropharyngeus muscle and horizontal
fibers of cricopharyngeus muscle.
SS Diverticulum develops due to loss of coordination during the second stage of swallowing.
Loss of coordination during 2nd stage of swallowing
Loss of tissue elasticity (in old age) Killian triangle is exposed to high pressure
Diverticula formation—Diverticula emerges through

the left side of the esophagus into the superior
mediastinum
SS Patients present with progressive cervical dysphagia, cough on recumbent position, spontaneous regurgitation of
undigested food.
SS Barium esophagogram is useful modality for diagnosis.
SS Esophagoscopy is indicated only when malignancy is

suspected.
SS Surgical or endoscopic repair is the treatment, regardless
of size. [Dohlman procedure]
SS If diverticulum is small (< 2 cm), myotomy alone is
sufficient.
SS If diverticulum is large, myotomy and diverticulectomy or diverticulopexy is indicated.

Midesophageal (Parabronchial) Diverticula
SS It is a traction diverticula.
SS Develops in conjunction with mediastinal granulomatous diseases (eg. tuberculosis, histoplasmosis).
SS Most of the patients are asymptomatic.

SS Lateral view of barium esophagogram is needed to assess the size and location of diverticula.
SS CT is helpful to identify mediastinal structures as well as diverticula. Manometric study is required in all patients to
rule out primary motor disorder.
SS Diverticulum < 2 cm — Can be observed.
SS Diverticulum > 2 cm — Diverticulopexy is indicated.
Epiphrenic Diverticulum
SS Itis a pulsion diverticulum

SS Typically present within the distal 10 cm of thoracic esophagus.
SS Develops due to high intraluminal pressure secondary to a relatively distal obstructon.
SS Most patients are asymptomatic. The diverticulum is often diagnosed as incidental finding during workup of a
motility disorder.
SS Contrast esophagogram is essential for diagnosis, but manometric study and endoscopic examination are also
indicated to assess the underlying physiology.
SS Asymptomatic, small (< 2 cm) diverticula do not need any surgical intervention.
SS Patients with symptoms, documented motor abnormality warrants surgical intervention.
Esophageal Perforation
It is a surgical emergency.
SS Etiologies:
Intraluminal causes—
SS Instrumentation (75%)
zz Endoscopy
zz Dilatation for stricture
zz Sclerotherapy for varices
zz Stent insertion.
SS Ingested caustic substances (Alkali)
zz Causes liquefaction necrosis.
SS Foreign bodies—From sharp objects (e.g. fish bone)
zz Erosion due to impacted bolus.
SS Barotrauma —Induced by Heimlich maneuver, forceful vomiting, during childbirth
SS Cancer of esophagus
SS Medications — NSAIDS, etidronate, potassium chloride.
Extraluminal causes—
SS Penetrating injuries, most commonly gunshot wounds
SS Blunt trauma — Due to compression between sternum and spine
SS Iatrogenic — During thyroidectomy, vagotomy, fundoplication.
[Absence of true serosa makes the esophagus more susceptible to perforation.]

SS Site of perforation—
SS Clinical presentation depends on the location of injury and time interval since occurence of injury
zz Injuries in cervical esophagus usually present with subcutaneous emphysema in neck, dysphagia or odynophagia,
pain in neck and stiffness.
zz Thoracic perforations present with shortness of breath and retrosternal chest pain.
zz Abdominal perforations usually present with symptoms and signs of acute abdomen.
zz History of recent esophageal instrumentation along with these symptoms and signs — Suspect esophageal
injury.
SS Make early diagnosis—
zz Early diagnosis can reduce the morbidity and mortality.
zz Plain X-ray of neck, chest may reveal subcutaneous emphysema in neck and mediastinum, free gas under
diaphragm, pleural effusion.
zz Contrast esophagogram (in upright and lateral decubitus position).
[Barium is used for suspected thoracic perforation and gastrograffin for abdominal perforation.]
[Barium is inert in chest but may cause peritonitis, gastrograffin can cause pneumonitis.]
zz High index of clinical suspicion but esophagogram is equivocal ⇒ CT chest is indicated.
zz Endoscopy is planned when esophagogram is inconclusive and surgical intervention is planned.
SS Management: 1. Conservative 2. Surgical

zz Conservative management—
[All patients with suspected perforations need initial conservative measures]

IV fluids
Broad-spectrum antibiotics
Catheterization
Nil per mouth
Access for TPN
Nasogastric decompression.
SS Then think —Conservative measures to be continued? Or proceed to surgical intervention?
SS Consider following points to take decision—
zz Patient stable or not?
zz Location of perforation
zz Leakage is contained or not?
zz Underlying esophageal disease (e.g. distal obstruction, malignancy) present or not?
SS Stable patient with minimal symptoms and contained perforation may be treated with conservative measures
SS If surgery is planned, consider which one is appropriate—
Primary repair
SS The first 24 hours is the golden period for primary closure
SS At any time, during surgical exploration, healthy tissue bed is found—Primary closure may be considered.
Muscle flap
SS If tissue bed is friable, severe mediastinitis—Muscle flap to be considered.
Exclusion? resection?
SS If primary repair not feasible or muscle flap fails —Cervical esophagostomy + gastrostomy/feeding jejunostomy
⇒ Delayed reconstruction.
Management of Cervical Perforation
SS Approach—Incision parallel to the anterior border

of left sternocleidomastoid.
SS Basic steps of repair — Thyroid, trachea and larynx

are retracted medially and carotid sheath laterally
zz Primary repair + drainage (closed suction drain)
zz If no perforation is identified, only drainage.

Management of Thoracic Perforation
SS Approach—
zz Through right chest for upper two-thirds of esophagus.

zz Through left chest for lower third of esophagus.
SS Different methods—
zz Primary closure with muscle patch
zz T-tube enterocutaneous fistula formation
zz Exclusion and diversion
zz Resection.
Primary closure with muscle flap
T-tube enterocutaneous fistula formation
SS In extensive injuries, perforation associated with malignancy—Resection may be considered if patient is stable.
SS In unstable patient with severe contamination and delayed presentation—Cervical esophagostomy + drainage of
mediastinum + gastrostomy + feeding jejunostomy.
Management of Abdominal Perforation
SS Approach through chest or abdomen

SS Basic principles are same.
What is Boerhaave’s Syndrome?
SS Professor Hermann Boerhaave first described this syndrome.

SS Postemetic rupture of esophagus is classically described as Boerhaave’s syndrome. Similar events occur after blunt
thoracic injury, seizure, childbirth.
SS Increased intrathoracic esophageal pressure causes perforation.
What is Mallory-Weiss Tear?
SS Tear in esophageal mucosa following persistent retching, paroxysmal coughing.

SS Mallory and Weiss first described this syndrome.
SS This tear is characterized by arterial bleeding, so bleeding may be severe.
SS Upper GI endoscopy confirms the diagnosis (one or more longitudinal fissures in the mucosa which are the source
of bleeding.)
SS In most of the cases, bleeding stop spontaneously.
SS Endoscopic epinephrine injection in the tear site is helpful. In some cases, surgical intervention (oversewing the
tear) is indicated.
Stricture of esophagus
Malignant Benign
Congential Acquired
• Due to presence of congenital web (as a result of 1. GERD

inappropriate canalization of esophagus during de- 2. Corrosive ingestion
velopment) 3. Iatrogenic (after esophagectomy, scle-
rotherapy for varices, after radiation
therapy)
4. Schatzki’s ring
5. Medications (potassium chloride, qui-
nidine, ferrous sulfate, NSAIDs)
6. Sarcoidosis
7. Infection (Candida albicans)
Schatzki’s ring—A concentric ring at the squamocolumnar junction, consists of inflammatory cells and fibrous tissue
in mucosa and submucosa.
Commonly found in association with hiatus hernia.
Usually detected in barium swallow study and in esophagoscopy]
SS Clinicalpresentation
zz Dysphagia to solid food is the typical presenting feature
zz In advanced stage, dysphagia to liquid develops.
SS Diagnosis
zz Barium swallow should be the initial investigation —Can evaluate the location, number and length of strictures
zz Esophagoscopy is also essential to assess the location, length, distensibility and to obtain biopsy or brushings.
Treatment
Dilatation Surgery
• Most of the strictures are amena- • Indicated for recurrent or persis-

ble to dilatation tent strictures
• 2 types of dilators (dilators fracture • The preferred technique is es-
the fibrous tissue of stricture) ophagectomy followed by colon
interposition between cervical
esophagus and stomach
Bougies Balloon dilators
What is Barrett Esophagus?
SS Replacement of distal esophageal stratified squamous epithelium by metaplastic columnar epithelium containing
goblet cells.
SS It is a complication of long standing GERD.
SS Many patients are asymptomatic and undiagnosed

SS White males are commonly affected.
SS Complications—
1. Barrett ulcer
Penetrating ulcer in metaplastic columnar epithelium
Can cause bleeding, perforation.
2. Stricture
Located in squamocolumnar junction.
3. Dysplasia
Dysplasia may be low or high grade.
4. Carcinoma
Risk of developing adenocarcinoma is 50–100 times that of general population.
SS Diagnosis—By endoscopy and biopsy. Repeat endoscopy and biopsy often required as Barrett mucosa is quite
focal and variable.
Identification of dysplastic changes in Barrett mucosa is very much crucial for early detection of malignant
change.
Digital chromoendoscopy (narrowband imaging type) paired with manification endoscopy has high diagnostic
precision for the diagnosis of high grade dysplasia in Barrett’s esophagus.
SS Treatment—
1. Asymptomatic patient, no complication

No specific therapy
Annual endoscopic surveillance and biopsy.
2. Symptomatic patient, no complication

Antireflux surgery + annual endoscopic surveillance and biopsy.
3. Barrett ulcer
Proton pump inhibitors
Nonhealing ulcer warrants rebiopsy from ulcer + antireflux surgery.
4. Stricture
Esophageal dilation + medical therapy
Recurrent stricture needs antireflux surgery and repeated dilation.
5. Dysphagia
Low grade dysplasia needs 3 monthly surveillance endoscopy and biopsy + medical therapy for GERD
High grade dysplasia needs definite intervention (surgery/photodynamic therapy).
6. Carcinoma
Esophagectomy.
Cancer of Esophagus
SS Esophagus is a unique organ because it covers three anatomic compartments: Neck, thorax and abdomen.
SS Esophageal cancer is unique among GI malignancies because it may present two distinct histopathologic varieties—
Squamous cell carcinoma and adenocarcinoma.
Risk Factors
Tobacco and alcohol use

SS Independent risk factor for squamous cell carcinoma
SS Risk factor for adenocarcinoma
SS Quiting smoking decrease the risk of squamous cell carcinoma, but not the risk of adenocarcinoma.
[Tobacco + alcohol – highest risk of squamous cell carcinoma]

SS Alcohol is an independent risk factor for squamous cell carcinoma
SS Amount of alcohol, type of beverage have relationship with risk
SS No risk of adenocarcinoma in use of alcohol.
Dietary factors
SS Deficiency of vitamins (A, C, E)
SS Deficiency of trace metals (zinc, molybdenum, selenium)
SS Fungal contamination of foods
SS Presence of nitrosamines and their precursors (nitrate, nitrite).
Esophageal disorders
SS GERD—One of the strongest risk factors of adenocarcinoma
SS H. pylori infection—H. pylori (particularly cag A + strain) is related to adenocarcinoma
SS Barrett esophagus—Single most important risk factor for adenocarcinoma
SS Tylosis—An autosomal dominant disorder characterized by hyperkeratosis of palm, sole and esophageal papilloma.
SS Plummer-Vinson syndrome—Characterized by iron-deficiency anemia, glossitis, cheilitis, splenomegaly and

esophageal webs.
[About 10% of patient develop esophageal epidermoid carcinoma.]
SS Corrosive stricture—Squamous cell carcinoma may develop after lye stricture, usually 40–50 years after injury
SS Achalasia—16–30 fold ↑ risk of developing squamous cell carcinoma.
Human papillomavirus infection

SS Responsible for squamous cell carcinoma in high-incidence regions.
Other aerodigestive malignancies

SS Patient with other aerodigestive malignancies are at a risk of developing squamous cell carcinoma, most likely due
to exposure to similar environment carcinogens and field cancerization.
Pathology
SS Squamous cell carcinoma and adenocarcinoma are the commonest types.
SS Squamous cell carcinoma usually affects the upper two-thirds (cervical, upper and middle third of thoracic
esophagus). Adenocarcinoma affects the lower one-third.
SS Incidence of adenocarcinoma is in a increasing trend.
Classification of Esophageal Tumors
SS Most commonly present with progressive dysphagia—Initially difficulty in swallowing solids, then liquids and lastly
saliva.
SS Weight loss.
SS Symptoms of local invasion and distant metastases—
zz Odynophagia, dull retrosternal pain, cough, hoarseness of voice.
SS Unusual presentation—
zz Pneumonia (due to tracheoesophageal fistula)
zz Exsanguinating hemorrhage (due to aortic invasion).
[Dysphagia usually develops late in the disease process, because lack of serosal layer allows smooth muscle to dilate
more.]
SS Esophagogram—
zz Barium esophagogram must be the initial study in any patient with dysphagia
zz Helpful to differentiate whether the lesion is intraluminal or extraluminal
zz The classic ‘apple-core lesion’ is highly suggestive.
SS Endoscopy and Endoscopy guided biopsy—
zz Location or site of the lesion
zz Nature of the lesion can be assessed

zz Relationship of lesion to the cricopharyngeus, GE junction and cardia.
SS Biopsy along with cytologic brushings—Can be performed.

Pretreatment Staging
SS Staging is for determination of

zz Extent of disease
zz Depth of esophageal wall involved
zz Regional lymph node status
zz Presence or absence of distant metastases.
SS For staging, following investigations are helpful:
1. CT scan of chest, abdomen and pelvis

Can detect liver and lung metastases
Can detect peritoneal carcinomatosis
Highly accurate for detection of aortic and tracheobronchial involvement.
2. Endoscopic ultrasonography
EUS is highly accurate in both T and N staging and is superior to CT.
Biopsy can be taken from the tumor mass as well as from the lymph node.
3. FDG–PET
The accuracy in assessing regional lymph nodal status is superior than CT, but not so accurate like EUS
Superior to CT in detecting distant metastases
Useful modality for evaluating response to chemo and radiotherapy.
4. Bronchoscopy
Indicated for tumors in upper and middle esophagus to rule out involvement of membranous trachea and
tracheoesophageal fistula.
Treatment
1. Treatment of high grade dysplasia and T1 disease—

zz Different options:
a. Intensive surveillance
b. Mucosal ablation
c. Endoscopic mucosal resection (EMR)
d. Minimally invasive esophagectomy.
a. Intensive surveillance
Serial endoscopy at 3 – 6 monthly interval + multiple four-quadrant biopsies.
[Serial endoscopy can detect the cancer at an earlier stage.]

b. Mucosal ablation
This method eliminates the premalignant mucosa and allows to regenerate squamous epithelium.
Different techniques of ablation:
−− Photodynamic therapy
−− Multipolar electrocoagulation
−− Laser (Nd : YAG)
−− Argon beam.
c. Endoscopic mucosal resection (EMR)

By separating the lesion from underlying muscular layer using submucosal injection of fluid Or, by using
suction to trap the mucosal lesion.
d. Minimally invasive esophagectomy
Most definite intervention
Different approaches:
−− Laparoscopic
−− Thoracoscopic
−− Combined laparoscopic and thoracoscopic.
[No significant role of radiation therapy and chemotherapy in T1 disease]

2. Treatment of localized resectable disease (T1–2, N0)—
zz Localized, resectable cancer in cervical esophagus is rarely found at the time of management because of early
invasion of larynx, trachea and great vessels.
zz T1–2 and without lymph node involvement in middle third of esophagus—Resection is the treatment (transhiatal
esophagectomy or transthoracic esophagectomy video assisted thoracic surgery).
zz T1–T2 in lower esophagus and cardia – Resection includes cervical division of esophagus and proximal
gastrectomy.
[GI tumors have increased propensity to submucosal spread]
3. Treatment of locally advanced disease– (T1–3, N1)
between 6–8 weeks
zz Preoperative chemotherapy (cisplatin + 5-FU) + radiation, Resection
[Before 6 weeks, due to inflammation, resection because hazordous. After 8 weeks, scarring in the perioesophageal
tissue makes dissection difficult].
4. Treatment of disseminated disease (any T, any N, M1)
zz Grade I – III dysphagia—Chemoradiation
zz Grade IV and more—Indwelling esophageal stents
zz Dysphagia due to cancer at GE junction—Stent must be avoided to prevent severe gastroesophageal reflux.
Radiation therapy alone is sufficient.
zz For feeding access—Laparoscopic jejunostomy.
Minimally invasive transhiatal esophagectomy
SS Five or six small incisions in upper abdomen for port introduction and
one transverse cervical incision for removal of specimen and for cervical
esophagogastrostomy.
SS Laparoscopic creation of 4 cm neoesophagus (gastric conduit).
SS A vein stripper is passed from the neck down into the abdomen followed by
inversion of the esophagus in the posterior mediastinum and removal through
the neck.
SS Gastric conduit is delivered to the neck with a chest tube and anastomosed to
the cervical esophagus in a end-to-side fashion.
Minimally invasive two and three field esophagectomy
SS In three field esophagectomy, the esophagus is dissected along its length with dissection of lymph nodes in upper,
middle and lower posterior mediastinum, with division of azygos vein—
zz Thoracic dissection—Is done through a mini thoracotomy at sixth intercostal space (right) with the help of
conventional surgical instruments. Videoscope is accessed through the ninth intercostal space (right).
zz Abdominal—Abdominal part of the operation is similar to minimally invasive transhiatal esophagectomy.
zz Cervical gastric conduit is delivered to the neck and anastomosed to the cervical esophagus.
SS In two-field esophagectomy—
zz Abdominal—Creation of gastric conduit.
zz Thoracic—Through right thoracotomy, the esophagus is dissected and then anastomosis (stapled) is done in
high thorax.
Open transhiatal esophagectomy
SS Division of the diaphragmatic crus allows enlargement of the hiatus. This is essential because, the esophageal
dissection is performed with the finger tips rather than surgical instruments.
SS Lower mediastinal and upper abdominal lymph node basins can be resected. The mediastinal lymph nodes above
the inferior pulmonary vein can not be resected.
SS Creation of gastric conduit and techniques of anastomosis are same as minimally invasive transhiatal esophagectomy.
Ivor Lewis (en bloc) esophagectomy
SS Midline laparotomy
zz Lymphnode dissection around celiac trunk and its branches, around porta hepatis and along the splenic artery,
along lesser curvature of stomach
⇓
zz Greater curvature gastric conduit is constructed
SS Anterolateral thoracotomy [through right 6th intercostal space]
SS Azygos vein is divided ⇒ Resection of thoracic duct; periaortic tissues; peribronchial, hilar and tracheal lymph nodal
basins ⇒ Gastric conduit is pulled up into the thorax and anastomosis is done between upper thoracic esophogus
and gastric conduit.
Three field open esophagectomy
SS Similarto minimally invasive three field esophagectomy except that all accesses are through open incisions.
[The advantage of placing a anastomosis in neck—Leakage of anastomosis is unlikely to create a severe systemic ef-
fect.]
SS Anastomosis in high chest minimized the risk of injury to vital structures of neck particularly RLN.
MIS 3 field esophagectomy MIS 2 field esophagectomy
Open transhiatal esophagectomy [orringer’s]
Ivor Lewis (en bloc) esophagectomy

Three field open (Mckeown’s) esophagectomy
Creation of gastric conduit

Chapter 22
Diseases of the Salivary

Gland
Important Topics
zzInflammatory Pathologies
zzObstructive Pathologies
zzSalivary Gland Tumors
zzSurgical Procedures
‘Education is what remains after one has forgotten everything he learned in school.’
Salivary Gland Pathologies
SS Salivaryglands consist of—

zz Paired parotid, submandibular,
sublingual glands.
zz Tiny accessory glands all over the
oral mucosa.
SS Diseases of salivary glands are due
to—
zz Inflammation
zz Obstruction and trauma
zz Neoplasm.
Inflammatory Pathologies
SS Inflammatory pathology of salivary gland are due to—

zz Viral infection
zz Bacterial infection
zz Autoimmune causes.
Viral Sialadenitis
SS Most commonly caused by mumps virus (a paramyxo virus)
SS May affect all salivary glands but predominantly affects both parotid glands
SS Childhood mumps is a self-limited disease. In adults, it may cause bilateral orchitis.
Acute Ascending Bacterial Sialadenitis

SS Mostlyaffects the parotid glands.
SS Reduced salivary flow and oral sepsis resulting in bacterial colonisation in parotid duct, gradually parotid
parenchyma is affected (pathophysiology of acute sialoadenitis in postoperative patients).
Diseases of the Salivary Gland 867
SS Nowadays, poorly fitting dentures is one of the causes of acute sialoadenitis
SS Infecting organism is Staphylococcus aureus or Streptococcus viridans
SS Patients present with tender, red parotid swelling associated with fever and regional lymphadenopathy.
SS USG shows characteristic dilation of the acini

[Sialography should not be done during acute phase of infection.]
SS If patient presents before abscess formation, antibiotics are useful
SS If abscess develops, the pus must be drained
SS Small transverse incision to avoid injury to facial nerve.

[As abscess develops in the superficial part of the gland, during drainage, chance of facial nerve injury is low.]
Chronic Bacterial Sialadenitis

SS Morecommon in the submandibular salivary gland and usually secondary to chronic obstruction
SS Submandibular gland has increased tendency to chronicity following infection.
Autoimmune Sialadenitis
SS Seen in Sjögren syndrome
SS Sjögren syndrome is characterized by—
zz Keratoconjunctivitis sicca
zz Xerostomia
zz Bilateral parotid swelling
zz Rheumatoid arthritis.
Rare Causes of Sialadenitis

SS Infectivecauses
zz Mycobacteria
zz Cat-scratch disease (caused by Bartonella henselae)
zz Syphilis
zz Toxoplasmosis (caused by T. gondii)
zz Deep mycoses
zz Sarcoidosis.
SS Radiation sialoadenitis
SS HIV-associated sialoadenitis.
Obstructive Pathology
SS Sialolithiasis
SS Mucoceles.
Sialolithiasis
SS About 80% of sialolithiasis occur in the submandibular gland, 10% in the parotid gland, rest in the minor salivary
gland.
SS Most of the sialolithiasis occur in the submandibular gland, because—
zz Secretions contain mucus and more viscous
zz Gland lies below the opening of its duct.
[Calculus composed of: Mucus, bacteria, calcium and magnesium phosphates, cellular debris.]
SS Classic presentation is acute pain and appearance of swelling beneath the

jaw within a minute of starting the meal; both pain and swelling resolves
after the meal but the pain resolves earlier.
SS This classic presentation is seen only when there is complete obstruction.
SS On examination, in early periods of obstruction, the gland is not palpable in between meals
SS Later, a chronically infected gland becomes palpable with rubbery hard consistency.
Bimanual palpation
SS To know the relations of the lump to the floor of the mouth and tongue
SS To feel the course of the duct in the floor of the mouth to note any discharge from the orifice of the duct.
SS PlainX-ray of jaw is all that is required, because most of the submandibular calculi (about 80%) are radioopaque.
No further investigation is necessary.
SS Majority of parotid stones are radiolucent.
SS In equivocal cases, sialography is indicated.
Treatment
Mucoceles
SS Mucus retention or extravasation cysts arise as a result of

damage of minor salivary gland or its ducts.
SS Most commonly present on the mucosal aspect of lower lip
and in the posterior buccal mucosa.
SS Treatment is excision of the cyst along with underlying minor
glands.
SS Ranula is a large mucocele arising as a result of ruptured

sublingual gland.
SS Classically, ranula presents as large, tense, bluish, translucent,
spherical swelling in the floor of the mouth.
SS Occasionally, ranula extends through the myelohyoid muscle
and enter the submental space, presenting as a swelling in upper
neck. This type of ranula is called ‘plunging ranula’.
SS Treatment is excision of ranula along with sublingual gland.
Salvary Gland
Treatment
Salivary GlandTumors
Tumors
SS Tumors arise from both major salivary gland (parotid, submandibular and sublingual) as well as from minor salivary
glands.
SS Majority of salivary gland tumors arise from parotid gland.
zz Majority of parotid gland tumors are benign (about 70–80%), about 50% tumors of submandibular and
sublingual glands are benign, whereas only 25% tumors arising from minor salivary glands are benign.
[Smaller the salivary gland, more likely the tumor to be malignant.]
SS Most of the salivary gland tumors arise from ductal lining epithelium and underlying myoepithelial cells.
Classification of salivary gland tumors
Benign Malignant
Epithelial tumors Nonepithelial tumors

• Pleomorphic adenoma • Neural sheath tumor
• Warthin’s tumor • Hemangioma
• Oncocytoma • Lipoma
• Basal cell adenoma • Lymphangioma
• Clear cell adenoma
Low grade High grade

• Mucoepidermoid carcinoma • Adenoid cystic carcinoma
• Acinic cell carcinoma • Adenocarcinoma
• Squamous cell carcinoma
• Undifferentiated carcino-
ma
SS Parotid tumor usually present with slow growing, well-circumscribed painless swelling in the parotid region with
rubbery hard consistency.
SS Facial nerve palsy, skin invasion are suggestive of
malignancy. Lymph node metastasis is uncommon in low
grade salivary malignant tumor (intra and periglandular,
level II).
SS Submandibular and sublingual gland tumors present with
slow-growing, well circumscribed, painless swelling in the
neck or floor of the mouth.
zz Bimanual palpation is essential to evaluate the
relationship of the tumor with floor of mouth, tongue
and mandible.
zz Numbness in anterior two-thirds of the tongue
suggests infiltration of the lingual nerve by malignant
submandibular tumor. Level Ia, Ib, II, III groups of lymph
nodes may be involved.
Minor salivary gland tumors present as painless mass
in the oral cavity, mostly at the junction of hard and
soft palate.
Investigation
SS CT and MRI, both are useful maging methods. They can define the extent of tumor, relationship of tumor to adjacent
structures, status of cervical lymph nodes. MRI is more sensitive than CT.
zz FNAC is useful to rule out malignancy. As facial nerve sacrifice may be necessary in malignant parotid tumors,
preoperative councelling is Indicated when a surgeon is planning for resection of malignant tumor.
SS Open surgical biopsy is contraindicated to avoid microscopic spillage of tumor cells in surrounding tissues.
Pleomorphic Adenoma
SS It is a true adenoma of the parotid gland.

SS It consists of epithelial cells mixed with myxoid, mucoid and chordroid elements (that is why termed as pleomorphic’
or mixed).
SS It is a well demarcated encapsulated lesion wtih incomplete capsule. The tumor has projections that protrude
beyond the capsule through the defects.
[This feature limits the scope of enucleation of the tumor and warrants excision of the involved lobe of the
gland.]
SS This tumor develops at any age with equal male: female ratio.
SS About two-third of parotid tumors and half of submandibular tumors are pleomorphic adenoma.
SS A slow growing, painless smooth mass rubbery hard consistency, present in the typical site-between angle of
mandible and mastoid process.
SS Rarely, this tumor may undergo malignant change.
SS This tumor is susceptible to recurrence.

Warthin’s Tumor (Adenolymphoma)
SS Itis benign tumor of the parotid gland.

SS Itdevelops only in the parotid gland.
SS A tumor of elderly population with a male: female ratio 4:1.
SS This tumor contains 2 components:
1. Epithelial element (originated from embryonic parotid ducts

which have separated from main ductal system).
2. Lymphoid element (originated from normal lymph tissues).
SS Usually develops in the lower part of the parotid gland, level with
the lower border of the mandible, soft in consistency.
SS Malignant transformation is rare.
Oncocytoma
SS A benign slow growing tumor of the major salivary gland

SS The tumor consists of acini or tubules of large cells with glandular eosinophilic cytoplasm (termed as ‘oncocyte’).
Carcinoma of Salivary Glands
SS Can be classified as low grade and agressive carcinoma.

SS Low grade malignancies are mucoepidermoid carcinoma and acinic cell carcinoma.
SS Aggressive malignancies are adenoid cystic carcinoma, adenocarcinoma, squamous cell carcinoma and
undifferentiated carcinoma.
SS These aggressive malignancies have a poor prognosis regardless of treatment.
SS Mucoepidermoid carcinoma
zz It is the most common malignant salivary gland tumor.
zz Adults (age 30–60 years) are more commonly affected, but it is also the most common malignant salivary tumor
in pediatric population.
zz Based on aggressiveness, this tumor exists in any form: Low grade and high grade. Low grade mucoepidermoid
carcinoma is composed of predominantly mucin secreting cells, whereas in high grade tumors, epidermoid cells
are more abundant.
SS Adenoid cystic carcinoma
zz Second most common malignant salivary gland tumor
zz This tumor has typical propensity for neural invasion
zz Distant metastasis is more common than other maligant salivary tumors.
SS Carcinoma ex pleomorphic adenoma
zz An aggressive malignant tumor arises from a benign mixed tumor.
zz Malignant transformation develops in later age (6th decade)
zz It more often develops in recurrent tumors.

Nonepithelial Tumors
SS Inchilhood, hemangioma and lymphangioma may develop in the salivary gland
SS Hemangioma usually regresses by the age of 2 years, but lymphangioma needs excision
SS Neurofibroma and neurilemmomas may develop in the adults.
Malignant lymphoma
SS Most of the salivary gland lymphomas develop in the parotids
SS Treatment is total parotidectomy and adjuvant radiotherapy.
Surgical Procedures for Salivary Gland Pathology
Excision of Sublingual Gland
SS A linear incision is made

in the floor of the mouth
just lateral and parallel to
the submandibular duct.
The incision should not be
extended beyond the 1st
molar tooth to avoid injury
to the lingual nerve.
SS The submandibular duct, sublingual gland and lingual nerve is

identified
SS The sublingual gland is mobilised from the inner cortex of the
mandible.
[Avoid injury to the submandibular duct and lingual nerve.]
Excision of Submandibular Gland
SS A horizontal skin crease incision atleast 3 cm

below the ramus of the maindible to avoid injury
to the mandibular branch of facial nerve.
[Avoid injury to marginal mandibular branch of

facial nerve]
SS Facial vein lies superficial to the gland and it is ligated and divided.
SS Facialartery is dissected from the deeper surface of the gland and is ligated above and below.
SS The superficial part of the gland is dissected off mylohyoid.
SS Mylohyoid is retracted anteriorly to expose the deeper part of

the gland and its duct. Lingual nerve is now becomes visible.
[Avoid injury to lingual nerve]
SS Hypoglossal nerve is also visible at the lower part of the

operative field, but in a deeper plane.
[Avoid injury to the hypoglossal nerve.]
zz Submandibular duct is ligated as anterior as possible.

zz The only attachment of the gland, part of facial artery
is again ligated at the lower border of the posterior
pole of the gland, and is removed along with the
gland.
Superficial Parotidectomy
SS Preauricular incision extending downwards in the neck (lazy ‘S’ incision)
SS Anteriorly, skin and platysma flap is elevated to expose the parotid gland along with parotid fascia.
[Avoid injury to the branches of facial nerve emerging from the anterior border of the gland.]
The principle of superficial parotidectomy is to—

1. Identification of facial nerve before it enters the gland
2. Following the nerve and it’s branches, the gland is dissected superficial to the fasciovenous plane.
Identification of facial nerve

SS Method No. 1 A plane is made anterior to the external auditory meatus and dissection is done just superficial to
styloid process and stylomastoid formen. This plane is then opened in inferior direction by blunt dissection till facial
nerve is visible.
SS Method No. 2 This method is particularly suitable when the tumor is large with posterior extension. Inferior pole of
parotid is lifted off from sternocleidomastoid muscle through the cervical extension of the incision. Great auricular
nerve is visible in this stage and needs sacrifice. Anterior border of sternocleidomastoid is retracted inferiorly, then
posterior belly of digastric is identified.
SS Digastric muscle is traced upwards to backwards upto its insertion to mastoid which lies immediately below the
stylomastoid foramen.
zz The nerve can also be located 1 cm medial and inferior to the ‘pointer’ of tragal cartilage.
SS After leaving the stylomastoid foramen, the nerve becomes more superficial and divides into zygomaticofacial
trunk and cervicofacial trank.
Dissection of parotid
SS The five branches of facial nerve are followed peripherally throughout the parotid.
SS Between each branch of the nerve, the parotid tissue bridging between superficial and deep lobe must be divided
carefully.
SS Use of unipolar diathermy is contraindicated during dissection. Ligature or bipolar diathermy must be used for
hemostasis.
SS Following removal of superficial lobe, the nerve trunk and its branches can be seen.
SS If deep lobe is involved, total parotidectomy to be done by retracting the nerve with slings.
SS If nerve is injured or partially excised, primary suturing or nerve grafting (using great auricular nerve or sural nerve)
using operating microscope.
SS During total parotidectomy for malignant tumor, only branches that directly invaded must be sacrificed without
disturbing others.
Chapter 23
Skin and Adnexal Lesion

Important Topics
zzCystic Lesions of the Skin

zzGanglion
zzVascular Lesions of the Skin

zzBenign Tumors
zzSkin Infection
zzBenign Pigmented Lesions
zzPremalignant Lesions
zzMalignant Lesions
‘If you cannot explain it to a six year old, you don’t understand it yourself.’
Skin and Adnexal Lesion 881
Diseases of the Skin and its Adnexa
Cystic Lesions of the Skin
Sebaceous cyst (epidermal inclusion cyst)

SS A retention cyst formed as a result of obstruction of the pilosebaceous follicles → gland becomes distended by its
own secretion.
SS Develop in all ages.
SS Can develop wherever there are sebaceous gland, but commonly occur in face, scalp, neck, scrotum.
[Palm of hands and sole of the feet devoid of sebaceous glands.]

SS On clinical examination, the cyst is smooth, soft or firm and sometimes a pathognomonic punctum (attached to
skin).
Sebaceous cyst with punctum
SS Complications are infection, Cock’s peculiar tumor and sebaceous horn.

SS Treatment is excision of the cyst with complete cyst wall removal. [retained cyst wall may cause cyst recurrence.]
SS Infected cyst (commonly found organisms are Staphylococcus, group A streptococcus, E. Coli, peptostreptococcus,
bacteroides) can be safely excised with antibiotic coverage and proper wound care.
[A length to width ratio of 3:1 is

necessary to make the ellipse]
What is sebaceous horn?

SS Content of the cyst exudes slowly from a large punctum
⇓
become dry and harden to take a shape of conical spike
What is Cock’s peculiar tumor?

SS An infected, open, granulating sebaceous cyst.
SS Granulation tissue arising from the lining of the cyst

bursts through ruptured cyst and makes the lesion
an angry looking lesion with an everted edge.
SS It looks like a squamous cell carcinoma.
[Epidermal inclusion cyst may be associated with Gardner syndrome, so individuals with extensive cysts warrant GI
neoplasm work up.]
Dermoid Cyst
Congenital dermoid cyst
SS Congenital dermoid cyst arise from separated epidermal cells during fusion
of the embryonic clefts and therefore found at the lines of fusion.
SS External angular and at the root of the nose are two most common sites of
this cyst.
SS Cyst contain thick opaque mixture of sebum, sweat and desquamated
epithelial cells.
SS Soft, nontender, cystic swelling, not fixed to the skin but fixed to the
underlying bone.
SS Rarely, the cyst has a intracranial communication. So a skull X-ray or CT is
essential to exclude this.
SS Excision of the cyst is the treatment of choice.
Dermoid cyst in external angular region Skull CT is indicated to exclude extracranial communication
Implantation dermoid cyst
SS It is an acquired dermoid cyst, develops following an injury.

SS Injury results in implantation of epithelial cells into the subcutaneous
tissue.
SS The cysts are often found in tailors, gardeners.
SS In most of the cases, patient can’t remember the event of injury.
SS Overlying skin is often scarred.
SS Excision is the treatmentof choice.
Ganglion
SS A unilocular, nonneoplastic, pseudocystic swelling as a

result of cystic, myxomatous degeneration of synovial
tissue in relation to joints or tendons.
SS Most commonly located in dorsum of the wrist, followed
by volar wrist, flexor tendon sheath.
SS Clinically, it is a nontender, smooth, firm swelling not
fixed to the overlying skin.
SS On compression, a ganglion may slip away between
deeper structures, giving the false impression that the
contents have reduced into the joint.
[A true ganglion is not connected with the joint.]
Ganglion in dorsum of wrist

SS Mobility of ganglion is restricted when the underlying structures (joint capsule, tendon sheath) becomes tense.
SS Treatment is excision or threading or intralesional sclerosant injection.
SS Definite therapy is excision of the stalk of the ganglion and debridement of the synovial origin.
SS In Dorsal wrist ganglion—Excision of the stalk followed by debridement of dorsal wrist capsule over the scapholunate
ligament.
SS In volar wrist ganglion—Excision of the stalk followed by debridement of volar wrist capsule over the
radioscaphocapitate ligament.
[Protection of radial artery and superficial radial nerve is crucial during excision.]
After excision of ganglion
Vascular Lesions of the Skin
SS Hemangiomas
SS Vascular malformations
SS Ectasia
SS Other lesions.
Hemangiomas
SS They basically arises due to endothelial hyperplasia

SS They are benign vascular neoplasm.
Strawberry nevus (Capillarycavernous angioma)
SS Small red mark is noted usually 1–3 weeks after birth, that rapidly increasing in size over a few weeks to take the
shape of a strawberry.
Strawberry nevus is intradermal collection of dilated vessels
SS Raised, compressible, nonpulsatile lesion covered with smooth, pitted epithelium, commonly found in face, scalp
and neck region.
SS About 90% of the lesions regress spontaneously over time (within 5–9 years) with accepted cosmetic outcome.
SS Treatment is conservative except in lesions causing difficulty in vision, feeding.
Those lesions warrant early surgical intervention.
Strawberry nevus
Vascular Malformations
Vascular malformations
SS Structural abnormalities due to aberrant morphogenesis in embryological period.

SS Lesions present at birth, grow in proportion to the body and do not regress.
SS Different types according to hemodynamic characteristics—
zz High-flow lesion
[Arteriovenous malformation, arteriovenous fistula.]

zz Low-flow lesion
[Capillary malformation, venous malformation, lymphatic malformation]

Port-wine stain
These are intradermal capillary malformation.

––
Histologically, they are collections of ectatic capillaries

––
lined by mature endothelium.
Commonly present in face, shoulder, neck. Sometimes,
––
they are confined to a single dermatome (along a
trigeminal distribution in face).
Occasionally, they present as a part of syndromes—
––
Sturge-Weber syndrome (leptomeningeal angioma-

``
tosis, epilepsy, glaucoma).
Klippel-Trenaunay syndrome (varicose vein, limb
``
hypertrophy, port-wine stain). Port-wine stain is intradermal collection of ectatic
Treatment is pulsed dye laser therapy.
–– capillaries
Ectasia

Dilated vessels but normal endothelial turnover.

––
Spider nevus
SS They are solitary dilated skin arteriole feeding a number of small branches.
SS Thislesion typically found in preschool and school-aged children.

SS They are present in the drainage area of SVC (upper half of trunk, face, arm).
SS After release of compression, it fills from the center outwards.
[Systemic examination should be done becaue it is associated with liver diseases (cirrhosis, hepatic tumors).
SS Spontaneous resolution may happen; if treatment is indicated, pulsed dye laser is the treatment.
zz Venous malformations
Most common type of vascular anomalies.
Venous malformations usually present as blue, soft, compressible lesion.
Histologically, venous malformations are composed of thin-walled, dilated, sponge-like alonormal channels
with surrounding smooth muscle.
MRI is the most useful imaging modality.
Treatment is sclerotherapy and surgery.

Lymphangioma
SS Cluster of dilated lymph sacs in the skin and subcutaneous tissues, not connected with the main lymphatic system.
SS Large, translucent lymph cysts mostly found in the neck—Known as ‘Cystic hygroma’.
SS Lymphangioma is classified according to size—
1. Microcystic (<1 cm)

2. Macrocystic (>1 cm)
3. Combined.
SS Lymphangiomas are commonly located in cervicofacial region (70%–80%), axilla, chest, mediastinum, buttock.
SS Prenatal USG can detect macrocystic lymphangiomas at second or third trimester.
USG can detect presence of macrocystic lymphangiomas, but MRI is the most useful imaging modality.
SS Treatment—(1) Sclerotherapy (2) Surgery
zz Sclerotherapy—Sclerotherapy acts by obliterating lymphatic lumen by endothelial destruction followed by

fibrosis.
Commonly used sclerosants are—sodium tetradecylsulfate, ethanol, bleomycin.
Sclerotherapy is more effective in macrocystic lymphangiomas. Repeated sessions of sclerotherapy are

required to achieve satisfying result.
zz Surgery—Staged excision is often necessary. During surgery, surgeon must keep in mind few principles—
Attempts to minimize blood loss, focus on a defined anatomic region, thorough dissection as possible.
Other Vascular Lesions
a. Campbell de Morgan spots

zz Bright red, small spots in upper half of the trunk, in middle aged and elderly persons
zz No clinical significance.
b. Salmon patch
zz Present at birth and regresses completely at the age of 1 year
zz Found in forehead and occipital region.
c. Pyogenic granuloma
zz Acquired lesion of skin and mucous membrane develops after a minor trauma.
zz At the phase of healing of ulcer or wound, sometimes capillary loops grow rapidly, thereby forming a protruding
lesion consists of capillaries covered by epithelium. This mass becomes infected and forms a pyogenic granuloma.
zz Typical natural history is usually present—
History of minor injury → appearance of nontender lump that rapidly grows → bleeds on minor touch.
zz Treatment is excision.
Pyogenic granuloma
d. Glomus tumor
zz A tumor arises from glomus body [glomus body, an arteriovenous
shunt in the skin that have a role in temperature regulation, are present
throughout the skin with special preference in fingers and toes]
zz Small, firm, bluish-gray, extremely tender nodules mostly found in
subungual region. The clinical triad of— (1) Hypersensitivity to cold
(2) Paroxysmal pain and (3) Pin point pain suggestive of glomus tumor.
zz Three clinical tests can be performed for diagnosis—
1. Love's test— Pressure is applied over the tumor by pin/paper clip
⇒ severe pain (positive result).
2. Hildreth's test—Touruiquet is applied proximal to the tumor site ⇒ Love's test is performed ⇒ No pain
(positive result).
3. Cold sensitivity test—Increased pain with exposure to cold.
zz As they are extremely tender, these malformations must be excised.
Arteriovenous malformations
zz
AVMs are high-flow vascular malformations consist of disorganized arteries and veins that communicate.

AVMs are manifested as warm, pink patch in the skin with underlying thrill or bruit.
A clinical staging system exists:
Schobinger clinical staging system for AVMs

Stage I (quiescence) Pink-bluish stain, warmth, and arteriovascular
shunting by continuous Doppler scanning or
20 MHZ color Doppler scanning.
Stage II (expansion) Same as stage I plus enlargement, pulsations, thrill,
bruit and tortuous/tense veins.
Stage III (destruction) Same as stage II plus either dystrophic skin changes,
ulceration, bleeding, persistent pain, or tissue necrosis.
Stage IV (decompensation) Same as stage III plus cardiac failure.
SS Doppler USG can detect the fast flow of AVM. CT, MR angiograply can also detect the presence of AVMs.
SS Treatment is angiographic embolization alone or in combination with surgical excision.
zz Treatment is indicated if symptoms (e.g. ischemic changes, pain, intermittent bleeding, ulceration) are present or
endangering signs (e.g. recurrent ulceration, increased cardiac output, Schobinger stage III and IV) are present.
Benign Tumors
Papilloma
SS Overgrowth of all layers of skin with a central core of cannective tissue, blood vessels and lymphatics.
SS With epithelial proliferation, it is thrown into folds and takes the shape of a papilloma. Along with epithelial
proliferation, the connective tissue and blood vessels grow.
Papilloma
SS It may present as sessile or pedunculated polypoidal lesion.
SS Surgery is indicated if the lesion is cosmetically unacceptable or vulnerable to injury.

Lipoma
SS Itis composed of adult type fat cells.

SS Lipoma may present any where in the body, that is why it is also called 'universal tumor'.
SS Different types—
1. According to presence of edge
Encapsulated lipoma [has a definite edge]
Diffuse lipoma [no definite edge].
2. According to number
Solitary.
Multiple lipomatosis [multiple lipomas of different

sizes are present particularly in the trunk].
3. According to presence of other tissues
Angiolipoma
Plemorphic lipoma
Fibrolipoma
Neurolipoma
Nevolipoma
Lipoma
Myelolipoma.
4. According to location
Subcutaneous lipoma
– Commonest type
– Commonly found in the shoulder, back.
Subfascial lipoma
– Present deep to palmar and plantar fascia.

Subsynovial lipoma—in the knee.
Intraarticular lipoma.
Intermuscular lipoma—In thigh or shoulder.
Retroperitoneal lipoma.
Submucous lipoma—Deep to mucous membrane

of alimentary tract or respiratory tract.
Lipoma after excision–lobulated pattern is obvious
SS Complications—
zz Myxomatous degeneration
zz Saponification
zz Calcification
zz Sarcomatous change (rare).
SS On clinical examination, lipomas are usually spherical shaped, lobulated, slips away from examining finger (slip
sign).
SS Investigation—
zz Typical subcutaneous lipoma does not need preoperative imaging. Imaging (USG/CT/MRI) is indicated if lipoma
> 5 cm, irregular in shape or myofascial involvement. MRI is the most sensitive imaging modality.
SS Surgery is mostly indicated for cosmetic reason. Other indications of surgery are—Nerve impingement, pain,
functional limitation, increase in size, case needle biopsy showing atypical histology, involvement of deep fascia.
SS Uncommon varieties of lipoma—
zz Adiposis dolorosa (Dercum’s disease)—It is characterized by tender multiple lipomas in the trunk.
zz ‘Lipoma aborescens’—Pedunculated subcutaneous lipoma.
SS Uncommon varieties of adipose tissue tumors—
zz Hibernoma—Benign tumor composed of brown fat
zz Lipoblastoma—Benign tumor composed of immature adipocytes.
SS Syndromes associated with lipoma—
1. Adiposis dolorosa
2. Gardner syndrome
3. Madelung disease
4. Bannayan-Riley-Ruvalcaba syndrome (BRRS).
Neurofibroma
SS Solitary benign tumor arising from connective tissue of a nerve sheath (epineurium)

SS Contains both neural (ectodermal) and fibrous (mesodermal) elements
SS Present as tender, subcutaneous, nodular swelling, most freely moves in right angle to the course of the nerve
Patient may present with tingling sensation in the distribution of the nerve from which it arises.
SS Treatment is excision of the tumor

zz Increased tendency for local recurrence
zz Sarcomatous changes rerely develop in neurofibroma, particularly in multiple neurofibromatosis.
Multiple Neurofibromatosis
SS This multiple, congenital, familial (autosomal dominant inheritance) neurofibromatosis is also called von
Recklinghausen’s disease.
SS This is type 1 neurofibromatosis with mutation in chromosome 17.
SS It arises from endoneurium.
Multiple neurofibromatosis–some nodules having malignant

transformation
SS Characterized by
zz Multiple cutaneous neurofibromas
zz Cutaneous hyperpigmented macules ('cafe' au 'lait spot)
zz Pigmented nodules of the iris (lisch nodule)
zz Gliomas of the optic nerve.
SS Patients present with nodules of varying sizes from a milimeter sized to large varieties. Some of them in the skin,
some are subcutaneous and few of them become pedunculated.
SS Examination of the spinal nerve and hearing tests are essential to exclude major nerve involvement.
SS Patient with NF 1 gene have a greater chance of malignant transformation of the tumors.
SS Tumor with ulceration, large pedunculated and tumor with sarcomatous changes need excision.
Plexiform Neurofibromatosis
SS Excessive overgrowth of neural tissue in subcutaneous fat

SS More commonly seen in relation to distribution of trigeminal nerve, sometimes seen in extremities
SS Presents as a folded, irregular mass hanging from the face with hyperpigmentation
SS The nerves are heavily thickened due to myxomatous degeneration of endoneurium
SS Very rarely, sarcomatous changes may develop.

Elephantiasis Neurofibromatosis
SS Rare,congenital variety of plexiform neurofibromatosis

SS Skin becomes coarse, dry and thickened and resembles an elephant’s skin.
Skin Infection
Furuncle (boil)
SS Staphylococcal infection of pilosebaceous unit with perifolliculitis.

SS Infection proceeds to suppuration and then central necrosis.
SS Commonly present in back and neck.
SS Usually presents as tender, indurated swelling around a hair follicle with

surrounding edema. Within a few days, the center softens, after that it
bursts spontaneously.
SS Commonly associated with generalised debility and diabetes mellitus.
SS Incision is usually not necessary for drainage of pus. Local application of

iodine aggravates spontaneous rupture.
SS Removal of affected hair follicle also helps in drainage.
SS Antibiotics coverage against staphylococcus is indicated in blind boil (boil

without suppuration).
Impetigo
SS Intradermal bacterial infection caused by staphylococcus and streptococci.

SS Commonly involves the hand and face.
SS Presents as vesiculopustular lesion and then ruptures and then formation of characteristic yellowish crust.
SS Treatment is washing the lesion and removal of crust with chlorhexidine lotion.
Carbuncle
SS Infectivegangrene of the subcutaneous tissue with multiple openings in the skin.

SS Usually caused by Staphylococcus aureus, sometimes streptococci and gram-negative bacilli are responsible.
SS Commonly found in back, nape of the neck (vitality of the tissues are less in these region).
SS Older diabetic patients are commonly affected.

SS Antibiotics and local application of magnesium sulfate (helps
to decrease the edema and softening the center of carbuncle)
is necessary in initial stage.
SS Surgical intervention is needed if the infection not responds to
conservative management.
Carbuncle
Hidradenitis Suppurativa
SS Chronic infection of the apocrine sweat glands due to blockage of the ducts of apocrine glands (compound sweat
glands).
SS More common in women in tropical countries. Perianal hidradenitis suppurativa is more common in men.
SS Most commonly found in axilla, but may also develop in groins, perianal regions (all apocrine gland bearing regions).
SS Patients present with multiple swellings in the axilla, which eventually discharges pus and then subsides
spontaneously or after treatment. The swellings again appear after a few months.
SS Maintaining local hygiene and avoiding of deodorant, depilation, shaving is important for preventing recurrence.
Erythromycin along with metronidazole are useful for controlling infection.

SS If conservative treatment fails and there is frequent episodes of infection, excision of the affected skin followed by
split thickness skin grafting is indicated.
Necrotizing Fasciitis (Fournier’s Gangrene)

SS Invasive infection of skin, subcutaneous tissue and deep fascia but sparing of muscle
SS Caused by beta hemolytic streptococci, coliforms and anaerobes.
SS Common sites are Genitalia, groin and lower abdomen.
SS Predisposing factors are – Diabetes mellitus

– Corticosteroid use
– Malnutrition
– Immunodeficiency disorders.
SS Treatment is wide excision of all infected tissues along with parenteral antibiotics.
[Mortality is significantly high.]

Benign Pigmented Lesions
SS Naevi are benign pigmented lesions of the skin

due to increased number of melanocytes.
SS Normally, melanocytes are present in the basal
layer of the epidermis.
SS Different types (according to microscopic
appearance)—
a. Lentigo: Increased number of melanocytes within the basal layer of epidermis.

SS Usually found in face and hand of elderly person.
b. Junctional nevus: Develops due to increased number of melano-

cytes at dermo-epidermal junction.
SS Usually found during or before puberty, as a smooth, flat pigmented
lesion.
[Majority of malignant melanoma arise from junctional nevus.]
c. Dermal nevus: Excess number of melanocytes cluster within the dermis.

SS Presents as pigmented, elevated fleshy lesion in adults.
d. Compound nevus: Excess melanocytes both at the dermo-epidermal junction

and within the dermis.
SS Presents as dermal nevus or junctional nevus.
e. Blue nevus: Excess melanocytes in the deeper layer of dermis.

SS Most commonly found in face, dorsum of hand and feet.
SS As the clusters of melanocytes present deep in the dermis, the lesion appears
bluish rather than brown.
SS Different types (according to clinical presentation):
a. Hairy mole
SS Flat, slightly raised lesion with warty epidermal covering
SS Hairs grow from its surface
SS Microscopically, intradermal nevi.
b. Nonhairy mole
SS Epithelium is smooth and not elevated
SS Microscopically, junctional or compound nevi.
c. Blue nevus
SS Overlying skin is smooth and shiny.
SS More often seen in children.
SS Commonly found in face, dorsum of hands and feet, over the sacrum
(mongolian blue spot).
d. Hutchinson’s lentigo
SS Large area of hyperpigmentation.
SS Seen in face and neck of older people.
SS Surface is smooth, but may be raised (areas of junctional activity)

as well as pale areas (areas of regression).
[Increased chance of malignant transformation.]
Treatment
SS Most of the nevus are benign and do not require treatment

SS Conditions where excision is indicated:
zz Patient wants for aesthetic reasons.
zz Recently discovered lesion in an adult.
zz Lesions undergone change in color (more darker), change in surface (loss of skin crease), increase in size, shape
and thickness.
zz Lesion starts itching (early symptom).
zz Lesion starts bleeding (a late symptom).
zz Lesion in sole of foot or palm of the hand.

Premalignant Lesions
Solar Keratosis (Actinic Keratosis, Senile Keratosis)
SS Areas of epidermal dysplasia and hyperkeratosis in sunexposed areas of skin in elderly fair skinned males
SS UltravioletB-induced P53 mutation have been observed in these lesions
SS Commonly seen in back of fingers and hands, face, rim of ears
SS Presents as raised erythematous plaque of skin with rough surface
SS Three possible behavior patterns Spontaneous regression
Persistence
Progression to carcinoma
SS These lesions are potentially malignant (squamous/basal cell carcinoma)
SS Prevention—
zz Use of hat
zz Use of sunprotective clothings, sunscreen.
SS Treatment—
zz Cryotherapy with CO or liquid nitrogen (in solitary lesion)

2
zz Topical 5–FU cream application (in multiple lesion)
zz Thermocautery + curettage
zz Topical imiquimod
zz Photodynamic therapy.
Solar keratosis not responding to treatment or presents with bleeding, rapid growth or pain—Think of SCC and should
be confirmed by biopsy.
Bowen’s Disease
SS Itis an intraepidermal squamous cell carcinoma in situ

SS Clinically presents as flat, pink papular patches with well-defined margins, covered with crusts
SS Exposure to arsenic is sometimes associated as an etiological factor
SS Local cytotoxic therapy e.g. 5-FU, cryotherapy, cauterisation is useful but increased chance of recurrence
SS Surgical excision is the best treatment option.
Erythroplasia of Queyrat
SS It
is the Bowen’s disease of glans penis
SS Most commonly found in uncircumcised males.
Xeroderma Pigmentosum
SS Autosomal recessive disorder where sunexposed skin is mostly affected

SS Patients are in increased risk of developing squamous cell carcinoma, basal cell carcinoma and malignant melanoma.
Malignant Lesions
Basal Cell Carcinoma (Rodent Ulcer)
SS Commonest of all skin cancers.

SS Locally invasive malignancy of skin arising from basal layer of
the epidermis.
SS Most commonly seen in middle aged fair-skinned male
person who have prolonged exposure to bright sunlight (U–V
irradiation).
Arsenic exposure is sometimes a risk factor.
Other risk factor—Psoralen-plus UVA therapy.
SS Most common location is face, specially a zone above a line
from lobe of the ear to corner of mouth.
Skin of all regions are susceptible.
SS Pathology—
zz Characteristic feature is proliferation of basaloid cells resembling basal layer of epidermis.
zz Masses of basaloid cells with single, outer layer of cells with palisaded appearance in dermis.
Different types
According to clinical appearances According to histologic types
1. Nodular (most common) 1. Basosquamous (rare)

2. Cystic 2. Morpheaform
3. Pigmented 3. Adenoid
4. Deeply eroding ulcer 4. Infiltrative
5. Geographical
Pigmented basal cell carcinoma should be distinguished from malignant melanoma.

Basosquamous basal cell carcinoma behaves more like a squamous cell carcinoma. So this type of carcinoma should
be treated aggressively.
SS Clinically starts as nodular lesion (covered by fine vessels which give it a pink hue), that soon become ulcerated
centrally. The resulting ulcer has a rolled pearly edge.
In advanced stage, the tumor erodes bone, muscle, cartilage.

BCC grows slowly, BCC does not metastasize.
SS Biopsy must be obtained prior to definite treatment.

SS Different methods of treatment—
zz Curettage and electrodesiccation
zz Cryotherapy
zz Laser ablation
zz Topical application of 5-FU
These methods of treatment can be employed for smaller lesions, but no tissue for histology is obtained and
clearance of tumor margin become uncertain.
zz Radiotherapy—
Bcc is highly radiosensitive.
Indicated in patients not fit for surgery.
Usually 40–60 Gy radiation dose is given for a period of 2–3 weeks.
zz Surgical excision—
Larger lesions, lesions involving adjacent structures, aggressive histologic

types (basosquamous, infiltrative) need excision with 2–4 mm margin.
zz Moh’s micrographic surgery—
Serial horizontal excision

⇓
Each piece of tissue is undergone frozen section biopsy [entire margin of
resection is examined]
⇓
Resection process to be continued until the margin is free.
This technique is particularly useful for BCC in eyelids and nose where tissue loss is
undesirable, in recurrent lesions and in lesion with indistinct borders (morpheaform).
Least sacrifice of uninvolved tissue.
The procedure is lengthy (takes upto several days).
SS No need of follow-up except in Gorlin’s syndrome (Familial BCC), nevoid BCC syndromes tumors in high risk areas.
Squamous Cell Carcinoma
SS SCC of skin arises from the keratinocytes in epidermis

SS Commonly found in men than women.
Risk factors
SS Prolonged exposure to sunlight (SCC is less aggressive)

zz Amount of exposure is proportional to risk.
zz Persons with fair complexion, blonde hair are more susceptible than individual with dark complexion.
SS Solar keratoses
SS Bowen’s disease
SS Xeroderma pigmentosa (1000 fold increased risk)
SS Oculocutaneous albinism
SS Immunosuppression (4 fold increased risk)
zz Risk is related to degree of and duration of immunosuppression.
zz Patient of organ transplantation (on immunosuppressive drugs, e.g. azathioprine, cyclosporine, prednisolone).
zz Patient with immunosuppressive diseases (e.g. HIV and HPV infection, autoimmune diseases, lymphoma,
leukemia).
SS Exposure to certain chemicals (e.g. organic hydrocarbons)
SS Exposure to arsenic
SS Old burn scar (higher incidence of metastases)
SS Long standing venous ulcer
SS Chronic osteomyelitis (higher incidence of metastases)
SS Tobacco use.
Site of tumor
SS Most commonly found in exposed areas—

zz Head region (about 75%)
zz Face, Pinna, back of hands
zz Mucocutaneous junctions—Lip, anal canal, glans penis.
SCC in external ear have increased tendency to recur and regional lymph node metastasis.
Chimney-sweeper’s cancer—Cancer of scrotal skin due to repeated exposure to soot.
Kangari cancer—SCC of skin of inner side of thigh and lower abdomen in natives of kashmir (Kangari is an earthen-
ware pot containing glowing charcoal– people keep this pot close to abdomen to keep warm).
Marjolin’s ulcer—SCC in old burn scar.
SS Microscopically, well differentiated SCC have a characteristic appearance—Whorled arrangement of malignant

squamous cells, in which the center of it contains laminated keratin material.
[SCC stains positive for

cylokeration 1 and 10]
SS Regional lymph nodes may become involved, either due to metastasis or from infection.
SCC in hand–ulcerated growth with everted edge are

characteristic
SS Clinically
presents as slightly raised hyperkeratotic macule or papule. Gradually the surface breaks down and an
ulcerated growth with everted edge with indurated base develops.
SS Diagnosis—Any lesion suspicious for SCC should be biopsied (shave biopsy).
Treatment 2. Radiotherapy
SS In head and neck SCC with no evidence of

local invasion or metastasis.
SS In elderly patients who are not fit for
surgery or unwilling to surgery.
1. Surgery
3. Electrodesiccation and curettage or

Cryosurgery
SSElectrodesiccation is indicated in well differenti-

ated SCC < 1 cm.
SSSCC-in-situ can be treated by cryosurgery.
Traditional excision
Mohs’ micrographic surgery
SS Tumor size> 1 cm. SS Large primary or recurrent SCC in those sites where
SS Tumor in high risk areas (in old burn scar, conservation of normal tissue is essential.
chronic osteomyelitis, in external ear). SS Invasive lesion, poorly differentiated lesion,
Margin must be at least 4 mm. lesion in high risk anatomic sites where surgery
is indicated but traditional excision can affect the
function or cosmesis.
SS Treatment of nodal metastasis— Radiotherapy, Lymph node dissection or both

SS Invasive SCC need close followup
zz Every 3 months during the 1st year after treatment
zz Every 6 months during the 2nd year
zz Then annually.
Verrucous carcinoma
SS A special variety of SCC which is well-differentiated, invade locally and rarely metastasize
SS Commonly found in palms and soles
SS Superficial part of the tumor resembles verruca (hyperkeratosis, parakeratosis, acanthosis, papillomatosis)
SS Treatment is surgical excision.

Cutaneous Melanoma
SS Melanoma is a malignant neoplasm arising from melanocytes.
SS Cutaneous melanoma arises from malignant transformation of melanocytes at the dermoepidermal junction.
SS More than 98% of melanomas are cutaneous melanomas.
[Melanocytes also found in meninges, upper esophagus and eyes (sites where precursor melanocytes migrate from
neural crest during embryonic development)].
Pathophysiology
SS Progressionfrom normal melanocytes to metastatic melonoma is a stepwise process induced by multiple genetic
mutations and involves several histologic intermediates.
Genetic mutations responsible:

1. Germline mutations in CDKN2A gene
(located in 9p21)
2. Suppression of PTEN gene
3. Polymorphism in melanocortin–1 receptor
(MC1R) locus.
[Mutation in p53 is quite uncommon.]
Cells in the vertical growth phase are different from cells in radial growth phase in respect of morphology, cell surface
antigens, behavior in cell culture.
SS Most of the melanomas arise de novo, few are hereditary.
Risk factors
SS Exposure to UV (UV–B) irradiation—most important risk factor

SS Presence of dysplastic nevus (more nevus, more risk)
SS Family members with dysplastic nevi and malignant melanoma
SS Xeroderma pigmentosa
SS History of other skin cancers associated with UV exposure
SS History of high dose irradiation in childhood
SS Genetic predisposition (e.g. mutation in CDKN2A and B-RAF gene).
SS Cutaneous melanoma most commonly develop in back and head-neck regions in male and in lower extremities
(below the knee) in female.
Malignant melanoma in face

Etiology of acral lentigenous melanoma (ALM) is most likely independent of UV exposure.

ALM is more common in African, Asian and Hispanic population than in fair skinned population.
Subungual lesions present as blue-black discoloration of the posterior nail fold. Additional presence of discoloration in
proximal or lateral nail folds (Hutchinson’s sign) is diagnostic of subungual melanoma.
Any pigmented subungual lesion should be biopsied.
Prognostic factors
SS Depth of invasion
zz Best prognostic indicator of metastatic risk.
zz Clark used the histologic level to measure the depth of invasion.
zz Breslow used the thickness of lesion (from granular layer of the epidermis to the base of the lesion)—with the
help of an ocular micrometer.
zz TNM classification is the modification of these classifications.
SS Metastasis
zz Lymph node metastasis– Regional lymph node involvement is a poor prognostic sign. The number of positive
lymph nodes is related with survival rates.
zz Distant metastasis is also a grave prognostic sign.
SS Ulceration—Ulceration of the lesion is a negative prognostic indicator.
SS Gender—Prognosis is better in women.
SS Location of tumor
zz Prognosis is bettter in melanoma on extremities in comparison to melanoma in trunk, head neck
zz Melanoma on acral sites have also poorer prognosis
zz Significant poor prognosis in mucosal melanoma.
SS Histologic growth pattern— Lentigo maligna melanoma have a better prognosis and acral lentigenous melanoma
have a worse prognosis independent of Breslow thickness.
SS Age of the patient—Melanoma—Associated mortality increases with age.
Spread of tumor
SS Lymphatic spread—Tumor may spread to regional lymph

node by embolism.
zz Lymphatic permeation causes local satellite lesion.
SS Hematogenous spread—Lungs, liver, brain, spinal cord,

adrenals are common sites of metastasis.
Unusual sites of metastasis—Small intestine, heart, breast.
Diagnosis
SS Malignant melanoma can be differentiated from benign

pigmented lesions by examining the features: Asymmetry,
Border irregularity, Color change, Diameter > 6 mm, Elevation
(ABCDE).
SS Clinical examination is to be done to assess the site of primary
lesion, any satellite lesion, all major lymph nodal basins and
thorough evaluation of regional lymph node basins.
SS If melanoma is suspected clinically, a full thickness biopsy of
skin and underlying fatty tissue along with all the visible lesion
is done. If complete excision is not possible, then excision
of a part of the lesion along with adjacent normal skin (full
thickness) is indicated.
Treatment
1. Surgery
SS Excision of primary lesion—
zz Surgical excision is the treatment of choice for all type of melanomas.
zz Lateral margin of 2 cm is recommended and the vertical extension of the excision must be include subcutaneous
tissue. No necessity to excise the fascia or muscle beneath the lesion.
zz The defect is closed by either primary closure or by skin graft or local
flap.
SS Lymph node dissection—
zz Clinically positive lymph nodes must be removed by regional nodal

dissection. Removal of lymphatics between the primary lesion and
regional lymph nodes is also recommended.
zz In lower extremity lesion, iliac lymph nodes have to be removed along
with inguinal lymph nodes.
zz In lesion on the face, anterior scalp and ear. superficial parotidectomy to
remove parotid nodes and modified radical neck dissection in clinically
negative lymph nodes is usually recommended in intermediate
thickness lesion (1–4 mm).
[lesion <1 mm thick are very unlikely to develop nodal metastasis and lesion > 4 mm are more likely to develop distant
metastasis]
[Sentinel lymphadenectomy is an accepted surgical option in malignant melanoma]

Metasectomy—Solitary metastatic lesion in brain, GI tract or skin should be excised if possible.
2. Immunotherapy— Interferon–α (INF–α) 26 is recommended for stage IIB and III
3. Radiotherapy
SS Radiotherapy is the treatment of choice in multiple brain metastasis.
SS Adjuvant Radiotherapy to the neck or axilla after radical lymph node dissection decreases regional recurrence rate.
4. Hyperthermic regional perfusion— Hyperthermic regional perfusion of the affected limb with a chemotherapeu-
tic agent (melphalan) is indicated in local recurrence or in transit lesion that is not amenable to excision.
Heated Melphalan (upto 41.5°C) is preferred for 60–90 minutes.
The advantage of regional perfusion is to increase the dose of chemotherapeutic agent without increasing systemic
side effects.
Other Malignancies of the Skin
Kaposi’s Sarcoma
SS Multicentric angiosarcoma affecting the skin and viscera

SS Clinically
presents as rubbery bluish nodules in the extremities
SS Four form of kaposi’s sarcoma—
1. Classic (European)— Locally aggressive, visceral involvement is rare

2. African (Endemic)— More aggressive than classic form, predilection to spread to lymph nodes
3. Epidemic (AIDS–associated)— Occurs exclusively in male homosexuals. Not in IV drug abusers and hemophiliacs
4. In renal transplant patients.
SS Treatment is surgical excision. Other treatment options are—
zz Radiotherapy
zz Cryosurgery
zz Laser ablation.
Angiosarcoma
SS Highly aggressive malignant tumor of endothelial cells

SS Clinically presents as ‘bruise’ like lesion that spontaneously bleeds or enlarges, in elderly males
SS Four forms of angiosarcoma—
1. As of scalp and face

2. As associated with lymphedema
3. Radiation induced AS
4. Epithelioid AS.
SS Radical excision is the treatment of choice
SS Prognosis is poor.
Lymphangiosarcoma
SS It may arise in areas of prior radiation therapy or in areas of lymphedema of the arm following mastectomy (Stewart–
Treves syndrome).
SS Prognosis is very poor. Chemotherapy and radiotherapy are used for palliation.
Cutaneous Metastases
SS Common primary sites—
} }
Lungs Breast
Color in male Colon in female
Melanoma Melanoma
SS Sister Mary Joseph nodule, a specific variety of cutaneous metastasis, presents as indurated umbilical nodule.
Chapter 24
Ulcer, Sinus and Fistula

Important Topics
zzDifferent Types of Ulcer

zzBasic Principles of Ulcer Dressing
zzSinus
zzFistula
‘Learn from yesterday, live for today, hope for tomorrow. The important thing is to not stop questioning.’
Ulcer
SS An ulcer is a discontinuity of an epithelial surface.

SS UIcer has some features that must be examined in clinical examination:
1. Edge— It is the junction between healthy and diseased tissue

It takes characteristic form according to underlying disease:
Sloping edge—The edge gently slopes from normal
epithelium to base of the ulcer.
All healing ulcers have sloping edge
Punched-out edge—The edge drops down at right angles to the skin surface.
Example – Deep trophic ulcer

– Gummatous ulcer
Undermined edge—The disease destroys the subcutaneous tissue faster than the overlying skin.
Example–Tuberculous ulcer
Rolled edge—Lesion becomes necrotic at its center, but grows rapidly at its periphery.
Everted edge—When ulcer caused by fast growing disease, the edge of the ulcer heaps up due to excessive
growth.
Typically found in basal cell carcinoma
Example – Squamous cell carcinoma

– Ulcerated adenocarcinoma
Ulcer, Sinus and Fistula 915
2. Floor—Floor is that which is seen by a clinician
Floor may be covered by—
Granulation tissue—In healing ulcer
Dead tissues (slough)—In active ulcer
Malignant tissue—In malignant ulcer.
3. Base—Base is that which can be palpated.

Marked induration of the base— In squamous cell carcinoma.
Base is attached to deeper structures—Varicose ulcer (attached

to tibia).
4. Discharge—Serous, serosanguinous, purulent, offensive.
Dicharge should be sent for culture-sensitivity.
Traumatic Ulcer
SS The ulcer may present in the body but more commonly found where skin is closely
applied to the bony prominences, e.g. shin, medial and lateral malleoli, back of
heel.
SS They are painful, circular-shaped ulcers.
Arterial Ulcer (Ischemic Ulcer)
SS An ulcer that develops due to inadequate blood supply

SS Causes Large artery occlusion
• Atherosclerosis
• Embolism
Small artery occlusion
zz Buerger’s disease
zz Raynaud’s disease
zz Diabetes
zz Embolism
zz Pressure necrosis
SS Found in the tip of the toes and fingers and over the pressure areas.
SS Floor is often infected, the blood supply is not adequate enough to form healthy granulation tissue.
SS Clinically presents as painful, deep ulcer in the distal part of the extremities associated with symptoms of PAD
(intermittent claudication, rest pain, exacerbation of pain at night) and signs of peripheral ischemia (dryness of skin,
hair loss, blackish discoloration, gangrene).
SS Treatment— Care of the ulcer + revascularization.
Unless revascularization is successful, the healing of ulcer is not satisfactory.
Venous Ulcer
Venous ulcer in typical location
SS Commonly found around the ‘gaiter’ area of the lower leg (lower third) and on the medial side of the leg.
The ulcers particularly develop at the sites of incompetent perforators—Most common over Cockett’s perforator
(above the medial malleolus).
SS The typical location of ulcer, characteristic skin changes and history of venous incompetence—Suggestive of
venous ulcer.
SS Treatment—Care of the ulcer + compression therapy.
Neuropathic Ulcer
SS The ulcer develops due to repeated injury or pressure in an area unable to appreciate pain.
SS Causes Spinal cord lesion
 Spina bifida
 Syringomyelia

Peripheral nerve lesion  Tabes dorsalis
zz Diabetes  Paraplegia
zz Leprosy
zz Alcoholic neuropathy
zz Peripheral nerve injury
SS The ulcers are seen on the heel, base of 5th metatarsal, head
of 1st metarsal in ambulatory patients; on the buttock and
on the back of the heel in nonambulatory patients.
SS Characteristic features of this ulcer—
zz Painless ulcer
Neuropathic ulcer at the head of 1st metatarsal
zz Loss of sensation in the surrounding tissues
zz Normal vascularity in the surrounding tissues.
SS Clinically, neuropathic ulcers must be differentiated from ischemic ulcer by through neurological examination.
SS Treatment—Care of the ulcer + use of applicances to reduce pressure + treatment of the cause.
Diabetic Ulcer
SS Sensory neuropathy causes unrecognized injury due to ill-fitting shoes, trauma and foreign bodies. Impaired
proprioception causes abnormal weight-bearing during walking. Neuropathy affects pain and temperature fibers
in initial phase.
SS Motor neuropathy (Charcot's foot, hammer toe, claw toe deformity) causes loss of arch of foot due to dislocation of
metatarsophalangeal and interphalangeal joints leads to excess pressure—Leads to ulcer formation.
SS Autonomic neuropathy causes anhidrosis and decreased cutaneous blood flow in the foot—Drying of skin and
fissure formation.
SS Micro and macroangiopathy leads to impaired wound healing.

SS Most commonly present in great toe and metatarsophalangeal joint areas.
Risk factors for development of ulcer
SS Male sex
SS Diabetes mellitus > 10 years
SS Poor glycemic control
SS History of smoking.
[About 14–24% risk of subsequent amputation following development of ulcer.]
Preventive measures
SS Risk factor modification—

zz Avoidance of smoking
zz Proper glycemic control
zz Treatment of hypertension, dyslipidemia
zz Use of orthotic shoes and devices
zz Nail care
SS Patient education—
zz Proper selection of footwear
zz Daily inspection of feet to detect any minor injury
zz Keep the foot skin clean and moist
zz Avoidance of bare foot walking
zz Consultation with a physician if any abnormality detected.
[Once ulcer develops, chance of healing is poor.]
Treatment
SS Proper control of blood sugar
SS Off-loading—Complete avoidance of weight-bearing on the ulcer—Can be done by using orthotic shoes/casts
SS Debridement—Wide debridement of all necrotic and infected tissues.
SS Dressing of ulcer—
zz Topical antibiotics have limited role.
zz Topical application of PDGF and granulocyte-macrophage colony stimulating factor has promising results.
[Antiseptic agents should be avoided.]

SS Antibiotics—
zz Oral or IV antibiotics according to severity of infection
zz Antibiotics should be used with coverage against gram (+ ve), gram (–ve) and anaerobes.
SS Revascularization
SS Limited amputation.
Decubitus Ulcer
SS Ulcer develops when tissue necrosis develops following compression between bony prominences and external
surface.
[Capillary occlusive pressure–30 mmHg]
SS 4stages of ulcer formation—

zz Stage I — Nonblanchable erythema, intact skin
zz Stage II — Partial thickness skin loss involving epidermis, dermis or both
zz Stage III— Full thickness skin loss
zz Stage IV— Full thickness skin loss with involvement of muscle and bone.
SS Usually presents over the sacrum, over the ischial tuberosity, posterior aspect of heel, buttocks, over the shoulder,
occiput.
SS This ulcers have punched out edge.
SS Treatment—
zz Nutritional supplementation
zz Debridement of ulcer
zz Flap coverage or skin grafting may needed
zz Care of the patient—
Change in position every 2 hours
Use of water bed/air bed
Maintenance of hygiene
Keeping the skin clean and dry.
Tuberculous Ulcer
SS Usually develops following bursting of cold abscess in neck, chest wall, groin.
SS Ulceris often multiple, oval-shaped with irregular crescentic border and undermined edge.
Tender ulcer with caseating material in the floor.
Slight induration is the characteristic feature.
SS Regional lymph nodes are often enlarged.
Bazin's Ulcer
SS Associated with 'Erythrocyanosis frigida'.

SS E.Frigida is a disease exclusively occurs in young women with thick ankles (due to increased subcutaneous fat),
characterized by diminished arterial supply to the ankle skin as a result of absence or small perforators arising from
posterior tibial and peroneal arteries.
SS Clinicallypresents as blue, tender, cold ankle in cold weather and hot, swollen, tender ankle in hot weather.
SS Superficial, tender nodules around the ankle develops, which breakdown to form small, multiple ulcers.
SS Sympathectomy is necessary, particularly if patient lives in a cold climate.
SS Tuberculosis is responsible in many of these patients. ATD is effective in that patients.
Martorell's Ulcer
SS These ulcer develop in patients of older age group with history of hypertension or atherosclerosis.
SS Ulcer develops due to sudden obliteration of end arterioles of the skin of outer or back side of calf
⇓
Skin and soft tissue sloughs away
⇓
Punched-out ulcer
SS Patients present with painful ulcer in calf of one side or both sides and it takes months to heal.
Cryopathic Ulcer
Cryopathic ulcer
Chilblains Frost bite

Chilblains (perniosis)
Meleney's ulcer
SS These ulcers seen in the postoperative wounds after surgery for peritonitis or after drainage of empyema thoracis
SS Caused by symbiotic action of microaerophilic nonhemolytic streptococci and hemolytic Staph. aureus
⇓
Infection causing endarteritis of skin of postoperative wounds
⇓
Ulcer formation
SS Undermined ulcer with plenty of granulation tissue in the floor
SS Patient presents with painful ulcer with features of toxemia.

Tropical Ulcer
SS Acute ulcerative lesion of the skin found in patients of tropical regions (Africa, India)
SS Usually caused by Vincent's organisms (Fusobacterium fusiformis) and Borrelia vincentii.
SS Ulcer with undermined and slightly raised edge, copious serosangineous discharge, significant pain—Characteristic
features.
[Ulcer refuses to heal for months and even years.]
Syphilitic Ulcer
Syphilis has 3 stages
Primary Secondary Tertiary
Ulcer develops in all 3 stages.
In primary syphilis
SS Hard chancre or Hunterian chancre develops at the site of entry of Treponema pallidum after 3–4 weeks of exposure.
SS They usually develops in external genital areas, but may also found in extragenital sites, e.g. lip, tongue, nipple and
perianal region.
SS They are usually single, nontender, oval or round shaped, raised hyperemic margin with an indurated base.
SS Regional lymph nodes are enlarged which are nontender and firm.
In secondary syphilis
SS Ulcersdevelop in the form of white mucous patches, snail-track ulcers (narrow, curved and shallow ulcers), or as
condyloma lata (fleshy, warty growth at the mucocutaneous junction).
SS Nontender, generalized lymphadenopathy—Particularly epitrochlear and suboccipital group of lymph nodes are
enlarged.
In tertiary syphilis
SS Gummatous ulcer develops (typically present over subcutaneous bones, e.g. tibia, sternum, ulna, skull and anterior
surface of scrotum).
SS It develops due to delayed hypersensitivity reaction with endartitis obliterans and vasculitis.
SS The ulcer is nontender, punched-out edge with wash leathers slough in the floor.
SS After healing, silvery 'tissue paper' scar develops.
SS Lymph nodes are not enlarged.
Soft Chancre (Ducrey's Ulcer)
SS Caused by Haemophilus ducreyi.

SS Regional lymph nodes become enlarged and tender.
Actinomycosis
SS Caused by gram-positive mycelia (Actinomyces israelii).
SS Multiple ulcer develops which discharge granules ('sulfur granules')
SS Commonly found in— Facio cervical region (most common)
– Thorax
– Liver.
SS Presence of 'sulfur granules' in the discharge is almost diagnostic. On microscopy, the granules consist of gram
positive mycelia.
Basic Priniciples of Ulcer Dressing
SS Primary aim of ulcer dressing—

zz To remove the dead, necrotic tissues
zz To hasten the granulation process
zz To accelerate the healing.
SS During dressing, followings must be kept in mind:
zz Excess exudate to be removed
zz All dead and necrotic tissues should be excised
zz Dressing must be permeable to oxygen, CO , moisture and impermeable to microorganisms

2
zz Dressing must be such that there will be minimal trauma during dressing change.
Sinuses and Fistula
Sinus
SS A blind track lined by granulation tissue from an epithelial surface into surrounding tissues.
Fistula
SS A communicating track lined by granulation tissue between two epithelial surfaces.

SS Communication may develop between hollow viscus and skin (external fistula) and between two hollow viscus
(internal fistula).
Causes of Peristence of Sinus or Fistula
SS Presence of foreign body or necrotic tissue (e.g. suture material, sequestrum, tuft of hair)
SS Presence of distal obstruction
SS Chronic infection (e.g. tuberculosis, actinomycosis)
SS History of radiotherapy
SS Nondependant drainage
SS Malignancy.
CHAPTER 25
Urology
Important Topics
z Urinary Symptoms
zCongenital Malformations
zCystic Disease of Kidney
zHydronephrosis
zRenal Stone
zInfections of Kidney
zTuberculosis of Kidney
zKidney Tumors
zUreferal Calculi
zUrethelial Tumors of Renal Pelvis and Ureter
zCongenital Anomalies of Urinary Bladder
zBladder Calculi
zSchistosomiasis of the Urinary Bladder
zBladder Tumor
zDiseases of Prostate
zUrethral Stricture
zHypospadias
zPriapism
zPeyronie's Disease
zCarcinoma of Penis
zTesticular Neoplasm
‘The person who never made a mistake never tried anything new.’
Urology 931
Diseases of the Kidney
Urinary Symptoms
1. Hematuria
S Presence of blood in the urine is called hematuria.

[In adults, hematuria of any degree must be regarded as symptom of urologic malignancy until proved otherwise.]
S Evaluation—Search the answers of following queries:
S Gross hematuria is commonly associated with significant pathology in comparison to microscopic hematuria.
z Hematuria associated with pain is commonly due to obstruction by clots or due to inflammation.
Malignancies of kidney and bladder usually present with painless hematuria.
[Patients with gross painless hematuria have a urinary tract malignancy until proved otherwise.]
z Clot indicates significant degree of hematuria
Amorphous clot—Bladder or prostatic urethral origin
Vermiform clot—Upper urinary tract origin.
Causes of Hematuria
Other causes of discoloration of urine—Must be excluded

S Paroxysmal hemoglobinuria
S Excess beetroot consumption
S Porphyria.
2. Pain
a. Renal Pain
S Caused by acute distension of renal capsule due
to obstruction or inflammation.
S Pain due to inflammation is steady; pain due to
obstruction is colicky.
Urology 933
Pain is usually located in the ipsilateral renal

angle (junction of lateral border of erector spi-
nae and 12th rib)
Renal pain may be associated with GI symptoms due to—

S Reflex stimulation of celiac ganglion
S Proximity of organs of GI system.
b. Ureteral pain
S Acute colicky pain in the loin that usually radiates to the ipsilateral groin and genitalia. The patient rolls around in
agony. Pain-free periods persist between each attack.
S Site of radiation of pain is determined by site of obstruction. In obstruction of right midureter, pain is referred
to right iliac fossa (simulate appendicitis) and in obstruction of left midureter, pain is referred to left iliac fossa
(simulate diverticulitis).
In midureter obstruction, pain may also referred to scrotum and labium.
In obstruction of lower ureter, patient may experience pain that radiates along the urethra to the tip of penis, along
with frequency, urgency.
S Pain is due to hyperperistalsis of the ureter to relieve the obstruction.
c. Vesical pain
S Usually caused by overdistension of urinary bladder or by inflammation of urinary bladder.
S Pain is felt at suprapubic region and is most severe when bladder is full.
S Sometimes, in cystitis, patient may complain sharp, stabbing suprapubic pain at the end of micturition—called
'Strangury'.
d. Prostatic pain
S Usually caused by distension of prostatic capsule as a result of inflammation.
S Patient experiences a penetrating ache in perineum or rectum that is poorly localized and usually associated with
dysuria and frequency.
e. Urethral pain
S Scalding or burning sensation in penis or vulva during voiding due to inflammation of bladder or urethra.
3. Irritative Symptoms
Nocturia without frequency—

S CHF and in peripheral edema (intravascular volume along with urine output increases in supine position).
S Geriatric patient (renal blood flow is increased in recumbent position, renal concentrating ability is decreased in
older age).
S Consumption of caffeinated and alcoholic beverages in evening (due to diuretic effect).
4. Obstructive Symptoms
Urology 935
5. Incontinence
a. Continuous incontinence
S Due to vesicovaginal fistula secondary to gynecological procedure, radiation, after obstructed labor
S Due to ectopic ureter that enters the urethra or female genital tract.
b. Stress incontinence: Leakage of urine with cough- c. Urgency incontinence: Strong urge to void followed
ing, sneezing or other activities that increase intraab- by passage of urine.
dominal pressure. S Found in cystitis, neurogenic bladder and in bladder
S Develops in women after childbearing or menopause outlet obstruction.
[due to weakening of pelvic tissues].
S After radical prostatectomy.
d. Overflow incontinence—
6. Enuresis
Urinary incontinence during sleep.

Children older than 6 years with enuresis warrants thorough urologic evaluation.
Diseases of Kidney and Ureter

Congenital Malformations
Anomalies in number
Anomalies of ascent
Congenital malformations Anomalies of form and

fusion
Cystic diseases
Anomalies of renal
vasculature
Other malformations
Anomalies in number
Bilateral renal Unilateral renal Supernumerary Duplication of Duplication of renal

agenesis agenesis kidney ureter pelvis
Urology 937
Bilateral Renal Agenesis
S Children who born alive can't survive beyond 48 hours due to

associated pulmonary hypoplasia.
S Presence of oligohydramnios and Potter facies (prominent fold and
skin crease beneath eyes, blunt nose, depression between lower lip
and chin, low set ears) are pathognomonic.
Unilateral Renal Agenesis
S Occurs once in 1100 births.

S Sometimes GI system and musculoskeletal systems are
affected.
S Unilateral agenesis with contralateral normal kidney can
lead to normal life.
S Contact sports or strenuous physical exertion must be
avoided.
Supernumerary Kidney
S Veryrare anomaly (about 100 cases have been reported).

S Supernumerary kidney has its own collecting system, blood supply and distinct capsule.
S The kidney is located either separately or loosely attached to the main kidney of the ipsilateral side, commonly
caudal to the dominant kidney.
Duplication of Renal Pelvis
S Most common congenital deformity of upper renal tract.
Duplication of Ureter
S In most of the cases, the ureters join in the lower third of their course.
Sometimes, the ureters open independently into the bladder. Ureter from the upper pelvis opens distal and medial
to the ureter from lower pelvis.
S Infection, stone formation and PUJ obstruction are more common in duplication of renal pelvis or ureter.
S In male, the aberrant opening may be above the external urethral sphincter, at the apex of bladder trigone, in the
posterior urethra (most common site of termination of ectopic ureter), in seminal vesicle or ejaculatory duct.
S In female, ectopic opening may be below the urethral sphincter or into the vagina [urethra and vestibule are the
most common site of termination of ectopic ureter.]
Urology 939
Treatment
S Ifatrophic or nonfunctioning chronically infected segment of kidney is present—Partial nephrectomy

S Incontinence due to ectopic ureter—Implantation of ureter into bladder or into the fellow ureter.
Anomalies of ascent
Simple renal ectopia Cephalad renal ectopia Thoracic kidney
Simple Renal Ectopia
S Kidney fails to reach its normal location (renal fossa) from pelvis and arrest at any level along its path of ascent.
S Usually smaller than normal kidney, renal pelvis is anterior to the parenchyma. About half of the ectopic kidneys
have dilated pelvicalyceal system due to ureteropelvic or ureterovesical junction.
S Associatedgenital anomalies are usually present.

S More susceptible for development of hydronephrosis and stone formation. No increased risk for malignant
transformation.
Cephalad Renal Ectopia
S Both kidneys are located just beneath the diaphragm.

S Ureters are excessively long and origin of renal arteries are more
cephalad.
Thoracic Kidney
S Partialor complete protrusion of kidney through the diaphragm into the

posterior mediastinum (through foramen of Bochdalek).
Anomalies of form and fusion
Crossed renal ectopia with and Horseshoe kidney

without fusion
Urology 941
Crossed Renal Ectopia with and without Fusion
S When a kidney located on the side opposite from which its ureter inserts into the bladder, it is called Crossed
ectopia.
Different types of crossed ectopia
S About ninety percent of crossed ectopic kidneys are fused with the normally positioned kidney
S Associated anomalies (genitalia and skeletal system) are common in solitary crossed renal ectopia
S Most of the patients have normal prognosis.
Horseshoe Kidney
S Most common of all renal fusion anomalies.

S Most medial subdivisions of the mesonephric bud meet and fuse in the midline. The fusion occurs before the
rotation on their long axis.
S The kidneys usually fused at their lower poles. The inferior mesenteric artery prevents ascent by obstructing the
isthmus.
S As kidneys fail to rotate, the calyces are pointed posteriorly.

The ureter may insert high on the pelvis and a characteristic angulation while crossing over and anterior to isthmus.
Ureter enters the bladder normally.
S The blood supply is variable. Sometimes duplicate and triplicate renal arteries supply the kidneys.
Isthmus is supplied by main renal artery or artery originating from aorta and sometimes branches arising from
inferior mesenteric artery or common iliac artery.
S Associated anomalies present—Genitourinary, skeletal, cardiovascular and CNS defects.
S Patient may presents with vague abdominal pain radiated to lumbar area. Sometimes, patient may present with
midline abdominal mass.
Many of the patients with ureteropelvic junction obstruction. As a result, increased incidence of infection and calcu-
lus formation.
S Classic radiologic features (in Urogram) — Lower pole calyces on both sides are directed towards midline
— Ureters have vase-like curves.

S Division of isthmus is not indicated for relief of pain.
Anomalies of Renal Vasculature [Accessory, Aberrant, Multiple Vessels]
S Accessory vessel— Two or more arterial branches

supplying the same renal segment.
S Aberrant vessel— Kidney supplied by vessels
originate from other than aorta or main renal artery.
S Multiple vessels—Any kidney supplied by more
than one vessel.
Urology 943
Cystic Disease of Kidney
Cystic diseases of kidney
Congenital/Acquired Nonneoplastic/Neoplastic
S Most of the cystic lesions are congenital and nonneoplastic

S Most of the cystic lesions arise from nephrons and collecting ducts.
Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD)
S An important cause of end-stage renal failure.

S Pattern of inheritance is autosomal dominant with mutation in
PKD gene. Three PKD genes are identified:
1. PKD1 gene (in 85% cases)—Located in chromosome 16
2. PKD2 gene (5–10% cases)—Located in chromosome 4
3. PKD3 gene—About 5% cases.
S Symptoms and signs usually manifest between 30 to 50 years. A
number of associated anomalies are present:
z Multiple cysts in liver, pancreas; spleen, lungs (appears later
than renal cysts).
z Aneurysm of the circle of Willis.
z Colonic diverticula.
z Aortic aneurysm.
z Mitral valve prolapse.
S Patients present with—
z Dull aching pain in the lumbar region
z Irregular abdominal mass
z Hematuria
z Infection
z Hypertension.
z Subarachnoid hemorrhage (due to rupture of berry aneurysm)
z End-stage renal failure.

CT scan showing multiple cysts in liver, spleen

and kidneys
S Kidneys are bilaterally enlarged and lobulated appearance due to underlying cyst.
Cysts are of varying sizes, from few mm to 4–5 cm in diameter.
Cysts do not communicate with the pelvis of the kidney.
Cysts derived from entire nephron. [Only 1% of nephrons changed into cysts].
S For diagnosis, positive family history is important but not essential.

Bilateral renal cysts associated with 3 or more hepatic cyst, presence of berry aneurysm or solitary cyst in pancreas
or spleen are sufficient enough for establish the diagnosis.
S Ultrasonography and CT abdomen reveals multiple cysts in both kidneys and sometimes cysts in liver, pancreas.
On intravenous urography — Bilateral renal enlargement

— Calyceal distortion (like spiders' legs)
— Swiss cheese appearance in nephrogram phase.
MRI is helpful when patient is in compromised renal function.
S Treatment — According to symptoms
— No definite surgical procedure is helpful.
[50% of the children of patient will be affected. The children should be screened by ultrasonography.]
Urology 945
Autosomal Recessive (Infantile) Polycystic Kidney Disease (ADPKD)
S A rare disease— 1 of every 40,000 live births.

S Pattern of inheritance is autosomal recessive.
Mutations of a single gene PKHD1, located on chromosome 6 is responsible.
S Age of presentation may be—
z Perinatal
z Neonatal [Earlier the disease presents, more severe the disease.]

z Infantile
z Juvenile.
S Clinical manifestations depend on when the disease presents.
Newborn presents with huge, normal reniform-shaped, nonbosselated, hard flank mass and sometimes history of dif-
ficult delivery due to the mass. Also history of oligohydramnios.
If disease appears later in childhood, patient may present with renal failure and hypertension.
All affected individuals have associated congenital hepatic fibrosis, which may lead to portal hypertension and sple-
nomegaly.
S Cysts are formed from dilatation of collecting tubules.
S The disease may be suspected during prenatal USG screening. Newborn presenting with ARPKD can be diagnosed
by USG.
In delayed films of IVU—Functioning kidneys with characteristic radial streaking (sunburst pattern).
S Patients to be treated for hypertension, renal and hepatic failure. Hemodialysis and renal transplantation may be
considered in some of these patients.
Simple Cyst of the Kidney
S A common incidental finding in USG imaging of abdomen.

S Rarely seen in infants and children.
S If cyst causes pain or pressure effects, laparoscopic unroofing either transperitoneally or retroperitoneally, is the
treatment.
[A simple cyst must be differentiated from a cystic neoplasm or early stage of ADPKD.]
Other Malformations
Congenital Megaureter
Urology 947
Postcaval Ureter (Also Termed Retrocaval Ureter or Preureteral Vena Cava)
S Rightureter passes behind the IVC instead of right of it.

S In
this disorder, the right ureter deviates medially behind the IVC, winding about and crossing in front of it form a
medial to lateral direction, then follows the normal course to drain in the bladder.
S Most of the patients present in 3rd or 4th decades. Patient may present with pain in the flank or hydronephrosis.
S MRI is superior to demonstrate the course of IVC and ureter in comparison to CT and retrograde pyelography.
S Treatment is excision of retrocaval segment of ureter followed by ureteral relocation.
Ureteroceles
S A cystic dilatation of the intramural part of ureter, associated with stenotic ureteral opening.
S Found mostly in females (4 :1).
S Large ureterocele can obstruct the bladder neck or contralateral

ureteral orifice resulting in hydroureter and hydronephrosis.
S The 'adder head' finding in IUV is typical. Voiding cystourethrography
can delineate the size and location of ureterocele and also can detect
the presence or absence of vesicoureteral reflux.
S Treatment is indicated for symptomatic ureterocele (bilateral
hydronephrosis).
Endoscopic incision (transverse incision) through the full thickness of ureterocele using cutting diathermy is the
preferred surgical approach.
Hydronephrosis
S Aseptic dilatation of the calyces and pelvis of the kidney due to partial or complete obstruction to the outflow of
urine.
Cause of Hydronephrosis
Unilateral hydronephrosis
z Tumor infiltrating the ureter e.g.

carcinoma cervix, rectum, colon
prostate.
z Retrocaval ureter.
Bilateral hydronephrosis
z Congenital PUJ stenosis.
z Calculus in renal pelvis or ureter.

z Carcinoma bladder.
z Ureterocele.
z Bladder neck contracture.
z Neoplasm of ureter.
z Prostatic enlargement (benign
z Neoplasm of bladder involving or malignant).
ureteric orifice. z Urethral stricture.
z Posterior urethral valve.
z Retroperitoneal fibrosis.
Pathophysiology
Urology 949
Clinical Features
S Insidious onset of dull, persistent aching pain in the loin is the commonest symptom
S Sensation of dragging heaviness
S Pain or heaviness may be exacerbated by taking excess water or alcohol.
S Intermittent hydronephrosis—After attack of pain, swelling appears in loin
S Fewhours later, after passage of large amount of urine, the pain relieved and swelling disappears
– Also called 'Dietl's crisis'.
Diagnosis
S USG imaging—
z Initial screening test for detection of hydronephrosis
z Can also detect hydronephrosis in utero.
S Intravenous urography—Pelvis appears dilated and calyces lose their cupping and become clubbed.
S DTPA (diethylenetriaminepentaacetic acid) Renography—99mTC labelled DTPA is injected intravenously. If there is

distal obstruction, the marker is trapped in renal pelvis and will not be washed out even after diuresis.
Treatment
S Indicationsfor surgical intervention:

z Recurrent episodes of pain
z Progressive hydronephrosis
z Pyonephrosis
z Evidence of parenchymal damage.
S Surgical options— Management of hydronephrosis + definite management of cause of hydronephrosis.

Renal Stone
S Stonedisease is one of the common urologic diseases

S Commonly affects adult men than adult women
S How stone develops?
Stone formation process is a complex cascade of events

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What is Randall’s plaque?
S According to Randall, initial event may be an erosion at the tip of a renal papilla. Deposition of calcium on this
erosion produces a lesion called ‘Randall’s plaque’.
Risk Factors
1.
2.
3. Hyperuricosuria
S Due to nn dietary purine intake
S Diseases associated with hyperuricosuria:
z Gout
z Myeloproliferative disorders
z Multiple myeloma
z Hemolytic disorders.
4. Low urine pH (<5.5)

5. Dehydration
6. Urinary tract infection—Urinary tract infected with urea-splitting organisms—Proteus, Klebsiella, Pseudomonas,
Staph. sp.
[Bacteria commonly found in the nuclei of stones — E.coli, staphylococci.]
7. Type I renal tubular acidosis.
Composition of Calculus
Matrix substance A is a unique protein, composed of three or four distinct antigens and found in all renal stones.
Types of Renal Calculi
Calcium is the major component of about 75% of stones.
Calcium oxalate stone
S Most common type of calcium containing stone.

S Most of the calcium oxalate stones are formed due to idiopathic hypercalciuria without hypercalcemia.
In few patients, stones are formed due to absorptive or renal hypercalciuria.

S Oxalate stones are usually small, hard, irregular in shape and surface covered with
sharp projections. These projections tend to cause bleeding due to repeated trauma.
Surface is dark brown colored due to pigments of altered blood.
S These stones are radiopaque.
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Uric acid stone
S Formed due to hyperuricemia and hyperuricosuria in gout, myeloproliferative disorders (e.g. leukemia), patient on
chemotherapy, use of uricosuric drugs (e.g. salicylates and probenecid).
In acidic urinary pH, the solubility of uric acid decreases, resulting in precipitation of uric acid crystals.
S Three determinant factors of uric acid stone formation—
z Acidic urinary pH
z Low urine volume
z Hyperuricosuria.
S These stones are hard, smooth, yellow to reddish brown in color and often multiple.
On cut section, they have multifaceted appearance.

z Pure uric acid stones are radiolucent.
z In IVU, they appear as filling defect.
Struvite stone
S Struvite stones are composed of magnesium ammonium-calcium phosphate.

[A Swedish Geologist discovered magnesium-ammonium phosphate and named it ‘struvite’ after his mentor, Naturalist
HCG Von Struve]
S Infection of the urinary tract with urea-splitting organisms is a prerequisite for formation of struvite stones, also
called infection stones.
Urease producing bacterias—
z Proteus mirabilis (most common)
z Klebsiella
z Pseudomonas
z Staphylococcal species.
Urease splits urea into ammonia and then ammonium. Despite the alkaline environment, due to presence of urease,
ammonia continues to be produced. Thereafter, precipitation of components of struvite stone develops.
S Stones are dirty white and smooth.
Sometimes, large solitary stone takes the shape of renal pelvis and major calyces— ‘Staghorn calculus’. [‘Stag'– male-
deer].
S They are radiopaque stones.

Cystine stone
S Due to cystinuria as a result of congenital defect in transport of cystine and other amino acids
S They are small, rounded, smooth, multiple and very hard
S They are radiopaque because of its sulfur content.
Xanthine stone
S Develops as a result of hereditary xanthinuria
S They are radiolucent stones.
S Silentstone—large staghorn calculi causes no symptoms for a long period.

S Pain—
z Most common symptom
z Fixed renal pain is experienced in the renal angle.
S Hematuria— Most often microscopic hematuria is associated with renal stone. Gross hematuria is uncommon.
Complication
Diagnosis
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Management
S Pain can be managed with parenteral or oral narcotics.

S All first-time stone formers should limit protein and salt intake.
S Obstructed urinary tract with infection should be emergently drained by percutaneous nephrostomy tube or
ureteral stent.
Surgical management
S Primary goal of surgical management is maximum stone clearance with minimum morbidity
S Preoperative evaluation—
z Bacteriologic evaluation of urine
z Complete blood count, blood biochemistry
z 24 hr urinary calcium, oxalate, magnesium, phosphorus, uric acid and creatinine.

Open surgery is indicated where the staghorn calculus is not expected to be removed by repeated PCNL or PCNL
followed by ESWL.
Factors to be considered for choosing treatment
S ESWL should be considered in a background of sterile urine and absence of distal obstruction
S Stone-free rate for ESWL to lower pole calculi is lower (60%) in comparison to PNL (90%).
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In morbid obese patients, ureteroscopic approach is preferable.
In patient with uncorrected coagulopathy, holmium: YAG laser intracorporeal lithotripsy is preferable.
S If minimally invasive approach is preferred, but which one?
Staghorn calculi Nonstaghorn calculi

– PNL followed by ESWL <10 mm — ESWL
or 10–20 mm — ESWL, PNL/ ureteroscopy may be considered
PNL followed by repeat PNL > 20 mm — PNL
What is ESWL? (Extracorporeal Shock Wave Lithotripsy)
Shock waves are generated by an source external to the patient's body
Shock wave is propagated into the body focusing on the stone

*Shock waves harmlessly propagate through the body tissues
*Stone is positioned in the focal point of shock waves
*Shock waves is focused by using USG or fluoroscopy or USG + Fluoroscopy.
Electromagnetic shock wave generator

Piezoelectric shock wave generator
Shock waves break stones by different mechanisms:

1. Spall fracture—At the sites of impedance mismatch (stone-fluid interface, crystalline-matrix interface)
2. Circumferential compression
3. Shear stress
4. Cavitation
5. Dynamic fracture.
Side effects— Most common side effects are hemorrhage, edema within and around kidney.
Fragmentation depends on—
S Consistency of stone
S Size of stone
S Site of stone
S Obesity.
Most oxalate and phosphate stones are well-fragmented after ESWL

Cystine stones are not so well-fragmented
Stones in the pelvis are cleared within few days after fragmentation. Stones in the calyces take months.
Urology 959
After ESWL
Percutaneous Nephrolithotomy
1. PNL is initiated by placement of 7 Fr occlusion balloon catheter—

z To prevent migration of fragments into the ureter
z To instill contrast during the procedure.

2. Selection of point of puncture and selection of calyx—A posterior calyx is the preferred site of entry.
3. Introduction of nephroscope
4. Removal of stone
z Stones upto 1 cm can be grasped with graspers or stone baskets
z Stones> 1 cm require fragmentation by intracorporeal lithotripters.

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5. Introduction of nephrostomy tube—
Open Surgery for Renal Stone
S Indicated only where multiple PNL or ESWL may needed.
1. Pyelolithotomy
2. Nephrolithotomy
3. Partial Nephrectomy
S Stone in the lowermost calyx and that part of renal parenchyma is damaged.
4. Nephrectomy
S Poorly functioning kidney with staghorn calculi with contralateral normally functioning kidney.
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Prevention of Recurrence
S Obesity is an independant risk factor

S Dietary sodium restriction is helpful to prevent recurrence
S Fluid intake must be such that urine output > 2 liters/day
S Avoid—
z High protein, low carbohydrate diet
z Excess milk products
z Oxalate-rich foods (e.g. spinach, beet, chocolate and nuts)
z Vit C over intake (should be < 2 gm/day)
z Red meat, fish— in patient with hyperuricemia.
S Citrus juice (particularly lemon juice) intake prevents recurrence.
S All patients with bilateral and recurrent stone formers should be investigated:
1. Serum calcium—Three occasions

2. Serum uric acid
3. 24 hours urinary excretion of urate, calcium, phosphate and cystine.
Infections of Kidney
Different Routes of Infection

Acute Pyelonephritis
S Acute suppurative inflammation of kidney and renal pelvis.
Causes
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2. Hematogenous infection
S Susceptibility of infection increased in — Diabetes mellitus

— Pregnancy
— After instrumentation
Pathology
S Patientpresent with abrupt onset of fever, chill, pain and tenderness in renal angle
S Dysuria, increased frequency and urgency are often present.
Sequelae of acute pylonephritis

Diagnosis
Treatment
S Iffever persists more than 72 hours, radiologic investigation (USG/CT) have to be done to rule out obstructive
uropathy, anatomic abnormalities or perirenal infections.
S Repeat urine culture on 5th–7th day, on 10th–14th day and 4th–6th week.
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Chronic Pyelonephritis
S A chronic tubulointerstitial disease resulting from repeated attacks of inflammation and healing.
S According to etiology, 2 types—
According to etiology
Chronic obstructive 5HÀX[DVVRFLDWHGS\HORQHSKULWLV

pyelonephritis >UHÀX[QHSKURSDWK\@
Obstruction at different levels of urinary z Major cause of chronic pyelonephritis.

tract results in recurrent episodes of in- z Reflux may be unilateral or bilateral.
fection
z VUR is common in girl child, due to
absence or shortening of intramural
past or ureter. VUR is also associated
Fibrosis with UTI.
Scarring of cortex
S Generalized characteristics of chronic pyelonephritis:

z One or both kidneys may affected. Either kidney is diffusely or scatteredly involved.
z Grossly, the kidney is small, contracted with irregular scarring.
z Chronic interstitial inflammation is present.
z Tubules show varying degrees of atrophy and dilatation. Glomeruli are usually unaffected except in advanced
stage.
[Hyaline casts are sometimes present in the tubules resembling thyroid colloid— Renal thyroidization.]
Clinical features
S Usually no symptoms are present until chronic renal failure develops.

S If it is a sequele of recurrent attacks of acute pyelonephritis, then symptoms like fever, loin pain and dysuria may be
present.
S Hypertension is present in about 40% of patient and may be of malignant type.
Diagnosis
S Urine culture commonly reveals presence of E.coli, Proteus, Pseudomonas. Urine culture may be negative.
S Casts are usually absent. Plenty of WBCs are found in microscopical examination of urine.
S IVU findings are almost diagnostic. The usual findings are:
z Asymmetrical kidney outline.
z Blunting or dilatation of one or more calyces and cortical scars at the corresponding site.
Treatment
S Treatment of bacterial infection (emperical o then according to C/S report)

S Prevention of future infections
S Treatment of causative factors (stone/VUR)
S Nephrectomy/partial nephrectomy
S Renal transplantation (in patient with end stage renal failure).

Urology 969
Perinephric Abscess
Causes
Mycobacterial perinephric abscess

may develop from a nearby spinal
tuberculous focus.
Symptoms and signs
S High swinging pyrexia

S Abdominal or flank mass
S Tenderness in loin.
[Psoas abscess is to be differentiated by limping gait and flexion and externally rotated ipsilateral hip.]
Diagnosis
Laboratory investigation—
S Leukocytosis
S Serum creatinine.
Urine examination—
S Pyuria
S Culture of urine– E.coli, Proteus, S. aureus are found in most of the cases.
Plain X-ray of KUB—

S Absence of psoas shadow
S Reactionary scoliosis—Concavity of vertebral column toward the abscess
S Elevated and immobile diaphragm on the affected side.
CT is specifically helpful to identify the abscess as well as detailed information about the spread of infection.
This is very much helpful for planning surgical drainage.
Treatment
Antimicrobial therapy
+
Drainage of abscess + Treatment of cause of abscess
USG or CT guided drainage (for small abscess) Surgical drainage (through lumbar incision)
Pus sent for C/S Pus sent for C/S
[Nephrectomy is indicated for pyonephrosis of nonfunctioning kidney.]
Pyonephrosis
S Pyonephrosis is infected hydronephrosis along with suppurative destruction of renal parenchyma

S Patient looks toxic, high rise of temperature with chill, flank pain, tenderness in loin, swelling in loin
S History of urinary tract calculi, UTI may be present
S USG reveals dilated pelvicalyceal system
S CT is nonspecific
S IVU shows a poorly functioning or nonfunctioning hydronephrotic kidney.

Urology 971
Antimicrobial therapy (parenteral)
+
Surgical intervention (urgent)
Drainage of pus through percutaneous nephrostomy Treatment of cause of obstruction and source of infection
[Nephrectomy to be considered in a nonfunctioning

kidney where the contralateral kidney is functioning
normally.]
Renal Abscess or Carbuncle
S Collection of purulent material confined to renal parenchyma.
Etiopathogenesis
Etiopathogenesis
Hematogenous spread Ascending infection VUR

(associated with obstruction/stasis)
Due to calculi, pregnancy Due to neurogenic bladder
[Commonly seen in diabetic patients, IV drug abusers, immunosuppressive patients.]

S Feverwith chill, flank pain, tender swelling in loin are the usual symptoms and signs.
S Diagnosis Lab investigations
• Marked leukocytosis
• Positive blood culture
Imaging • Urine culture Gram + ve (if hematogenous spread)
Gram –ve (if ascending infection)
S USG and CT helps to differentiate renal abscess from other inflammatory renal diseases
S CT is the investigation of choice.
S Treatment Parenteral antimicrobial therapy (selection of antimicrobial agent according to presumed
source of infection)
Abscess < 3 cm Abscess > 3 cm
Abscess in immunosuppressed patient
Parenteral antibiotic
patient not responding
therapy Drainage of abscess (CT/USG guided or open drainage)
Tuberculosis of Kidney
Etiopathogenesis
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How the Tubercular Ulcer Develops?
Different Types of Tubercular Lesion in Kidney

Clinical Features
S Usually common in 20–40 years of age.

[Genitourinary TB is very uncommon in children.]
S More common in men (2 :1)
S Right kidney is more affected
S Increased frequency of micturition—Often the earliest symptom
S Hematuria
S Dull aching pain in loin
S Constitutional symptom—Weight loss, evening rise of temperature.
[Suspect genitourinary TB if patient presenting with vague, persistent urinary symptoms without any obvious cause.]
Diagnosis
S Diagnosis Urine examination

• Sterile pyuria is the classic finding on routine urinalysis and culture.
Imaging
• Plain X-ray—Calcification in • Z–N staining rarely shows presence of acid-fast bacilli.
kidney.
• IVU— Distortion of calyx, calyceal • Urine culture—Culture on Lowenstein- Jensen medium take
and parenchymal destruction. 6–8 weeks as the bacteria is slow growing.
• CT—Imaging modality of choice.
3D reconstruction of CT image is 3–5 consecutive early morning samples of urine should be cultured
helpful to identify calyceal abnor- [because the organism is intermittently excreted].
malities, hydronephrosis, hydro-
ureter.
• Chest X-ray—To exclude an • Fluorescence microscopy.
active lung lesion. • Radiometric culture method.
• PCR of DNA or rRNA.
Treatment
S Prognosis is good if patient completes the course of ATD (6–9) months

S Surgical intervention—Aim is to preserve the organ and reconstruction rather than excision
z Surgery should be done at least after 4–6 weeks of chemotherapy
z Nephrectomy or partial nephrectomy may be indicated.

Urology 975
Kidney Tumors
Kidney tumors
Benign Malignant
Epithelial tumor of renal parenchyma
z Adenoma z Renal cell carcinoma

z Oncocytoma
Epithelial tumor of renal pelvis
z Transitional cell papilloma z Transitional cell carcinoma
Embryonal tumor
z Mesoblastic nephroma z Wilms' tumor
Nonepithelial tumor
z Angiomyolipoma
Metastatic tumor
z Most common malignant tumor of kidney.
z Usually, hematogenous route of spread.
z Lung, breast, GI tumors, malignant

melanoma are the common primary sites.
Benign Renal Tumor
They are usually an incidental finding during radiological imaging, after nephrectomy or at autopsy.
Oncocytoma
S A benign epithelial tumor arising from collecting ducts.

S Ultrastructurally, these tumors are packed with numerous large mitochondrias.
[Most of the oncocytomas cannot be differentiated from RCC by clinical or radiological means.]
That is why, most urologists treat this tumor aggressively (thermal ablation, partial nephrectomy, radical nephrec-
tomy).
Angiomyolipoma
S A benign clonal neoplasm that contains mature adipose tissue, smooth muscle and thick-walled vessels.
S This tumor is often associated with tuberous sclerosis (20–30%)
[Tuberous sclerosis syndrome—An autosomal dominant disorder is characterized by mental retardation, epilepsy, ad-
enoma sebaceum]
S AML associated with tuberous sclerosis is more likely to be bilateral and multicentric. Their growth rate is higher
in comparison to solitary AML.
S Its fat content gives it a characteristic appearance in CT.
On CT scan, presence of fat within a renal lesion is diagnostic of AML and excludes RCC.
S Positivity to HMB–45, a monoclonal antibody is characteristic for AML.
S Small (< 4 cm), asymptomatic AML can be observed expectantly with close surveillance.
Solitary, large, symptomatic (e.g. life-threatening hemorrhage) AML needs total nephrectomy.
S In tuberous sclerosis patients, bilateral AML, patients with pre-existing renal insufficiency— A nephron-sparing
approach) selective embolization/partial nephrectomy) should be considered.
Renal Cell Carcinoma (Hypernephroma, Grawitz Tumor)
S Most lethal of all the urologic malignancies

S Common in elderly patients— in 6th and 7th decades
S Male-female ratio 3:2
S Most of the RCCs are sporadic
S These tumors are derived from tubular epithelium. So they are located predominantly in the cortex
S Usually arises from poles of the kidney, usually from the upper pole
S Most sporadic RCCs are unilateral and unifocal.

Urology 977
Risk factor
Pathology
S Most RCCs are round to avoid in shape, golden

yellow in color, usually varies in size from 5–8 cm,
circumscribed by a pseudocapsule (composed of
compressed parenchyma and fibrous tissue).
z Cut section shows areas of necrosis,
hemorrhage and cystic changes.
[RCC with cystic degeneration is associated with bet-
ter prognosis than solid RCC.]
S Based on cytogenetics, RCC is classified into:

z Clear cell type (70%) —
Most common type.
The cells contain lipid, glycogen which are removed during processing of tissues, thus appears as cells with
clear cytoplasm (clear cell).
z Papillary type (10–15%)—
The tumor cells arranged in papillary pattern over fibrovascular stalks.
They tend to be bilateral and multiple.
z Chromophobe type (5%)—
Arise from intercalated cells of collecting ducts.
Stains more darkly than clear cell type.
Perinuclear halo and presence of numerous microvesicles are distinctive features.
Better prognosis.
z Granular cell type (8%)—
Abundant acidophilic cytoplasm with marked atypia present.
z Sarcomatoid type— Most anaplastic variety of RCC.
z Collecting duct type (<1%)—
Rare type
Derived from medulla.
Spread of tumor
Urology 979
1. Classic triad of Flank pain, gross hematuria and palpable abdominal mass
z Also called ‘too late triad’
z Found in advanced stage of RCC.
2. Other symptoms due to advanced disease—

z Weight loss Varicocele (left)
z Fever Bilateral lower extremity edema
z Night sweat.
3. Symptoms due to metastatic disease—

z Bone pain
z Persistent cough.
4. Paraneoplastic syndrome—
z Hypercalcemia—Nausea, anorexia, fatigue, decreased deep tendon reflexes.
z Hypertension
z Polycythemia
z Nonmetastatic hepatic dysfunction (Stauffer’s syndrome).
Staging
S Robson’smodification of the system of Flacks and Kadesky

S TNM staging.
Investigation (for diagnosis and staging)
S USG— Can detect a SOL in kidney as well as gives information about its cystic/solid nature
S CECT abdomen— Can demonstrate the extent of lesion, hilar lymphadenopathy and renal vein involvement
S Multiplanar CT is more accurate regarding detection of venous thrombus
S MRI—Imaging of choice for evaluation and staging of IVC thrombus
S Metastatic evaluation— Chest X-ray and isotope bone scan.

Treatment
Urology 981
3. Treatment of metastatic RCC
Cytoreductive nephrectomy followed by systemic treatment

S Radiation therapy
S Immunotherapy (interleukin–2)
S Targeted therapy (bevacizumab, sumitinib and pazopinib).
[RCC is a chemotherapy resistant tumor.]

Wilms’ Tumor [Nephroblastoma]
S Thisis a embryonal tumor originated from remnants of immature kidney.

S Most common primary malignant renal tumor of childhood.
S Most commonly seen in children between 1–5 years.
S Syndromes associated with increased incidence of Wilms’ tumor—
z Beckwith-Wiedemann syndrome (omphalocele, nephromegaly, hepatomegaly, macroglossia and hemi-

hypertrophy).
z Denys-Drash syndrome (male pseudohermaphroditism, renal mesangial sclerosis, nephroblastoma)
z WAGR syndrome (Wilms’ tumor, aniridia, genital anomalies and mental retardation).
S Genetics associated with Wilms’ tumor—
z More than 90% of Wilms’ tumor arise from somatic mutations
z Very few tumors arise as result of germline mutations. These tumors have a inherited predisposition
z Chromosomal abnormalities.
WT1 mutations (11 p13) WT2 gene (11p15) Familial Wilms' tumor gene
–associated with significant associated with BWS (FWT1 and FWT2)
genital abnormalities
S Pathological veriety
Favorable-histology Anaplastic Nephrogenic rests

• Predominant epithelial • Resistant to chemotherapy • Precursor lesion
differentiation
• Less aggressive
Grossly, the tumor is large, spheroidal, compresses the adjacent normal renal parenchyma to form a pseudocapsule.
Microscopically, it composed of primitive epithelial and mesenchymal elements (e.g. muscle, cartilage, bone and
fibrous tissue).
Urology 983
Clinical features
S Palpable abdominal lump—Most common presentation. The lump may be large comparing to the size of the
patient.
S Hypertension (due to n plasma renin).
S Hematuria.
S Pyrexia.
[During clinical examination, signs of associated Wilms' tumor syndomres must be searched—Aniridia, macroglossia,
genitourinary anomalies, hemihypertrophy).]
Diagnosis
S Ultrasonography—The initial imaging technique

z Whether the mass is originated from kidney
z Whether cystic or solid
z Doppler USG can also detect tumor thrombus in renal vein and IVC.
S MRI is the imaging of choice for detection of tumor thrombus.
S CT abdomen—To differentiate Wilms’ tumor from neuroblastoma.
Originated from adrenal or sympathetic ganglia.

S Urinary catecholamine measurement
Increased in neuroblastoma Normal—in Wilms’ tumor

S Chest X-ray or CT chest is to be done to rule out lung metastasis (lung is the most common site of metastasis).
Management
S Surgical intervention?
z Indicated for confirmation of diagnosis, assessment of contralateral kidney
z Radical nephroureterectomy is the ideal choice
z Ipsilateral adrenal gland is also removed en bloc

z Adjuvant therapy (according to stage) chemotherapy ± radiotherapy.
S Chemotherapy?
z Tumor is present in solitary kidney or both kidneys or in horse-shoe kidney
z Tumor thrombus extends above the level of hepatic veins.
z Extensive metastasis.
Diseases of Ureter
Ureteral Calculi
S Ureteral calculi almost always originated in kidney.

S Clinical features—
z Ureteric colic—Character and radiation of pain– described previously.
Pain is mediated by prostaglandins in response to obstruction. Prostaglandin in-

creases the ureteral peristalsis and sensitize nociceptors to stimuli such as brady-
kinin.
z Hematuria— Microscopic hematuria is commonly associated with attacks
of ureteric colic.
[If macroscopic hematuria is present, think of other causes of colicky pain (e.g.
clot) rather than stone.]
z On clinical examination, tenderness may be present over the course of
ureter according to the site of impaction of stone.
[Right sided ureteric colic and appendicitis are almost similar in clinical presen-
tation. Usually, the pain in ureteric colic is more but patient is less ill.]
S Diagnosis— Same as renal stone.
S Treatment—
z Goal of treatment is complete stone clearance with minimal morbidity.

Urology 985
S Ureteroscopy is more effective for larger stones.

S Calcium oxalate dihydrate stone (fragile)— SWL is a better option.
Cystine and brushite stone—Ureteroscopy ± intracorporeal lithotripsy.
S Severe symptoms refractory to conservative and medical therapy warrant active intervention.
Pyelonephritis or pyonephrosis due to obstruction needs urgent drainage of the tract (by ureteral catheter/percu-
taneous nephrolithotomy)— Definite treatment after infection resolves.
S Ureteral stone obstructing a solitary kidney warrants active intervention.
Urothelial Tumors of Renal Pelvis and Ureter
S Transitionalcell carcinoma (TCC) is the most common type of urothelial cancer.

[Renal pelvis, ureter, bladder and proximal urethra are lined by transitional epithelium]
S Men are commonly affected.
S About 70% tumors occur in distal ureter.

Risk Factors
S Genetics associated with urothelial tumor—

z p53 gene
z Retinoblastoma gene (RB)
z Abnormalities in chromosome 9.
S Clinical presentation—
z Hematuria (gross or microscopic)— Most common symptom
z Flank pain
z Abdominal mass, weight loss, bone pain—In advanced stage.
S Diagnosis—
z IVU—Traditional imaging method.
z CT urography—A three–dimensional image can be obtained, thereby sensitivity for detecting upper tract tumor
is very high.
z Ureteroscopy and guided biopsy—If diagnostic dilemma is still present after imaging.
[Cystoscopy is mandatory in all patients of upper tract tumors to rule out coexisting bladder tumor.]
S Treatment—
1. Endoscopic treatment—
Indicated in patient with solitary kidney, bilateral upper tract tumor or patient with contralateral
nonfunctioning kidney.
Also indicated in low-stage, low-grade lesions.
Urology 987
2. Segmental ureterectomy—Indicated in low-grade tumor.

3. Radical nephroureterectomy—Indicated in high grade, large and invasive tumors.
Urinary Bladder
Congenital Anomalies
Patent Urachus
S Due to failure of urachal canal to obliterate.

S Clinically presents as continuous or intermittent discharging umbilicus.
May present as edematous umbilicus with delayed healing of cord stump.
S Diagnosisis done by retrograde fistulogram or voiding cystourethrogram.

S Treatment is complete excision of patent urachus including a bladder cuff.
Urology 989
Ectopia Vesicae (Exstrophy of the Bladder)
S Exstrophy of the bladder is one of the components of exstrophy–epispadias complex of genitourinary malformations.
S Inclassic bladder exstrophy, the defects are in the bladder, abdominal wall, pelvic skeletal structure, pelvic floor,
anorectum and genitourinary tract.
1. Skeletal defects—
2. Pelvic floor defects—

Levator ani group is more posteriorly placed
Puborectal sling becomes flattened than its normal conical shape.
3. Abdominal wall defects—

Triangular defect in the abdominal wall occupied by exstrophy bladder and posterior urethra.
At the upper end of the fascial defect, umbilicus is present.

Umbilical hernia is usually present.
Indirect inguinal hernia (unilateral/bilateral) is usually associated.
z Anorectal defects—
Perineum is short and broad
Anus is present directly behind the urogenital diaphragm.
z Genital defects—
In male—
–Epispadias
–Prominent dorsal chordee
–Wide separation of crural attachments
–Deficiency of anterior corporal tissue
–Shorter penis.
In female—

–Bifid clitoris
–Shorter vagina
–Stenotic and anteriorly placed vaginal orifice.
z Urinary defect—
Horseshoe kidney, hypoplastic kidney or pelvic kidney may present
Ureters are abnormally terminated resulting in VUR in all patients.

S Diagnosis
z In conventional USG imaging, prenatal diagnosis is difficult

z 3-D USG and fetal MRI is helpful in prenatal diagnosis.
S Treatment— Staged surgical approach
}
z Bladder closure
z Abdominal wall closure

In newborn period
z Urethral closure onto the penis
z Bilateral innominate and vertical iliac osteotomy
z Epispadias repair— 6 months—1 year of age

(testosterone secretion starts)
z Bladder neck reconstruction— 4–5 years
(child has adequate bladder capacity)
z Postoperative voiding program
Bladder Calculi
S Among the lower urinary tract, calculi develops mostly in the bladder.
Urology 991
S Different types of bladder calculi
Secondary Calculi
S Related to bladder outlet obstruction—

z Main cause of bladder calculi
z Mostly related to BHP
z Stones are composed of uric acid, calcium oxalate or triple phosphate.
S Related to infection—
z Urease producing bacterias are responsible
z Usually triple phosphate and carbonate apatite calculi are found.
S Related to catheterization—
z Patient with urethra or suprapubic catheter have increased (nine fold) risk of stone formation.
S Calculi related to foreign body—
z Calculi may develop following self-induced (e.g. hairpin, pen) foreign body or iatrogenic FB (e.g. balloon catheter,
ureteral stent).
S Calculi related to bladder augmentation and urinary diversion.
Clinical Features
S Most of the bladder calculi are asymptomatic.

S Symptomatic presentation:
z Pain— Usually located in the lower abdomen, exacerbated after exercise and sudden movement, usually felt at
the end of micturition.
Pain may be referred to the tip of penis, scrotum, labia majora or perineum.
z Frequency—More common during daytime.
z Hematuria— Terminal hematuria is due to abrasion of bladder trigone by the stone.
z Interruption of urinary stream.
z Symptoms of UTI.
Diagnosis
S X-rayof KUB— Most of the bladder calculi are radiopaque

S IVU— Radiolucent calculi may be detected as filling defects
S Cystoscopy—Most accurate method of detecting bladder calculi.
X-ray of KUB showing bladder calculi

Urology 993
Management
Schistosomiasis of the Urinary Bladder
S Schistosomiasis is a disease caused by Schistosomes, a digenetic trematodes.

S S. haematobium pairs (adult male and female) reside in the prevesical venous plexus—Urinary schistosomiasis.
S. mansoni and S. japonicum reside in the mesenteric veins— GI and hepatic schistosomiasis.
S Urinary schistosomiasis is endemic in parts of Africa and Middle East.
Mode of Infestation
S Man is the definitive host and freshwater snail (Bulinus truncatus) is the intermediate host.
S Free-swimming bifid-tailed cercaria is the infective stage. Cercaria penetrate the unbroken skin while bathing in
infected water. It losts its tail during penetration.
S Cercaria enters into the circulation and reaches to the liver where it develops into male and female worms.
S In liver, it attains sexual maturity and leaves the liver and enters the portal vein.
Urology 995
S In portal vein, the male worm bends to take the shape of a gutter (the gynecophonic canal), into which the female
worm rests, and then the pair proceed to the inferior mesenteric vein.
S Through the portosystemic anastomotic channel, the pair ultimately reaches the vesical venous plexus.
S After reaching the vesical venous plexus, the female worm moves forword and enters into the submucous venule
and then lay ovas in a chain (each ovum has a terminal spine). This ova penetrate the wall of venules and reaches
the urinary bladder.
S An infected person excretes hundreds of ova through urine. If the ova reaches fresh water, the envelope bursts and
ciliated miracidium emerges.
S To survive, the miracidium must reach the intermediate host (snails of Bulinus species), where they develop into
sporocyst, daughter sporocysts and then cercariae. These cercariae emerge into the water from snail’s surface.
S The cercariae, if fail to penetrate human skin within a few hours, they die.
Clinical Features
S Men are commonly affected.

S Urticaria may develop at the site of penetration by cercaria, (Swimmer's itch)
S Classic presentation is hematuria with terminal dysuria.
S Polypoidal lesion in bladder may develop.
S Bladder ulcer—Usually develops in the posterior bladder wall and clinically presents as dysuria, intense pelvic and
suprapubic pain.
S ‘Contracted bladder’ syndrome presents as lower abdominal pain, frequency, urgency and incontinence.
Diagnosis
S Examination of urine— Terminally spined eggs in urinary sediment is diagnostic of active S. haematobium infection
(egg excretion peaks between 10 AM – 2PM).
S Imaging—
z Plain X-ray—A calcified bladder which looks like a fetal head is diagnostic of chronic urinary schistosomiasis.
z USG—Can detect focal thickening of urinary bladder, polypoidal lesion, as well as hydroureter or hydronephrosis.
z IVU— Can detect hydroureter, hydronephrosis or polypoidal lesions.
S Serology—Western blot technique is highly sensitive and specific for diagnosing chronic inactive urinary
schistosomiasis (egg excretion is uncommon).
Treatment
S Medical
z Praziquantel is the drug of choice (active in all stages of diseases)

z 2 oral dose– 40 mg/kg for 1 day.
S Surgical
z Indicated for complications and for intractable bladder hemorrhage
z ‘Contracted bladder’ warrants surgical intervention
z Residual ureteral stenosis after chemotherapy may need reconstruction.

Bladder Tumor
Types of Bladder Tumor
Transitional Cell Papilloma
z Very rare bladder tumor.

z Usually solitary, small (0.2–1 cm), frond like structure
having a delicate fibrovascular core covered by multi–
layered (d 7), well differentiated transitional epithelium.
z Looks like a red sea-anemone.
z Noninvasive.
z Almost never recurs after endoscopic resection.
Bladder Cancer
S More common in men (3 times)

S Incidence increases with age.
[Younger patients have more favorable prognosis as they present with well-differentiated tumors.]
Urology 997
Risk factor
S Genetic factor—
z RAS (oncogene) mutation
z Absence or abnormal expression of tumor suppressor genes (TP53, and retinoblastoma gene)
z Overexpression of ERBB1 and ERBB2 oncogenes.
S Occupational factor—
z Workers with exposure to β-naphthylamine, aniline dyes, dyes used in rubber, textile industries.
S Cigaret smoking—
z Higher incidence (4 fold) of bladder carcinoma.
z Risk related with number of cigarets smoked, duration of smoking, degree of inhalation of smoke.
S Other bladder lesions—
z Chronic cystitis in presence of catheter or calculi is associated with increased risk of SCC of urinary bladder.
z Cystitis caused by S. haematobium is associated with increased risk of SCC.
z Ectopia vesicae, diverticulum, urinary diversion in defunctionalized bladder are associated with increased risk.
S Cyclophosphamide— 9 fold nrisk of bladder carcinoma.
S Pelvic irradiation—Radiation for carcinoma cervix or ovary is associated with nrisk.
S Arsenic— Ingestion of high arsenic contaminated water is associated with nrisk.
S Analgesic abuse— Large amount of phenacetin containing analgesic use is associated with TCC of bladder.
S Renal transplant recipients.
Pathology
S Transitional
cell carcinoma [commonest of all bladder carcinoma (> 90%)]
S Adenocarcinoma.
Different patterns of tumor growth

SCCs are usually sessile and associated with muscle invasion.

Nonbilharzial SCCs are caused by urinary calculi, indwelling catheter, chronic UTI and bladder diverticula.
Bilharzial SCCs are usually exophytic, fungating lesions (caused by S. haematobium) and present early (10–20 years
earlier than TCC). Prognosis not good.
S Adenocarcinomas arise in exstrophic bladder, urachal remnants and in intestinal urinary conduits and augmenta-
tions.
S Secondary metastasis in bladder–Primary sites are rectum, stomach, breast and prostate.
Clinical features
S Mostcommon presentation is painless hematuria.
S Symptom complex of frequency, urgency and dysuria are usually present.
S Symptoms of advanced disease—Flank pain due to obstructive uropathy, lower extremity edema and pelvic mass.
[An elderly patient with painless hematuria—Think of bladder carcinoma unless proved otherwise.]
Diagnosis
S Urine examination for malignant cells—

z Conventional microscopic cytology— of urinary sediment or bladder washings. This test is more sensitive for
high grade tumors or CIS. Chance of false-positivity and fake-negativity is high.
z Flow cytometry—Not much valuable.
Urology 999
z Cystoscopy— is the mainstay of diagnosis.
Location, number and nature of tumor can be assessed. Local invasion such as involvement of ureteral orifices
or prostatic urethra also can be assessed.
z Imaging—IVU is usually performed to identify other lesions of the upper urinary tract.
Staging
Treatment decision is based on whether tumor is muscle invasive or not.

Primary TUR of the tumor (TURBT) is done to assess the depth of tumor invasion and also to remove all visible tu-
mors.
After TURBT, persistence of a palpable mass suggests locally advanced disease.
Then, assessment of local extension and distant metastasis is done by—
Treatment
S Treatment of nonmuscle invasive bladder cancer (Ta, T1, ClS)—

1. Endoscopic management
2. Laser ablation—Nd: YAG laser is useful for ablation of tumor
upto 2.5 cm.
3. Immunotherapy—
Intravesical BCG (Live attenuated vaccine derived from M.
bovis) is not a substitute of TURBT.
Indicated in CIS, T , high risk tumors (large, high
1
grade,recurrent).
Intravesical BCG therapy is started 2–4 weeks after TURBT
and the reconstituted BCG solution must be retained in the
bladder for 2 hours.
BCG therapy reduces recurrence as well as risk of progression.
BCG + interferon-D therapy is superior to BCG therapy alone.
4. Intravesical chemotherapy—Intravesical thiotepa, mitomycin C

epirubicin, valrubicin decreases the chance of recurrence, but
cannot prevent progression.
S Treatment of muscle-invasive bladder cancer (T2– T4)—

z Radical cystoprostatectomy in male patient and anterior exenteration in the female patient along with pelvic
lymphadenectomy (en bloc) is the treatment of choice.
Anterior exenteration means removal of uterus, fallopian tubes, ovaries, bladder, urethra, segment of anterior
vaginal wall.
S Treatment of metastatic bladder carcinoma—

z MVAC (methotrexate, vinblastine, doxorubicin and cisplatin)
z GC (gemcitabine, cisplatin)—Survival similar to MVAC but better tolerability and safety.
Diseases of Prostate
Benign Prostatic Hyperplasia
S Characterized by both glandular and stromal hyperplasia resulting in enlargement of the gland.
Normal Prostate Benign Prostatic Hyperplasia

Urology 1001
S Prostate is divided into several biologically distinct regions— Peripheral, central, transitional and periurethral zone.
S Hyperplasia initially develops in the periurethral transition zone of the prostate, resulting in nodular enlargement.
Glandular and stromal component of peripheral zone are compressed and take the appearance of typical 'lateral
lobe' enlargement.
If hyperplasia primarily affects the central zone, 'middle lobe' develops.
Sometimes both lateral and middle lobe enlargement develops.
Etiology (How BPH Develops)?
Assess – which one?
Clinically enlarged prostate? Histologic BPH?
BOO ? LUTS ?
Patient may develop any one or combination of the above presentations.
What is LUTS (Lower Urinary Tract Symptoms)?

S Previously, termed as 'Prostatism'.
Causes of LUTS
S BPH
S Carcinoma of prostate
S Bladder neck contracture
S Neurogenic bladder
S Bladder carcinoma
S Bladder calculi
S UTI.
Urology 1003
Clinical Manifestations of BPH
S LUTS
S UTI
S Hematuria
S Retention of urine.
Initial Evaluation
S History—
z History of hematuria, UTI, retention of urine

z History of lower urinary tract surgery (to exclude the possibility of urethral stricture or bladder neck contracture)
z History of medical illness (e.g. diabetes, Parkinson's disease and CVA)
z History of medication (e.g. anticholinergics, D–adrenergics).
S Clinical examination— Examination of nervous system—To exclude tabes

dorsalis, Parkinson's disease, cervical spondylosis (these diseases may
present as prostatic obstruction). Elicitation of perianal sensation and anal
tone is helpful to detect Cauda equina lesion.
Examination of lower abdomen and external genitalia—
z To detect palpable bladder
z To exclude meatal stenosis, palpable urethral mass.
Digital rectal examination (DRE)—

z To assess the size, consistency and nodularity of prostate.
z In BPH, the posterior surface of prostate is convex, smooth. Rectal mucosa

can be moved over the prostate.
S Symptom assessment—
z Symptom severity is assessed by IPSS (International Prostate Symptom

Scare) or AUA symptom index.
z 7 symptoms related questions are scored (score 0–5). According to scoring, symptoms are classified as mild
(0–7), moderate (8–19) and severe (20–35).
z IPSS is used to grade symptom severity, to choose the optimal treatment, assess the response to therapy and
assess disease progression in the follow-up period.
S Urinalysis— To exclude UTI and microscopic hematuria.
Urine cytology should be done in patient with severe irritable symptoms and dysuria.
S Prostate–specific antigen (PSA)—
z Prostate carcinoma may coexist with BPH. So measurement of PSA in patient with greater life expectancy should
be done to detect early prostate carcinoma.
z PSA velocity, free versus complexed PSA ratio, PSA density are more specific than serum PSA.
S Additional evaluation?
S Uroflowmetry— A noninvasive urodynamic test to record the urinary flow rate throughout the act of micturition.
S Postvoid residual urine (PVR)— Urine remains in the bladder immediately after completion of micturition. PVR
measurement is done by noninvasive method (ultrasound) or invasive method (catheterization).
S Pressure-flow urodynamic studies—If an invasive treatment is planned and flow rate and PVR are not suggestive
of BOO.
Management
Watchful waiting
[Carcinoma of prostate or other serious pathologies must be excluded before adopting this treatment policy.]
Indicated if— Patient is reluctant to follow medical therapy and IPSS d 7
Severity of symptoms can be managed by—
S Decreasing total fluid intake before bedtime
S Avoid over intake of alcohol and caffeine
S Follow time-voiding schedules.

Urology 1005
Medical therapy
S Medical therapy is the treatment of choice except absolute indications for surgery.
S Two classes of drugs have clinical importance.
S D-adrenergic antagonist 5-D reductase inhibitors

• Two types of D-adrenergic receptors • 5-D reductase inhibitors act by blocking the
(D1, D2) are abundant in prostate and base conversion of testosterone to DHT.
of the bladder.
• It acts against the fixed component (prostate size).

• Commonly used 5-D reductase inhibitors are finasteride
and dutasteride.
• D1 adrenergic antagonists act against the

dynamic component (tension of prostatic
smooth muscle on prostate and bladder neck)
• Commonly used D1 antagonists are terazosin,
doxazosin, tamsulosin.
Minimally invasive and endoscopic management
1. TURP (Transurethral resection of prostate)—

z Gold standard surgical management of BHP.
z Indicated in moderate to severe symptom severity and that interfere with quality of life.
z Absolute indications—
Acute retention
Recurrent UTI
Recurrent hematuria
Renal insufficiency.
[Not indicated if associated bladder diverticula or large bladder stone is present.]

S Prophylactic antibiotic is necessary (1st generation cephalosporin or cephalosporin + gentamicin)
S Commonly used irrigation fluid is 1.5% glycine (nonhemolytic, hypotonic)
S Standard technique is described by Nesbit (1943)—Nesbit technique is divided into 3 stages.
z Resection starts at the bladder neck at 12'O clock position.
z Verumontanum is the distal-most point of resection.
z Strips of prostatic tissue are resected from the bladder neck to verumontanum using diathermy.
z Irrigation with glycine is applied whenever necessary.

z At the end of the resection, 3-way self-retaining catheter is introduced into the bladder.
S Complications—
z TUR syndrome—
An immediate postoperative complication due to excess systemic absorption of glycine leads to dilutional
hyponatremia.
Risk is increased if gland >45 gm, resection time> 90 minutes, Irrigant fluid > 70 cm H O.
2
Syndrome is manifested as mental confusion nausea, vomiting, hypertension, bradycardia and visual
disturbance.
Treatment includes— Diuretic (furosemide)
+
Decreasing the fluid overload
In severe cases, 200 ml of 3% saline (very slow infusion)
z Hemorrhage—
After completion of TURP procedure, the color of irrigation fluid should be light pink.
Arterial bleeding must be controlled with electrocoagulation.
Venous bleeding can be controlled by placing the catheter on traction for few minutes and over inflating the
balloon of the catheter.
2. Transurethral needle ablation of the prostate (TUNA)—
z Low-level Radiofrequency energy (490KHZ) is delivered by needles into the prostatic tissue causing localized
necrosis.
Urology 1007
3. Transurethral microwave therapy (TUMT)—
z Microwave therapy uses heat energy thus
resulting in hemorrhagic necrosis and
sympathetic nerve degeneration.
4. Transurethral ultrasound-guided laser-induced prostatectomy (TULIP)—

z Different types of laser—
Nd-YAG laser
KTP laser
Ho: YAG laser
Diode laser.
Laser works on the prostatic tissue either by coagulation or vaporization.
5. Transurethral incision of the prostate (TUIP)—

z Incision is made at 5 and 7 o'clock positions,
starting just distal to ureteral orifice and end
just proximal to verumontanum.
Open prostatectomy
{
S Indications for prostatectomy 1. Acute retention
2. Recurrent UTI
3. Recurrent hematuria
TURP is the gold standard 4. IPSS symptom severtiy— moderate to severe, but patient
approach for prostatectomy not responding to medical therapy
5. Renal insufficiency
Open approach is only indicated when—

1. Prostate size > 75 gm
2. Associated bladder diverticula
3. Associated large bladder calculi.
Different approaches for open prostatectomy
Retropubic prostatectomy (Millin) Transvesical prostatectomy

(Frayer's)
Retropubic prostatectomy
Urology 1009
Suprapubic prostatectomy (transvesical)
S Complications—
z Hemorrhage
z Perforation of bladder or prostatic capsule
z Incontinence
z Urethral stricture
z Bladder neck stricture
z Retrograde ejaculation.
Prostate
Prostatitis
Types of Prostatitis
S Different types
S Traditionalclassification NIH classification

z Acute bacterial prostatitis { Category I
z Chronic bacterial prostatitis { Category II
z Nonbacterial prostatitis { Category III A (inflammatory CPPS)
z Prostatodynia { Category III B (noninflammatory CPPS)
Category IV (asymptomatic inflammatory prostatitis)
[CPPS– chronic pelvic pain syndrome]
S Category I— Acute onset of perineal or suprapubic pain associated with irritative and obstructive urinary symptoms
along with systemic symptoms (e.g. fever, malaise, nausea, vomiting).
S Category II—History of recurrent UTI.
S Category III A and B—
z Pain in the perineum, suprapubic area and penis.
z Pain during or after ejaculation.
S Category IV—
z Asymptomatic
z Evidence of prostatitis detected during workup for other prostatic pathologies.
Assessment of Symptoms
S Objective assessment of symptoms—

z By NIH—CPSI (The National Institutes of health-chronic prostatitis symptom Index)
z This symptom index covers 3 domains:
Pain (location, frequency, severity)
Urinary symptoms (irritative and obstructive symptoms)
Quality of impact.
Urology 1011
Diagnosis
S Inacute prostatitis, on DRE, prostate gland presents as a hot, boggy and exquisitely tender swelling.
[DRE is better avoided due to sphincter spasm.]
S 4-glass test (Meares Stamey test)— A four-glass collection technique to differentiate between urethral, bladder and
prostate infections.
S Urine culture—E. coli, Klebsiella, Proteus, Pseudomonas are the most common uropathogens found in prostate
specimens.
Gram-positive enterococci are the next common organisms.
S Cytology.
Treatment
S Antibiotics— Fluoroquinolones are effective in chronic prostatitis caused by Enterobacteriaceae, but not against
P. aeruginosa or enterococci.
S D-adrenergic blockers— May improve outflow obstruction and thereby intraprostatic ductal reflux is diminished.
Carcinoma of Prostate
S Carcinoma of prostate is the most common malignant tumor in men of 65 years or more.
S Itis predominantly a disease of older males.
S Prostate carcinoma is unique among solid tumors—it exists in two forms — (1) Histologic (Latent) form and
(2) Clinically evident form.
Risk Factors
S Genetic factors— Various susceptibility genes have been identified. Among them, HPC1 is best characterized.
Others are – SR–A/MSR and MIC–1 gene.
S Chronic inflammation— There is a significant association of prostate carcinoma with history of sexually transmitted
disease.
S Androgen— A variable lifetime exposure of prostate to androgens have important role in carcinogenesis. No dose-
response relationship is yet established.
S Estrogen— Estrogen increases risk by initiating inflammation and producing mutagenic metabolites.
S Vitamin D— Vitamin D deficiency is associated with increased risk of prostate carcinoma.
S Dietary factors— Diects rich in fat particularly polyunsaturated fat are associated with n risk.
S Obesity—Higher BMI is associated with nrisk.

Pathology
z Adenocarcinoma is the most common histologic type.

z The tumor may show variable degrees of differentiation and
based on that, a grading system was devised– Gleason system.
[Presence of osteoblastic metastases in older

male—Suspect prostate carcinoma with bony
metastases.]
Urology 1013
Clinical Features
S In early stage, patient become asymptomatic.

S Incidentally, it is detected during histologic examination of prostatic tissue excised for BPH.
S Clinically, it may be detected as hard nodular prostate during routine DRE.
S In locally advanced stage, patient may present with symptoms of LUTS, hematuria, local discomfort.
S In the stage of metastases, patient may present with bone pain.
S On DRE—Stony hard consistency with obliteration of median sulcus.
Staging
S TNM staging
T1— Clinically inapparent lesion
T1a
T1b
T1c
T2— Palpable cancer confined to prostate
T3— Extraprostatic extension (seminal vesicles)
T3a— Unilateral extracapsular extension

T3b— Bilateral extracapsular extension
T4— Extension to adjacent structures (not seminal vesicles)

T4a— Tumor invades bladder neck, external sphincter and /or rectum
T4b— Tumor invades levator muscle and/or fixed to pelvic wall.
S Investigations for diagnosis and staging—

S Triad of investigation for diagnosis DRE
Serum PSA
TRUS guided prostatic biopsy
[Bone scan is an additional investigation (if needed)]
1. DRE — n serum PSA along with DRE improves the positive predictive value of DRE.
2. PSA— (Prostate specific antigen)—
z A proteolytic enzyme produced by normal and neoplastic prostate epithelium.
z PSA is secreted in high concentration (mg/ml) in seminal fluid and maintains the seminal secretions in a liquid
phase.
z Serum PSA is elevated when normal prostatic architecture is disrupted and PSA is diffused from prostatic tissue
to circulation.
z Serum PSA is elevated in
Prostate disease After prostate manipulation

– BPH – Prostate massage
– Prostate carcinoma – Prostate biopsy
– Prostatitis – Transurethral resection
z Men with PSA > 4 ng/ml should undergo a TRUS-guided prostate biopsy.
z PSA velocity (rate of change of PSA values with time), PSA density (ratio of serum PSA value and volume of
prostate gland) and free versus bound forms of PSA— are the most useful tests when PSA is in between 4–10
ng/ml (Gray zone).
3. TRUS–guided prostate biopsy—
z TRUS is not helpful to detect early prostate carcinoma.
z TRUS is helpful to locate the suspicious lesions targeted for biopsy.
z A 18-gauge core biopsy device is attached to the ultrasound probe and biopsy is taken (sextant biopsy).
4. Bone scan—
z Standard imaging modality for detecting bony
metastases.
z Bone scan is not necessary if PSA < 10 ng/ml.
z Bone scan is indicated if PSA> 20 ng/ml or patient

presents with bone pain.
Urology 1015
Treatment
S Treatment of localized disease (T1a, T1b, T2)—

1. Active monitoring— is particularly indicated formen with life expectancy <10 years and low grade (Gleason
score 2–5) tumor.
Patient should be evaluated with DRE and serum PSA monitoring quarterly and prostatic biopsy annually.
2. Radical prostatectomy—is indicated for men with life expectancy > 10 years and without any comorbid illness.
Different techniques
Open (retropubic/perineal prostatectomy) Minimally invasive (laparoscopic/robotic)

Radical prostatectomy includes complete removal of prostate along with seminal vesicles + modified pelvic
lymph node dissection
Complications
Early Late
• Nerve injury (obturator nerve) • Erectile dysfunction
• Ureteral injury • Urinary incontinence
• Rectal injury • Urethral stricture
• Urinary fistula
3. Radiotherapy—Radical radiotherapy to the prostatic bed and pelvic lymph nodes.
4. Cryotherapy.
S Treatment of locally advanced disease (T , T )—
3 4
1. Radical prostatectomy—Most of the patients are not benefited by this treatment modality
2. Adjuvant radiotherapy—Improves local control after radical prostatectomy
3. Androgen deprivation.
S Treatment of metastatic disease—
Androgen ablation
By ablating the source Antiandrogens LHRH/RH inhibition Inhibition of androgen

Synthesis
– Bilateral subcapsular – Cyproterone acetate – Goserelin – Aminoglutethimide
orchiectomy – Flutamide – Leuprolide – Ketoconazole
– Bicalutamide – Cetrorelix
– Aborelix
Urethra
Urethral Stricture
S Classically, urethral stricture means scarring involving the anterior urethra and sometimes along with spongy
erectile tissue of corpus spongiosum.
Etiology
S Congenital—Rarest of all cases.
S Traumatic—following straddle trauma.
S Inflammatory—
z Postgonorrheal (less common nowadays)
z Lichen-sclerosus-balanitis xerotica obliterans.
S Iatrogenic—
z Indwelling catheter
z Endoscopic procedure.
Clinical Features
S Straining during micturition

S Poor urinary stream
S Increased urinary frequency
S Recurrent UTI
S Acute retention of urine
S In well-developed stricture, the stricture can be palpated along the line of urethra.
Evaluation
S Location, length, depth and density of the stricture must be determined to make appropriate line of management.
Urology 1017
Location Length Depth Density
{
Determined by— Determined by—
z USG z Clinical examination
z Dynamic retrograde urethrogram z Elasticity felt during urethroscopy
z Urethroscopy
Treatment
S Dilatation
S Internal urethrotomy
S Urethral stents
S Laser
S Reconstruction.
1.
Dilatation—Strictured urethra is stretched using graduated series of dilators.
[During dilatation, be cautious about making false passage.]

2.
Internal urethrotomy—
Urethrotomy— Transurethral incision through the scar to healthy tissue.
3.
Urethral stents
z Temporary
z Permanent.
4.
Laser
5.
Reconstruction
a. Excision and reanastomosis
b. Primary urethral reconstruction
with the help of graft.
Excision and reanastomosis

Urology 1019
Hypospadias
S A congenital abnormality in which urethral meatus open on the ventral aspect of the penis, scrotum or perineum.
S Commonly associated anomalies are—
z Abnormal ventral curvature of the penis (chordee).
z Abnormal distribution of foreskin—presence of dorsal hood and deficient ventral foreskin.

S Classification—Level of hypospadias can be accurately determined by only after correction penile curvature
(orthoplasty).
Hypospadias with chordee
S Development—Due to incomplete fusion of urethral plate during development of penis.

S Risk factor— Risk is increased by history of maternal intake of estrogen or progesterone during pregnancy.
S Associated anomalies include— Cryptorchidism
— Inguinal hernia
Syndromes where hypospadias is one of the features—
S Aniridia-Wilms' tumor association
S Beckwith-Wiedemann syndrome.
[Penoscrotal or perineal hypospadias may represent intersex state. Hypospadias along with cryptorchidism also may
represent intersex disorder. So chromosomal study must be done in these conditions.]
S The ideal age of surgery is between 6–12 months of age.
[Newborn with hypospadias should not be circumcised.]

S Principles of hypospadias repair—
1. Correction of penile curvature

2. Urethroplasty
z Correction of penile curvature is done by 2 steps—
Step 1 — Assessment of penile curvature—By inducing erection
By injecting normal saline By injecting arterial

into corpora cavernosa vasodilator (prostaglandin
E1) into corpora
cavernosa
Urology 1021
Urethroplasty
S For distal hypospadias

S For middle hypospadias
S For proximal hypospadias.
For distal hypospadias

S Meatoplasty and glanuloplasty (MAGPI)— All glanular and some coronal hypospadias are repaired by this technique.
S Tubularization technique— is a Snodgrass modification of Thiersch-Duplay technique.

Critical steps are:
z A 'relaxing' incision of the urethral plate distal to the hypospadias opening.
z Tubularization of the relaxed urethral plate.
For middle and proximal hypospadias:

z Onlay island flap is a useful technique
z Transverse preputial island flap (TPIF).
Priapism
S An erection that is unrelated to sexual activity or persists beyond that.

Urology 1023
Types Priapism
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•Due to venous occlusion and •'XH WR LQFUHDVHG DUWHULDO LQÀRZ DQG
ĹLQWUDFDYHUQRVDOSUHVVXUH LQFUHDVHGYHQRXVRXWÀRZ
•Characterized by erect painful penis • &KDUDFWHUL]HGE\QRQWHQGHUHUHFWLRQ*ODQV
ZLWKHQJRUJHGJODQV LVVRIW
•Causes— • &DXVHV²$UWHULRYHQRXV ¿VWXOD VHFRQGDU\
–Sickle cell disease WRSHQLOHRUSHULQHDOWUDXPD
–Leukemia
–Spinal cord injury
–0HGLFDWLRQV HJ VLOGHQD¿O
FKORUSURPD]LQHWUD]RGRQH
–,QWUDFDYHUQRVDO LQMHFWLRQV IRU
erectile dysfunction
–,GLRSDWKLF
[/RZÀRZSULDSLVPVKRXOGEHWUHDWHG
DVPHGLFDOHPHUJHQF\@
>/RZÀRZSULDSLVPLVEDVLFDOO\FRPSDUW-
PHQWV\QGURPHRISHQLV@
Diagnosis
S Low-flow priapism can be differentiated from high-flow priapism by
corporal blood gas analysis.
In high-flow priapism, corporal blood gas analysis is similar to arterial
blood gas.
In low-flow priapism, corporal blood gas analysis is similar to venous
blood (hypoxia, hypercapnia and acidosis).
High-flow priapism also can be confirmed by perineal Doppler USG.
Management of Low-Flow Priapism
S Intracorporal irrigation with D-adrenergic

agonist (e.g. phenylephrine, epinephrine,
ephedrine).
Repetition of this sequence every 5 minutes interval until detumescence.

BP and pulse should be monitored during this procedure.
,ILQWUDFRUSRUHDOLQMHFWLRQIDLOVVKXQWLV
necessary
Corporoglandular Corporospongiosal Corporosaphenous

(Winter shunt) (Sacher shunt) *UD\KDFNVKXQW
*=J=CAIAJPKB%ECDŃKS-NE=LEOI
S Can be treated expectantly

S Selective embolization of A-V fistula is effective. If this fails, the fistula is surgically ligated.
Management of Priapism due to Sickle Cell Disease
S Canbe managed conservatively with hydration, alkalinization with bicarbonate and oxygenation
S Chance of recurrent priapism is high, so transfusion or exchange transfusion should be considered.
Peyronie's Disease
S Dense fibrous plaque on the tunica albuginea, causing

curvature of the penis.
S Exact etiology is unknown. Plaque represents scar tissue
resulting from buckling trauma of the penis usually during
intercourse.
S Clinical presentation—
z Painful erection
z Deformity in penis (both in flaccid and erect state)
z Well-defined plaque or induration on the dorsal

surface of the penis.
Urology 1025
z In most of the cases, curvature is noted during erection, not in flaccid state.
S Efficacy of medical management is doubtful. Therapy with Vitamin E, colchicines. Tamoxifen may be effective in
some cases.
S Surgical interference is indicated if erectile dysfunction develops or curvature interferes with sexual intercourse.
Plication and corporoplasty. Incision and grafting have excellent results.

Significant erectile dysfunction in Peyronie's disease warrants penile prosthesis.
Carcinoma of Penis
S Commonly presents in the sixth decode of life, but may develop in earlier age.
S Etiology—
z Phimosis—Definitive role of smegma in carcinogenesis is still lacking.

Neonatal circumcision is protective for invasive penile carcinoma, not so much protective for CIS.
Circumcision at puberty or at adult life do not have any protective role.
z HPV infection—particularly HPV-16
z Exposure to tobacco products —cigaret smoking, chewing tobacco, snuff— all are associated with increased
risk.
z Ultraviolet light exposure.
z Balanitis xerotica obliterans
z Premalignant lesions of penis—
Leukoplakia of the glans
Erythroplasia of Querat.
S Pathology—Lesion usually arises in prepuce and glans, but extends to involve the shaft.
Two forms of growth—Exophytic and ulcerative.

S Distantmetastases to lungs, liver, bone and brain are uncommon

S More than 90% of carcinomas are squamous cell carcinoma.
Squamous cell carcinoma are graded using Broder's classification:
Low grade (Grade I and II)—Tumors are usually confined to prepuce and glans
High grade (Grade III)—Tumors are usually involve the shalf of penis.
[Verrucous carcinoma—An exuberant variety of squamous cell carcinoma with extremely low potential for lymph
node metastases.]
S Patient may present with small papular, warty growth or in advanced cases, an exophytic lesion.
[Phimosis may obscure the tumor.]
S Patient may present with inguinal lymph nodes or ulceration in the inguinal region.
S Urethral involvement is very rare.
S On clinical examination, location, fixity, involvement of corporal bodies must be assessed.
[Bilateral palpation of inguinal area must be done to assess lymphadenopathy.]
KJłNI=PEKJKB!E=CJKOEO=J@0P=CEJC
S For confirmation of diagnosis, assessment of depth of invasion and presence of vascular invasion, for histologic
grading— biopsy is essential.
S A dorsal slit is often necessary for adequate exposure for biopsy.
S In early-stage, small sized lesion in glans—No further radiologic workup is necessary.
S High grade lesions suspected of involving corporal bodies, and if partial penectomy is being considered—Contrast
enhanced MRI is helpful to give additional information.
S For assessment of inguinal lymph nodes, clinical assessment is sufficient enough. Abdominal and pelvic CT is
recommended in obese patients and in patients where inguinal lymphadenectomy is indicated.
Urology 1027
Treatment
S Treatment of primary tumor
S Treatment of regional lymph nodes.
Treatment of primary lesion

Different treatment options
Depending on the stage of tumor, different

treatment options
Mohs micrographic
Circumcision Local resection Laser ablation Partial penectomy Total penectomy
surgery
In CIS
S Circumcision (if preputial lesion)

S Topical 5-FU cream (minimal systemic absorption)
S Nd: YAG laser
S Mohs micrographic surgery
S Radiotherapy.
In invasive carcinoma
Different treatment options
Partial penectomy Total penectomy Radiotherapy
•Distal penile lesion •Lesion involving the •Young patient with small
midshaft and base of VXSHU¿FLDOOHVLRQLQGLVWDO
penis penis who is willing to
preserve his organ
• 3DWLHQWXQ¿WIRUVXUJHU\
Partial penectomy
The ability to void in standing position and to perform sexual intercourse is preserved.
Urology 1029
Total penectomy
Radiotherapy
S Plesiobrachytherapy (radioactive substance is molded around the tumor)

S Interstitial brachytherapy (placement of radioactive material within the tumor)
S External beam radiotherapy.
Advanced penile cancer
S Proximal tumor with involvement of adjacent structures—Total penectomy with scrotectomy with bilateral
orchiectomy is recommended.
Management of regional lymph nodes
Inguinal lymph node metastases is a important prognostic factor.

S Clinically NO–
z TIS, Ta, T tumor with grade 1 or 2 tumor histology— Watchful waiting

1
z T , T with grade 3 tumor and presence of vascular invasion—Superficial inguinal lymph node dissection
2 3
Lymph nodes sent for frozen section biopsy

If positive If negative
Modified No further procedure

inguinal lymphadenectomy needed
S Clinically
node positive (N1)—
Treatment of primary tumor
4–6 weeks of antibiotic (e.g. 1st or 2nd generation antibiotics)

Lymph nodes still palpable
Modified inguinal lymphadenectomy
Urology 1031
Role of Pelvic Lymphadenectomy
S To identify patient who should receive adjuvant combination chemotherapy

S Locoregional control can be achieved.
Neoplasms of Testis
S About 99% of testicular neoplasms are malignant type.

S About 95% of testicular tumors arise from germ cells and all are malignant.
S About 90% of germ cell tumors (GCT) arise in testicular tissue and rest are extragonadal (mediastinum,
retroperitoneum).
S Testicular GCT is the most common solid tumor in between 15–35 years.
Risk Factors
S Cryptorchidism—Risk of testicular cancer is 3–14 times in undescended testis, less risk is also present in contralateral
normally descended testis.
Orchiopexy cannot prevent the risk of carcinogenesis, but it allow the clinician to early detection of tumor growth.
S Androgen insensitivity syndrome and gonadal dysgenesis— associated with increased incidence.
H=OOEł?=PEKJ
S Tumors with one histologic pattern (60%)—

z Seminoma
}
z Teratoma
z Yolk sac tumor Nonseminomatous GCT

z Choriocarcinoma.
S Tumors of more than one histologic type (40%)—
z Leydig cell tumor
z Sertoli's cell tumor.

Seminoma
S Accounts for 50% of GCTs.

S Most frequently develops between 35–45 years of age.
S Arises from seminiferous tubules.
S Two variant forms—
z Classic seminoma
z Spermatocytic seminoma.
S On cut section
S Prognosis is better among all GCTs

S Highly radiosensitive.
Nonseminomatous GCT
S Comprises about 50% of all GCTs.

S Different types—
z Teratoma
z Choriocarcinoma
z Yolk sac tumor
z Embryonal carcinoma.
Teratoma
S Composed of two or more germ cell layers—Ectoderm, mesoderm, endoderm.

S Differenttypes—
z Mature teratoma
z Immature teratoma
z Teratoma with malignant transformation.

Urology 1033
S On cut section
S Usually develop in younger age.
Sex cord-stromal tumor
S Two types—
z Leydig cell tumor—Secretes androgen, thereby causes sexual precocity
z Sertoli cell tumor—Secretes estrogen, thereby causes gynecomastia and loss of libido.
Clinical Presentation of Testiclular Neoplasm
S The pathognomonic presentation is painless testicular mass.

S May present with features of epididymoorchitis.
S In advanced stage, patient may present with distant metastases (iliac and paraaortic lymph nodes, liver and lungs).
S On clinical examination, testis is enlarged and firm. Testicular sensation is lost.
Lax secondary hydrocele may present.

All testicular swellings are suspicious, particularly if persists after antibiotic treatment.
Diagnosis
Clinical findings, imaging studies and tumor markers are to be considered for diagnosis
All suspected testicular malignancies must be approached through an inguinal approach.
Radical inguinal orchiectomy (testis and spermatic cord en bloc) with early, high ligation of spermatic cord at the
deep inguinal ring is the only accepted diagnostic as well as initial therapeutic procedure.
The orchiectomy specimen must be examined by the pathologist for histologic

type and subtype, T stage of the tumor as well as lymphatic and vascular invasion.
Staging
Staging is important for planning the proper management.
AJCC staging system (TNMS)
Serum tumor marker

Tumor (T) Node (N) Meastasis (M)
(S)
Staging is done by
1. Radical inguinal orchiectomy—to know the 'T' status

2. Imaging— to know the 'N' and 'M' status
z Chest X-ray— PA and lateral view of chest X-ray should be done to detect pulmonary metastasis. If high index of
suspicion is present, chest CT to be considered.
z Abdominal CT— Most effective imaging modality to defect retroperitoneal lymph node involvement.
z MRI or PET— Offers no added value.

Urology 1035
3. Tumor markers—
a. D–fetoprotein—
Increased level of D–fetoprotein are never found in pure seminoma.
Nonseminomatous GCT (containing elements of yolk sac) produce AFP.
So, n AFP is a indicator of presence of nonseminomatous component in GCT.
[Persistently elevated AFP after orchiectomy—Think of liver metastases.]

b. Human chorionic gonadotropin (HCG)—
Produced by syncytiotrophoblasts.
In all choriocarcinomas, about 50% of patients with embryonal carcinoma and few percentage of patients
with seminomas have n level of HCG.
c. Lactate dehydrogenase (LDH)
Due to its low specificity, serum LDH level should be corroborated with other findings
A direct relationship is present between tumor burden and LDH level
Most useful surveillance marker to detect persistence as well as recurrent tumors.
Treatment
S Treatment of seminoma
S Treatment of nonseminomatous GCT.
Treatment of seminoma
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Low-stage disease
S Treatment of stage I and IIa—

1. Modified (template) retroperitoneal lymph node dissection through a transabdominal approach is the treat-
ment.
[In modified RPLND, postganglionic nerve fibers are spared.]
2. Retroperitoneal lymph node irradiation—Radiation to paraaortic and ipsilateral pelvic lymph nodes.
3. Chemotherapy—Chemotherapy with bleomycin, etoposide and cisplatin.
S Treatment of stage IIb—
1. Modified RPLND
2. Chemotherapy—Usually considered with nodes > 3 cm and patients with relapse.
S Treatment of stage IIc and stage III—
1. For good-risk patients—3 cycles of chemotherapy (bleomycin, etoposide, cisplatin)

2. For poor-risk patients— 4 cycles of chemotherapy (same regime).
Chapter 26
Minimally Invasive Surgery,

Robotic Surgery
Important Topics
zzDifferent Minimal Access Techniques

zzPhysiology of Pneumoperitoneum
zzLaparoscopic Access
zzPort Placement
zzInstrumentation
zzAdvantages and Disadvantages of MIS

zzNew Techniques of MIS
zzRobotic Surgery
‘The mind likes a strange idea as little as the body likes a strange protein and resists it with a similar energy. It would not
perhaps, be too fanciful to say that a new idea is the most quickly acting antigen known to science.’
Wilfrid Batten Lewis Trotter (1872–1939)
British Surgeon and Sociologist
Minimally Invasive Surgery, Robotic Surgery 1039
Minimally Invasive Surgery
SS It
is not a discipline of surgery, rather a philosophy of surgery.
SS The philosophy—
zz Small incision
zz Use of miniaturized sophisticated instuments and imaging techniques
zz Performing basic to complex surgical interventions
zz Less sufferings of the patient.
Different Minimal Access Techniques
Laparoscopy
Access to the inflated peritoneal cavity (pneumoperitoneum) through sleeve (metal or plastic)
Extracavitary Endoscopy
Body planes (retroperitoneal space, space of Retzius, extraperitoneal space, subfascial space of leg) are accessed, but
needs inflation to develop the working space.
Examples: TEP repair of inguinal hernia, Laparoscopic nephrectomy, subfascial perforator ligation.
Endoluminal Endoscopy
Rigid or flexible endoscopes are introduced into the urinary tract (e.g. cystoscopy), gastrointestinal tract (upper and
lower gastrointestinal endoscopy), respiratory tract (e.g. bronchoscopy).
Thoracoscopy
Thoracic cavity is accessed through a rigid endoscope.

Physiology of Pneumoperitoneum
Access
SS Laproscopic access
SS Extraperitoneal and subcutaneous access
SS Hand-assisted laparoscopic access.
Laparoscopic Access
Two techniques for abdominal

access
Direct puncture Open technique

(with Veress needle) (Hasson technique)
Direct puncture techique
SS Measures to be taken—
zz Site of incision—Umbilicus is one of the preferred point of access, because the abdominal wall is quite thin in
this location, even in obese patient.
Trajectory of Veress needle

Force and depth of insertion of needle—
Veress needle is inserted after lifting the abdominal wall with towel clips or firm hand grip.
Surgeon can feel two pops as the needle penetrate the fascia and peritoneum.
Confirmation of proper placement of needle—
Then the Veress needle is connected to the insufflation tubing.
Open technique (Hasson technique)
Particulary indicated in patient who have undergone abdominal operations previously.
Extraperitoneal and Subcutaneous Access
Extraperitoneal and subcutaneous access
Access to Access to preperitoneal Access to subcutane-

retroperitoneum space ous space
• For nephrectomy, uretero- • For TEP repair of inguinal • For subfascial perforator
lithotomy, adrenalectomy hernia ligation
• Minimally invasive thyroid
surgery
• Saphenous vein harvesting
Hand-assisted Laporoscopic Access
SS Inlaparoscopy, a 'port' for the hand is created in such a way that the pneumoperitoneum is preserved
SS Tactile advantages of open surgery can be achieved due to use of hand
SS Particularly indicated in advanced colon surgery.
Port Placement
Ideal trocar orientation will create an equilateral triangle between the surgeon's right hand, left hand and the tele-
scope. Each arm will be about 10–15 cm.
Instrumentation
1. Imaging system
zz Telescope—Standard laparoscope is a metal shaft containing a series of quartz-rod lenses and optical fibers.
SS Length of laparoscope—24 cm
SS Diameter of laparoscope—
zz 10 mm (most commonly used)
zz 5 mm (can be used through the 5 mm working ports)
zz 1.1 mm (used in pediatric laparoscopy).
SS End of laparoscope—
zz Flat-end (0°)—provides straight view
zz Angled end (30° or 45°)— Provides oblique view as well as provides wider field of view.
When diameter of the rod lens telescope is doubled, the illumination is 4 times greater.
SS Video camera:
zz Video camera is attached to the eyepiece of the telescope
zz For perfect color representation, three-chip camera is required—Red, green and blue (RGB) input
zz In minimally invasive techniques—
Priority is on— Illumination — 1st priority

Resolution — 2nd priority
Color — 3rd priority.
SS Light source:
zz Bulbs of mercury, halogen vapor or xenon— 150–300 watt
zz In large cavity, in procedure where bleeding may encountered, bright light source is indicated.
SS Video monitor:
zz To display the image.
[High definition monitors have a resolution of upto eight times more than a standard NTSC/ PAL monitors.]
2. Energy sources
a. Radiofrequency electrosurgery—
Most popular energy source in minimally invasive surgery.
RF electrosurgery delivers an alternating current of 500 000 cycles/s (Hz). This causes tissue heating that
results in coagulation (60°C), dessication (100°C) and carbonization (> 200°C).
The RF can be delivered by monopolar and bipolar electrodes.
A short, high voltage current (coagulation current) is used for coagulation necrosis of bleeding sources.
Lower voltage, higher-wattage current (cutting current) is used for tissue division.
Complications:
––Capacitive coupling
––Direct coupling.
Ligasure— A newer bipolar device—Both coagulates (larger vessels) as well as divides the tissue.
Argon beam coagulation—
––A special type of monopolar electrosurgery.
––Uniform field of electrons is delivered across a tissue surface with the help of a jet of argon gas.
––Not preferable in laparoscopic surgery because the argon gas increases the chance of gas embolism.
b. Ultrasonic shears (harmonic scalpel)—

Can coagulate and divide the blood vessels.
A generator produces an current (55,500 Hz) that transmits to the

piezoelectric crystal stack (in the transducer). The crystal stack converts
the electrical energy to mechanical vibration at the same frequency.
This vibration is further amplified as it traverses the active blade of the
harmonic scalpel. The shearing force separates the tissue and produces
heat, results in coagulation of bleeding vessels.
Damage to adjacent tissues is minimal.
3. Hand instruments
zz They are larger and narrower than conventional hand instruments (in open surgery).
zz Standard hand instruments are 30 cm long and 5 mm in diameter.
zz Shorter and narrower instruments are required for pediatric (2–3 mm) laparoscopy, whereas longer instruments
are required for bariatric surgery.
4. Ports
zz All ports have attachments for insufflation and valves to prevent gas leaks.
5. Insufflator
zz Rapid-flow insuflator supplies the CO2 and maintains the pneumoperitoneum.
zz It maintains the gas-flow according to present pressure values.
Advantages and Disadvantages
Advantages
 Disadvantages 
• Smaller incisions • Two dimensional representation of the operative field makes the
depth perception difficult
• Cosmetically better • Hand-eye coordination is required.
• Decreased tissue trauma • Loss of tactile feedback
• Earlier return to activity • Technical expertise and infrastructure facility is required
• Reduced hospital stay
• Video recording of the procedure is possible in all cases
• Decressed chance of contact with HIV and hepatitis B virus
Examples of Laparoscopic Procedures
Basic Advanced
• Cholecystectomy • Bile duct exploration
• Appendectomy • Nissen fundoplication
• Hernia repair (TEP and TAPP) • Splenectomy
• Diagnostic laparoscopy • Colectomy (hand assisted)
• Nephrectomy
• Adrenalectomy
Contraindications
Absolute × Relative ?
• Generalized peritonitis • Pregnancy
• Intestinal obstruction • History of multiple abdominal operations
• Cirrhosis of liver • Organomegaly
• Coagulopathy
Complications
Related to Related to port insertion Related to procedure Dlayed complications
pneumoperitoneum
• Damage to major vessels or • Injury to viscera, vessels • Diathermy related injury (direct • Port site infection (e.g. atypical my-
viscera coupling, capacitive coupling) cobacterial infection)
• CO2 embolus • Hemorrhage • Inadvertent organ injury or liga- • Port site hernia (commonly in um-
tion (e.g. CBD ligation) bilical part)
• Metabolic acidosis • Hemorrhage
• Cardiorespiratory
compromise
New Techniques of Minimally Invasive Surgery
1. Notes (Natural Orifice Transluminal Endoscopic Surgery)

2. SILS (Single Incision Laparoscopic Surgery).
Notes (Natural Orifice Transluminal Endoscopic Surgery)
SS This concept involves access within the abdominal cavity through a natural orifice (vagina, mouth, urethra) to
perform surgical procedures.
SS Transvaginal and transgastric approach are common in Notes.
SS TV Notes is a safe alternative to traditional

laparoscopic surgery in female patient.
zz Appendectomy, cholecystectomy,
nephrectomy, adrenalectomy, hernia repair
are now performed by TV Notes.
zz The advantages are better cosmetics outcome,
decreased postoperative pain and shorter
recovery period.
SS In transgastric Notes, dual channel flexible
endoscope is used and through the gastrostomy
wound, the endoscope along with instruments
reach to the target organ.
zz The site of gastrostomy depends on the type of surgery.
zz Cholecystectomy, appendectomy are performed by transgastric NOTES.

Single Incision Laparoscopic Surgery (SILS)
SS SILS involves use of single port device with multiple port sites. Umbilicus is often the site of single incision and port
insertion.
SS The challanges in this technique are close proximity of the instruments, difficulty in retraction of organs, increased
cost.
Robotic Surgery
SS Stillnow, robotic surgery is performed by a surgeon with the help of robotic arms, not by a preprogramed robots.
'surgeon with robotic arms'.
SS Two surgical robotic system—
zz Zeus robotic surgical system
zz da Vinci surgical robotic system

(the robotic system now used.)
SS How da Vinci surgical robotic
system works?
zz Its working principle is based on
the master-slave concept.
zz Made up of 3 components.
Components of da Vinci Robotic System
SS Surgeon console:
Viewing a 3-D image of the operative field, the surgeon moves the master controllers at the console. These
movement, are exactly translated to the robotic arm, but with more degree of movement, more preciseness and
without any tremor or fatigue.
SS The patient (robotic) cart: Consists of 4 arms—One for the camera and others for the instruments.
–– Each arm has 3 joints (resembling the human arm) Setup joint (shoulder)
Instrument clutch button (elbow)
Effector instrument (wrist)
–– Each instrument have a wrist—The wrist provides six degrees of freedom at the tip and the seventh
degree of freedom is by the instrument itself.
SS Vision cart: Consists of 3-D high resolution endoscope, camera (3-chip) with camera control unit, high intensity
illuminators.
––This system provides 3-D stereoscopic vision to the surgeon.
Advantages
SS 3-D stereoscopic vision to the surgeon—Depth perception of binocular vision can be achieved.
SS More degrees of freedom of instruments.
SS Improved hand-eye coordination due to visual and spatial alignment, the surgeon feel as though his hands are
inside the patient's body.
SS Motion scaling—A unique feature of da vinci system. It scales down coarse movements of the surgeon (master) to
smaller and finer movements made by the robotic arm (slave) and instrument tip.
SS Useful in difficult anatomic areas (e.g. pelvis) where extremely fine dissection is warranted (e.g. nerve sparing
dissection).
Disadvantages
SS Highercost
SS Needs expertise proper training
SS Needs adequate setup.

Chapter 27
Nerve Injury
Important Topics
zzClasification of Nerve Injuries

zzPrinciples of Nerve Repair
zzSpecific Nerve Injuries
‘Look at the sky. We are not alone. The whole universe is friendly to us and conspires only to give the best to those who dream
and work.’
Introduction
SS A peripheral nerve trunk is made up of many nerve fibers.

SS Each nerve fiber consists of an axon which is surrounded by myelin sheath formed by Schwann cells.
SS Axon is the process of a nerve cell (neuron). Each neuron consists of a cell body, dendrites and one axon.
SS Group of nerve fibers form fascicles. Each fascicle is surrounded by a layer of connective tissue, the perineurium.
Many such fascicles are surrounded by connective tissue sheath, called the epineurium.
Fascicles surrounded by the epineurium form the nerve fiber.
[Connective sheath of peripheral nerve are very much strong.]
Classification of Nerve Injuries
SS Seddon's classification
zz Neuropraxia
zz Axonotmesis
zz Neurotmesis.
SS Sunderland's classification
zz 1st degree
zz 2nd degree
zz 3rd degree
zz 4th degree
zz 5th degree.
Nerve Injury 1057
Neuropraxia
SS Localblock of conduction of nerve fibers due to localized demyelination of axon.

SS Caused by compression of the nerve, mild stretching, etc.
SS Recovery occurs spontaneously (takes days to weeks).
Axonotmesis
SS Disruption of axons and myelin sheath but perineurium and epineurium is intact
SS Wallerian degeneration occurs distal to the site of injury, so distal conduction is lost
SS Recovery occurs by spontaneous regeneration (1–2 mm/day)
SS Restoration of motor and sensory function is almost normal
SS Caused by severe stretch injury of the nerve.

Neurotmesis
SS The nerve is completely severed

SS No recovery is possible unless surgical repair is undertaken
SS Recovery is not so perfect, in aspect of both motor and sensory function
SS Caused by cut injury (after trauma or iatrogenic), severe traction injury.
Sunderland's Classification
SS 1stdegree ≡ Neuropraxia
SS 2nd degree ≡ Axonotmesis
SS 3rd degree ≡ Disruption of axon and endoneurial tube, intact perineurium and epineurium
[Schwann cell basement membrane along with endoneurial collagen fiber form the endoneurial tube]
SS 4th degree ≡ Only epineurium is intact
SS 5th degree ≡ Epineurium is also disrupted.
Clinical Features
SS In neuropraxia, paralysis of specific muscle groups but sensory and autonomic function is preserved.
SS In axonotmesis, complete paralysis of specific muscle groups, sensory function and autonomic function (e.g.
sweating) is also lost.
Nerve Injury 1059
Management of Nerve Injury in Closed Injury
SS A loss of nerve function in a closed injury is usually due to stretch or compression.

SS The type of injury is usually neuropraxia a axonotmesis.
SS These type of injuries recover spontaneously, but you have to wait for few weeks if it is axonotmesis.
SS If any doubt about neurotmesis, the wound should be explored for surgical repair of the nerve, as early repair carries
better prognosis.
Management of Nerve Injury in Open Injury
SS After control of hemorrhage, the surgical exploration should be continued for search of injured nerve, if any clinical
evidence of nerve injury is present.
SS Routine exploration without any evidence of neurological deficit should be done in flexor compartment of forearm
(in this region, nerves are vulnerable to damage.
Principles of Nerve Repair
SS Timing of repair
zz Primary repair is indicated if—
Clean, incised wound
Surgeon has proper expertise
Proper instruments (e.g. loupes, operating microscopes) available.
zz Secondary repair is perferable if—
Highly contaminated wound
Proper expertise and instruments not available.
SS Type of repair
zz Nerve suturing
Clean division of the nerve
After mobilization, suturing is technically not possible.
zz Nerve grafting
Length of nerve is lost
After mobilization, suturing is technically not possible.
SS Choice of suture material
zz Fine (8/0 or fine), nonabsorbable (e.g. prolene or nylon) suture is preferable for median nerve, 6/0 for sciatic
nerve and 10/0 for digital nerve.
SS Basic steps of primary suturing

zz Minimal trimming of nerve ends.
zz Correct orientation of the nerve ends to minimise crossover during

recovery (pattern of nerve fascicles and surface blood vessels act as
guide for proper alignment).
zz Sutures are placed in the epineurium (epineurial repair). No need of
interfascicular repair.
zz Sufficient suturing to provide epineurial cover.
zz Excessive suturing must be avoided.
SS Basicsteps of secondary repair—

zz During wound exploration, it primary repair is technically not feasible, secondary repair to be planned.
zz The severed ends should be fixed to surrounding tissue to prevent further retraction.
zz During secondary repair, first to identify the nerve before dissecting the scar tissue.
zz The neuroma of both ends must be excised until nerve bundles sprout from the cut surface.
zz Orientation and suturing techniques are same as primary suturing.

Nerve Injury 1061
SS Nerve grafting—
zz When direct nerve suturing is technically not feasible (defect > 3 cm), nerve grafting (cable grafting) is indicated.
zz The nerves that can be used as graft are sural nerve, saphenous nerve, medial cutaneous nerve of forearm (these
are nerves of long length carries sensation of small areas).
SS Postoperative management—
zz Immobilization for 3 weeks to protect the suture line from undue tension
zz Regular physiotherapy to prevent contracture and muscle atrophy
zz Tinel's sign is regularly elicited to monitor axon regeneration.
SS Specific nerve injuries

zz Facial nerve—
Neuropraxia after superficial parotidectomy is not uncommon. Recovery within few days is the rule.
If nerve is damaged or sacrificed for treatment purpose (involvement of facial nerve in carcinoma parotid),
nerve graft is indicated (great auricular nerve is the preferable nerve for grafting).
zz Recurrent laryngeal nerve—
Chance of injury is more in thyroid surgery (particularly in total thyroidectomy or re-do thyroid surgery).
Neuropraxia due to dissection recovers spontaneously.
In unilateral axonotmesis or neurotmesis, force of voice is reduced.
In bilateral injury, both vocal cords is shifted medially. Thereby, tracheostomy is indicated to maintain the
airway.
zz Brachial plexus—
Caused by—
––Traction injuries (in motor cycle accidents)

––Penetrating injuries in axilla
––Iatrogenic (during axillary lymph node dissection).
In traction injury, any grade of injury like neuropraxia, axonotmesis, neurotmesis,
preganglionic injury (avulsion of the roots from the spinal cord) may occur.
According to degree of injury, the neurological deficit varies from paralysis and
sensory loss of whole upper limb to only a specific group of muscles.
zz Median nerve—
Usually injured at elbow (fracture distal humerus or dislocation of elbow joint) or

at wrist (laceration or fracture distal radius).
Paralysis of pronators and flexor muscles of wrist and fingers (except flexor carpi
ulnaris and medial part of flexor digitorum profundus). Thenar muscles are also
paralyzed.
Sensory loss over the palmar aspect of thumb, index, middle finger and radial half
of ring finger.
zz Radial nerve—
Commonly injured in the radial groove in fracture of humeral shaft.
Recovery after repair is satisfactory.
'Saturday night palsy' is neuropraxia or axonotmesis of radial nerve due to pressure over the nerve, as arm is
placed over the sharp back of a chair in deep sleep.
Paralysis of brachioradialis, extensor digitorum and extensors of wrist.
Sensory loss over the dorsum of the thumb and first webspace.
zz Ulnar nerve—
Commonly injured following lacerations in forearm
Paralysis of small muscles of hand (except thenar muscles and lateral two lumbricals)
Sensory loss over the medial one and half of the ring finger.
zz Sciatic nerve—
Rarely injured after posterior dislocation of hip and fracture pelvis
Prognosis after repair is poor.

Chapter 28
Surgery of Hand
Important Topics
zzPrinciples of Hand Surgery

zzInfections in Hand
zzHand Injuries
‘However many holy words you read, however many you speak, what good will they do you if you do not act on upon them?’
Surgery of Hand 1065
Introduction
SS Anesthesia in hand surgery.
Different types
anesthesia
Digital nerve block (with-

Brachial plexus block General anesthesia
out adrenalin)
SS Tourniquet—To make a bloodless operative field for better visualization of structures.
SS Incisions—
zz Shorter incision in palmar aspect is better placed through flexion crease

zz If longer exposure is needed, a 'mid-lateral incision' is preferable
zz To prevent scar contracture formation, the incision should not cross the skin creases at right angle
zz Incision should not cross the wrist at right angles.

SS Instrumentation—
zz General instruments are used but that must be of delicate variety (e.g. scissors, forceps)
zz Bipolar diathermy is preferable
zz Loupes and sometimes microscopes are required.
SS Position of immobilization—
The position of immobilization is maintained by boxing glove dressing along with plaster back slab.
SS Measures to prevent swelling and

stiffness—
zz Elevation—Hand must be elevated
in a high sling.
zz Position of immobilization—
Previously described.
zz Early joint movement—Movement
of the joints should be stored as
early as possible.
Infections in Hand
SS Acute paronychia—
zz Acute infection of the nail fold.

zz Mild infection can be treated by antibiotics.
zz If any pus collection, it must be drained by either separating the nail from nail bed or by partial excision of
proximal part of nail.
SS Chronic paronychia—
zz A chronic fungal infection of the nail fold

zz Treatment–keep the hands dry and application of antifungal ointment.
SS Pulp space infection—
zz Infection of the terminal pulp space does not spread proximally into the other pulp spaces due to fibrous septa,
but it causes a rapid rise of pressure with sloughing of skin and osteomyelitis of terminal phalanx.
zz Incision is made over the maximum point of tenderness.
SS Web space infection—
zz The web spaces are connected with the dorsum of the

hand and proximal pulp spaces of the fingers. Natatory
ligament is a fascial support in web space and acts as
a partial barrier between volar and dorsal web space.
zz At the stage of cellulitis, antibiotic therapy is sufficient.
zz If abscess develops, it must be drained.
The abscess should be drained through the most direct

route.
Incision should be in such position that digital nerves and
vessels will least likely injured.
zz Flexor tendon sheath infection—

The synovial sheath of the flexor tendons, those of index, middle and ring finger end proximally at the level
of metacarpophalangeal joints.
The synovial sheath of thumb is continuous with the radial bursa and synovial sheath of little finger is continuous
with ulnar bursa.
Infection in the tendon sheath of index, middle and ring finger can't spread to the palm or forearm.
Infection in the tendon sheaths of thumb and little finger can spread to the palm and forearm.
Patient complains of throbbing pain and swelling of the fingers. Passive movements cause severe pain.
Infection of synovial sheath of thumb or radial bursa causes swelling of thumb and thenar eminence and makes the
thumb slightly flexed.
Infection of the ulnar bursa causes swelling of the whole hand, sometimes involvement of the wrist.
Surgical exploration of the affected tendon sheath or infected bursa is mandatory if the infection has not
subsided after 48 hours of antibiotic management.
zz Palmar space infection—
The deep fascial spaces are consist of hypothenar, midpalmar and thenar spaces.
These spaces are prone to infection by penetrating trauma or from spreading from a neighboring
compartment.
The characteristic presentation is loss of normal concavity of the palm along with swelling of the dorsum of
the hand.
Passive movements of the fingers cause extreme pain.
Drainage of the pus is done through appropriate lumbrical canal.
Injuries in Hand
SS Nerve injury:
zz Median nerve injury—
Wasting of thenar eminence
Inability to abduction and opposition of thumb
Absence of flexion of terminal interphalangeal joint of index finger.
zz Ulnar nerve injury—
Wasting of hypothenar eminence
Inability to flexion of little and ring fingers
Inability to adduct and abduct the fingers.
zz Radial nerve injury—
Inability to extend the wrist
Inability to extend the MCP joint of digits and interphalangeal joint of thumb.
Tests to check the integrity of median, ulnar and radial nerve—
Tendon injury
zz Injury of extensor tendons—
Repair is done by classic tendon suturing technique. (with nonabsorbable, monofilament suture—
Polypropylene).
Recovery is satisfactory.
zz Injury of flexor tendons—
Injury in zone 2 and 4— Primary repair should not be attempted, repair should be done by a tendon graft of
palmaris longus or plantaris.
Injury in zone 1, 3 and 5— Primary repair is satisfactory.
Vascular Injury
Chapter 29
Neck Swelling
Important Topics
zzAnatomy of Neck
zzNeck Swellings
‘Technology is just a tool. In terms of getting the kids working together and motivating them, the teacher is the most
important.’
Neck
Anatomy of Neck
SS Neck is divided into two triangles:
SS Neck is divided by multiple fascial layers:

Neck Swelling 1075
SS Neck is divided into seven lymphatic levels:
Neck Swellings
[Among 800 lymph nodes in the body, about 300 of them are present in the neck]
Lymphadenopathy
SS Enlargement of the cervical lymph node is the most common cause of neck swelling
SS Causes—
zz Infection: Tuberculosis, tonsillitis, infective focus in oral and nasal cavity, larynx, pharynx, ear, face, toxoplasmosis.
zz Metastatic deposit: Carcinoma in head-neck region (nasopharynx, tonsil, piriform fossa, supraglottic larynx),
carcinoma in chest and abdomen.
zz Primary neoplasms of lymphatic system: Hodgkin's lymphoma and nonhodgkin's lymphoma.
zz Sarcoidosis
Nonspecific lymphadenitis
SS Due to infective focus in oral and nasal cavity, larynx, pharynx and face
SS Enlarged lymph nodes are tender
SS Systemic symptoms like fever, malaise are usually present
SS Treatment is—
zz Treatment of the infective focus with appropriate antibiotics
zz If abscess develops, then incision and drainage is indicated along with antibiotics.
Tuberculous lymphadenitis
SS Common cause of cervical lymphadenopathy in developing countries.

SS Both human and bovine strain may be responsible.
SS Tubercular bacilli can enter the body through the tonsil, from where it enters the cervical lymph nodes.
SS In most of the cases, disease is limited to clinically affected cervical lymph nodes. Associated pulmonary and renal
tuberculosis is rare. If any suspicion, then it have to be investigated.
SS Common in children and young adults, but can occur at any ages.
SS The upper deep cervical lymph nodes are most commonly affected.
SS In the early stage, the nodes are appeared firm and discrete.
If no treatment is instituted, caseation increases, infection spreads beyond the capsule of nodes. The nodes now
become coalesce and appear as matted.
Abscess develops in the center of the matted glands.
Initially, the pus is confined by the deep cervical fascia, but later it bursts through it and reach the subcutaneous
tissue. Now it has two compartments, one on either side of the deep fascia connected by a track. This is now called
'collarstud abscess'.
The superficial abscess gradually enlarges, the skin overlying the abscess becomes eroded and then the discharging
sinus develops.
Neck Swelling 1077
SS Treatment is antitubercular chemotherapy.
Metastatic deposit in cervical lymph node
SS Commonest cause of cervical lymphadenopathy in adults.

SS The primary one is most oftently present in the buccal cavity (tongue, lip, buccal mucosa) and larynx.
Other sites that have to be searched for—

zz Skin of scalp, ear and external auditory meatus
zz Nose, nasopharynx and maxillary antrum
zz Thyroid
zz Upper limb and both sides of chest wall
zz Lungs
zz Breast
zz Stomach, pancreas, ovaries
zz Testis.
SS Presentsas painless lump in neck. They are hard, irregular, tethered to the surrounding structures.
SS Enlarged left supraclavicular lymph node is called Virchow's node.
SS Presence of Virchow's node is called Troisier's sign.
SS Treatment— Treatment of the primary disease.
Radiotherapy/neck dissection for the lymph node.

Primary neoplasm of lymph node
SS Malignant lymphoma (Hodgkin's lymphoma and Non-Hodgkin's lymphoma) are most common primary tumor of
lymphoid tissue.
SS Painless lymphadenopathy, particularly in the posterior triangle along with systemic symptoms (e.g. fever, malaise,
weight loss, pallor).
SS Lymph nodes are smooth, discrete and rubbery in consistency.
SS Other groups of lymph nodes (e.g. inguinal, axillary) are commonly enlarged.
SS Chemotherapy is the treatment of choice.
Branchial Cyst
SS It is a remnant of a branchial cleft, usually the second

branchial cleft.
SS It is lined by squamous epithelium and contains turbid,
thick white fluid full of fat globules and cholesterol crystals
secreted by sebaceous glands of epithelial lining.
SS Presents in adult life, a painless cystic swelling in upper
lateral part of neck, appears beneath the junction of upper
one-third and lower two-third of sternomastoid at its
anterior border.
SS USG and FNAC are useful methods for diagnosis.
SS Excision is the treatment of choice.

Neck Swelling 1079
zz Incision over the cyst along the skin crease.
Incision should be atleast 2 cm below the angle of jaw
to avoid the injury of marginal mandibular branch of facial
nerve.
zz The anterior (superficial) part of the cyst can be easily
enucleated. If deep extension is present, then it must be
excised with careful dissection.
zz The deeper part of the cyst extends backwards and
upwards in between the internal and enternal carotid
artery to the region of tonsillar fossa.
The hypoglossal and spinal accessory nerves are en-
countered during dissection of deeper extension of cyst.
Branchial Fistula
SS Itis due to persistence of second branchial cleft.

SS The external opening is near the lower third of sternomastoid at its anterior border, the internal opening in the
tonsillar fossa.
SS The tract is lined by ciliated columnar epithelium.

SS Patient presents with small dimple in the lower part of the neck that discharges mucous or mucopurulent discharge
with recurrent interval.
SS If the upper end of the fistula obliterates, then it is called branchial sinus.
SS Treatment is excision of sinus.

Carotid Body Tumor (Chemodectoma)
SS Itis the tumor of the chemoreceptor tissue of the carotid body.

SS Carotid body usually presents on the posterior aspect of the bifurcation of common carotid artery, and adherent to
the carotid wall.
SS Patient presents with nontender, slowly growing lump.
On examination, the lump is palpable at the level of hyoid bone, beneath the anterior border of sternomastoid
muscle.
Most of these tumors are hard, pulsatile. The common carotid artery is below the lump and the external carotid
artery may pass over the lump.
SS Carotid body tumors are also called 'Potato tumor', because of its shape and firm consistency.
Most of these tumors are mistaken as cervical lymphadenopathy.

SS Duplex study is to be done to delineate the nature of tumor. Carotid angiogram is indicated to demonstrate the
carotid bifurcation and its relationship with the tumor.
[FNAC is contraindicated.]
Neck Swelling 1081
Cystic Hygroma
SS Congenital cystic abnormalities of lymphatic channels, develops due to failure of a cluster of lymphatic channels
(jugular lymph sac) to connect into normal lymphatic pathways.
SS It is composed of multiple uni and multiloculor cysts, each cyst contain clear lymph.
SS Other sites of cystic hygroma—Axilla
Groin
Mediastinum.
SS It may present at birth, may be so large to obstruct the delivery of the baby.
May present in early infancy.

SS Commonly located in the lower third of neck, at the base of the posterior triangle.
SS Treatment is—Excision of all of the cyst.

This excision demands a meticulous neck dissection.
Injection of sclerosant before planning the surgery may diminish the size of the tumor, but it destroys the normal
tissue planes, makes further surgery more cumbersome.
Sternomastoid Tumor
SS Swelling in the middle third of sternomastoid muscle, found in the neonates.

SS It is due to infarcted segment of muscle following trauma of birth.
SS Mother notice a lump in neck with slight torticollis.
SS If muscle damage is more and causes fibrosis, the tilting of head to one side will become prominent as the child
grows.
Thyroglossal Cyst
SS Most common congenital anomaly of the neck.

SS The cyst represents the persistence of a part of thyroglossal
duct, which begins at the foramen cecum and ends at the
thyroid isthmus.
SS The cyst can present anywhere between base of tongue and isthmus of thyroid.
The two sites are common–subhyoid and suprahyoid at the midline.
SS The swelling moves with deglutition as well as with protrusion of tongue.
[Thyroglossal cyst may be the only thyroid

tissue present in the body. So, before exci-
sion, thyroid scan should be done.]
SS Treatment is excision of cyst along with whole thyroglossal tract including the body of hyoid bone. This is called
Sistrunk's operation.
Chapter 30
Cleft Lip and Palate

Important Topics
zzClassification of Cleft Lip

zzManagement of Cleft Lip
zzClassification of Cleft Palate
zzManagement of Cleft Palate
‘When books are opened, we discover that we have wings.’

Cleft Lip and Palate 1085
Cleft Lip
SS Congenitaldefects in head and neck is one of the common pathologies encountered by Pediatric and Plastic
surgeons.
Among head-neck defects, cleft lip and palate is the most common problem encountered.
SS During embryogenesis, the five facial elements (one frontonasal, two lateral maxillary and two mandibular
segments) merge to form the face and jaw.
The frontonasal process forms the nose, the nasal septum, the nostrils, the philtrum of the upper lip and the pre-
maxilla.
The maxillary process form the cheek, the upper lip (except the philtrum), the upper jaw and palate.
The mandibular processes form the lower jaw and lower lip.
SS In classic theory, failure of fusion of the maxillary process and frontonasal process causes the cleft.
SS Incidence—
zz Racial difference is noted in prevalence

zz Cleft lip and palate—45%
zz Isolated cleft lip—15%
zz Isolated cleft palate—40%
zz Cleft lip and other malformations is about 14%
zz In cleft lip, the deformity in left side is about 60%.
Etiology
Classification
SS Defects in cleft lip (unilateral)—
zz Ill-defined philtral ridge on the cleft side
zz Columella shorter on cleft side
zz Lateral inferior and posterior displacement of the alar cartilage
zz Vermilion thining
zz Nasal floor defect
zz Hypoplastic muscles and abnormal muscle insertions.
SS Defects in cleft lip (bilateral)—
zz Premaxilla is outwardly rotated and projected
zz Prolabium is devoid of muscle
zz Short columella.
Treatment
SS A multidisciplinary team consists of plastic surgeon, pediatric dentist, otorhinolaryngologist, speech therapist,
pediatrician and psychologist is necessary for highest level of care.
SS Timing of repair— Usually follow the 'rule of tens'
10 weeks of age
10 lbs body weight
Hb% 10 mg/dl.
SS Presurgical procedure— Presurgical orthodontics such as nasoalveolar segment alignment.
SS Goal of repair—To make the appearance of lip, nose and face normal and also to make the development of speech,
dentition and facial growth almost normal.
SS Principles of cleft lip repair—
zz Layered repair of skin, muscles and mucous membrane to restore symmetric shape and function
zz To level cupid's bow and reconstruct the central philtrum of the lip
zz Primary closure of the alveolar cleft (gingivoperiosteoplasty) at the time of primary lip repair
zz Primary nasoplasty at the time of lip repair.
SS The Millard rotation—Advancement flap technique is widely used for unilateral cleft lip repair.
SS Delaire technique is another option.
SS Mulliken technique is commonly used for bilateral cleft lip repair.
Cleft Palate
SS Due to failure of fusion of the two palatal processes

SS Etiology—Multifactorial.
Classification
SS Problems due to cleft palate—
zz Ineffective suckling and feeding (due to failure of
creating negative intraoral pressure because of
nasal and oral cavity continuity).
zz Speech difficulties (due to velopharyngeal
incompetence).
zz Improper facial growth.
zz Recurrent otitis media.
SS Timing of repair— Before speech development (6–

18 months of age)
SS Goal of surgical repair—To separate the oral and
nasal cavities and formation of tight velopharyngeal
valve.
SS Different techniques of repair—
zz Furlow palatoplasty—Double opposing z-plasty

of soft palate.
zz Von Langenbeck repair—Bipedicled hard palate mucoperiosteal flap repair.
zz Wardill-Veau-Kilner repair—Unipedicled hard palate mucoperiosteal flap repair.
SS Secondary management—
zz Hearing difficulty—Child with cleft lip and palate are at increased risk of sensorineural deafness and conductive
deafness (due to secretory otitis media).
All children with cleft lip and palate should undergo assessment for deafness by auditory brainstem responses
(ABR) and tympanometry before 1 year of age.
Sensorineural deafness are treated with hearing aid and treatment of conductive deafness is controversial.
zz Speech difficulty—Speech assessment should be started from 1½ years of age and at regular interval.
Assessment is done by—

Videofluoroscopy
Aerophonoscopy
Nasoendoscopy.
Difficulties are managed by—

Speech therapy
Veloplasty
Pharyngoplasty.
SS Dental abnormalities—
zz Child with cleft lip and palate should undergo regular dental examination.
zz Delayed eruption, variation in number and ill health teeth may present.
zz Preventive measures, e.g. fluoride supplements, maintenance of dental hygiene is essential for disease-free
dentition.
SS Orthodontic management—By alveolar bone graft/maxillary osteotomy.
Chapter 31
Anesthesia
Important Topics
zzTypes of Anesthesia
zzLocal Anesthesia
zzSpinal Anesthesia
zzEpidural Anesthesia
zzGeneral Anesthesia
zzPreoperative Evaluation
zzComplication of GA
‘I keep six honest serving men; they taught me all I know. Their names are what, why, when, how where and who.’
Introduction
SS The discipline of anesthesia mainly controls three components during any surgical procedure:
zz Pain
zz Consciousness
zz Movement.
Types of Anesthesia
Anesthesia
Local Regional (spinal/epidural) General
Local Anesthesia
SS Local anesthesia reversibly block impulse conductions along nerve axons by blocking voltage-gated sodium
channels (small-diameter unmyelinated fibers, such as type C pain fibers are most sensitive whereas heavily
myelinated, thicker fibers are least).
SS 2 classes of local anesthetics (according to chemical structure).
Amides Esters
• Lidocaine • Cocaine
• Bupivacaine • Procaine
• Prilocaine • Benzocaine
• Ropivacaine
Anesthesia 1093
SS Amides are metabolized in the liver
SS Esters are hydrolyzed in the blood by pseudocholinesterase.
Local anesthetics can be used in various routes
Nerve block
EMLA cream is composed of 2.5% lidocaine and 2.5% prilocaine. Its topical use is very much useful for anesthetizing the
skin before minor vascular access, superficial laser skin treatment.
Systemic toxicity
CNS manifestations CVS manifestations
• Sleepiness • Hypotension
• Circumoral and tongue numbness • ↑P–R interval
• Metallic taste • Bradycardia
• Tinnitus • Cardiac arrest
• Visual disturbances [Bupivacaine is more cardiotoxic than other local
• Slurred speech anesthetics.]
• Seizures [Inadvertent IV injection of bupivacaine results in
profound hypotension, VT, VF, complete A–V block
that is refractory to treatment.]
SS Treatment of toxicity—
zz Oxygen and airway support
zz For seizure—Bezodiazepine or thiopental
zz Cardiovascular support.
SS Precautions to be taken to avoid toxicity—
zz Before injecting local anesthetic, always aspirate

to exclude vascular entry.
SS Calculation of the toxic dose of the local anesthetic—
zz Toxic dose of lidocaine 5 mg/kg [1% = 10 mg/

ml]
zz Toxic dose of bupivacaine 3 mg/kg.
Anesthesia 1095
SS Epinephrine as an additive:
zz Advantages
Reduces local bleeding
Absorption of local anesthetic from injection site is delayed, so the anesthetic will work for a longer period
Systemic absorption is delayed, so chance of toxicity will be less.
Epinephrine containing anesthetics should not be injected in body parts which are supplied by end arteries.
Spinal Anesthesia
SS Local anesthetics is injected into the CSF surrounding the spinal cord, in the subarachnoid space resulting in
sensory, motor and sympathetic blockade below the level of block.
SS Site of injection is usually below L1 or L2 (needle is passed between two lumbar spinous processes).
SS Lidocaine, bupivacaine are the commonly used anesthetic agents.
SS Indicated in lower abdominal operations, in urologic surgery, surgery in perineum and lower extremity.
Advantages
SS Complications of general anesthesia can be avoided

SS Patient is awake.
Complications
SS Hypotension (particularly if patient is not adequately prehydrated)

SS Bradycardia
SS Postdural puncture headache (is related to diameter of spinal needle, female gender, younger age)
SS Radicular neuropathy (temporary)
SS Backache
SS Cardiorespiratory compromise (if more cephaled spread).

Spinal anesthesia Epidural anesthesia
Epidural Anesthesia
SS Localanesthetic is injected into lumbar or thoracic epidural space

SS A epidural catheter is placed into epidural space after locating the space with needle
SS Catheter can be used for repeated dosing
SS Postop analgesics can be administered for several days through this catheter.
Advantages
SS The onset of sympathetic blockade and hypotension is slower in comparison to spinal anesthesia.
Anesthesia 1097
Complications
SS Similar to spinal anesthesia.
Specific complications
SS Epidural hematoma (in patient receiving oral or parenteral anticoagulants)

SS Epidural abscess.
General Anesthesia
General anesthesia produce three separate effects:
Effect of general anesthesia
Unconsciousness and
Analgesia Muscle relaxation
amnesia
General anesthesia
SS General anesthesia is achieved by both intravenous and inhalational agents.

SS Intravenous agents—Used for induction of anesthesia.
SS IVagents (causing unconsciousness and amnesia)—

1. Barbiturates— Thiopental is a barbiturate that is commonly used. They act on GABA receptor, resulting in
inhibition of excitatory synaptic transmission.
Barbiturates are anticonvulsants and reduces cerebral metabolism
In higher doses, it is myocardial depressant.
2. Propofol— It acts on GABA receptor resulting in inhibition of synaptic transmission.

It has bronchodilator property
It may cause hypotension.
Anesthesia of choice for ambulatory surgery.

3. Etomidate— It acts on GABA receptor.
4. Ketamine—
zz It acts on NMDA receptor
zz It is a dissociative anesthetic, producing analgesia also
zz Patient may present with delirium and hallucinations while regaining consciousness
zz It increases heart rate and BP
zz It can maintain BP in hypovolemic patients by sympathetic stimulation
zz It is myocardial depressant.
IV Agents (Causing Reduction of Anxiety as well as Amnesia)

Benzodiazepines
SS Actson GABA receptor

SS Commonly used benzodiazepines are—Diazepam, lorazepam, midazolam
SS Cause peripheral vasodilation and hypotension
SS They are also good anticonvulsants
SS When it is combined with opioid analgesics, it may cause respiratory depression.
IV Agents (Causing Analgesia)

Opioid analgesics
SS Actson μ-receptor in brain and spinal cord

SS Commonly used opiod analgesics are: morphine, codein, fentanyl (Synthetic opiod).
[Remifentanil (a fentanyl analog) undergo rapid hydrolysis that is not affected by age, weight, renal or hepatic func-
tion.]
Anesthesia 1099
Nonopioid analgesics
SS Ketamine—Previously described
SS Ketorolac—Acts by inhibiting both COX-1 and COX-2.
IV Agents (Causing Neuromuscular Block)
SS Acts on postsynaptic receptors in the neuromuscular junction to antogonize the effects acetylcholine.
SS 2 types of neuromuscular blockers—
zz Nondepolarizing agents
Vecuronium
Pancuronium
Atracuronium.
zz Depolarizing agents
Succinylcholine.
SS Succinylcholine—
zz Rapid acting (< 60 seconds) depolarizing neuromuscular blocker. Also rapid offset (5–8 minutes).
zz Rapidly hydrolyzed by plasma cholinesterase.
zz Causes hyperkalemia. Patient with severe burn

or trauma may develop arrhythmia or cardiac
arrest.
zz Can cause increase in intraocular, intracranial
and intragastric pressures.
zz Malignant hyperthemia—A rare but fatal
complication.
SS Vecuronium—
zz Intermediate duration (<1 hour), nondepolar-

izing neuromuscular blocker.
zz Metabolized by both kidneys and liver.
SS Pancuronium—
zz Longest-acting (> 1 hour) nondepolarizing

blocker.
zz Excreted by kidneys in unchanged form.
SS Atracurium—
zz Intermediate-acting (<1 hour) nondepolarizing

blocker.
zz Metabolized in plasma by a unique method—
Hofmann elimination.
SS Reversal of neuromuscular blockade—
Neostigmine, pyridostigmine inhibit the
acetylcholinestease, there by increased circulatory
level of acetylcholine. So, more acetylcholine
is available for competition for postsynaptic
receptors.
Inhalational Agents
zz It produce three aspects of GA—unconsciousness, analgesia and muscle relaxation.

zz Acts on GABAA receptor–chloride channel, resulting in inhibition of synaptic transmission.
zz Inhalational agents are:
Nitrous oxide
Halothane
Sevoflurane
Desflurane
Isoflurane.
zz To provide adequate anesthesia, the anesthetic agent requires transfer from the alveolar air to the blood and
from the blood to the brain.
zz Minimum alveolar concentration (MAC) is the measure of potency of a inhalational anesthetic.

Higher the MAC, less potent the agent is.
zz Nitrous oxide (MAC 105%)—
A weak anesthetic agent.
Most rapid onset and offset.
When combined with other inhalational agents, it reduces the required dose and side effects of other
inhalational agents.
It readily diffuses into any closed gas space, thereby increases the presence of the space.
[It should not be administered in intestinal obstruction or pneumothorax.]

zz Halothane (MAC 0.75%)— Rapid onset of action.
It is a preferable induction agent in pediatric patients due to less irritating effect on airway
A preferable agent for asthmatics due to its bronchial smooth muscle relaxing properties.
[Increased chance of ventricular arrhythmia.]

It increases intracranial pressure. So, it should be used cautiously in patients with brain lesions.
zz Isoflurane (MAC 1.15%)—
Less cardiovascular depression
Low rate of metabolism.
zz Sevoflurane (MAC 1.17%)
Pleasant smell, therefore ideal for mask induction
Decreased tissue and blood solubility, therefore rapid induction and recovery.
zz Desflurane (MAC 6%)
Rapid induction and recovery
Causes increase in cerebral blood flow. So it is better avoided in patients with intracranial lesion
Causes upper airway irritation (cough, bronchospasm).
[So it is not used as an induction agent, used for maintenance of anesthesia.]

Anesthesia 1101
Preoperative Evaluation
SS History taking—
zz Detailed medical history also includes any history of exposure to anesthesia
zz History of atopy (atopy to food, medications, etc.)
zz History of medication (e.g. anticoagulants, antihypertensives, antidiabetics).
SS Physical examination— Examination of CNS, CVS and respiratory system.
SS Investigations—
zz Specific investigations
zz Routine investigations.
SS Risk assessment—
zz ASA physical status scale is to assess the risk of an individual during anesthesia and surgery.
Scale: P1 P6
P1 — Normal healthy patient
P2 — Patient with mild systemic disease
P3 — Patient with severe systemic disease
P4 — Patient with severe systemic disease that is a constant threat to life
P5 — Moribund patient who is not expected to survive without the operation
P6 — A declared braindead paitent whose organs are being removed for donor purposes.
SS Assessment of the airway—
zz Is important to identify the chance of difficulty during conventional endotracheal intubation.
zz Mallampati classification is based on how much posterior pharynx is visualized after maximal mouth opening
and tongue protrusion in sitting position.
SS Assessment of patient with comorbid illness—

zz Ischemic heart disease— Assessment of severity and functional limitations induced by the disease.
zz Pulmonary disease— Assessment is essential for thoracic and upper abdominal surgical procedures.
zz Renal disease— Patient with chronic renal disease needs vigorous attention to intraoperative fluid management
and control of ventilation.
Doses of anesthetic agents, particularly opioids and neuromuscular blockers must be reduced.
zz Hepatobiliary disease—Selection of a proper inhalational anesthetic is crucial. Halothane has the greatest
potential and desflurane has the least potential for hepatotoxicity.
Selection of neuromuscular blocker (e.g. vecuronium, pancuronium) is better avoided in impaired hepatic
funtion.
zz Metabolic disease—The three metabolic diseases, diabetes mellitus, hypothyroidism and obesity are mostly
associated with increased risk.
zz CNS disease— Propofol decreases cerebral blood flow, intracranial pressure.
zz Etomidate also decreases cerebral blood flow and ICP. It has also excitatory effect on the brain.
Intraoperative Management
1. Induction of anesthesia—
zz Most vital phase of anesthesia, as most of the catastrophes occur during this phase.
zz During induction, patient becomes unconscious and apneic, myocardial function is being depressed.
2.
Anesthesia 1103
3. Neuromuscular blockade—
zz It optimizes ventilatory support
zz It relaxes the muscles, thereby provides satisfactory working conditions
zz Done by nondepolarizing neuromuscular blockers.
4. Maintenance of anesthesia—
zz With the help of both inhalational as well as intravenous agents.
5. Fluid therapy—Is to replace the perioperative fluid losses.
6. Recovery from anesthesia—
zz The goal of smooth recovery is to achieve a smooth and rapid return to consciousness, stable hemodynamics,
return of protective airway reflexes and continued analgesia.
7. Postanesthesia care unit (PACU)—
zz All patients awakening from anesthesia are to be observed in PACU, to detect immediate postoperative nausea
and vomiting, hypotension requiring pharmacologic support, abnormal bleeding, dysrhythmia.
zz Once patient become oriented, hemodynamically stable and without signs of anesthetic or surgical
complications, patient can be shifted to the ward.
Complications of General Anesthesia
SS Malignant hyperthermia
SS Postoperativenausea and vomiting
SS Hypothermia
SS Nerve injury
SS Laryngospasm.
Chapter 32
Instrument
Important Topics
zzParts of an Instrument
zzInstruments used for Antiseptic Dressing and Draping
zzInstruments used for Fixation
zzInstruments used for Skin Incision
zzInstruments used for Hemostasis
zzInstruments used for Holding Tissues
zzInstruments used for Suturing
zzOther Methods of Skin Closure
zzRetractor
zzScissors
zzSuture Material
‘Medicine rests upon four pillars — philosophy, astronomy, alchemy, and ethics ……………….. , the fourth shows
the physician those virtues which must stay with him up until his death, and it should support and complete the three other
pillars.’
Paracelsus (C. 1493–1541)
Swiss Doctor and Chemist
Surgical Instruments
Parts of an Instrument
SS Blades—A pair of blades

SS Joint
zz Box joint— Slot in each shaft, fits with each other

zz Pivot joint— Two shafts are joined by a screw at one point.
SS Shaft—A pair of shafts
SS Catch or ratchet
SS Finger bow—Two finger bows.
Instruments Used for Antiseptic Dressing and Draping
Rampley's Swab Holding Forceps
SS Blades are oval, fenestrated and serrations on the inner aspect

SS Uses—
zz Antiseptic dressing prior to any surgical procedure [antiseptic most commonly used is povidone–iodine (both
antibacterial and antifungal)].
[Antiseptic dressing is essential to remove the transient and resident bacterial flora of skin]
zz During blunt dissection of Calot's triangle in open cholecystectomy.
zz During retroperitoneal dissection-to strip off the peritoneum.
zz For removal of laminated membrane and daughter cyst of hydatid cyst.
zz May be used as a substitute of Moynihan's cholecystectomy forceps.
SS Sterilization—Autoclaving.
Instrument 1107
Instruments Used for Fixation
Towel Clip
Towel Clip
Doyen's cross action

Corner Clip
type
SS Uses—
zz For fixing the draping sheets

zz For fixing the diathermy cables, suction tubes and other cables
zz May be used as a tongue holding forceps.
Instruments Used for Giving Incision Over the Skin

Bard Parkers Handle
SS Ithas a slot on one end for attachment of the surgical blade

SS Various sizes are available—
zz No. 3 and No. 4 are commonly used
zz Others are No. 5 and No. 7.
Surgical Blades (Scalpel Blade)
'Scalpel' arises from Latin word 'Scalpere'— to cut.

SS Blades are of varying sizes and slots, for attachment with the BP handles
of different sizes.
SS Uses—
zz To make skin incisions in all operations.
zz To make skin flaps in mastectomy, thyroidectomy, neck dissection.
zz For incision and drainage of abscess (by blade number 11— also
called 'stab knife').
zz Scalpel has 2 parts— a handle and a blade (disposable).
Pen holding fashion
Instruments Used for Hemostasis

Instrument 1109
Spencer Well's Hemostatic Forceps
Medium size curved Spencer Well's hemostatic forceps
SS Useof Spencer Well's hemostatic forceps—

zz Used to hold the bleeding points
zz Used to hold the vessel and ligate it
zz To hold the cut margins of rectus sheath, aponeurosis and peritoneum
zz For blunt dissection during excision of lipoma, sebaceous cyst
zz May be used in drainage of abscess as an after native to sinus forceps
zz To hold the end of a ligature during anastomosis, sheath or skin closure.
Use of Spencer Well's hemostatic forceps

SS Steritization—Autoclaving
Instrument 1111
Mosquito Hemostatic Forceps
SS Lighter and smaller than Spencer Well's hemostatic forceps.

SS 2 varieties:
zz Straight
zz Curved.
SS Uses—
zz In appendicectomy, mesoappendix is punctured by mosquito forceps for tying the appendicular artery
zz In circumcision
zz In cleft lip operation
zz For holding delicate vessels.
Use of mosquito forceps
Kocher's Hemostatic Forceps

SS Uses—
zz To hold the bleeding vessels in palm, sole and scalp (vessels tend to retract)
zz To crush the base of appendix
zz In subtotal thyroidectomy.
Instruments Used for Holding Tissues
SS The function of these instruments are to hold the tissues firmly with minimal damage
SS Varieties—
zz Allis' tissue forceps
zz Babcock's tissue forceps
zz Lane's tissue forceps.
Allis' Tissue Forceps

SS Uses—
zz During mastectomy or thyroidectomy, to raise the skin flaps

zz During midline incision, the skin margins are retracted by it when linea alba is incised
zz During closing the midline incision, the linea alba is held by this instrument
zz During excision of lipoma, sebaceous cyst, the skin margins are held by it
zz During creation of stoma, the skin is grasped by it.
Use of Allis' tissue forceps

Instrument 1113
Babcock's Tissue Forceps
SS No teeth in blades, so minimal trauma to the tissues

SS Fenestration in the blade allows tissues to be accomodated
SS Uses—
zz In appendectomy
zz During resection anastomosis
zz During gastrectomy
zz During open prostatectomy or suprapubic cystostomy.
Use of Babcock's tissue forceps
Lanes' Tissue Forceps
SS At the tip of the blade, tooth in one blade and grove in other blade
SS Uses—
zz As an alternative to towel clip
zz During mastectomy, to hold the brest tissue when dissecting it

from the pectoral muscle.
Dissecting forceps
Toothed dissecting—Grip-
Plain dissecting
ping is better due to tooth
SS Use of plain dissecting forceps—

zz During hernia repair, to dissect the sac from cord structures as well as during ligation of the sac
zz During resection anastomosis or in gastrojejunostomy, to hold the gut margins during suturing
zz During choledocholithotomy, to hold the cut margins of common bile duct for closure.
SS Use of toothed dissecting forceps—
zz To hold the skin margins during skin closure
zz Suturing of aponeurosis in appendectomy
zz During closure of midline incision, to hold the linea alba.
Use of toothed dissecting forceps

Instrument 1115
Instruments Used for Suturing
Needle Holder
Medium sized curved needle holder
Use of needle holder

SS How to hold the needle by needle holder?
SS Movement of the hand during suturing

Start with hand fully pronated
⇓
Progressive supination of the hand
⇓
Full supination
SS Use— To hold the needle for suturing.
Hand fully pronated Progressive supination of hand
Hand fully supinated

Instrument 1117
Needle
SS Parts of a needle—(1) Eye (2) Body (3) Point (extends from the tip to the maximum cross-sectional area of the
body).
SS Needle performance is determined by—(1) Sharpness (2) Strength (3) Surface finish (4) Temper (5) Rigidity (6)
Malleability (7) Ductility.
SS Round bodied needle—
Use— For suturing delicate tissues like intestines, vessels
SS Cutting needle—
Use— For suturing tough structures, e.g. fascia, aponeurosis and skin
SS Reverse cutting needle—
Use— During closure of midline in mass closure technique
SS Taper cut needle—
Use— Particularly used in vascular surgery
SS Eyed and swaged (atraumatic) needle—
SS Needle with different curvature—
Sterilization of eyed needle —Lysol

Sterilization of eyeless needle—Packed after sterilization (Gamma radiation)
Instrument 1119
Other Methods of Skin Closure
1. By skin stapler—
zz These staples can close the skin with satisfactory wound edge eversion without strangulation of tissue.
zz Crosshatch scarring is minimal.
zz Contaminated wounds closed with staples have lower wound infection rate than closure with sutures.
zz No risk of needle prick.
zz Specially designed staple extractor is available, but hemostatic forceps can be used.
2. Topical tissue adhesives—

zz Chemically, it is 2-Octyl cyanoacrylate.
zz In comparison to sutures, staples, steristrips; adhesives provide faster closure.
zz Infection rate, dehiscence rate, cosmetic outcome is almost equivalent to other modes of skin closure.
zz Adhesives are contraindicated in—
Contaminated wounds
Deep wounds
Wounds under tension
Mucous membranes.
zz Particularly useful in superficial wounds or wounds in which deep dermis is closed with sutures.
3. Steristrips—
zz Steristrips maintain integrity of the epidermis.
zz This technique cannot be used in—
Moist areas
Wound under tension.
zz Wound edge approximation is satisfactory, if it is supported by sutures.
zz Blistering at the tap margin may develop if there is wound edema.
Retractor
SS Use of Langenbeck retractor—

zz During appendicectomy, the abdominal wall is retracted
to visualize the cecum.
zz During modified radical mastectomy, pectoralis major and
minor is retracted for proper axillary dissection.
zz During hernia repair, retraction is required for repair of the
posterior wall of inguinal canal.
zz During neck dissection, retraction of sternocleidomastoid
is required for adequate exposure.
SS Sterilization—Autoclaving
SS Use of Czerney's retractor—
zz Same as Langenbach's retractor.
SS Use of Deaver's retractor—
zz During open cholecystectomy, to retract the right lobe of

liver. From left to right: Deaver's refractor (1) , Czerney's re-
tractor (2), Double hook retractor (3, 4),Langenbeck
zz During right hemicolectomy, to retract the abdominal wall retractor (5)
laterally, during mobilization of colon.
zz During APR or anterior resection, to retract the urinary
bladder or pelvis during pelvic dissection.
SS Use of hook retractor—
zz To retract the skin flap during excision of sebaceous cyst,

lipoma.
zz To retract the skin and isthmus of thyroid during
tracheostomy.
SS Use of self retaining retractor—
zz During truncal vagotomy and gastrectomy
zz During hepatic resection
zz During APR and anterior resection of rectum.
Sterilization of retractors—Autoclaving.
Use of Deaver's retractor
Self-retaining retractor
Instrument 1121
Scissors
Scissors
Mayo's scissors Mcindoe scissors Metzenbaum scissors
SS Use of Mayo's scissors—

zz To cut extenal oblique aponeurosis, rectus sheath.
zz To cut sutures.
SS Use of Mcindoe scissors—
zz To raise the skin flap during thyroidectomy and mastectomy.
zz To cut the cystic duct and artery during cholecystectomy,

to cut the splenic artery and vein during splenectomy.
SS Use of Metzenbaum scissors— same as Mcindoe scissors.
Sterilization—Lysol.
Use of Mayo's scissors
Moynihan's Cholecystectomy Forceps
SS Use— During open cholecystectomy, for traction of

gallbladder.
Desjardin's Choledocholithotomy Forceps
SS Use—
zz During choledocholithotomy, to remove the

stones from the common bile duct.
zz During laparoscopic cholecystectomy, while
extracting the gall bladder through umbilical
or epigastric part, the stones are removed
from the gallbladdder for easy delivery of the
gallbladder specimen from port site.
Right Angled Forceps
SS Use—
zz During Truncal vagotomy, to dissect the anterior and posterior

vagal trunk.
zz During open cholecystectomy, to dissect the cystic duct and
artery.
zz During thyroidectomy, to dissect the middle thyroid vein,
superior thyroid pedicle and Inferior thyroid pedicle.
zz During gastrectomy, to dissect the vascular pedictes.
Use of right angled forceps

Instrument 1123
T-tube
SS Made up of PVC/Latex/Silastic
SS Uses—During open choledocholithotomy, to place it as a stent as well as drainage.
SS Sterilization—Supplied in pack (Sterilized pack).
Use of gastric occlusion clamp

Simple Rubber Catheter
SS Made of India rubber

SS Variety of sizes— No. 8, 10, etc.
No. of catheter
SS The diameter of catheter = +1
2
(in mm)
10
Diameter of no 10 catheter = + 1 = 6 mm
2
SS Uses—
zz To differentiate between anuria and retention of urine
zz In acute retention of urine (particularly in females)
zz For performing cystography
zz May be used as a substitute of umbilical tape to sling the esophagus during truncal vagotomy.
zz Used to flush the bile duct during open choledocholithotomy.
Foley's Self Retaining Catheter
SS 2-way catheter
SS 3-way catheter.
SS Size of catheter–in french (Fr)
(circumference of catheter)
French scale
Diameter of catheter =
3
(in mm)
16
16 Fr = = 5.33 mm
3
SS Balloon capacity varies according to size of catheter
In 2-way catheter In 3-way catheter, the third one is for irrigation

One for drainage of One for inflation of
urine balloon
SS Uses of 2-way catheter—
zz In retention of urine, for relief the retention
zz In postoperative patient, for proper monitoring of urine output
zz In suprapubic cystostomy
zz In feeding jejunostomy, as feeding tube.
SS Use of 3-way catheter—
zz For bladder irrigation in patient with hematuria
zz After open prostatectomy.
SS Sterilization—by gamma irradiation.

Instrument 1125
Malaecot's Catheter
SS Ithas the self retaining property by its winged end

SS Uses—Can be used as a suprapubic cystostomy catheter
SS Uses—
zz For dilatation in urethral stricture

zz For dilatation prior to cystoscopy.
Rectal Speculum (Proctoscope)
SS Two part
zz Speculum
zz Obturator.
SS Uses—
zz Diagnosis of anorectal pathologies (e.g. hemorrhoids,

carcinoma rectum, internal opening of fistula-in-
ano).
zz For sclerosant injection in hemorrhoids (in 2nd
degree).
zz To take biopsy from rectal and anal canal growth.
Suture Material
Properties of suture material
1. Tensile strength—The force that the suture will withstand before it breaks.
2. Tissue absorption—A nonabsorbable suture is resistant to tissue absorption, whereas an absorbable suture is
absorbed in tissue and elicit a tissue reaction.
3. Tissue reactivity—Suture materials are foreign to tissue and elicit a tissue reaction. An ideal suture stimulates
minimal tissue reaction.
4. Memory—Capacity of a suture to remain free of curling. Surgeons face difficulty with a suture with significant
memory, needs more knots (polypropylene, nylon have significant memory).
Instrument 1127
5. Knot security—Is the quality of a suture material that allows it to be tied securely with a minimum number of
throws per knot.
Suture with smooth surface and significant memory has less knot security and so extra throws are needed.
6. Elasticity—Is the ability of a suture material to return to its original length after stretching.
A highly elastic suture material stretches with wound edema and return to its original form when edema subsides.
7. Cross sectional diameter—When suture size is selected, the diameter should be the minimum necessary for
approximation of wound edges.
1–0 is larger than 5–0 and so on.
8. Color—Different suture material have different color; silk is black, polypopylene is blue, vicryl is violet, etc.
9. Capillarity—Is an inherent property of polyfilament sutures (due to its interstitial space).
A braided nylon could transport upto three times as many microorganisms as monofilament nylon.
10. Physical configuration—Suture material is composed of either single filament (monofilament) or multiple filament
(polyfilament).
Monofilament sutures have some extra advantages—(a) more tensile strength (b) low tissue drag (c) low propensity
to harbor microorganisms.
SS Advantages and disadvantages of monofilament suture—

zz Chance of bacterial infection is less
zz Knot tying is more difficult
zz Higher tensile strength
zz Low tissue drag.
SS Advantages and disadvantages of polyfilament suture—
zz Knot tying is easier
zz Bacteria may lodge in the crevices of sutures, thereby increased chance of bacterial infection in the ground.
SS Principles of choicing a suture material—
zz Slowly healing tissues, e.g. skin, tendon must be sutured with nonabsorbable suture.
zz Rapidly healing tissues, e.g. intestines, urinary bladder must be sutured with absorbable suture.
zz In presence of contamination, monofilament suture is preferable.
zz Nonabsorbable suture should not be used in suturing duct, e.g. common bile duct, as this suture acts as a nidus
for precipitating stone formation.
Catgut
SS Natural, absorbable, monofilament suture.

SS Derived from the submucosa of sheep's intestine, or serosal layer of small intestine of cattle.
SS Two types—
zz Plain catgut
zz Chromic catgut (is tanned with chromic salts).
SS Chromic catgut is absorbed in tissues in 21 days.
SS Uses—
zz Mesoappendix is tied with 1–0 chromic catgut during appendicectomy
zz In herniotomy, the sac is tied with 2–0 chromic atraumatic catgut
zz In circumcision with 3–0 atraumatic catgut.
SS Sterilization—by gamma irradiation (in sterilized pack).

Polyglactic 910 (Vicryl rapide)
SS Synthetic, absorbable, polyfilament suture

SS It is derived from polyglactin 910
SS 50% of tensile strength is retained at 5 days, tensile strength is 0% at 2 weeks
SS It gets absorbed in 7–14 days.
Polyglactin 910 (Vicryl)
SS Synthetic, delayed absorbable, polyfilament suture.

SS It gets absorbed in 90 days.
SS It retain 65% of its tensile strength at 2 weeks and 40% at 3

weeks.
SS Available in clear undyed or violet–dyed form.
SS Used—
zz For closure of right or left subcostal incision (with 1–0

vicryl).
zz In biliary-enteric anastomosis (with 3–0 suture).
zz In small and large gut anastomosis.
SS Sterilization—by gamma irradiation (in sterilized pack).
Polydioxanone suture (PDS)
SS Synthetic, delayed absorbable, monofilament suture.

SS PDS is absorbed in tissues within 6–7 months.
SS Retain 74% of its tensile strength after 2 weeks, 50% after 4 weeks, 25% after 6 weeks.
SS Its tissue reactivity is low, maintains its integrity in the presence of bacterial infection.
SS Uses—
zz Same as polyglactin suture
zz Is used to close the midline or para median incisions.
Poliglecaprone (monocryl)
SS Synthetic, delayed absorbable, monofilament suture.

SS It has significant initial tensile strength.
SS Dyed monocryl retains 30–40% of its tensile strength at 2 weeks.
SS Monocryl is absorbed in 90–120 days.
SS Use—
zz Subcuticular skin closure.

Instrument 1129
Silk
SS Natural, nonabsorbable, polyfilament suture,

extruded by silk worm larvae.
SS Available in various forms:
zz Only silk in sterile pack (sutupak)
zz Only silk in reel (unsterilized)
zz Silk mounted on a atraumatic needle – in

sterile pack (mersilk).
SS Knot tying is easy and it knots very securely.
SS As it is a polyfilament suture, it harbor microor-

ganism.
SS Uses—
zz To ligate the cystic duct and artery during open cholecystectomy
zz To ligate the appendicular artery during appendicectomy
zz To ligate the vessels during resection anastomosis and colectomy
zz For skin closure
zz Mersilk is used for suturing seromuscular layer in gut anastomosis.
Polypropylene (prolene)
SS Synthetic, nonabsorbable, monofilament suture, made by

catalytic polymerization of propylene.
SS It is inert and low reactivity to tissues, high tensile strength,
significant memory.
SS Extremely smooth surface and less knot security. Extra
throws are needed during knotting.
SS High plasticity and ability to accomodate wound edema.
SS Uses—
zz For herniorrhapy
zz For closure of midline incision
zz For repair of nerve and tendon injuries
zz For anatomical repair of epigastric hernia, umbilical or

incisional hernia.
Monofilament polyamide (ethilon)
SS Synthetic, nonabsorbable, monofilament suture

SS It is inert and low reactivity to tissues
SS Uses—For closure of skin incision.

Tracheostomy Tube
SS Differentvarieties:
zz Metallic tracheostomy tube
zz Cuffed portex tracheostomy tube.
SS Two parts
zz Inner tube
zz Outer tube.
SS Uses—
zz Emergency indications
Acute laryngeal edema
Airway obstruction following RTA
Ludwig's angina causing laryngeal obstruction
Foreign body in larynx
Cut throat injury
Bilateral recurrent laryngeal nerve palsy.
zz Elective indications
Following laryngectomy
Following respiratory paralysis in GB syndrome, bulbar palsy.
IV Cannula
SS Consists of plastic cannula and metal needle

SS Differentsizes of cannula—color codes according to the size:
Green— 18 gauge Grey 16 gauge
Pink— 20 gauge Brown 14 gauge.
Blue— 22 gauge
Yellow— 24 gauge
SS Uses—
zz For intravenous fluid infusion
zz For blood transfusion.

Instrument 1131
Ryle's Tube
SS One meter long plastic tube with lead shots (radiopaque) near the rounded tip of the tube
SS A number of side holes near the tip of the tube
SS The body of the tube has 4 black circular markings:
zz First mark—40 cm from the tip–when tube is inserted upto this mark, the tip of the tube lies at G-E junction.
zz Second mark— 50 cm from the tip–when tube is inserted upto this mark, the tip of the tube lies at body of the
stomach.
zz Third mark— 60 cm from the tip–when tube is inserted upto this mark, the tip of the tube lies at the pylorus of
the stomach.
zz Fourth mark— 70 cm from the tip–when tube is inserted upto this mark, the tip of the tube lies at the duodenum.
SS Uses—
zz For nasogastric suction
zz For feeding through the tube.

Index
Page number followed by f refer to figure
A Alvarado scoring 384

Anal cushion 413
Anesthesia 1090
Abdominal wall 220
epidural 1096
acquired abnormalities
general 1097
diastasis recti 227
complications 1103
rectus sheath hematoma 227
intraoperative management 1102
congenital defect
local 1092
exomphalos 220
preoperative evaluation 1101
gastroschisis 221
spinal 1095
infantile umbilical hernia 222
Anomalous anatomy 96
desmoid tumor 228
Anterior cord syndrome 609
omphalomesenteric duct persists 223
Appendix 376
urachus 226
acute appendicitis 378
Acidosis and alkalosis
clinical presentation 380
metabolic acidosis 25
investigations 381
metabolic alkalosis 26
tratment 385
respiratory acidosis 26
appendicular lump 390
respiratory alkalosis 27
neoplasm
Acquired hemorrhagic disorders
carcinoid tumor 392
anticoagulant drugs 31
liver diseases 32
thrombocytopenia 32 B
vitamin k deficiency 31
Acute acalculous cholecystitis Balloon tamponade 167
treatment 58 Bascom’s theory 420
Acute cholangitis 67 BCT 464
Acute cholecystitis 44 Biliary dyskinesia
clinical presentation 45 treatment 59
investigations 46 Birads 460
pathophysiology 45 Bladder injuries 659
treatment 47 Body fluids 15
Adenoma-carcinoma sequence 364 hypovolemia 17
Adrenal gland 531 input-output 16
adrenal crisis 545 volume overload 18
adrenal insufficiency 544 Borrmann’s classification system 269
adrenogenital syndrome 543 Brown-Séquard syndrome 609
anatomical variations 531 Burn 674
Cushing syndrome 537 chemical 692
clinical presentation 540 different mechanisms of burn injury 676
investigations 541 electric 689
treatment 542 late complications 692
types 537 management 677
hyperaldosteronism 534 systemic changes 688
microscopic features 533
pheochromocytoma 546
clinical presentation 547 C
etiology 547
investigations 548 Calcium oxalate stone 952
treatment 549 Cauda equina syndrome 610
CEAP classification 756 ANDI 449
Central cord syndrome 609 breast carcinoma 450
Chest drain 616 clinical presentation 453
Cholangiocarcinoma 86 diagnosis 454
clinical presentation 88 pathology 450
investigations 88 prognostic factors 472
pathology 87 risk factors 450
risk factor 87 spread 453
Cholecystoses treatment 462
cholesterol polyposis 57 breast lump 441
strawberry gallbladder 57 breast cyst 444
Choledochal cyst 69 fat necrosis 445
clinical presentation 70 fibroadenoma 442
investigations 71 galactocele 445
treatment 72 phyllodes tumor 443
Choledocholithiasis 60 sclerosing adenosis 445
clinical features 61 duct ectasia 437
investigations 62 gynecomastia 445
primary bile duct stone 60 lactational breast abscess 434
secondary bile duct stone 60 mastalgia
treatment 64 cyclical 448
Chronic cholecystitis noncyclical 449
clinical presentation 49 Mondor’s disease 441
pathophysiology 49 nipple discharge 447
treatment 50 nonlactational breast abscess 437
Chvostek’s sign 530 periductal mastitis 437
Cleft lip 1085 Diseases of the esophagus 832
classification 1086 achalasia (faliure to relax) 841
etiology 1085 Barrett esophagus 855
treatment 1088 Boerhaave’s syndrome 853
Cleft palate cancer of esophagus 857
classification 1088 classification 858
different techniques of repair 1089 clinical presentation 858
Closed loop obstruction 297 investigations 858
Congenital hemorrhagic disorders pathology 857
hemophilia 31 pretreatment staging 859
B 31 risk factors 857
von Willebrand's disease 31 treatment 859
diffuse esophageal spasm 845
epiphrenic diverticulum 848
D esophageal perforation 849
gastroesophageal reflux disease (GERD) 837
Diagnostic peritoneal lavage 627 hiatus hernia 834
Diseases of the arteries 696 Mallory-Weiss tear 853
aneurysmal vascular disease 724 midesophageal (parabronchial) diverticula 848
abdominal aortic aneurysms 726 nutcracker esophagus 846
femoral artery aneurysm 737 pharyngoesophageal (Zenker’s) diverticulum 846
iliac artery aneurysm 736 stricture of esophagus 854
popliteal artery aneurysm 737 vigorous achalasia 845
splanchnic artery aneurysms 737 Diseases of the intestine 294
upper extremity aneurysms 737 cancer of colon 361
arterial occlusive diseases 696 clinical presentation 367
mesenteric arterial insufficiency 721 investigations 367
peripheral arterial occlusive 697 risk factors 362
renovascular occlusive 718 spread of colon cancer 366
diseases of thoracic aorta 738 treatment 369
aortic dissection 742 cecal volvulus
thoracic aortic aneurysm 739 management 343
vascular trauma 746 colorectal polyp 353
Diseases of the breast 434 familial juvenile 355
Index 1135
hyperplastic 353 infections 963
inflammatory 355 acute pyelonephritis 964
juvenile 354 chronic pyelonephritis 967
tubular adenoma 356 perinephric abscess 969
villous adenoma 357 pyonephrosis 970
Crohn’s disease 309 renal abscess or carbuncle 971
clinical presentation 312 kidney tumors 975
investigations 314 angiomyolipoma 976
macroscopic and microscopic features 310 oncocytoma 976
treatment 314 renal cell carcinoma 976
diverticular disease of colon 333 Wilms’ tumor 982
clinical presentation 334 other malformations 946
management 334 renal stone 950
diverticulitis 335 tuberculosis of kidney 972
complicated 336 urinary symptoms 931
investigations 335 Diseases of the liver 122
treatment 336 amebic liver abscess 131
duodenal diverticula 325 clinical presentation 133
familial adenomatous polyposis (FAP) 359 diagnosis 133
extracolonic manifestations 360 management 134
screening 360 congenital liver cyst 148
treatment 361 clinical presentation 149
variants 361 investigation 149
ileosigmoid knotting 344 treatment 149
intestinal obstruction Couinaud system of segmental nomenclature 122
small intestinal obstruction 294 cystadenoma 151
intestinal tuberculosis 321 focal nodular hyperplasia 152
intussusception 306 hemangioma 153
clinical presentation 307 hepatocellular carcinoma 153
investigations 307 clinical presentation 154
treatment 308 diagnosis 156
jejunal and ileal diverticula 324 treatment 157
large bowel obstruction 344 hydatid cyst 136
Meckel’s diverticulum clinical presentation 138
clinical presentation 326 diagnosis 139
diagnosis 328 Gharbi classification 140
treatment 329 management 141
neoplasm of small intestine WHO classification of hydatid cyst 140
benign 330 liver cell adenoma 152
malignant 330 liver metastases 161
metastatic tumor 331 polycystic liver disease associated with polycystic kidney
short bowel syndrome disease
causes 331 clinical presentation 150
clinical presentation 332 investigations 150
treatment 332 treatment 151
sigmoid volvulus 340 portal hypertension 162
clinical presentation 341 Budd-Chiari syndrome 164
investigations 341 cirrhosis 165
management 341 extrahepatic portal vein obstruction 164
predisposing factors 340 noncirrhotic portal 164
typhoid enteritis 320 pyogenic abscess of liver 125
ulcerative colitis 345 clinical presentation 128
clinical presentation 347 investigation 128
investigations 349 treatment 129
macroscopic appearance 346 treatment 162
treatment 350 Diseases of the pancreas
Diseases of the kidney 931 acute pancreatitis 175
congenital malformations 936 assessment of severity 178
cystic disease 943 clinical presentation 176
hydronephrosis 948 complications 181
diagnosis 176 gastric lymphoma 283
management 179 gastric outlet obstruction
chronic pancreatitis 187 causes 263
clinical presentation 188 clinical presentation 263
diagnosis 190 diagnosis 264
treatment 191 investigations 264
intraductal papillary mucinous tumor 197 treatment 264
gastric varices 287
mucinous cystadenoma 196
gastric volvulus 285
pancreatic carcinoma 199
gastritis
clinical presentation 200 erosive 266
investigations 201 reflux 266
pathology 199 stress 266
treatment 204 type a 266
serous cystadenoma 198 type b 266
Diseases of the prostate gastrointestinal stromal tumor 280
benign prostatic hyperplasia 1000 clinical presentation 281
Diseases of the skin and its adnexa 881 immunology 281
benign pigmented lesions 898 investigations 281
benign tumors 890 prognostic factors 282
elephantiasis neurofibromatosis 895 treatment 283
lipoma 891 malignant neoplasms 267
multiple neurofibromatosis 894 clinical presentation 273
investigations 274
neurofibroma 893
risk factors 268
papilloma 890
treatment 275
plexiform neurofibromatosis 894 Mallory-Weiss tear 284
cystic lesions of the skin 881 Ménètrier’s disease 284
dermoid cyst 882 peptic ulcer disease 243
sebaceous cyst 881 clinical presentations 247
ganglion 883 investigations 248
malignant lesions pathophysiology 246
basal cell carcinoma 901 treatment 251
cutaneous melanoma 906 perforation
squamous cell carcinoma 903 diagnosis 258
other malignancies of the skin treatment 258
angiosarcoma 910 postvagotomy syndromes 287
cutaneous metastases 911 early dumping 289
Kaposi’s sarcoma 910 late dumping 290
Diseases of the testes 815
lymphangiosarcoma 911
chylocele 828
premalignant lesions
Fournier's gangrene 829
Bowen’s disease 900 hematocele 828
erythroplasia of Queyrat 900 hydrocele 825
solar keratosis 900 primary vaginal 826
xeroderma pigmentosum 901 secondary 828
skin infection 895 other scrotal swellings 828
carbuncle 896 paraphimosis 831
furuncle (boil) 895 phimosis 830
hidradenitis suppurativa 897 pyocele 828
impetigo 896 sebaceous cyst in scrotum 829
necrotizing fasciitis (Fournier’s gangrene) 897 torsion of the testis 822
vascular lesions of the skin undescended testis 815
hemangiomas 884 complications 818
other vascular lesions 888 factors responsible for testicular descent 817
Fowler-Stephens orchiopexy 821
vascular malformations 886
standard orchiopexy (open approach) 821
Diseases of the stomach 243
varicocele 823
bezoars 286 Diseases of the thyroid gland 475
bleeding peptic ulcer 262 cretinism 476
management 262 hypothyroidism 475
Dieulafoy’s gastric 285 neoplasm of thyroid 496
Index 1137
anaplastic thyroid carcinoma 507 Fibrolamellar HCC 154
follicular adenoma 496 Fistula 927
follicular carcinoma 503 causes of persistence of sinus or fistula 928
medullary carcinoma of thyroid 505 Flail chest 575
papillary thyroid carcinoma 500
pathogenesis of primary thyroid malignancy 498
staging system 499
G
types of primary thyroid malignancy 498
nontoxic goiter Gallbladder carcinoma 78
nontoxic diffuse (simple goiter) 490
investigations 80
nontoxic multinodular goiter 490
pathology 79
surgical approaches to thyroid 509
risk factors 78
thyroiditis
treatment 82
acute (suppurative) 491
Gallstone 41
chronic lymphocytic (Hashimoto) thyroiditis 494
in Ileus 55
Riedel’s 495
subacute 492 pathophysiology 55
thyrotoxicosis 478 treatment 56
Graves’ disease 479 pancreatitis
toxic adenoma 489 how it develops 51
toxic multinodular goiter 488 investigations 53
Diseases of ureter treatment 54
ureteral calculi 984 pathogenesis 42
urothelial tumors of renal pelvis and ureter 985 risk factors 41
Disorders of lymphatic system 765 varieties
acute lymphangitis 766 black pigment 41
lymphedema 766 brown pigment 41
tumors of the lymphatics 773 cholesterol 41
Diverticulitis 333 Goodsall’s rule 410
Diverticulosis 333
Dukes classification system 374
H
E Hemorrhage
management 32
Electrolyte imbalance 18 Hepatectomy 158
hypercalcemia 23 Hernia 774
hyperkalemia 21 anatomy of the groin 783
hypermagnesemia 25 epigastric 801
hypernatremia 19 fermoral 797
hypocalcemia 22 incisional 802
hypokalemia 20 inguinal 785
hypomagnesemia 24 sliding 795
hyponatremia 18 strangulated 795
Endocrine pancreas 553 interparietal 812
glucagonoma 559 Littre's 796
insulinoma 554 lumbar 811
multiple endocrine neoplasia (MEN) syndromes 560 Maydl's 796
type I 561 obturator 808
type II 562 perineal 809
somatostatinoma 559 sciatic 811
VIPoma 559 spigelian 810
Zollinger-Ellison syndrome 555 umbilical 799
Endoscopic therapeutic approaches to biliary system 98 Hinchey staging system 336
ESWL 957 H. pylori 243
F I
FAST 626 Incidentaloma 550
K sternomastoid tumor 1081

thyroglossal cyst 1082
Neoplasms of testis 1031
Karydakis’s explanation 421
Nerve injury 1054
classification of nerve injuries 1056
L axonotmesis 1057
neuropraxia 1057
Lauren classification system 269 neurotmesis 1058
Linitis plastica 270 principles of nerve repair 1059
Liver transplantation 159 Nigro regime 431
M O
Mammography 459 Ogilvie’s syndrome 345
Massive hemothorax 576 Omentum
Ménètrier’s disease 267 omental cyst 235
Mesentery omental graft and transpositions 236
acute mesenteric lymphadenitis 234 omental infarction 235
cyst 234 Open pneumothorax 575
malignancies 235 Organ of Zuckerkandl 546f
panniculitis 235 Ormond disease 238
Mesorectum 427
Minimally invasive surgery 1039 P
access 1042
extraperitoneal and subcutaneous 1044 PAIR 141, 142
hand-assisted laparoscopic 1045 Pancreaticoduodenectomy 204
laparoscopic 1042 Pantaloon hernia 796
advantages and disadvantages 1049 Parathyroid 516
complications 1050 hypoparathyroidism 529
contraindications 1050 primary 518
different minimal access techniques 1039 secondary 527
endoluminal endoscopy 1040 tertiary 528
extracavitary endoscopy 1039 Pediatric appendicitis score 384
laparoscopy 1039 Peritoneal cavity 229
thoracoscopy 1040 abdominal abscess 230
examples of laparoscopic procedures 1049 pelvic abscess 232
instrumentation 1045 malignant peritoneal mesothelioma 233
new techniques of minimally invasive surgery pseudomyxoma peritonei 233
NOTES 1050 Peutz-Jeghers syndrome 353
SILS 1051 Primary sclerosing cholangitis 77
physiology of pneumoperitoneum 1041 investigations 78
port placement 1045 Prostate 1010
robotic surgery 1051 carcinoma 1011
advantages 1053 prostatitis 1010
components of Da Vinci robotic system 1052 Pseudocyst 182
disadvantages 1053 Pugh’s modification of child’s grading 157
Myopectineal orifice of Fruchaud 783
R
N
Rectum and anal canal 393
Neck anorectal abscess
anatomy 1074 clinical presentation 404
swellings 1075 investigations 404
branchial cyst 1078 treatment 405
branchial fistula 1079 cancer of the anus 429
carotid body tumor 1080 clinical presentation 430
cystic hygroma 1081 risk factors 429
lymphadenopathy 1075 treatment 431
Index 1139
fissure-in-ano 400 accessory spleen 212
clinical presentation 401 anatomy 209
treatment 402 cyst and tumors 214
fistula-in-ano functions of spleen 211
classification 406 splenectomy 213, 215, 216
clinical presentation 407 postsplenectomy blood picture 217
investigation 409 prophylaxis 215
treatment 410 splenosis 212
hemorrhoids or piles 413 wandering spleen 212
clinical presentation 415 Strangulation obstruction 296
treatment 416 Struvite stone 953
types 414 Surgery of hand 1063
pilonidal sinus 420 infections in hand 1067
clinical presentation 421 injuries in hand 1069
treatment 421 Surgical approaches to gallbladder and biliary system 101
prolapse of the rectum 395 CBD stone (open approach) 115
clinical presentation 397 cholecystectomy 101
investigation 398 choledochoduodenostomy 117
treatment 398 laparoscopic management of CBD stones 112
rectal cancer 423
Roux-en-Y hepaticojejunostomy 118
why bile duct injury 107
preoperative staging 425
Surgical instruments 1106
spread 423
catheter 1123
treatment 425
Foley's self retaining 1124
solitary rectal ulcer syndrome 399
Malaecot's 1125
Recurrent pyogenic cholangitis (cholangiohepatitis) 76
simple rubber 1124
treatment 77
Renal injuries 654 Desjardin's choledocholithotomy forceps 1122
Retroperitoneum dissecting forceps 1114
abscess 236 instruments used for antiseptic dressing and draping
fibrosis 237 Rampley's swab holding forceps 1106
hematoma 236 instruments used for fixation
neoplasm 239 towel clip 1107
Richter’s hernia 796 instruments used for giving incision over the skin
Rule of ‘2’ 326 Bard-Parker's handle 1107
surgical blades (scalpel blade) 1108
instruments used for hemostasis 1108
S Kocher's hemostatic forceps 1111
mosquito hemostatic forceps 1111
Salivary gland pathologies Spencer Well's hemostatic forceps 1109
acute ascending bacterial sialadenitis 866 instruments used for holding tissues
autoimmune sialadenitis 867 Allis' tissue forceps 1112
chronic bacterial sialadenitis 867 Babcock's tissue forceps 1113
mucoceles 870 Lanes' tissue forceps 1113
salivary gland tumors 871 instruments used for suturing 1115
carcinoma of salivary gland 874 needle 1117
nonepithelial tumors 875 needle holder 1115
oncocytoma 874 IV cannula 1130
pleomorphic adenoma 873 Moynihan's cholecystectomy forceps 1121
Warthin’s tumor 874 occlusion clamp 1123
sialolithiasis 868 other methods of skin closure 1119
surgical procedures for salivary gland pathology parts of an instrument 1106
excision of sublingual gland 875 rectal speculum (proctoscope) 1126
superficial parotidectomy 877 retractor 1119
viral sialadenitis 866 right angled forceps 1122
Schatzki’s ring 854 Ryle's tube 1131
SEPS 764 scissors 1121
Seton 411 suture material 1126
Sinus 927 tracheostomy tube 1130
Splenic pathologies 209 t-tube 1123
T U
Tension pneumothorax 574 Ulcer 914
Tetany 530 actinomycosis 926
TIPS 169 arterial 916
TME 426 basic principles of ulcer dressing 926
Toxic megacolon 348 Bazin's 922
Transfusion of blood and its components 33 cryopathic 922
complications 34 decubitus 920
indications 33 diabetic 919
Trauma 563 Martorell's 922
abdominal compartment syndrome
neuropathic 918
risk factors 673
soft chancre 925
abdominal injuries 624
syphilitic 924
colon injuries 639
duodenal injuries 630 traumatic 915
gallbladder and extrahepatic bile duct injury 629 tropical 924
genitourinary injuries 653 tuberculous 921
liver injuries 643 venous 917
pancreatic injuries 634 Urethra 1016
rectal injuries 641 carcinoma of penis 1025
retroperitoneal injuries 652 hypospadias 1019
small bowel injuries 637 Peyronie's disease 1024
splenic injuries 649 priapism 1022
stomach injuries 628 urethral stricture 1016
damage control surgery 670 Urethral injuries 662
head injury 582 Uric acid stone 953
assessment of severity 595 Urinary bladder 988
concussion 595 bladder calculi 990
contusion 595 bladder tumor 996
diffuse axonal injury 595 ectopia vesicae 989
extradural hematoma 588 patent urachus 988
intracerebral hematoma 594 schistosomiasis of the urinary bladder 994
skull fracture 585
subdural hematoma 591
treatment 596 V
hospital care 572
maxillofacial injuries 597 Venous diseases 749
fracture maxilla 600 deep vein thrombosis 750
fracture nasal bone 600 venous insufficiency 754
fracture of mandible 599 venous ulcer 765
neck injury 602
prehospital management 570
spinal injury 606 W
management 611
thoracic 612 Wound closure techniques 11
cardiac injury 620 Wound healing 1
diaphragmatic injuries 623 classification 4
esophageal injuries 623 complications 9
great vessel injury 622 factors affecting 8
hemothorax 615 growth factors 8
pneumothorax 614 phases
pulmonary parenchymal injury 618 inflammatory 5
rib fracture 612 maturational 7
sternal fracture 613 proliferative 6
tracheobronchial injuries 619 processes
types of injury 565 regeneration 3
Treatment of wound 12 repair 3
Trendelenburg’s surgery 762 types 4

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Illustrated Surgery

Nilay Mandal MS (General Surgery)

The Health Sciences Publisher

Jaypee Medical Inc Jaypee Brothers Medical Publishers (P) Ltd

0Chapter 1 Wound Healing 1–12

0Chapter 2 Fluid, Electrolyte and Acid-base Balance 13–27

Chapter 3 Hemostasis-Coagulation-Hemorrhage 28–35

Chapter 4 Gallbladder and Extrahepatic Biliary System 36–119

Chapter 6 Pancreas 173–206

Chapter 7 Spleen 207–217

Chapter 8 Abdominal Wall, Peritoneum, Mesentery, Retroperitoneum 218–240

Malignant peritoneal mesothelioma 233

0Chapter 9 Stomach 241–291

Chapter 10 Intestine 292–375

Chapter 11 Appendix 376–392

Chapter 12 Rectum and Anal Canal 393–431

Solitary Rectal Ulcer Syndrome 399

Chapter 14 Thyroid 473–513

Chapter 15 Parathyroid, Adrenal, Endocrine Pancreas and MEN 514–562

Chapter 16 Trauma 563–673

Abdominal injuries 624

Chapter 17 Burn 674–693

Chapter 18 Arterial Diseases, Venous Diseases and Diseases

Chapter 19 Hernia 774–812

Chapter 20 Diseases of the Testes, Scrotum and Penis 813–831

Chapter 21 Diseases of the Esophagus 832–863

Chapter 22 Diseases of the Salivary Gland 864–878

Chapter 23 Skin and Adnexal Lesion 879–911

Benign tumors 890

Chapter 24 Ulcer, Sinus and Fistula 912–928

Chapter 25 Urology 929–1036

Chapter 26 Minimally Invasive Surgery, Robotic Surgery 1037–1053

Chapter 27 Nerve Injury 1054–1062

Chapter 28 Surgery of Hand 1063–1071

Chapter 29 Neck Swelling 1072–1082

Chapter 30 Cleft Lip and Palate 1083–1089

Chapter 31 Anesthesia 1090–1103

Chapter 32 Instrument 1104–1131

zzProcess of Wound Healing

Wound Healing Involves Any of the Two Processes

Types of Wound Healing

zz Inflammatory (reactive) phase

Inflammatory (Reactive) Phase

Proliferative (Reparative) Phase

SS It is the second phase of healing.

Maturational (Remodeling) Phase

zz Matrix metalloproteinases (MMPs) are important factors for wound contraction.

zz The process begins about 21 days after injury.

zz As a result, a mature, avascular, acellular collagen rich scar develops.

SS Healing by secondary intention:

Role of Growth Factors in Healing

SS Differentgrowth factors are:

zz Fibroblast growth factor (FGF)

zz Vascular endothelial growth factor (VEGF)

zz Granulocyte-macrophage colony-stimulating factor (GM-CSF)

zz Insulin-like growth factor (IGF-1, IGF-2).

SS Growth factors act on cells by surface receptor binding.

SS Growth factors have different actions on different cells:

zz Chemotaxis of PMNs, macrophages, fibroblasts

zz Stimulation of fibroblasts leads to replication and proliferation

Permeable to gases and water vapor

Minimal pain during change of dressing.

Occlusive and semiocclusive dressing

Hydrophilic and hydrophobic dressing

As effervesent tablet or syrup.

Potassium concentration in IV solution should be ≤ 40 mEq/l.