STP Book PDF

STANDARD TREATMENT
PROTOCOL
Public Health Department

Government of Maharashtra
Message
There has been an increase in the expenditure on healthcare, especially in view of the growing
rate of urbanisation and rise in the number of lifestyle diseases. Within the limited financial allocation
in the Public Health Sector, health care services are needed to cater to majority of the population. This
demands rational and efficient utilisation of the limited resources.
Standard treatment protocols aim to ensure efficient utilisation of essential drugs to treat
majority of population in a standardised manner. Thus, more people can be treated, limiting the
wastage of resources over unstandardized treatment modalities. It also ensures that treatment quality
& standards are followed. They serve as a guide for health care providers in deciding the best possible
approaches for diagnosis, management and prevention of the health issues.
I greatly appreciate the work done by the Public Health Department for coming up with the
Standard Treatment Protocols for common health issues experienced by the people in the State. I hope
that they help the care providers in rational use of treatment modalities and lay the standards for
quality health services.

M essage
W orldwide more than 50% of all medicines are prescribed, dispensed or sold inappropriately,
while 50% of patients fail to take them correctly. M oreover, about one-third of the world's population
lacks access to essential m edicines. In Public Health Care system, which caters to the majority of the
population and given the constraint of availability of drugs and com modities, rational use of medicine
in treatment and managem ent of illness has attained even more significance. M oreover, the quality of
the treatment needs to be standardised for all the levels of health care. The health care provider must
have updated knowledge about the latest developm ents in the treatment modalities and ascertain
treatment regimen suitable for the disease.
This Standard Treatment Protocols book is meant for medical officers and health care
providers from different levels in the public health care system, to refer information about the
condition from a concise source. It is supposed to be a guide and aid for making decisions on
diagnosis and management of conditions for majority of the population. The management of
individual cases would ultimately depend on clinical judgement and skills of the health care provider.
I would like to express m y appreciation to all those who have participated in various
workshops, meetings and video conferences despite their demanding schedule for producing a
valuable document. I am positive that this book will be useful to all Health care providers working in
m y department and ultimately contribute to attain positive health for the patients.
Foreword
Sustainable Development Goal 3 aims to ensure healthy lives and promote well-being for all
ages. The strategic approach currently adopted is maintaining continuum of care throughout the various
levels of Healthcare and over the life cycle of the individual. The Public Health Department has been
working diligently with the goal of provision of effective and affordable quality health care which is
easily accessible to all age groups. The work done is reflected in the SRS reports and the IIMA report
for States. Still sustained and vigorous efforts are needed to reach the last mile.
To better utilise our resource pool in terms of drugs, laboratory services and human resources
while maintaining the qualrty of care, there was a need of a standardised system. There are various
guidelines and protocols available for all the diseases. To keep in pace with the recent changes in
treatment regimens and technological progress, it was necessary to have Standard Treatnent Protocols
(STP) for all diseases of public health importance in the State.
With the extensive efforts from specialists working in the Public Health Departmen! Professors
from Government, Private Medical Colleges as well as under the guidance of Dr. Prakash Doke, Ex-
Director of Health Services, Ex-Bureau Chiefs and department heads, the Standard Treatment Protocols
came into fruition. Over a period of 2 years, various deliberations were held in the form of meetings,
workshops and video conferences to add the latest changes in the field and include references for further
reading of the Health Care provider. I would like to highlight the guidance from our former Principal
Secretary, Mrs. Sujata Saunik and our Additional Chief Secretary, Dr. Vijay Satbir Singh who shared
their vision for developing this STP.
I sincerely hope that the Standard Treatment Protocols would be helpful for effective decision
making and in day to day working of the Healthcare providers.
,.c9
(Dr.76charfa Patil)
Additional Director,
SFWB,Pune.
STP
Team No.1 Gen. Medicine, ICU, CCU, ICCU, ARV/ASV
Sr.
Name Post Place of post Mobile No.
No.
1 Dr. N. J. Rathod (Team Leader) Ex. Addl. DHS Mumbai 9322890107
2 Dr. A.L. Kakrani Prof. Medicine Dr. D. Y. Patil Medical 9823972424
College, Pimpri
3 Dr. Umakant Shetkar Prof. Medicine Smt. Kashibai Navale 9960011820
Medical College, Pune
4 Dr. Mrs. Swati C. Aundhekar Prof. Medicine KIMS, Karad 9766535255
5 Dr. Priti Dave Prof. Dept. of Bharati Vidyapeeth Medical 9822790490
Medicine College, Pune
6 Dr. (Col) P.K. Sharma Asso. Prof. MD AFMC, Pune 9823071758
(Med)
7 Dr. Mrs. Priti P. Dhande Asso. Prof. Bharati Vidyapeeth Medical 9922426840
(Pharmacology) College, Pune
8 Dr. Sujata Abhay Jadhav Asso. Prof. M.D. KIMS, Karad 9423262871
Pharmacology
9 Dr. Madhulika Mahashabde Asso. Prof. Dept. of Dr. D. Y. Patil Medical 9850015831
Medicine College, Pimpri
10 Dr. Kiran K. Khalate Class I, Physician D.H. Ratnagiri 9850493260
11 Dr. Shyamsundar H. Nikam Physician, Medical RRH Amravati 9423124973
Superintendent
12 Dr. Sukrut V. Purandare Lecturer, Medicine Dinanath Mangeshkar 9881568748
Hospital, Pune
13 Dr. Shingade Madhuri M. Physician T.C.M. Hospital, Pune 9763825105
14 Dr. Khalate Physician Civil Hospital, Ratnagiri 9850493260
15 Dr. Nikam Medical VSSH, Amravati 9423124973
Superintendent
16 Dr. Miss Rande Physician District Hospital, Pune
Team No.2 National Health Programme, NRHM

Sr.
No.
1 Dr. Dodwad Ex. Addl.DHS Pune 9421014106

Dr. Vandana A. Kakrani Prof. Community Dr. D. Y. Patil Medical 9373324064
2 Medicine College, Pimpri
(Team Leader)
Dr. Prasad D. Pore Prof. Community Bharati Vidyapeeth 9921073540
3
Medicine Medical College, Pune
Dr. Abhay Mane Professor MD (PSM) Smt. Kashibai Navale 8975008663
4
5 Dr. Uddhav T. Kumbhar Asst. Prof. MD (PSM) KIMS, Karad 8983374099
6 Dr. Pavan Salve Addl. MOH PCMC 9922501584
7 Dr. Rahul D. Anerao MO PHC, MD (PSM) PHC Hasegaon, Latur 9881337338
8 Dr. Mangesh A Patil MO, PHC MD (PSM) Jalgaon 9403313482
9 Dr. Ganesh S. Lokhande THO, MD (PSM) THO Patoda, Beed 9922373120
Sr.
No.
10 Dr. R.G. Chaudhari MO PHC, MD (PSM) Nashik 9403505910
11 Dr. Sanjiv Kamble Jt. Director (TB & TB & Lep. Office Pune 9869972056
Leprosy)
12 Dr. Madhukar Pawar Dy. Director (TB & TB & Lep. Office Pune 9404194042
Leprosy)
13 Dr. Pradeep Aawte SSO IDSP Pune 9423337556
Team No.3 General Surgery, Ortho., Burn & Trauma

General Surgery
Sr.
No.
1 Dr. Mrunal N. Ketkar Prof. Surgery Bharati Vidyapeeth Medical 9623019743
College, Pune
2 Dr. D.P. Pande (Team Leader) Prof. Surgery Smt. Kashibai Navale 9422320164
3 Dr. Nitin Bilolikar OSD to Hon. Health Mantralaya, Mumbai 9422189337
Minister
4 Dr. N.L. Vyas Prof. Surgery Navi Mumbai 9322956914
5 Dr. S.R. Kulkarni Prof. Surgery KIMS Karad 9423606439
6 Dr. K. Sahoo Prof. Radiologist KIMS Karad 9970173439
7 Dr. Sanjay Padale Surgeon YCMH Pimpri 9922501324
8 Dr. Bolde A.N. Surgeon CS Beed 9822195062
9 Dr. B.H. Shinde Surgeon DH Pune 9420202731
10 Dr. Ajit Gawali Surgeon CS Raigad 9422096363
11 Dr. Ashish Chitharanjan Surgeon Pune 9822931328
12 Dr. Shinde Med. Superintendent District Hospital, Pune 9420202731
13 Dr. Rathod Addl. Civil Surgeon Civil Hospital, Thane 9422877733
14 Dr. Sonar Med. Superintendent VSSH, Amravati 9422754136
Orthopedic
Sr.
No.
1 Dr. M.S. Diggikar Jt. Dir (NVBDCP) Pune 9325398011
2 Dr. Hemant Parekh Asso. Prof. Ortho. Smt. Kashibai Navale 9011020901
3 Dr. Chintamani Latkar Asso. Prof. Ortho. Bharati Vidyapeeth Medical 9823028036
College, Pune
4 Dr. Piyush P. Jakkal Ortho. Surgeon, Cl.I D.H. Bhandara 8888865848

Sr.
No.
5 Dr. Ranjit Deshmukh Consultant Dinanath Mangeshkar 9822058954
Hospital, Pune
6 Dr. P.K. Dake Med. Superintendent Ortho. Hosp. Parbhani 9823529336
7 Dr. Anupam Hivlekar Class I, Ortho Surgeon D.H. Wardha 9422841044
8 Dr. Ravindra Gunaki (Team Orthopedician KIMS Karad 9422039510
Leader)
9 Dr. Saurabh Kale Orthopedician YCMH Pimpri 9960902842
11 Dr. A. K. Bnajdr Orthopedician YCMH 9552595521
12 Dr. Sanjog Kadam Orthopedician DH Satara 9422606782
13 Dr. Santpure Orthopedician DH Pune 8308667603
Team No.4 Pediatric & Neonatology

Sr.
No.
1 Dr. Dilip N. Patil (Team Ex. Dy. Director Aurangabad 9421407574
Leader)
2 Dr. C. D. Aundhekar Prof. Paed. KIMS, Karad 9960697814
3 Dr. Maya Borle Assoc. Prof. Pune 9890192458
4 Dr. Kavita Srivastava Assoc. Prof. (Paed.) Bharati Vidyapeeth Medical 9850825791
College, Pune
5 Dr. M. V. Deshpande DCH YCMH, Pune 9922501322
6 Dr. Rohini Nagarkar Paediatrician YCMH, Pune 9922501571
7 Dr. Sagar Khedu Paediatrician D.H. Alibag 9224367253
8379006796
8 Damale Kalpana T. Dietician Osmanabad 9423073368
9 Dr. Lohare B.S. M.O. Pediatrician RH Panvel 8655007705
10 Dr. Sanjay Jaiswal Paediatrician Daga Hospital, Nagpur 9422150677
11 Dr. Anupama Nadkarni Paediatrician Dinanath Mangeshkar Hospital, 9890599646
Pune
12 Dr. Ramdas N. Khune Med. Superintendent SDH Pen, Dist. Raigad 9271705557
13 Dr. Manoj Patil Paediatrician Dr. D. Y. Patil Medical College, 9922417017
Pimpri
14 Dr. Tahsim F. Khan Paediatrician Class-I Maternity Hosp. U'nagar-4 9325329874
15 Dr. Kadam Pediatrician Civil Hospital, Hingoli 8007001525
16 Dr. Purushottam Darshne Med. Superintendent Rural Hospital Shikrapur, Pune 9823307703
17 Dr. Pankaj Gajre Pediatrician Civil Hospital, Nashik 9822965458
18 Dr. Chandrakala Jaiswal Pediatrician SFWB Pune 9822496233
19 Dr. Navale Pediatrician SFWB Pune 9326874228
20 Dr. Baviskar ADHS SFWB Pune 7738362899
Team No.5 Ophthalmic
Sr.
No.
1 Dr. Varsha N Kulkarni Prof. Ophthalmology Bharati Vidyapeeth Medical 9423009019
College, Pune
2 Dr. Mrs. Smita D Javdekar Asso. Prof. of KIMS, Karad 9422613592
Ophthalmology
3 Dr. Pramod M. Sonune Civil Surgeon D.H, Chandrapur 9561962697
4 Dr. Satish Kumar Sriwastav Ophthalmologist Smt. Kashibai Navale 9881067666
(Team Leader) Medical College, Pune
5 Dr. Madhav J. Bhat DMH Consultant Dinanath Mangeshkar 9822323530
Hospital, Pune
6 Dr. S.B. Andhare Ophthalmic Surgeon G.H, Wardha 9823248623
Class-I
7 Dr. P. Jogewar Ophthalmic Surgeon DAGA Hospital Nagpur 9422131577
Class-I
ENT
Sr.
No.
1 Dr. G. D. Mahajan Prof. ENT Dr. D. Y. Patil Medical 9850038510
College, Pimpri
2 Dr. Havle Abhay D. Prof. ENT KIMS, Karad 9423263164
3 Dr. Sanjana Nemade Asso. Prof.ENT Pune 9923730525
4 Dr. Sarika Dhoot Asst. Prof.ENT Bharati Vidyapeeth Medical 9326349006

College, Pune
5 Dr. N. B. Patel M.S. (ENT) RMO (OR) DH Beed 9370066114
6 Dr. Manoj Deshmukh M.S. (ENT) YCMH Pimpri 9922501564
7 Dr. S. M. Mahalle Class-I, ENT Surgeon C.H. Amravati 9423124812
8 Dr. Kamble A.G. (Team Leader) MO ENT C.H. Pune 9823174647
9 Dr. Vikram Oak DMH Consultant Dinanath Mangeshkar 9822031070

Hospital, Pune
10 Dr. Yadav Physician VSS Hospital, Amravati 8308667603
11 Dr. Kamble Physician Civil Hospital Thane 9823776442

Team No.6 Obs/Gyn
Sr.
No.
1 Dr. G.S. Shekhawat Prof. (Obst. &Gyn) Smt. Kashibai Navale Medical 9372897090
College, Pune
2 Dr. Aparna N. Shrotri (Retd.) Prof. BJMC, Pune 9422513482
(Team Leader) OBGY. Consultant 020-25433233
3 Dr. Suchita Dabhadkar Asst. Prof.OBGY Bharati Vidyapeeth Medical 9422304399
College, Pune
4 Dr. Dileep P. Javadekar Asst. Prof MD KIMS, Karad 9423871993
(Gyn).
5 Dr. Mangal Santosh Supe MD OBGY YCMH Pimpri Pune 9604167167
6 Dr. Shubhang Mhasde MBBS DGO M.O. Govt. Maternity Hosp. & 7303170483
Dispensary, Ulhasnagar
7 Dr. Vaishali P. Khedikar Med. DAGA Hosp., Nagpur 9096724121
Superintendent
8 Dr. Ratna Raokhande Obst. &Gyn ADHS Thane 8080001530
9422030810
9 Dr. Arundhati Kanade OBGYN Consultant Dinanath Mangeshkar 9822614612
Hospital, Pune
10 Dr. Miss Dikshit Obst. &Gyn District Hospital, Pune 9503486712
11 Dr. S.M. Sonawne Obst. &Gyn District Hospital, Satara 9422029973
12 Dr. D. Kangule ADHS SFWB, Pune 7875185846
13 Dr. M.V. Karnataki UNICEF SFWB, Pune 9324341580

Consultant
Team No.7 Anesthesiology

Sr.
No.
1 Dr. Vithal K. Dhulkhed Prof. Anaesthesia KIMS, Karad 7588953396
2 Dr. Noopur Singh Prof. Anaesthesia Smt. Kashibai Navale 9011070600
3 Dr. Pooja N. Bhosle Asso. Prof. Anesthesia Bharati Vidyapeeth 9860835279
4 Dr. B. Nagaonkar ADHS RGJAY Mumbai 7738574849
5 Dr. Kore B.S. Civil Surgeon Latur 9011430402
6 Dr. Pradeep M. Kulkarni M.D. Anaesthesia Women Hosp. Jalna 9421448716
7 Dr. Patil Makarand P (Team Anaesthesia DH Alibag-Raigad 9822509077
Leader)
8 Dr. Dhangekar Anaesthesia DH Pune 9822616930
9 Dr. Bhabhul Gaonkar Anaesthesia DH Thane 9892007704
Team No.8 Dental, Chest & TB
Sr.
No.
Dental
1 Dr. Kharat (Team Leader) Dental Surgeon D.H. Beed 9423450077
2 Dr. Supriya Mahajan Dental Surgeon UH-3 Thane 8108715475
3 Dr. Dinesh Ashok Dhole Dental Surgeon D.H. Nashik 9923551519
Chest & TB
1 Dr. Ramkrishnan V. Ghubde Asso. Professor Smt. Kashibai Navale 9822462536

(Team Leader) Medical College, Pune
2 Dr. Ramesh L. Pawar M.O. RRH Nashik 9420335958
3 Dr. Anita Kharat Dental Surgeon D.H. Jalna 9423450077
4 Dr. Zapkar Dental Surgeon D.H. Thane 9029083693
5 Dr. Shegavkar Dental Surgeon RH, Igatpuri, Nashik 9890317834
Team No.9 Psychiatry

Sr.
No.
1 Dr. Sharmishta S. Deshpande Prof. (Psychiatry) Smt. Kashibai Navale 9890381144

2 Dr. Jyoti Shetty Prof. (Psychiatry) Bharati Vidyapeeth 9822326019

3 Dr. Khandekar (Team NRHM Psychiatrist Thane 9821351712

Leader)
4 Dr. Amit Nagarkar Class I, Psychiatrist Regional Mental Hospital, 9579591936

Nagpur
5 Dr. Hemant Sonanis Psychiatrist D.H. Nashik 9922069966
6 Dr. Amol Gulhane Psychiatrist GH Amravati 9881424080
7 Dr. Divekar Psychiatrist D.H. Thane 9619388012
8 Dr. M. Bahale Psychiatrist D.H. Thane 9850411911
9 Dr. Shirsath Med. Superintendent D.H. Thane 9096726700

Team No.10 Nephrology, Haematology& Pathology
Sr.
No.
1 Dr. R. C. Nimbargi Prof. & Head Bharati Vidyapeeth 9422069392
Pathology Medical College, Pune
2 Dr. Sunil V. Jagtap Asso. Prof. Patho. KIMS Karad 9960628672
3 Dr. Sunita M. Assoc. Prof. Bharati Vidyapeeth 9922913622
Bhatawadekar Microbiology Medical College, Pune
4 Dr. Satish V. Shimpi Pathologist Nashik 9890304750
5 Dr. P. V. Puri M.O. Nashik 9850632960
6 Dr. Deepak N. Gosavi Pathology D.H. Alibag 9881671533
7 Dr. S.K. Pawar Microbiologist KIMS, Karad 9423034094
8 Dr. V.V. Jadhav Pathologist G.H. Amravati 9763599173
(Team Leader)
9 Dr. Bhamre Pathologist DH, Nandurbar 9823100333
10 Dr. M.M. Kulkarni Pathologist DH, Pune 9623690256
11 Dr. Padmakar Kadam Pathologist DH, Satara 9822637176
Team No.11 Dermatology

Sr.
Name Post Place of post Mobile No
No.
1 Dr. N.D. Chaudhari Prof. Dermatology Dr. D. Y. Patil 9422331015
Medical College,
Pimpri
2 Dr. N.R. Gokhale Prof. Dermatology Smt. Kashibai 9823154022
Navale Medical
College, Pune
3 Dr. S.T. Vandav(Team Leader) Dermatologist D.H. Sindhudurg 9422052644
4 Dr. A.D. Ingale MO, Class-I. Skin DH Pune 9850556079
5 Dr. P.P. Ghushe Prof. Dermatology DH, Thane 9930661664
6 Dr. Vaishali Giri Prof. Dermatology DH, Nashik 8149904659
Special Thanks to Hon. Dean Seth G.S. Medical College and KEM Hospital Mumbai, Dr. Shinde
(Prof and Head Department of PSM) and all Professors and their colleagues of the Medical College
for their contribution for Standard Treatment Protocol Book. Without their contribution, it would
have been not possible to develop this book.
Editors
Sr.
No.
1 Dr. Archana Patil Addl Director SFWB, Pune 9869394115

(Editor in chief)
2 Dr. Tanaji Mane DDHS SBHIVS 9422746567

3 Dr Umesh Shirodkar ADHS DHS, Mumbai 9892726618
4 Dr Madhusudan Karnataki UNICEF Consultant SFWB, Pune 9324341580
5 Dr Chandrakala Jaiswal UNICEF Consultant SFWB, Pune 9822496233

6 Dr Ravindra Bagal UNICEF Consultant SFWB, Pune 7720009948
7 Dr Aparna Deshpande UNICEF Consultant SFWB, Pune 9373089938

8 Dr Pushkar Deshmukh UNICEF Consultant Jalgaon 9028198508
9 Dr Neha Wagh UNICEF Consultant Aurangabad 9673527421
10 Dr Vinay Koparde UNICEF Consultant Nanded 9168849555
11 Dr Vaibhav Mahatme UNICEF Consultant Beed 9096309076
12 Dr Prashant Hingankar UNICEF Consultant Nandurbar 8879597487

MASTER INDEX
Sr.
Contents Page No.
No.
Preface i-x
1 Medicine 1-165
2 Pediatrics 166-269
3 Obstetrics and Gynaecology 270-335
4 Dermatology 336-362
5 Psychiatry 363-391
6 ENT 392-438
7 Ophthalmology 439-480
8 Surgery 481-529
9 Orthopaedics 530-571
10 Anaesthesiology 572-598
11 Pathology 599-626
12 Dentistry 627-661
Abbreviations Used
Sr. No. Abbreviation Forms
1 ASHA Accredited Social Health Activist
2 AFB Acid-Fast Bacillus
3 AFP Acute Flaccid Paralysis
4 AIDS Acquired Immuno Deficiency Syndrome
5 AMTSL Active Management of Third Stage of Labour
6 ANC Ante Natal Care
7 AOM Acute Otitis Media
8 APH Ante Partum Haemorrhage
9 ARDS Acute Respiratory Distress Syndrome
10 ARF Acute Renal Failure
11 ARM Artificial Rupture of Membranes
12 ART Anti-Retroviral Treatment
13 ARV Anti-Rabies Vaccine
14 ASV Anti-Snake Venom
15 ATT/AKT Anti-Tuberculosis/ Anti-Koch Treatment
16 BERA Brainstem Evoked Response Audiometry
17 BMI Body Mass Index
18 BSL Blood Sugar Level
19 BT Bleeding time
20 BUN Blood Urea Nitrogen
21 CAP Community Acquired Pneumonia
22 CBC Complete Blood Count
23 CCF Congestive Cardiac Failure
24 CIN Cervical Intraepithelial Neoplasia
25 CMV Cyto Megalo Virus
26 COPD Chronic Obstructive Pulmonary Disease
27 CPAP Continuous Positive Airway Pressure
28 CPD Cephalo-Pelvic Disproportion
29 CPK Creatinine Phospho Kinase
30 CRF Chronic Renal Failure
31 CRP C-Reactive Protein
32 CRT Capillary Refill Time
33 CS Caesarean Section
34 CSOM Chronic Suppurative Otitis Media
35 CT Clotting time
36 CT Scan Computerized Tomography
37 CTEV Congenital Talipes Equino Varus
38 CVA Cerebro Vascular Accident
39 D&C Dilatation and Curettage
40 DHF Dengue Haemorrhagic Fever
41 DIC Disseminated Intravascular Coagulation
42 DMARDs Disease Modifying Anti Rheumatic Drugs
43 DNS Dextrose Normal Saline
44 DOTS Directly Observed Treatment, Short Course
45 DUB Dysfunctional Uterine Bleeding
46 EBM Expressed Breast Milk
47 EBV Epstein Barr Virus
48 ECG Electro Cardio Gram
49 EDD Expected Date of Delivery
50 EEG Electro Encephalo Graphy
51 ELISA Enzyme Linked Immuno-Assay
52 ENG Electro Nystagmo Graphy
53 ESR Erythrocyte Sedimentation Rate
54 FFP Fresh Frozen Plasma
55 FHR Fetal Heart Rate
56 FHS Fetal Heart Sound
57 F-IMNCI Faculty based Integrated Management of Newborn Child Illness
58 FNAC Fine Needle Aspiration Cytology
59 FRU First Referral Unit
60 GDM Gestational Diabetes Mellitus
61 GERD Gastro Esophageal Reflux Disease
62 GFR Glomerular Filtration Rate
63 GIT Gastro Intestinal Tract
64 HA Health Assistant
65 HCC Hepato Cellular Cancer
66 HCG Human Chorionic Gonadotropins
67 HDCV Human Diploid Cell Vaccine
68 HDL High Density Lipids
69 HDN Haemolytic Disease of Newborn
70 HE Hepatic Encephalopathy
71 HIV Human Immune Deficiency Virus
72 HPV Human Papilloma Virus
73 HSG Hystero Salpingo Graphy
74 HSV Herpes Simplex Virus
75 HTN Hypertension
76 IBS Irritable Bowel syndrome
77 ICCU Intensive Coronary Care Unit
78 ICTC Integrated Counselling and Testing Centre
79 ICU Intensive Care Unit
80 IDA Iron Deficiency Anemia
81 IDDM Insulin Dependent Diabetes Mellitus
82 IFA Iron Folic Acid
83 IG Immunoglobulin
84 IHBD Intra Hepatic Biliary Duct
85 IHD Ischemic Heart Disease
86 IMNCI Integrated Management of Newborn and Childhood Illness
87 IPPR Intermittent Positive Pressure Respiration
88 IUD Intra Uterine Death
89 IUGR Intra Uterine Growth Retardation
90 IUI Intra Uterine Insemination
91 IVC Inferior Vena Cava
92 IVF In Vitro Fertilization
93 JVP Jugular Venus Pressure
94 KFT Kidney Function Test
95 KMC Kangaroo Mother Care
96 LBW Low Birth Weight
97 LDL Low Density Lipids
98 LFT Liver Function Test
99 LMP Last Menstrual Period
100 LRTI Lower Respiratory Tract Infections
101 LSCS Lower Segment Cesarean Section
102 LVH Left Ventricular Hypertrophy
103 MAM Moderate Acute Malnutrition
104 MCHC Mean Corpuscular Hemoglobin Concentration
105 MCV Mean Corpuscular Volume
106 MDR-TB Multi Drug Resistant Tuberculosis
107 MI Myocardial Infraction
108 MMR Vaccine Measles, Mumps, Rubella Vaccine
109 MOHFW Ministry of Health and Family Welfare
110 MPW Multi-Purpose Worker
111 MRI Magnetic Resonance Imaging
112 MTP Medical Termination of Pregnancy
113 MVA Manual Vacuum Aspiration
114 NACP National Aids Control Programme
115 NBCC New Born Care Corner
116 NBSU New Born Stabilization Unit
117 NGO Non-Government Organization
118 NICU Neonatal Intensive Care Unit
119 NSAID Non-Steroidal Anti Inflammatory Drug
120 OAE Oto Acoustic Emission
121 OCPs Oral Contraceptive Pills
122 ORS Oral Rehydration Salt
123 PCR Polymerase Chain Reaction
124 PCV Packed Cell Volume
125 PEEP Positive End Expiratory Pressure
126 PEF Peak Expiratory Flow
127 PEFR Peak Expiratory Flow Rate
128 PEP Post Exposure Prophylaxis
129 PET Scan Positron Emission Tomography Scan
130 PID Pelvic Inflammatory disease
131 PID Prolapse Intervertebral disc
132 PMN Poly Morpho-Nuclear
133 PNS Para Nasal Sinuses
134 PPD Purified Protein Derivative
135 PPH Post-Partum Haemorrhage
136 PROM Premature Rupture of Membranes
137 PT Prothrombin Time
138 PUD Peptic Ulcer Disease
139 RDT Radical Drug Treatment
140 RF Renal Failure
141 RL Ringer Lactate
142 RNTCP Revised National Tuberculosis Control Programme
143 RVH Right Ventricular Hypertrophy
144 SAH Sub Arachnoid Hemorrhage
145 SAM Severe Acute Malnutrition
146 SGA Small for Gestational Age
147 SLR Test Straight Leg Raising Test
148 SNCU Special New Born Care Unit
149 STD Sexually Transmitted Disease
150 STI Sexually Transmitted Infections
151 SVC Superior Vena Cava
152 TIA Transient Ischemic Attack
153 TSH Thyroid Stimulating Hormone
154 UC Ulcerative Colitis
155 URTI Upper Respiratory Tract Infections
156 USG Ultrasonography
157 VIA Visual Inspection of Cervix with Acetic Acid
158 VLBW Very Low Birth Weight
159 WHO World Health Organization
160 XDR-TB Extensive Drug Resistant Tuberculosis
Preface
I. HOW TO USE THE BOOK
The Standard Treatment Protocol booklet was developed to serve as a comprehensive index of
protocols for the common conditions, syndromes and ailments. Each condition is individually dealt with clearly
presented information on definitions, classification, symptoms, signs, investigation and advice on diagnosis and
treatment. At the end of each chapter, books and journals referred by the specialists during the formulation are
mentioned in bibliography along with additional reading material links and references are provided. Simplified
Flowcharts, Algorithms and Tables have been used to depict contents in a comprehensive manner. The most
effective and feasible therapy is chosen in case if several modalities of therapy are available. When to refer a
case is also indicated. Drugs & dosages as well as alternatives are provided clearly. Photographs for reference
are also included where required.
This booklet is intended as a ready reference for the clinical aspects of the conditions included in the
book. It is meant for medical officers and health care providers from different levels in the public health care
system, who wants to refer information about the condition from a concise source.
At the beginning of the booklet a list of conditions as per speciality are indexed for rapid referencing.
Apart from this, section-wise contents are also provided in between sections. Abbreviations used throughout the
booklet are also mentioned in the initial pages after master index. Introduction, concept of essential medicines,
benefits of standard treatment protocol and rational prescription practices along with common prescription
terminologies are listed next. Each section documents the nature and magnitude of the condition and provides
basic approaches to the diagnosis and management. Bibliography mentions the source of information for the
chapter along with further reading material sources for in depth reading for interested readers is provided at the
end of each chapter of the booklet. The emphasis of the protocols is on rapid assessment and decision making, in
order to prioritise the patients and the urgency of action required. It helps to easily identify the conditions that
require referral to a higher level of health care.
This booklet is intended for health care providers who diagnose and treat patients at various levels of
health care in a practical manner. The booklet is supposed to be guide and aid for making decisions on diagnosis
and management of conditions for majority of the population. The management of individual cases would
depend on clinical judgement and skills of the health care provider.
Page i
II. STANDARD TREATMENT PROTOCOLS
The terms standard treatment protocols, treatment guidelines, and prescribing policies are all used to
indicate systematically developed statements to help practitioners or prescribers make decisions about
appropriate treatments for specific clinical conditions. Treatment guidelines exist for different levels of health
care, ranging from general treatment guidelines for sub centre to detailed protocols for Tertiary level healthcare
institutes.
Advantages
Sr No. Group Benefits
1 Health Care Managers • Deciding most effective, economical treatment for a specific
setting
2 Health Care providers • Gives opportunity to concentrate on correct diagnosis
3 Supply system managers • Helps in calculation of demand based on the utilisation
pattern of the drugs for treating conditions
4 Patients • Ensures consistency among prescribers for treatment through
provision of most cost-effective treatments
• Encourages adherence to treatment thus improving the
availability of drugs and ensuring better treatment outcome
5 Overall • Helps to integrate the technical advices of specialists from
different disease programmes into an overall training policy
• Can be used as the basis for training, for supervision
• For medical audit to assess and compare quality of care
Page ii
III. ESSENTIAL MEDICINES
The Alma-Ata declaration during the International Conference on Primary Health Care in 1978
reaffirms that health is a fundamental human right and the attainment of the highest possible level of health is a
most important worldwide social goal. Provision of essential medicines is one of the eight essential components
of primary health care outlined in The Alma Ata declaration. Medicines are integral parts of the health care and
the modern health care is unthinkable without the availability of necessary medicines. The medicines are
undoubtedly one of the weapons of mankind to fight disease and illness. They not only save lives and promote
health, but prevent epidemics and diseases too. Accessibility to medicines is one of the fundamental right of
every person.
The concept of essential medicines
World Health Organization (WHO) introduced the concept of essential medicines in 1977.
Essential medicines, as defined by the World Health Organization (WHO) are those that satisfy the priority
health care needs of the population. They are selected with due regard to public health relevance, evidence on
efficacy and safety, and comparative cost-effectiveness. Essential medicines are intended to be available within
the context of functioning health systems at all times in adequate amounts, in the appropriate dosage forms, with
assured quality and adequate information, and at a price the individual and the community can afford. The
implementation of the concept of essential medicines is intended to be flexible and adaptable to many different
situations.
While the open pharmaceutical market is flooded with large number of medicines many of which are of
doubtful value, an essential medicine list contains limited cost-effective and safe medicines. The concept of
essential medicines has been worldwide accepted as a powerful tool to promote health equity and its impact is
remarkable as the essential medicines are proved to be one of the most cost-effective elements in health care.
Several factors like efficacy, safety, public health relevance and comparative cost-effectiveness of
available treatments determine the selection of essential medicines. Other factors which are also considered
include factors such as local demography and pattern of disease, treatment facilities, training and experience of
the available personnel, local availability of individual pharmaceutical products, financial resources and
environmental factor. The generic name of the medicine is considered in selecting medicines for the List.
Lists of essential medicines also guide the procurement and supply of medicines in the public sector.
Bibliography
1. World Health Organization. Declaration of Alma Ata. International conference on primary health care,
Alma-Ata, USSR, 6-12 September 1978. Geneva: WHO, 1978. (Cited 2016 June 28)
Available from: www.who.int/hpr/NPH/docs/declaration_almaata.pdf
Further reading
1. World Health Organization. The selection and use of essential medicines. Report of the WHO Expert
Committee, 2002 (including the 12th Model List of Essential Medicines). Technical Report Series No
914. Geneva: WHO

Page iii
IV. RATIONAL USE OF MEDICINE
Rational use of medicine is defined by WHO as "Patients receive medications appropriate to their
clinical needs, in doses that meet their own individual requirements, for an adequate period of time, and at the
lowest cost to them and their community."
Worldwide more than 50% of all medicines are prescribed, dispensed, or sold inappropriately, while
50% of patients fail to take them correctly. Moreover, about one-third of the world's population lacks access to
essential medicines.
Rational use of medicine has attained more significance now-a-days in terms of medical, socio-
economical and legal aspects. Factors leading to need for rational use of medicines are:
1. Drug explosion: Increase in the number of medicine available for a particular indication complicates
choice of appropriate drug dosage.
2. Prevention of development of resistance: Irrational use of medicine may lead development of resistance
to highly effective medicines prematurely
3. Growing awareness: With the rapid spread of technology, information about drug development, its uses
and adverse effects can be accessed by any part of the world and is available at the fingertips of
consumers
4. Increased cost of the treatment: Rational use of medicine can reduce the economic burden on the public
as well as on the Government.
5. Consumer Protection Act (CPA): Extension of CPA in medical profession may restrict the irrational
use of medicines.
Common types of irrational medicines use are:
• The use of too many medicines per patient (poly-pharmacy);

• Inappropriate use of antimicrobials, often in inadequate dosage, for non-bacterial infections;
• Over-use of injections when oral formulations would be more appropriate;
• Failure to prescribe in accordance with clinical guidelines;
• Inappropriate self-medication, often for prescription-only medicines.
Reasons for irrational use of medicines are:
• Lack of information
• Faulty and inadequate training and education of medical graduates
• Poor communication between health professional and patients
• Uncertainty of diagnosis
• Demand from the patient
• Defective drug supply system and ineffective drug regulation
• Promotional activities of pharmaceuticals
Page iv
Irrational use of medicine may lead to
• Adverse, possibly lethal effects due to antibiotic misuse or inappropriate use of drugs
• Limited efficacy of treatment regimen
• Antibiotic resistance due to overuse as well as under-therapeutic dosage
• Drug dependence
• Risk of infections due to improper use of injections
• Waste of resources leading to medicine stock-outs and increased cost of treatment
• Exacerbation or prolongation of illness
• Distress and harm to patient leading loss of patient confidence in the health system
Bibliography
1. World Health Organization. Promoting Rational Use of Medicines: Core Components. [Internet] [cited
2016 June 27]
Available from: http://apps.who.int/medicinedocs/en/d/Jh3011e/2.html.
2. Brahma D, Marak M, Wahlang J. Rational Use of Drugs and Irrational Drug Combinations. The
Internet Journal of Pharmacology. 2012: Vol 10; Number 1.
Further reading
1. World Health Organization. The selection and use of essential medicines. Report of the WHO Expert
Committee, 2002 (including the 12th Model List of Essential Medicines). Technical Report Series No
914. Geneva: WHO

Page v
V. RATIONAL PRESCRIBING
WHO "Guide to good prescribing" provides step by step process of rational treatment.
Step 1: Define the patient's problem: A patient usually presents with a complaint or problem. Making a right
diagnosis is crucial for starting a correct treatment strategy. This is based on integrating many pieces of
information: the complaint as described by the patient; a detailed history; physical examination; laboratory tests;
X-rays and other investigations.
Step 2: Specify the therapeutic objective: Before choosing a treatment it is essential to specify your
therapeutic objective. Specifying therapeutic objective will prevent a lot of unnecessary drug use and helps to
avoid unnecessary prophylactic prescribing. Discussing therapeutic objective with patient before starting
treatment makes them an informed partner in the therapy and improves adherence to treatment.
Step 3: Selecting a suitable drug regimen: First confirm if drug is really needed. Very often, health problems
can be resolved by a change in lifestyle or diet, use of physiotherapy or exercise, provision of adequate
psychological support, and other non-pharmacological treatments; these have the same importance as a
prescription of drug and instructions must be written, explained and monitored in the same way. Depending on
the indication, suitable dosage schedule for suitable duration is selected taking into consideration factors like
safety, efficacy, interactions and contra indications. If necessary the dosage form, the dosage schedule and the
duration of treatment can be changed as per need of each patient. The selected strategy should be agreed with
the patient; this agreement on outcome, and how it may be achieved, is termed concordance.
Step 4: Write a prescription: A prescription is an instruction from a prescriber to a dispenser. It is a

medicolegal document which links prescriber, dispenser and patient. This step is covered in detail in the next
section.
Step 5: Giving information, instructions and warning: This step is important to ensure patient adherence
and helps create a good doctor-patient relationship This step is covered in detail in the next section.
Step 6: Monitoring treatment. Monitoring the treatment enables you to determine whether it has been
successful or whether additional action is needed. Monitoring interval depends on the type of illness, the
duration of treatment, and the maximum quantity of drugs to prescribe. At the start of treatment, the interval is
usually short; it may gradually become longer, if needed.
Knowledge and ideas about drugs are constantly changing. New drugs come in the market and
experience with existing drugs expands. Side effects become better known and new indications or ways of using
existing drugs are developed. A physician is expected to know about developments in drug therapy.
Bibliography
1. World Health Organization. Guide to Good Prescribing - A Practical Manual. [Internet] [cited 2016
June 27]
Available from: http://apps.who.int/medicinedocs/en/d/Jwhozip23e/5.html

Page vi
VI. PRESCRIPTION WRITING
A prescription is an instruction from a prescriber to a dispenser. The prescriber is not always a doctor
but can also be a paramedical worker, such as a lady health visitor, an auxiliary nurse midwife or a staff nurse.
The dispenser is not always a pharmacist, but can be a pharmacy technician, an assistant or a nurse. All
prescriptions orders should be comprehensible, clear-cut, dated (and time in the case of chart order), and signed
clearly for optimal communication between prescriber, pharmacist, and nurse. A good prescription or chart
order should contain sufficient information to permit the pharmacist or nurse to avoid possible errors during
dispensing or administering the drug.
Information on a prescription form
The most important requirement is that the prescription be clear. It should be legible and indicate precisely what
should be given.
The following details should be shown on the form:
• Name, address, telephone of prescriber

• Date
• Generic name of the drug, strength
• Dosage form, total amount
• Label: instructions, warnings
• Name, address, age of patient
• Signature or initials of prescriber
The prescriber’s name, address and telephone number - This will allow either the patient or the
dispenser to contact the prescriber for any clarification or potential problem with the prescription. 
Date of the prescription
Name, form, strength of the drug and duration of treatment.
• The Generic (non-proprietary) name of the drug should always be used. It also enables the pharmacist
to maintain stock of drugs, or dispense the drug easily. If there is a specific reason to prescribe a special
brand, the trade name can be added.
• The pharmaceutical form (for example ‘tablet’, ‘oral solution’, ‘eye ointment’) should also be stated.
• The strength of the drug should be stated in standard units using abbreviations that are consistent with
the International System of Units (SI). ‘Microgram’ and ‘nanogram’ should not be abbreviated since
abbreviated form (“μg”) is very easily misread as “mg”, a 1000-fold overdose. Also, ‘units’ should not
be abbreviated.
• Try to avoid decimals whenever possible. If unavoidable, a zero should be written in front of the
decimal point. Use ballpoint pen to avoid ink spread.
Specific areas for filling in details about the patient including name, address and age.
Page vii
Directions
• Directions should be written out in full in English, many Latin abbreviations are still in use (some
common terms are listed in Table 1). Knowledge of these abbreviations is essential for the dispensing
pharmacist and often useful for the prescriber .
• The abbreviation “OD” should be used only to mean “the right eye’ (if used); it has been used for
“every day” and has caused inappropriate administration of drugs into the eye. Acronyms such as ASA
(aspirin), 5-ASA (5-Aminosalicylic acid), PCM (paracetamol), CPM (chlorpheniramine), CPZ
(chlorpromazine) etc., should not be used; drug names should be written out.
• Unclear handwriting can be lethal when drugs with similar names especially brand names but very
different effects are available e.g., Daonil, Duodil and Diovol. In this situation, errors are best avoided
by noting the indication for the drug in the body of the prescription e.g., “Daonil (Glibenclamide), for
diabetes”.
• Directions specifying the route, dose and frequency should be clear and explicit; use of phrases such as
‘take as directed’ or ‘take as before’ should be avoided.
• For preparations which are to be taken on an ‘as required’ basis the quantity should be specified with
maximum limit and minimum interval. It is good practice to specify the purpose of the medication (for
example ‘every 6 hours as required for pain’, or ‘at night as required to sleep’).
• Where possible, usage directions should specify times (7 am, 3 pm, 11 pm) rather than simply
frequency (thrice a day) and especially relationship to meals for orally consumed medication.
• Avoid units such as "teaspoons" or "tablespoons."
• The length of the treatment course may be stated
• For liquid preparations, the quantity should be stated in millilitres (abbreviated as ‘ml’) or litres
(abbreviated as ‘L’, since the letter ‘l’ could be confused with the figure ‘1’).
• Explain the directions to the patient. The directions should be reinforced by the label on the medicinal
product and by appropriate counselling by the dispenser.
Narcotics and controlled substances
Under Narcotic Drugs and Psychotropic Substances Act, 1985; the prescribing of a medicinal product that is
liable to abuse requires special attention and may be subject to specific statutory requirements. In particular, the
strength, directions and the quantity of the controlled substance to be dispensed should be stated clearly, with all
quantities written in words as well as in figures to prevent alteration. Other details such as patient particulars and
date should also be filled in carefully to avoid alteration.
Page viii
Table 1. List of abbreviations used in medical prescriptions
Abbreviation From the Latin Explanation Abbreviation From the Latin Explanation
a.c. ante cibum before meals o.u. oculus uterque Both eyes
use as much as
ad lib. ad libitum oz ounce
one desires
bid bis in die twice a day per Per by or through
as a large single
bol. bolus dose (usually p.c. post cibum After meals
intravenously)
cap capsula capsule prn pro re nata as needed
dil. dilute p.o. per os by mouth or orally
disp. dispense p.r. By rectum
div. divide q Quaque every
every day before

quoque die ante
D.W. distilled water q.a.m noon. every
meridiem
morning
g gram q.d. quaque die every day
gr grain q.h, q1h quaque hora every hour
gtt (s) gutta (e) drop (s) q.i.d. quater in die four times a day
hr hour q.s. quantum sufficiat sufficient quantity
at bedtime right
h.s. hora somni Rx Take
eye
ID intradermal RL, R/L Ringer's lactate
Intramuscular
IM (with respect to SC subcutaneous
injections)
inj. injection injection s.o.s. si opus sit if there is a need
IP intraperitoneal stat Statim at once
IV intravenous supp suppositorium suppository
liq liquor solution susp suspension
min minimum a minimum syr Syrupus syrup
mcg microgram tab Tabella tablet
tablespoon (always
mEq milliequivalent Tbsp, T
write out “15 ml”)
mL millilitre tid three times a day
teaspoon (always
noct. nocte at night tsp
write out “5 ml”)
Normal saline ter in die/ ter die

NS t.i.d/t.d.s Three times a day
(0.9%) sumendum
o.d. oculus dexter Right eye top. topical
units (always write

o.s. oculus sinister Left eye U
out “units”)
Page ix
Bibliography
1. World Health Organization. Guide to Good Prescribing - A Practical Manual. [Internet] [cited 2016
June 27]
Available from: http://apps.who.int/medicinedocs/en/d/Jwhozip23e/5.4.html
Further reading
1. Johnston, Mike (2006). The pharmacy technician series: Fundamentals of pharmacy practice. Pearson
Prentice Hall. p. 24
2. Aronson JK. A prescription for better prescribing. British Journal of Clinical Pharmacology.
2006;61(5):487-491.
Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885053/pdf/bcp0061-0487.pdf
3. Scobie SD, Lawson M, Cavell G, Taylor K, Jackson SH, Roberts TE. Meeting the challenge of
prescribing and administering medicines safely: structured teaching and assessment for final year
medical students. Med Educ. 2003; 37: 434–7
Page x
Medicine
1. Medicine
Sr. No. Contents Page No.
1 Fever 1
2 Community Acquired Pneumonia (CAP) 6
3 Bronchial Asthma 9
4 Pleural Effusion 12
5 Chronic Obstructive Pulmonary Disease (COPD) 14
6 Bronchiectasis 16
7 Lung Abscess 18
8 Pneumothorax 20
9 Lung Cancer 23
10 Pulmonary Embolism 25
11 Hypertension 27
12 Heart Failure 32
13 Ischaemic Heart Disease and Acute Coronary Syndrome 34
14 Acute Rheumatic Fever 37
15 Infective Endocarditis 39
16 Diabetes Mellitus 43
17 Thyroid Disorders 55
18 Cerebrovascular Accidents 58
19 Subarachnoid Haemorrhage (SAH) 60
20 Pyogenic Meningitis 62
21 Tuberculous Meningitis 64
22 Viral Meningitis 65
23 Viral Encephalitis 67
24 Epilepsy 69
25 Guillain Barre Syndrome (GBS) 73
26 Aphthous Ulcers 75
27 Oesophageal Candidiasis 76
28 Dyspepsia 77
29 Gastro oesophageal Reflux 78
30 Peptic Ulcer Disease 79
31 Vomiting 82
32 Constipation 83
33 Irritable Bowel Syndrome 84
34 Ulcerative Colitis 85
35 Amoebic Liver Abscess 87
36 Pyogenic Liver Abscess 89
37 Intestinal Protozoal Infection 91
38 Ascites 95
39 Hepatitis 97
40 Hepatic Coma 99
41 Nephrotic Syndrome 101
42 Acute Nephritic Syndrome 102
43 Acute Renal Failure/Acute Kidney Injury 103
44 Chronic Kidney Disease 106
45 Malaria 108
46 Dengue 116
47 Leptospirosis 121
48 Influenza AHN (Swine Flu) 123
49 Diarrhoeal Diseases 126
50 Rheumatoid Arthritis 132
51 Snake Bite 134
52 Scorpion Sting 138
53 Dog Bite (Rabies) 140
54 Poisoning 143
55 Alcohol Intoxication / Alcohol Withdrawal 147
56 Anaemia 148
57 Heat Stroke 150
58 Tuberculosis (RNTCP) 154
59 Leprosy (NLEP) 163
1. FEVER
Body temperature is controlled by the hypothalamus.
The normal core body temperature is 36.5-37.5⁰C
2. Causes
• Malaria
(97.7-99.5⁰F). The morning temperature of >98.9⁰F
• Sepsis
and the evening temperature of >99.9⁰F defines
fever. • Abscess
• Brucellosis
1. Definition • Lymphoma
Since an oral temperature is 0.5°F (0.3°C) to 1°F o Night sweats– Characteristic of Tuberculosis,
(0.6°C) lower than a rectal or tympanic temperature: but sweating from any cause is usually worse
Rectal temperature ≥ 100.4°F - Core temperature at night.
o Recurrent fever– Cholecystitis, Cholangitis
Tympanic temperature ≥ 100.4°F - Core Temperature and Urinary tract infection with obstruction or
calculi.
Oral temperature ≥ 99.5°F-99.9°F
o Headache– Fever due to any cause can
Axillary temperature ≥ 99.0°F-99.5°F produce headache. If severe and with
photophobia suspect- Meningitis.
Note:
o Delirium– Common in elderly and young
• This is not absolute, remember that fever is a ones.
relative condition.
o Muscle pain– Myalgia classical of viral fever,
• Have a lower threshold for fever at 6am or 6pm. Influenza, Malaria, Leptospirosis and
• Keep antipyretics and recent intake in mind Brucellosis.
when considering fever.
• Feeling hot- does not necessarily imply fever.
• Rigors – profound chills accompanied by 3. Evaluation of Febrile Patient
chattering of teeth & severe shivering implies a Although fever is a “normal response”, prolonged
rapid rise in body temperature. episodes can cause damage so always evaluate for
stability of patient (regardless of what you think is
the cause).
Table 1: Evaluation of fever patient
1.Temperature Axillary temperature >990F
2.White Blood Cell Count >12,000 or <4,000 or
>10% bands
3.Heart Rate >90 bpm*
4.Respiratory Rate >24 bpm^ or PaCO2<32mm Hg
Sepsis = SIRS** + infection
Severe sepsis = SIRS** + infection + end organ damage
Septic shock = Severe sepsis + refractory hypotension
(<90 mm Hg or 40% below baseline)
* beats per minute
^ breaths per minute
**SIRS- systemic inflammatory response syndrome
3.1. Fever Pattern 3.2. Relation to Pulse
It is important to note that the cycle of fever pattern is Liebermeister’s rule: For every one-degree Celsius
often not very helpful in determining the cause of the rise of temperature above normal, the pulse will
disease. increase by 8-10 beats per minute.
Possible exceptions are: Tertian and Quartan Malaria, Faget Sign: The exception to Liebermeiser’s Rule.
Abscesses, Pel-Ebstein fever and drug fever. This Relative bradycardia may be useful when
present, although it is associated with a substantial
Page 1
differential diagnosis, including Typhoid fever, • Neurologic
Rickettsial diseases, Yellow fever, Legionnaire's • Abdominal
disease, Psittacosis, Leptospirosis, Drug fever, • Pulmonary
Brucellosis, Mycoplasma infections, Neoplasm and • Rash
Factitious fever. • Haemorrhage
• Bone and joint
4. Types of fever • Gynaecologic
• Continuous fever - Does not fluctuate more than 6.1 Fever only
1⁰C in 24 hr. e.g. Lobar Pneumonia, Typhoid • Malaria
fever, Brucellosis, Urinary tract infection. • Typhoid fever
• Intermittent fever- Temperature elevation for a • Dengue
certain period then returning to normal. e.g. • Leptospirosis
Malaria, Pyaemia, Septicaemia. • Rickettsia
• Quotidian- Periodicity of 24 hours - • Relapsing fever
Plasmodium Falciparum Malaria. • Other viral illnesses
• Tertian fever- 48-hour periodicity - Plasmodium • HIV
Vivax and Ovale.
• Quartan fever – 72-hour periodicity -
Plasmodium Malaria 6.2 Neurologic symptoms
• Remittent fever- Temperature remains above Fever, headache, altered mental status, convulsions,
normal throughout the day with fluctuations coma
more than 1⁰C in 24 hours e.g. Infective • Cerebral malaria
Endocarditis. • Meningitis
• Encephalitis
5. Hints to be obtained from • Chronic Meningitis: Tuberculous meningitis,
Cryptococcal Meningitis
history • Rabies
• Japanese Encephalitis
(Since Presentation can be nonspecific)
• West Nile Encephalitis
• Detailed fever history • HIV
• Medication review • Toxoplasmosis
• Family illnesses • HIV dementia
• Ethnicity • Trypanosomiasis (Sleeping Sickness)
• Detailed history of past surgeries
• Recent sick contacts and TB contacts/risks
• Host factors (Immunocompromised) 6.3 Abdominal symptoms
• Recent travel Fever, abdominal pain
• Environmental exposures associated with jobs • Typhoid
or hobbies • Infectious colitis: Shigella, E. coli, salmonella,
• Animal exposure Campylobacter, Amoeba
• Unusual dietary habits • Amoebic liver abscess
• High risk behaviour • Abdominal TB
• Sexual history including Contraceptives • Appendicitis, Pyelonephritis
• Gynaecologic history • HIV
• Hypersensitivities to environmental agents /
medicines or family history of such diseases 6.4 Fever and rash
Fever and skin rash
6. Common associated • Chicken pox
• Measles
symptoms • Dengue
• Other viral diseases
• Fever only
Page 2
6.5 Haemorrhagic symptoms 7.3. Abdominal symptoms
Hematemesis, melena, epistaxis, petechiae, purpura, Diarrhoea with or without blood, weight loss
puncture site bleeding and abdominal pain
• Dengue • Gastroenteritis
• Relapsing fever • Intra-abdominal sepsis
• Ebola, Lassa, Marburg • Inflammatory bowel disease
• Yellow fever • Malignancy
6.6 Bone and Joint 7.4. Skin rash-appearance &

Fever with joint or bone pain distribution will give a clue
• Sickle cell disease • Macular - Measles, Rubella, Toxoplasmosis
• Septic arthritis • Haemorrhagic - Meningococcal, Viral
• Osteomyelitis haemorrhagic fever
• Pyomyositis • Vesicular - Chicken Pox, Shingles, Herpes
• Rheumatic fever Simplex
• Chikungunya • Nodular - Erythema Nodosum- TB & Leprosy
• Brucellosis • Erythematous - Drug rash and Dengue fever.
6.7 Gynaecological symptoms 7.5 Joint symptoms-

Fever, pelvic pain, vaginal discharge Joint pain, swelling or limitation of movement is
• PID suggestive of active arthritis
• Tubo-ovarian abscess • Distribution-mono, oligo, polyarticular
• Postpartum endometritis • Appearance-Fleeting-Rheumatic fever
• Septic abortion • Oligoarthritis-infective, Koch's
• Polyarticular-
Rheumatoid arthritis, Osteoarthritis
7. Symptom Analysis of Fever • Axial skeleton involvement:
• Verify presence of fever- true/factitious Spondyloarthropathy, Psoriatic
• Duration-acute/chronic
• Mode of onset- abrupt/gradual
• Progression- continuous/intermittent 8. Hints to obtain from
• Severity- how it affects the daily work / examination
physical activities?
• Relieving and aggravating factors • Vital Signs: Monitor all of the vital signs for
• Treatment received and outcome stability
• Associated symptoms- localizing features. • General appearance: Do they look sick?
Anxious? Do they have altered sensorium? look
for pallor, icterus, cyanosis, clubbing and
7.1. Respiratory tract symptoms lymphadenopathy.
• Sore throat, nasal discharge, sneezing - URTI • Oral examination: Oral cavity infections, dental
• Sinus pain & headache- Sinusitis examination, gum examination, sinuses
• Cough, sputum, wheeze or breathlessness - • Cardio vascular examination: Any murmurs
LRTI • Respiratory examination: Bronchial sounds,
Decreased breath sounds, Adventitious sounds
• Central nervous system examination: Fundus
7.2. Genitourinary Symptoms examination, Mental Status, Encephalopathy,
Frequency of micturition, loin pain, vaginal or look for any neurological deficit.
urethral discharge suggesting • Per abdomen: Tenderness, Organomegaly,
• Urinary tract infection Ascites
• Pelvic inflammatory disease • Skin: Rashes, Nail Exam, Wounds / Decubitus
• Sexually transmitted disease Ulcers
• Musculoskeletal examination: Joint
examination, Muscle tenderness.
Page 3
• Genital / pelvic examination and rectal 10.3. ESR
examination. Normal: Men = Age/2, Women = Age+10/2
• Look for indwelling devices. Elevated in:
• Acute or Chronic Inflammation
9. Differential diagnosis • Infection
• Tissue Injury
• Infection (TB, UTI/Prostatitis, Endocarditis, • Thyroid Disease
Abscess, Line Infection, Sinusitis, Meningitis, • Azotaemia
Arthritis, Osteomyelitis, Wound infectious,
An elevated ESR does not rule in or out disease.
Diarrhoea)
As opposed to the ESR, the CRP increases more
• Inflammatory (Rheumatic Disorders, Vasculitis) quickly with an acute process, and decreases for
• Drug Fever (Beta - Lactam antibiotics, quickly when the underlying state resolves.
Amphotericin B, Chemotherapy, Drug
Interactions) ESR > 100
• Thrombotic (DVT / PE / MI) T - TB
• Neurologic (Hypothalamic disorder, Spinal O - Osteoarthritis
Cord Injuries, ICH) E - Endocarditis
• Endocrine (Thyrotoxicosis, Adrenal Insufficiency, V - Vasculitis (Temporal Arteritis)
Subacute Thyroiditis) A - Abscess
• Gastrointestinal (IBD, Pancreatitis, Cholecystitis) N - Neoplasm (especially Lymphoma, Plasma
• Malignancy Cell dyscrasias)
10. Fever Workup 10.4. Blood cultures

• The bacteriologic burden is highest in the blood
10.1 Minimum in all patients stream approximately 1 hour before fever
spikes. So, collect blood cultures 1 hour before
• CBC with differential and reticulocyte count fever spike.
• Blood smear- for malarial parasites • If you are suspecting Endocarditis, tell the lab to
• CXR PA and Lateral. Add Decubitus if needed. continue following the cultures for at least 4
Infiltrates negative if dry weeks.
• Urine analysis (with Microscopy) and Urine
Culture 11. Treatment of Fever Itself
• 2 sets of blood cultures + Cultures from any
central catheter • Give empiric Antibiotics when there is high
• Electrolytes and Metabolic Panel, LFTs, suspicion of the source of infection or if the
Hepatitis Panel, HIV Test source is unknown and the patient is unstable.
• Tab Paracetamol 500 mg orally 4 times a day
10.2 Other Specific procedures/labs for most fevers with discomfort.
to obtain data • Don’t always lower the temperature so readily.
• Autoimmune Workup (RF, ANA, etc. as history
This decreases your ability to know when to draw
guide, ESR, CRP)
cultures and may lower the patient’s defence
• Specific Viral Serology
mechanism. Once workup has been performed (and
• Lumbar Puncture, Thoracentesis,
possibly repeated) then temperature can be lowered.
Arthrocentesis, Paracentesis
However, have low threshold for lowering the
• CT Scan of Head temperature when there is a hypermetabolic state that
• CT PE Protocol / Doppler of extremities would be damaging (i.e. concurrent MI, CVA) or if
• Echocardiogram the patient is very symptomatic.
• Stool Cultures - Gram Stain, Clostridium
difficile toxin etc.

• Sputum Cultures
• Skin biopsy
Page 4
Bibliography
1. Casper DL, Fauchi AS, Harrison’s Principles of Internal Medicine, 19 th edition, McGraw Hill
Professional. April 2015
2. Boon NA, Colledge NR, Walker BR. Davidson’s Principles and Practice of Medicine, 20 th edition,
Churchill Livingstone Elsevier
3. Munjal YP, Sharma SK, Agrawal AK, Singal RK, Gupta P, Sundar S et el. API Textbook of Medicine.
10th edition. JAYPEE Brothers. 2015
4. National Treatment Guidelines for antimicrobial use in infectious diseases – Version 1.0 (2016),
National Center for Disease Control, Ministry of Health and Family Welfare. [Cited 2016 July 7]
Available from: http://www.ncdc.gov.in/writereaddata/linkimages/AMR_guideline7001495889.pdf
Further reading
1. WHO Informal Consultation on Fever Management in Peripheral Health Care Settings a Global Review
of Evidence and Practice [Internet]. [cited 2016 Jul 4]
Available from: http://apps.who.int/iris/bitstream/10665/95116/1/9789241506489_eng.pdf

 
Page 5
2. COMMUNITY ACQUIRED PNEUMONIA
[CAP]
1. Introduction 3. Radiological imaging
• Pneumonia is an infection of pulmonary 3.1 Chest x ray (PA and Lateral)
parenchyma that causes them to function
abnormally • Lobar consolidation – more common in typical
pneumonia
• Classified as typical or atypical, although the
clinical presentations are often similar. • Bilateral, diffuse infiltrates – commonly seen in
Approximately 20-33% of episodes result in atypical pneumonia
hospitalization
If performed early in the course of the disease, may be
Typical: Up to 70% usually caused by Streptococcus negative
pneumoniae
Figure 2.1 - Chest X-Ray PA VIEW - CAP
Atypical: 30-40% (“My Lungs Contain Viruses”)
• Mycoplasma pneumoniae
• Legionella pneumophila
• Chlamydia pneumoniae
• Viruses: Influenza, Adenovirus
2. Clinical features
Symptoms:
• Cough, fever, chills, fatigue, dyspnoea, rigors, and
pleuritic chest pain
• Cough may be persistent and dry or it may produce
sputum
• Other presentations may include headache and
3.2 CT scan- Could be performed in patients with
a negative chest radiograph when there is a high clinical
myalgia
suspicion for pneumonia and to rule out other
• Certain aetiologies, such as legionella, also may pathologies.
produce gastrointestinal symptoms
Signs -
4. Laboratory Diagnosis
Complete blood count, sputum, gram stain and cultures,
• Tachycardia
blood sugars, blood urea, serum creatinine.
• Tachypnea
• Dullness to percussion of chest, crackles or rales on
5. Treatment
auscultation, bronchial breath sounds, tactile Initial treatment of CAP is based on physical
fremitus, and Egophony (“E” to “A” changes) examination findings, laboratory results and patient
characteristics. After examination, you must decide
• Patients with typical pneumonia are more likely to whether to treat patient on OPD basis or to admit the
present with dyspnoea and bronchial breath sounds patient.
on auscultation
Page 6
Patients with any one of following features must be OR
admitted
• Tab Levofloxacin 750 mg once a day, OR
• Respiratory rate >30/min Moxifloxacin 400 mg once a day, OR
• Systolic BP <90 mmHg or diastolic <60 mmHg Gemifloxacin 320 mg once a day x 5-7 days
• New onset confusion or impaired level of OR
consciousness • Tab Cefpodoxime 200 mg BD or Tab Cefuroxime
• Comorbid illness- Diabetes, Ischaemic Heart 500 mg BD Plus Macrolide antibiotics
Disease, Alcoholics, Immunocompromised,
Multilobar pneumonia 5.4. Inpatients
Therapy for pneumonia is empiric because specific • I.V. Cefotaxime 1-2 gm 8 hourly OR
pathogens usually are not identified at the time treatment
• I.V. Ceftriaxone 1-2 gm once a day OR
is initiated.
• I.V. Ampicillin 1-2 gm 4-6 hourly OR
5.1. Duration of therapy • I.V. Ampicillin Sulbactum 2 gm 8 hourly x 4 days
• S. pneumoniae: 7-10 days or until afebrile for 3 plus

days • Tab Azithromycin or in severe cases I.V.
• Mycoplasma/Chlamydia pneumoniae: 10-14 days, Azithromycin 1 gm on day one and then 500 mg
up to 21 days once a day for next 4 days or Tab Levofloxacin,
• Legionella: 10-21 days Moxifloxacin as above.
• After clinically stable (T<100.00F, HR<100
5.2. CAP, not hospitalized with No beats/min, RR<24/min, SBP>90mm of Hg, O2
comorbidities saturation>90%) and able to tolerate oral intake,
may be switched to oral antibiotics for remainder
• Cap Amoxicillin 500 mg three times a day x 5 days of therapy
• Tab Azithromycin 500 mg PO x 1, then 250mg • PPV23 vaccine is recommended for all adults ≥65
once a day -5 days OR years of age and in younger patients with a number
• Tab Clarithromycin 500 mg twice a day - 5 or 7 of conditions that increase the risk of invasive
days OR pneumococcal disease.
• Cap Doxycycline 100 mg twice a day -10 days
6. Complications
5.3. CAP, not hospitalized with
Lung abscess, pleural effusion, empyema. These patients
comorbidities need to be referred to district hospital.
• Cap Amoxicillin 1gm thrice a day x 5 days plus
Tab Azithromycin / Clarithromycin as above doses
OR
• Cap Amoxicillin and Clavulanate 2 gm twice a day
x 5 days plus a Tab Azithromycin / Clarithromycin
as above doses
Bibliography
1. Casper DL, Fauchi AS, Harrison’s Principles of Internal Medicine, 19th edition, McGraw Hill
2. Boon NA, Colledge NR, Walker BR. Davidson’s Principles and Practice of Medicine, 20th edition,
3. Munjal YP, Sharma SK, Agrawal AK, Singal RK, Gupta P, Sundar S, et.al. API Textbook of
Medicine. 10th edition. JAYPEE Brothers. 2015
Page 7
Further reading
1. Gupta D, Agarwal R, Aggarwal AN, Singh N, et el. Working Group Guidelines for Diagnosis and
Management of Community and Hospital Acquired Pneumonia in Adults: Joint ICS/ NCCP (I)
Recommendations [Internet]. Lung India 2012;29: S27-S62. [cited 2016 Jul 4]
Available from: http://medind.nic.in/iae/t12/i4/iaet12i4p267.pdf

Page 8
3. BRONCHIAL ASTHMA
• Simple spirometry shows air flow limitation with
1. Introduction decreased FEV1, FEV1 / FVC and PEF.
Asthma is defined as a chronic inflammatory disease
• Peak expiratory flow- by using peak expiratory
of airway that is characterized by increased
flow meter >20% of diurnal variation on ≥3 days
responsiveness of tracheobronchial tree to a
in a week for 2 weeks.
multiplicity of stimuli.
• Diagnosis of asthma is established by
2. Precipitating factors demonstrating reversible airway obstruction.
Reversibility is defined as a ≥ 12% increase in
• Childhood infections – Respiratory syncytial FEV1 15 minutes after two puffs of a β
virus adrenergic agonist (salbutamol) on spirometry.
• Allergen exposure – Allergy to feathers, animal
danders, dust mites, molds 6. Treatment
• NSAID, Aspirin, Beta blocker, Sulphite Drug treatment: Classified in to:
containing topical ophthalmic solution, food
preserving agent 6.1. Controller: To be taken on long term
basis to control asthma through their anti-
• Wood and vegetable dust, industrial chemicals inflammatory effects
and plastic
(a) Inhaled corticosteroids (ICS) –
• Exercise, emotional stress.
Beclomethasone 200 mcg/metered dose twice a day
3. Symptoms OR
Budesonide –200-400 mcg/metered dose twice a day
• Dyspnoea, cough and wheezing
OR
• Sense of constriction in the chest
• Cough that produces thick, stringy mucus. Fluticasone- 100-250 mcg/metered dose twice a day
Increase mucus production, typically tenacious (b) Systemic corticosteroids
mucus.
Oral Prednisone or Prednisolone 40-60 mg once daily
4. Signs for 5 to 10 days
Tachypnea, tachycardia, mild systolic hypertension (c) Leukotriene modifier –
Respiration become audibly harsh, rhonchi heard on Tab Montelukast 10 mg once a day X 5 days.
auscultation. (d) Long acting inhaled β2 agonist-
In severe cases - Accessory muscle become visibly -Salmeterol (MDI 21 mcg/puff, 2 puff 12 hourly OR
active, Paradoxical pulse, Cyanosis, Silent chest. In
some severe cases patients may land in to respiratory - Formoterol (1 to 2 puffs 12 hourly)
failure. (e) Theophylline-Tab Deriphyllin 150 mg twice a day
X 5 days.
5. Investigation
• Sputum and blood examination for eosinophilia
6.2. Reliever: Used on or as needed basis to
quickly relieve symptoms by their bronchodilator
• Chest X-ray showing hyper inflated lungs properties. These are:
Short acting inhaled β2 agonist (SABA) Salbutamol 100 mcg/metered dose 1-2 puffs, Levosalbutamol 50
mcg/metered dose 1-2 puffs as needed, Terbutaline
Systemic glucocorticoid - Tab Prednisolone 40-60mg/day
Page 9
Short acting oral β2 agonist - Tab Salbutamol 2-4mg/day
Anti-cholinergic - Ipratropium inhaler
Theophylline - 100-300 mg three times a day
6.3. Combinations available as Formoterol / Budesonide 1-2 puffs twice daily

Salbutamol / Beclomethasone.
inhaler and Rotacaps Inhaled drugs are preferred over oral due to less dose,
Salmeterol / Fluticasone 1-2 puffs twice daily less side effects, quick onset of action.
OCS
LABA LABA LABA
ICS ICS ICS ICS
Low dose Low dose High dose High dose
Short acting β2 agonist as required for symptom relief
Moderate Severe persistent Very severe
Mild intermittent
Mild persistent persistent persistent
Figure-3.1: Step wise approach to asthma therapy according to the severity of asthma and ability to
control symptoms.
ICS = Inhaled corticosteroid;

LABA = Long acting β2 agonist 7.3. Treatment
OCS = Oral corticosteroid
• Oxygen 40-60 % nasally to achieve oxygen
7. Acute severe asthma: (Status saturation >90%
• Inj. Hydrocortisone-200 mg I.V. stat and then
Asthmaticus) 100 mg 8 hourly
Can be fatal and must be treated promptly. • Salbutamol (2.5-5 mg) and Ipratropium
7.1. It is characterized by Bromide (0.5 mg) alternately inhaled through
• Severe dyspnoea the nebulizer.
• Respiratory rate ≥25/min • Inj. Aminophylline 500 mg in 500 ml of 5%
• Heart rate ≥110/min. Dextrose over 12 hours if patient is not
• Inability to complete sentence in single breath. receiving theophylline previously.
• PEF (peak expiratory flow)35-50% predicted • Inj. Ampicillin 500 mg 6 hourly till patient is
stable and then oral Ampicillin 500 mg TDS X
7.2. Life threatening features 5 days.
• PEF<33% predicted
• In very severe cases patient may require
• SpO2<92% silent chest ventilatory support.
• Cyanosis
• Normal or raised PaCO2 (suggests impending Refer to higher center with above life threatening
respiratory failure) signs.
• Feeble respiratory effort
• Bradycardia or arrhythmia
• Confusion, coma.
Page 10
Rotahaler Spacer Metered dose inhaler
Figure 3.2 – Types of Devices used in Bronchial Asthma
Bibliography
Further reading
1. Agarwal A, Dhooria S, Aggarwal AN et el. Guidelines for diagnosis and management of bronchial
asthma: Joint ICS/NCCP (I) recommendations. Lung India [Internet]. 2015 Apr; 32(Suppl 1): S3–S42.
[cited 2016 Jul 5]
Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405919/
2. WHO Guidelines, factsheets regarding Asthma [Internet]. [cited 2016 Jul 5]
Available from: http://www.who.int/respiratory/asthma/en/
3. Yash Pal Munjal, Surendra K. Sharma, A. K. Agrawal, R.K. Singal, Pritam Gupta, Shyam Sundar et
el. API Textbook of Medicine. 10th edition. JP Brothers.2015


Page 11
4. PLEURAL EFFUSION
A pleural effusion is an abnormal excess amount of fluid
in the pleural space
1. Symptoms
• Breathlessness
• Cough
• Fever
• Pleuritic chest pain
2. Signs
• Decreased breath sounds
• Stony dullness on percussion Figure 4.2: Massive right pleural effusion with shift
• Decreased vocal resonance of mediastinum towards left
3. Common Causes 4.2. Thoracocentesis

• Tuberculosis Once a pleural effusion is identified on imaging, a fluid
• Pneumonia sample is usually taken to determine the pleural
effusion's character and seriousness, a procedure called
• Cancer
Thoracocentesis.
• Liver disease (Cirrhosis)
• End-stage renal disease A sample of fluid is removed with a needle inserted
• Nephrotic syndrome between the ribs
• Congestive heart failure Pleural fluid tests: routine, microscopy, cytology and
• Pulmonary embolism ADA (Adenosine deaminase) levels
• Constrictive pericarditis
• Lupus and other autoimmune conditions There are two different types of fluid
Transudative or Exudative
4. Investigations
i. Transudative: clear fluid
4.1. Chest X-ray film Clear fluid, low protein content, cell count is low.
e.g. Congestive Cardiac Failure, Liver Cirrhosis,
PA view, lateral decubitus, lateral view Nephrotic Syndrome.
Blunting of CP angle, Ellis S shaped in large effusions
ii. Exudative:
• Straw coloured, high protein content, cell count
is high.
By the gross characteristics of the fluid.
• Frankly purulent fluid indicates an empyema.
• A putrid odour suggests an anaerobic empyema.
• A milky, opalescent fluid suggests a chylothorax,
resulting most often from lymphatic obstruction
by malignancy or thoracic duct injury by trauma
• Grossly bloody fluid result from trauma,
malignancy,
Figure 4.1: Chest radiograph showing left-sided
pleural effusion
5. Treatment
Management of common pleural effusions
Page 12
5.1. Tuberculosis • Cell count predominantly neutrophilic
• Appropriate antibiotics
Tuberculosis is the commonest cause of pleural effusion • Thoracocentesis to ensure that empyema has not
• Straw coloured effusion developed
• Cell count - lymphocyte predominance
• Pleural fluid protein > 3 g/dl
5.3. Malignant effusion
• Cob web formation • Cytology positive
• ADA level is high. • Refer to higher centre
Tubercular pleural effusion is treated as per RNTCP Treatment of underlying cause in heart failure, nephrotic
guidelines syndrome, liver cirrhosis
5.2. Para pneumonic effusion

• Chest X-ray consolidation features along with
effusion
Bibliography
Medicine. 10th edition. Jaypee Brothers. 2015
Further reading
1. WHO Guidelines for Respiratory tract diseases [Internet]. [cited 2016 Jul 5]
Available from: http://www.who.int/topics/respiratory_tract_diseases/en/

Page 13
5. CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
cause cough with expectoration on most days for at
1. Introduction least 3 months a year for more than 2 consecutive
COPD is a chronic lung disease characterized by years.
airflow limitation that is not fully reversible.
1.2. Emphysema
It includes chronic bronchitis and emphysema.
It is defined as distension of air spaces distal to the
1.1. Chronic Bronchitis terminal bronchiole with destruction of alveolar
septa.
This is a condition associated with excessive
tracheobronchial mucus production sufficient to
Table-1: Differentiating features between Emphysema and Bronchitis

Features Predominant emphysema (Pink Predominant bronchitis (Blue
puffer) bloater)
1. Age of onset 6th decade 5th decade
2. Cough After dyspnoea Before dyspnoea
3. Dyspnoea Severe Mild
4. Sputum Scanty, mucoid Copious, purulent
5. Infections Less common Common
6. Respiratory insufficiency Often terminal Repeated attacks
7. Chest x-ray Hyperinflation +/- bullous changes; Increased bronchovascular marking;
small heart large heart
8. PaCO2 (mm Hg) 35-40 50-60
PaO2 (mm Hg) 65-75 45-60
9. Pulmonary hypertension Mild Moderate to severe
10. Cor pulmonale Pre terminal stage Common
11. Diffusing capacity Decreased Normal to slight reduction
Table-2: Differences between Pink puffer and Blue bloater

Pink puffer Blue bloater
1. Course Progressive dyspnoea Intermittent dyspnoea
2. Sputum Scanty Profuse
3. Polycythaemia Uncommon Common
4. X-ray Attenuated peripheral vessels Normal peripheral vessels
5. pCO2 Normal Increased
6. Alveolar gas transfer Reduced Normal
• Sitting and bending forward with hands on
2. Aetiology knees (tripod position).
Smoking (active and passive), Smoke from biomass • Pursed lip breathing
fuel (firewood, burnt plastics) • Cyanosis (Ominous sign)
• Forced expiratory time Normal - 4 secs, COPD -
3. Signs 6 secs and above
• Barrel chest
Page 14
• Hyper resonant chest • Long acting beta agonist (Salmeterol,
• Diminished breath sound and bilateral wheeze Formoterol), 1-2 puffs twice a day
• Spirometry showing obstruction (FEV1/ FVC < • Short acting anticholinergics (Ipratropium) 1-2
70%) even after bronchodilator confirms the puffs, 2-3 times a day
diagnosis of COPD. • Long acting anticholinergic (Tiotropium) 1-2
puffs once a day.
4. Treatment 4.2.4. Theophylline
4.1. Non pharmacological • Inj. Aminophylline 250 mg in 500 ml of 5 %
• Rehabilitation Dextrose slowly over 8-10 hours in acute
attacks.
• Exercise
• Tab Theophylline 100-300 mg three times a day
• Nutrition
• Side effects: Tachycardia, nausea, arrhythmias
• Education
and convulsions
• Avoid smoking
4.2.5 Glucocorticoids
4.2. Pharmacological
• Inhaled corticosteroids should be given in
4.2.1. Oxygen therapy severe COPD or in those with repeated
exacerbation.
4.2.2. Antibiotics
• Fluticasone 1-2 puffs twice a day
Antibiotics are required as infection often precipitates • Budesonide 1-2 puffs twice a day
acute attacks. Inj. Benzyl Penicillin 10 lakhs units 6 • Systemic corticosteroids should be given only in
hourly 5-7 days or Inj. Ampicillin 500 mg 6 hourly patients with acute exacerbation of COPD.
5-7 days • Tab Prednisolone 30-40 mg /day for 8-10 days
4.2.3. Bronchodilators in tapering doses
Inhaled bronchodilators are preferred to oral 5. Complications

formulations in view of better efficacy and lesser side
effects. i. Pneumothorax
ii. Respiratory failure
Inhaled bronchodilators include - iii. Cor pulmonale
• Short acting beta agonists - Salbutamol, 1-2
puffs three times a day, Terbutaline 1.5 mg
three times a day
Bibliography
3. Munjal YP, Sharma SK, Agrawal AK, Singal RK, Gupta P, Sundar S, et al. API Textbook of
Further reading
1. Gupta D, Agarwal R, Aggarwal AN, et el. Guidelines for diagnosis and management of Chronic
Obstructive Pulmonary Disease: Joint recommendations of ICS and NCCP India, Special issue The
Indian Journal of Chest Diseases and Allied Sciences, Vol 56 [Internet] – 2014. [cited 2016 Jul 5]
Available from: http://medind.nic.in/iae/t14/s1/iaet14s1.pdf
2. World Health Organization (WHO) Guidelines and factsheets for COPD. [cited 2016 Jul 5]
Available from: http://www.who.int/topics/chronic_obstructive_pulmonary_disease/en/

Page 15
6. BRONCHIECTASIS
• Fever, generalized malaise, weight loss,
1. Definition haemoptysis
Bronchiectasis is chronic, irreversible dilation and • Dry bronchiectasis; usually involve the upper
distortion of the bronchi caused by inflammatory lobes
destruction of the muscular and elastic components of • Recurrent pneumonia
the bronchial walls. It may be focal or diffuse. It is
categorized as cylindrical, tubular, varicose or cystic. 4. Signs
2. Aetiology • Early phases or dry variety: Normal
• Severe or secondary infection: Persisting
Conditions associated with the development of crackling rales in the same part of lung
bronchiectasis • Later stage: Emphysema and Cor Pulmonale.
• Moist crackles at lung bases
2.1. Post infection • Halitosis, skin pallor
• Bacterial pneumonia
• Tuberculosis 5. Laboratory tests
• Pertussis
• Sputum for Gram stain, C&S, and acid-fast
• Measles bacteria (AFB)
• Influenza • CBC with differential (leucocytosis with left
• Fungus shift, anaemia).
• Serum protein electrophoresis to evaluate for
2.2. Proximal airway obstruction hypogammaglobinaemia.
• Foreign body aspiration • Antibody test for Aspergillosis.
• Benign airway tumours • Sweat test in patients with suspected Cystic
Fibrosis.
2.3. Abnormal host defence
• Ciliary dyskinesia (Kartagener’s syndrome)
6. Evaluation
• Alpha 1 antitrypsin deficiency 6.1. Chest x-ray:
2.4 Immunodeficiency Increase in size and number of bronchovascular
markings (quiet nonspecific). Presence of “Tram-
• HIV, Hypogammaglobinaemia track” indicates dilated airways suggestive of
bronchiectasis.
2.5 Genetic disorders
• Cystic fibrosis 6.2. CT or HRCT:
High sensitivity and specificity
3. Symptoms
• Cough with production of large quantities of
purulent and often foul-smelling sputum.
Page 16
Figure 6.1- HRCT showing Bronchiectasis
Tram track sign: The bronchial wall is thickened 8.2. Acute General Treatment
and visible; the bronchi lose the trend of narrowing
from proximal end to distal end. • Supplement oxygen for hypoxemia.
• The choice of antibiotics should be accurate by
Signet ring sign: Dilated bronchi appear as ring
the results of sputum culture and drug
structures with internal diameters greater than those
sensitivity test.
of them accompany pulmonary artery branches.
• Empirical therapy - Antipseudomonal
antibiotics, Ciprofloxacin and Gentamicin or
7. Differential diagnosis • Antibiotic therapy is based on the results of
Differentiate from: sputum, Gram stain, and C&S
Chronic bronchitis, Lung abscess, Tuberculosis, • Bronchodilators are useful in patients with
Congenital pulmonary cyst. demonstrable airflow obstruction.
8. Treatment 8.3. Chronic Treatment

• Avoidance of tobacco.
8.1. Non-Pharmacologic Therapy • Maintenance of proper nutrition and hydration
• Chest physiotherapy helps the Postural drainage • Prompt identification and treatment of
and enhances removal of respiratory secretions. infections.
• Adequate hydration, mucolytic administration • Pneumococcal vaccination and annual influenza
vaccination
Bibliography
Further reading

Page 17
7. LUNG ABSCESS
• Blood culture may be helpful in establishing the
1. Introduction aetiology.
• A lung abscess is an infection of the lung • Obtain sputum for ova & parasite whenever a
parenchyma resulting in a necrosis and cavitation of parasitic cause for lung abscess is suspected.
lung.
• Commonest site is right lung and involves the 5. Radiological imaging
posterior segment of the right upper lobe, the
superior segment of the lower lobe, or both 5.1. CXR
• The bacterial infection may reach the lungs in
several ways that most common is aspiration of Lung abscesses are most commonly found in the posterior
oro-pharyngeal contents. segment of the right upper lobe. They appear as
irregularly sharp cavity with an air-fluid level inside.
2. Microbiology
• The most common anaerobes are
Peptostreptococcus, Bacteroids, Fusobacterium
species & Microaerophilic streptococcus.
• Other organisms that may infrequently cause lung
abscess include Staphylococcus aureus,
Streptococcus pyogens, Streptococcus pneumoniae
(rarely), Hemophilus influenza, Actinomyces
species, Nocardia species, & Gram negative bacilli
(Pseudomonas)
• Mycobacterial tuberculosis is a common cause.
• Non-bacterial pathogens may also cause lung
Figure 7.1- X-Ray Showing Lung Abscess
abscesses. Parasites [Paragonimus, Entamoeba]
Fungi [Aspergillus, Cryptococcus, Histoplasma,
Blastomyces, Coccidioides] seen in 5.2. CT Scan
immunocompromised patients. An abscess is rounded radio-lucent lesion with a thick
wall & ill-defined irregular margins.
3. Clinical presentation
• Symptoms are generally insidious and prolonged,
occurring for weeks to months
• Fever, chills, and sweats
• Cough
• Sputum production (purulent with foul odour)
• Pleuritic chest pain
• Haemoptysis
• Dyspnoea
• Malaise, fatigue, and weakness
• Tachycardia and Tachypnea
Dullness to percussion, whispered pectoriloquy, and
bronchophony
Figure 7.2- CT Showing Lung Abscess
4. Lab Studies
6. Medical care
• CBC- leucocytosis
• Sputum for gram stain, culture & sensitivity. Antibiotic therapy:
• If T.B. is suspected, acid fast bacilli stain & • IV Clindamycin 600 mg 3 times a day, till afebrile
mycobacterial culture is requested. then oral 300 mg four times a day for 7 days.
Page 18
• Alternative is IV Amoxicillin / Clavulanate 1.2gm • Duration of therapy is generally for 4-6 weeks to
thrice a day or I.V. Ampicillin / Sulbactam 1.5gm as long as 14 weeks.
thrice a day then to oral Amoxicillin / Clavulanate
Antibiotic treatment should be continued until the chest
for 7 days, with I.V. Metronidazole 500 mg 8
radiograph has shown either the resolution of lung
hourly is an effective drug against anaerobic
abscess or the presence of a small stable lesion.
bacteria for 7 days.
• In hospitalized patients who have aspirated and Patients with poor response to antibiotic therapy include
developed a lung abscess, antibiotic therapy should bronchial obstruction with a foreign body or neoplasm
include coverage against Staphylococcus aureus or infection with resistant bacteria, Mycobacteria, or
and Enterobacter and Pseudomonas species and as fungi.
per the identified pathogen.
• Cephalosporin that have gram-positive, gram- 7. Complication
negative, and anaerobic coverage, may be used
Rupture into pleural space causing empyema, pleural
when a polymicrobial infection is suspected as
fibrosis, bronchopleural fistula.
cause of lung abscess.
Bibliography
Further reading
1. Kuhajda A, Zarogoulidis K, Isirgogianni K, et.al. Lung abscess – etiology, diagnostics and treatment
options, Ann Transl Med [Internet].2015 Aug; 3(13): 183. [Cited 2016 Jul 5]

Page 19
8. PNEUMOTHORAX
• Stature
1. Definition
The presence of air within the pleural cavity. 4.2. Secondary spontaneous - less
common
2.Classification
• Chronic bronchitis & emphysema, (35%).
2.1. Spontaneous • Asthma (0.8).
• Suppurative pneumonia like Staphylococci,
• Primary. Klebsiella, HIV (2-4%).
• Secondary. • TB of lungs.
2.2. Traumatic 4.3. Traumatic Iatrogenic
• Non-iatrogenic. • Paracentesis thoracis (28%).
• Iatrogenic. • Central venous cannulation, (22%).
• Barotrauma (mechanical ventilation).
3. Spontaneous Pneumothorax • Tracheostomy.
Pneumothorax occurring in the absence of trauma
may be described as spontaneous. 4.4. Traumatic Non-Iatrogenic
Presents in 3 ways: Pneumothorax
• Open Pneumothorax- air moves freely in & out
of pleural space during breathing. • Open & closed chest injury, (road traffic
• Closed pneumothorax- no movement of air accident).
from the pleural space due to closure of the • Stab or gunshot wounds.
communication, air slowly gets absorbed & the • Rib fractures.
lung re-expands.
• Tension pneumothorax- a check – valve 5. Symptoms
mechanism is produced; this allows air to enter • Small pneumothorax is asymptomatic.
pleura & accumulate to raise the intrapleural
• Chest pain - Sharp unilateral associated with
pressure above the atmospheric pressure and
shortness of breath is commonest presentation.
leads to compression on lung & shifting of
• Sharp & stabbing Chest pain exacerbated by
mediastinum to opposite side.
deep inspiration & postural change.
3.1. Primary spontaneous • Anxious, restless, tachypnoeic, struggling for
breath, rapid low volume pulse & hypotension.
pneumothorax • May large pneumothorax produce respiratory
• Commonly occurs in healthy subjects with no distress, signs of shock.
h/o of pre-existing lung disease. • Closed pneumothorax –usually does not
• Disease of young adult. produce severe symptoms.
• Tension pneumothorax –medical emergency.
3.2. Secondary spontaneous
pneumothorax 6. Physical signs
• Coexisting structural or functional abnormality • Small pneumothorax – Difficult to detect on
in the lung. physical examination.
• Stature. • Absence or diminished breath sounds on
affected side.
4. Causes of Pneumothorax • Chest movement diminished on affected side
• Decreased vocal fremitus.
4.1. Primary spontaneous • Hyper resonant percussion notes.
• Apical Blebs (90%)
Page 20
• Ipsilateral enlargement of chest due to decrease
elastic recoil of the collapsed lung.
7. Diagnosis
• Shift of mediastinum on opposite side. ECG- Diminished anterior QRS amplitude.
• Increased JVP.
Radiographic appearances.
• Respiratory distress.
• Diaphoresis X-ray chest-sharply defined lung edge convex
• Cyanosis. outwards separated from chest wall by translucency
• Hypotension. with no lung markings & mediastinal displacement
• Crepitus is seen if there is associated depending upon the extent of pneumothorax.
subcutaneous emphysema.
Plain X-ray film of the chest showing

hyperlucency without any lung markings
on right side of the chest (Pneumothorax)
Figure 8.1 – X-Ray Showing Pneumothorax
• If pneumothorax small but patient mild

8. Differential diagnosis symptomatic, admit the patient & administer
• Transmural myocardial infarction-ECG changes high–flow oxygen, resulting nitrogen gradient
& left sided pneumothorax changes resolve will speed resorption.
once re-expansions. • If pneumothorax larger than 15% to 20% or
• Emphysema confused with pneumothorax but x- more than mildly symptomatic, insert a
ray is main diagnostic tool. thoracostomy tube.
• Massive emphysematous bulla or congenital • Secondary pneumothorax - Patients are
cyst, when ruptures may be confused with symptomatic & require lung re-expansion.
pneumothorax but previous x-ray, lateral • Often bronchopleural fistula persists & larger
decubitus view is helpful in differentiating thoracostomy tube & suction are required.
upper lobe bulla/cyst. • Iatrogenic pneumothorax -- Due to barotrauma
from mechanical ventilation always persistent
9. Complications air leak & should be managed with a chest tube
& suction.
Recurrence, Haemopneumothorax, Pyopneumothorax • Tension pneumothorax--decompress the
and Respiratory failure –when tension pneumothorax affected hemithorax immediately with a 14-
present. gauge needle attached to a fluid filled syringe,
release of air with clinical improvement
10. Treatment confirms the diagnosis. Seal chest wound with
Treatment depends on cause, size, degree of an occlusive dressing & arrange the placement
physiological derangement. Primary pneumothorax- of a thoracostomy tube.
smaller without pleural air leak may resolve
spontaneously.
Page 21
Bibliography
Further reading


Page 22
9. LUNG CANCER
1. Definition 3. Risk factors

Uncontrolled growth of malignant cells in one or • Smoking: Smokers have 10 fold or greater
both lungs and tracheo-bronchial tree. increase in risk.
• Radiation Exposure.
2. Epidemiology • Family history: 1st degree relatives – 2 to 3-fold
increase risk.
• Lung cancer was initially thought to be
• Environmental/ Occupational Exposure:
infrequent in India.
Asbestos, Arsenic, Chromium, Mustard gas,
• Rare below age 40.
Nickel, Radon, Polycyclic Hydrocarbons.
• Increasing until age 80 after which rate tapers
• Scarring.
off.
• Probability developing lung cancer
approximately 8% & 6% in males & females.
4. Signs and Symptoms
Table No. 1
Signs & symptoms Range of frequency
Cough (persistent for > than 2 weeks) 8-75%
Weight loss 0-68%
Dyspnoea 3-60%
Chest pain (poorly localized deep chest discomfort) 20-49%
Haemoptysis (seen more in central tumours) 6-35%
Bone pain 6-25%
Clubbing 0-20%
Fever 0-20%
Weakness 0-10%
SVC syndrome 0-4%
Dysphagia 0-2%
Wheezing & stridor 0-2%
5. Types of Lung Cancer • Large cell Carcinoma – 10-15%,

undifferentiated, giant or clear cell
5.1. Non-small cell carcinoma
5.2. Small cell Carcinoma (20-25%,
• Squamous Cell Carcinoma (25-40%, epidermoid
derived). oat, intermediate cell)
• Adenocarcinoma (25-40%, bronchial, acinar,
papillary, solid, bronchoalveolar). 6. Diagnosis
History and Physical exam: Physical signs like
clubbing, lymphadenopathy, hoarseness of voice
(vocal cord palsy on indirect laryngoscopy) along
Page 23
with chest x-ray signs of mass lesion and collapse malignancy.
which are pointers towards the diagnosis of
non resolving pneumonia in an elderly individual or in • PET scan – helpful in staging to determine
smoker, lung malignancy needs to be excluded. degree of metastases
• MRI/CT brain – useful in looking at CNS
6.1. Diagnostic tests involvement.
• Chest X-ray – Identifies nodules usually >1cm
• HRCT Chest - Mass lesion along with its morphology 7. Clinical findings suggestive
and vascularity can be better visualised of metastatic disease
• Bronchoscopy - It is the most useful investigation.
• Pleural tapping - Cytological examination of the • Lymphadenopathy [>1 cm]
pleural fluid is necessary to establish the diagnosis. • Bone tenderness
• Hepatomegaly [>13 cm span]
• Focal neurologic signs, papilledema
• Soft tissue mass
• Haematocrit < 40% in men, < 35% in women.
• Elevated alkaline phosphatase, GGT, SGOT,
calcium levels.
• Oesophageal compression – Dysphagia.
• Laryngeal nerve paralysis – Hoarseness.
• Symptomatic nerve paralysis - Horner’s
syndrome.
• Cervical/thoracic nerve invasion - Pancoast
tumour.
• Lymphatic obstruction - Pleural effusion.
Figure 9.1: Chest X ray showing Left Para hilar lung • Vascular obstruction - SVC syndrome.
mass • Pericardial / cardiac extension - Effusion,
tamponade.
6.2. Staging tests
• CT chest/abdomen.
8. Treatment
• Bone scan. Medical, surgical and radiation therapy modalities
• Bone marrow aspiration. considered according to the type and stage of the
cancer.
Bibliography
Further reading
1. Malik PS, Raina V. Lung Cancer – Prevalent trends and emerging concepts, Indian J Med Res
[Internet]. 2015 Jan; 141(1): 5–7. [cited 2016 Jul 5]

Page 24
10. PULMONARY EMBOLISM
Sometimes patients are asymptomatic.

1. Introduction
Differential Diagnosis - Myocardial Ischemia -
Thrombosis that originates in the venous system and Angina, Myocardial Infarct, Pneumonia, Pericarditis,
embolizes to the pulmonary arterial circulation. DVT Congestive Heart Failure etc.
in veins of leg above the knee (>90%), DVT
elsewhere (pelvic, arm, calf veins, etc.), Cardiac 3. Investigations
thrombi.
Risk factors - Obesity, smoking, OC pills, surgery, • Chest x-ray- Atelectasis, Westermark sign –
trauma, malignancy, thrombophilia. increased lucency in area of embolism,
Hampton’s hump - peripheral wedge shaped
density above diaphragm, pleural effusion.
2. Signs and symptoms • ECG- Sinus tachycardia, Classic S1Q3T3
Massive PE – Severe dyspnoea, hypotension, pattern, signs of RV Strain-R in V1 V2 with t
cyanosis, tachycardia. inversion.
• ABG - Hypoxia, hypocapnia, respiratory
Moderate PE- Cough, pleuritic pain, haemoptysis,
alkalosis Normal does not rule out PE.
fever. Other signs are anxiety agitation, raised JVP,
loud P2, right ventricular heave.
ECG Findings
Figure-10.1: ECG changes seen in Pulmonary Embolism
Page 25
• D-dimer is raised (high sensitivity but poor
specificity).
4.Treatment
• CT Pulmonary Angiography is gold standard. • Thrombolysis in massive PE. Inj. Streptokinase
• V/Q Lung scan identifies areas of lung that are 2.5 lakhs bolus, then 1.0 lakh per hour.
ventilated but not perfused. • Unfractionated heparin 80 U/kg bolus, then 18
• US Venous Doppler to detect deep venous u/kg/hour with goal of PTT 46-70 secs.
thrombosis. • LMWH- Inj. Enoxaparin 1 mg/kg 12 hourly. To
overlap with warfarin and to continue it for 3-6
months.
Bibliography
Further reading
1. Dalal J J, Amin P. Management of Acute Pulmonary Embolism, Journal of The Association of
Physicians of India Vol. 63 [Internet]. December 2015. [cited 2016 Jul 5]
Available from: http://www.japi.org/december_2015/07_oa_management_of_acute.pdf

Page 26
11. HYPERTENSION
Blood pressure is lateral pressure exerted by column

The average of two or more seated blood pressure
of blood on the walls of artery when it flows through
during each of two or more outpatient visits.
it.
4.2. Basic investigations for initial
1. Definition
evaluation: Always includes
• Hypertension - Defined as any one of the • Haematocrit / Hb.
following:
• Serum BUN, Creatinine.
• Systolic blood pressure > 140 mmHg and / or
Diastolic blood pressure >90 mmHg, • Serum potassium.
• Patient taking antihypertensive medications. • Fasting blood sugar.
• Essential HT: When the cause is not known (90 • Total cholesterol, S Triglycerides.
to 95 % cases). • Urine analysis for albumin, blood, glucose.
• Secondary HT: Specific organ dysfunction is • ECG for left ventricular hypertrophy and ST-T
detected (5 to 10 % cases). changes.
2. Symptoms • Fundoscopy for HT retinopathy.
• Often asymptomatic (silent killer). 4.3. Investigations usually included

• Due to Elevated pressure: Headache (Occipital), depending on cost & other
vomiting, giddiness, breathlessness, factors
palpitations. i. TSH
• Due to Vascular disease: Cerebrovascular ii. Complete blood count.
accident, Acute Myocardial Infarction.
iii. HDL, LDL cholesterol.
• Due to Underlying disease: symptoms of
underlying organ affected. iv. Serum calcium, phosphorus.
v. Serum Uric Acid.
3. Signs
vi. Chest X-ray - Cardiomegaly.
• Blood vessels – Bruits over carotid.
vii. USG renal system - Cortical scarring,
• Abdominal Bruit – To rule out Renovascular shrunken size, obstructive uropathy.
hypertension.
viii. Echocardiography – LVH, Diastolic
• Spells of sweating, tachycardia – dysfunction, Ejection Fraction.
Pheochromocytoma.
4.4. Special tests to screen for
• Tremors, neck swelling– Thyroid Disorder.
secondary HT (only in
• Snoring, Daytime somnolence – Obstructive
sleep, Apnoea.
indicated cases)
• Renovascular disease: Renal Doppler, MR
• Asymmetry of pulses, Radiofemoral delay– angiography, DTPA scan.
Takayasu Disease, Coarctation of Aorta.
• Renal parenchymal: Kidney biopsy.
4. How to investigate? • Pheochromocytoma: 24-hour urine
metanephrine & catecholamine.
4.1. Accurate BP measurement
• Cushing’s syndrome: Serum cortisol,
Dexamethasone suppression test.
Page 27
• Aldosteronism: Plasma aldosterone: renin ratio. • ECG
4.5. Annual tests in hypertensive • Fundoscopy.

subjects 5. How to treat?
• Haemogram
• Renal profile 5.1. Goal BP – 150/90 mm Hg in elderly and
140/90 mmHg in all others (including DM, CKD).
• Lipid profile
5.2. Life style changes
• Urine analysis
Table 1: Lifestyle changes to manage hypertension
Modification Aim
Weight reduction Attain and maintain BMI < 25 kg/m2
Adopt DASH eating plan Diet rich in fruits, vegetables & low-fat dairy products with
reduced content of saturated and total fat
Dietary sodium reduction < 4.8-7.4 g NaCl/day
Physical activity Regular aerobic activity- brisk walking for 30 min/day
5.3. Guidelines for management

Table 2: Hypertension management guidelines
Lifestyle
BP Classification SBP mmHg DBP mmHg Drug Therapy
Modification
Normal <120 and <80 Encourage No
Prehypertension 120-139 or 80-89 Yes No
Stage 1 Hypertension 140-159 or 90-99 Yes Single Agent
Stage 2 Hypertension ≥ 160 or ≥ 100 Yes Combo
Page 28
5.4. Treatment protocol
Figure 11.1: Treatment Protocol for HT Age > 30 Years
History & Physical examination
Confirmation of diagnosis by
BP > 140/90 mm of Hg.
Educate Patient on nutrition, salt restrictions, physical activity

de-addiction and regular follow up. (Refer to Health Workers Manual)
Start the Treatment
Age ≥ 60 Yr. Age < 60 Yr.

Goal of Treatment Goal of Treatment
BP < 150/90 mm Hg. BP < 140/90 mm Hg.
1) IF BP is 140-160 1) IF BP is 140-100
Start CCB Start ACE inhibitors. *(Not recommended in Renal Failure)
T. Amlodipine 5mg once a day T. Enalapril 5 mg once a day
Goal achieved Goal achieved

Cont. Rx Cont. Rx
Goal Not Achieved Goal Not Achieved
T. Enalapril 10 mg once a day

T. Amlodipine 10 mg once a day
Goal achieved Goal achieved

Cont. Rx Cont. Rx
Goal Not Achieved

Goal Not Achieved
Goal achieved
Goal achieved Cont. Rx
Cont. Rx
T. Enalapril + T. Hydrochlorothiazide
T. Amlodipine + T. Hydrochlorothiazide 5 mg once a day + 12.5 mg once a day
5 mg once a day + 12.5 mg once a day
Goal not achieved

Goal Not Achieved
Page 29
Goal achieved
Cont. Rx
Age ≥ 60 Yr.
Goal of Treatment
BP < 150/90 mm Hg.
Age < 60 Yr.
Goal of Treatment
BP < 140/90 mm Hg.
2) If BP is>160 mm of Hg
2) If BP is >160 mm of Hg
Start with
Start with
T. Amlodipine + T. Hydrochlorothiazide
5 mg once a day + 12.5 mg once a day
Goal achieved 5 mg once a day + 12.5 mg once a day
Cont. Rx
Goal achieved
Goal not achieved Cont. Rx
Goal not achieved

T. Amlodipine + T. Hydrochlorothiazide
10 mg once a day + 25 mg once a day
10 mg once a day + 25 mg once a day
Goal achieved
Cont. Rx
Goal achieved cont.
T. Amlodipine + T. Hydrochlorothiazide + T. Enalapril Rx
10 mg once a day + 25 mg once a day + 5mg once a day
Goal not Achieved
T. Enalapril + T. Hydrochlorothiazide + T. Amlodipine

10 mg once a day + 25 mg once a day +5 mg once a day
Goal achieved
Cont. Rx
Goal achieved
Goal not Achieved Cont. Rx
Goal not Achieved

T. Amlodipine + T. Hydrochlorothiazide + T. Enalapril
T. Enalapril + T. Hydrochlorothiazide + T. Amlodipine
Refer to DH
Goal Achieved Refer to DH

Cont. Rx
Goal Achieved
Cont. Rx
Goal not achieved
Goal not achieved
Page 30
• If age < 30 years & BP > 140/90 - immediately
refer to DH (District hospital).
6. Vigilance for End Organ
• When patient is on drug if systolic BP is < 100 Damage in hypertensive
mm of Hg withhold the drugs (Anti-
Hypertensive drugs) and refer to DH. patients
• BP >160/100, Start min 2 Anti-Hypertensives • Congestive heart failure.
• If initial BP is > 200/100 refer to DH after a • IHD.
shot of Inj. Frusemide 60 mg stat. • Chronic Kidney Disease.
• If Sr. Creatinine > 1.5mg% refer to DH. • Stroke.
• Hypertensive Retinopathy.
5.5. Hypertension in Pregnancy
• Tablet Methyl Dopa – 500 mg-1000 mg/Day in 7. When to refer?
three divided dose.
• Tablet Nifedipine Extended Release Preparation • Annual Work-up of known Hypertensive
30 - 60 mg OD/BD. subjects.
• Other drugs that can be given - Labetalol, • Young Hypertensive/ secondary HT.
Hydralazine, Beta Blocker. • Resistant Hypertension (Target BP not achieved
• ACE inhibitors and ARBS avoided. with 3 drugs including diuretics).
• Pregnant subjects.
• Hypertensive emergencies (BP > 180/ 110 mm
Hg with e/o end organ damage).
Bibliography
Further reading
1. India. Ministry of Health and Family Welfare. NHM Standard Treatment Guidelines for Hypertension.
[cited 2016 Jul 5]
Available from: http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/hypertension.pdf
2. Hypertension guidelines. World Health Organization (WHO) [Internet]. [cited 2016 Jul 5]
Available from: http://www.who.int/topics/hypertension/en/
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Page 31
12. HEART FAILURE
i. Right heart failure should be suspected if the

1. Introduction clinical features are present like swelling in the
Heart failure (HF), often referred to as congestive legs and engorged neck vein.
heart failure (CHF), occurs when the heart is unable ii. Also, once the features can be demonstrated on
to pump sufficiently to maintain blood flow to meet clinical examination, the underlying causes of
the body's needs right heart failure should be looked for; e.g.
History of smoking and signs of COPD, or signs
2. Types of heart failure of Mitral Valve Disease.
The heart consists of two distinct parts; right and left 2.1.4. Investigations for Right Heart Failure
receiving blood from different venous system and The diagnosis of Right Heart failure is a clinical one.
perfusing distinct parts of the body; the right heart Investigations are basically to diagnose the
perfusing Heart Failure is a condition where the heart underlying cause of right heart failure.
is unable to perform its functions optimally; leading
to decreased perfusion of the tissues supplied by the 2.1.5. Treatment of Right Heart Failure
lungs for gaseous exchange and the left heart
Right heart failure is not a medical emergency and
perfusing the systemic circulation.
does not cause immediate fatality. There is no direct
Hence there are two types of heart failure. treatment of Right Heart failure. This condition is
alleviated by effective treatment of the cause of
• Right heart failure. failure.
• Left heart failure. Hence attempts should be made to manage COPD
effectively, like:
2.1 Right Heart Failure
• Antibiotics in acute exacerbation.
The right receives blood from the systemic veins and • Effective bronchodilation using inhalers and
pumps blood into the pulmonary artery through the oral long acting Xanthines (Deriphyllin).
pulmonary valve. • Low flow oxygen inhalation which is the
Hence the cause of Right heart failure would be; treatment of choice for Cor Pulmonale.
increased pressure in the pulmonary artery • Effective treatment of Mitral stenosis including
(Pulmonary Hypertension) or pulmonary valve Low salt diet, Diuretics, and Digoxin.
stenosis. 2.1.6. When to Refer a Case of Right Heart
2.1.1. Causes of Pulmonary Hypertension Failure to Higher Centre
i. Chronic Obstructive Pulmonary Disease
(COPD) seen commonly in smokers. Cor A case of right heart failure needs to be referred for
Pulmonale. specialized treatment only for management of non-
ii. Mitral valve stenosis seen in Rheumatic heart responsive chronic obstructive airway disease. In
diseases. case, the cause of right heart failure is Mitral valve
disease which is not amenable to medical
2.1.2. Clinical features of Right heart failure management, such cases should be referred to a
As the right heart receives blood from the systemic cardiac centre for definitive management of the
veins, the main clinical features involves features of condition.
congestion in the systemic venous system.
2.2. Left Heart Failure:
i. Raised Jugular Venous Pressure with engorged [Pulmonary Oedema]
superficial neck veins.
ii. Tender Hepatomegaly: Painful, soft liver The left heart receives blood from the pulmonary
palpable in the right hypochondrium. vein and pumps blood in the systemic circulation.
iii. Dependent Oedema: Pitting oedema
2.2.1. Causes of left heart failure
demonstrable on the shin of the tibia and ankles.
i. Systemic Hypertension is the commonest cause
2.1.3. When to Suspect Right Heart Failure for left ventricular failure
Page 32
ii. Valvular heart diseases: Aortic stenosis, Aortic i. The patient should be treated in the propped up
regurgitation and Mitral regurgitation are all position using a backrest or raised head end of
causes or acute left heart failure. the bed.
iii. Myocardial infarction involving significant part
ii. High flow Oxygen inhalation should be given.
of left ventricle can cause L.V. failure.
iii. Sedation preferably with Morphine 10 mg I.V
2.2.2. Clinical features or Pentazocin 30 mg is the management of
i. Sudden onset breathlessness is the main choice.
symptom. If these powerful narcotics are not available, any
ii. There may be continuous cough with pink form of sedation will be of help.
frothy sputum.
iii. The patient will be very anxious and restless. iv. Intravenous Frusemide (Lasix) 60 mg I.V
iv. The patient will choose to be in the sitting should be administered.
position and unable to lie down.
v. Acute reduction of blood pressure must be done
v. On auscultation of the chest, crepitation will be
if the cause of left heart failure is Hypertension:
heard most prominently in the bases.
I.V. infusion of Nitroglycerin (5 microgram/ kg)
vi. General examination will reveal high blood
by BP monitoring, should be tried for the
pressure which is the commonest cause.
purpose.
vii. Such patients are likely to present with
cyanosis. (Bluish discoloration of tongue, lip, vi. Anti-platelets, statins to be continued.
oral mucosa, fingers and toes).
2.2.5. When to Refer the Patient
2.2.3. Investigations
Treatment of left heart failure must be attempted at
Left ventricular failure is a medical emergency and the peripheral level. Once stabilized the patient may
time should not be wasted in any investigation. be referred to higher centre for management of the
underlying cause.
However, after stabilizing the patient investigations
may be carried out to find the underlying cause. Failure of the patient’s breathlessness to resolve, may
require, endotracheal intubation or non-invasive
2.2.4. Treatment positive pressure ventilation and patient should be
Left heart failure or Pulmonary oedema is a medical referred to such a centre if facilities for the same is
emergency and speed of administration of treatment not available.
is of paramount significance.
Bibliography
Further reading
1. Huffman MD, Prabhakaran D. Heart Failure: Epidemiology and prevention in India, Natl Med J India
[Internet]. 2010 Sep-Oct; 23(5): 283–288. [cited 2016 Jul 5]
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Page 33
13. ISCHAEMIC HEART DISEASE AND
ACUTE CORONARY SYNDROME
ECG taken at that time may show ST elevation or

1. Introduction depression or T inversion. In between anginal
episodes, the ECG may be normal.
1.1. Ischemic heart disease (IHD) A treadmill stress test would confirm angina in over
It is a condition in which there is an inadequate 95% of these cases in referral hospital.
supply of blood and oxygen to a portion of the Echocardiography to measure left ventricular
myocardium. It typically occurs when there is an function and rule out segmental dyskinesia
imbalance between myocardial oxygen supply and suggestive of earlier myocardial infarction.
demand.
1.2. Patients with ischemic heart 2.3. Treatment

disease fall into two large Daily exercise, Stop smoking, Dietary modification –
groups. low cholesterol, low fat diet with high roughage.
i. Patients with chronic coronary artery disease Control of hypertension, Diabetes Mellitus and
(CAD) who most commonly present with Dyslipidaemia.
stable angina.
Drug Treatment
ii. Patients with acute coronary syndromes
(ACSs). • Tab Aspirin 75 mg once daily.
a. Patients with acute myocardial infarction • Tab Clopidogrel 75 mg per day.

(MI) with ST-segment elevation on their • Tab Atorvastatin 40 mg per day.
presenting electrocardiogram (ECG).
• Nitrates -Sublingual Glyceryl Trinitrate 300-500
b. With unstable angina (UA) and non-ST- microgram t.i.d. or Isosorbide Dinitrate 10 mg
segment elevation MI. thrice a day. If there is headache lower dose of 5
mg twice or thrice daily can be tried.
2. Stable Angina
• Beta-blockers - Tab Metoprolol 50 –200 mg /
2.1. Clinical Presentation day (PO in divided dose).
Chest pain – Retrosternal, dull aching, constricting or
burning, radiating to neck, jaw, shoulders or arms • Potassium channel activators- Nicorandil 10mg
usually precipitated by exertion or stress and relieved BD.
by rest or nitrates. Angina is crescendo and
decrescendo in nature and typically last for 2-5 • Calcium channel blockers like Tab Amlodipine
minutes. 5-10 mg once a day.
The physical examination is often normal in patients Refer for coronary angiogram and revascularisation
when asymptomatic. Examination during an anginal therapy.
attack and transient left ventricular failure, there can
be a third, fourth heart sound, and systolic murmur of
mitral regurgitation. 3. Unstable Angina and Non-
2.2. Investigations ST-Segment Elevation
CBC, Urine, Blood sugar, Lipid profile, and X-ray
Myocardial Infarction
chest PA view may be helpful.
Page 34
UA is defined as angina pectoris or equivalent
ischemic discomfort with at least one of three
4. ST segment elevated
features: Myocardial Infarction
a. It occurs at rest (or with minimal exertion), 4.1. Clinical Presentation
usually lasting >10 minutes. • Chest Pain- commonly occurs at rest, severe,
b. It is severe and of new onset (i.e., within the and lasts longer. Typically, the pain involves the
prior 4–6 weeks); and/or central portion of the chest and/or the
epigastrium, and, on occasion, it radiates to the
c. It occurs with a crescendo pattern (i.e., arms, abdomen, back, lower jaw, and neck.
distinctly more severe, prolonged, or frequent
than previously). • Sudden-onset breathlessness, Sweating, loss of
consciousness, a confusional state.
• Sensation of profound weakness, the appearance
3.1. Clinical Presentation of an arrhythmia, an unexplained drop in arterial
Chest pain, typically located in the substernal region pressure.
or sometimes in the epigastrium that radiates to the
neck, left shoulder, and/or the left arm. 4.2. Laboratory Findings
• CBC, Blood sugar, lipid profile, X-ray chest.
3.2. Electrocardiogram
ST-segment depression, transient ST-segment • Cardiac markers - CPK-MB elevated.
elevation, and/or T-wave inversion.
• Troponin T and I released within 4-6 hours and
3.3. Cardiac Biomarkers elevated for 2 weeks.
CPK-MB and troponin raised in Non-ST segment • Electrocardiogram Convex ST – segment
elevated MI. elevation with either peaked upright or inverted
T waves. Q waves if necrosis occurs.
3.4. Treatment • Echocardiogram - regional wall motion
• Bed rest. abnormality.
• Sublingually Nitroglycerin .3-.6 mg stat can
repeat after 5 min - 3 Doses.
4.3. Complications
• If symptoms persist, intravenous Nitroglycerin • Arrhythmias.
infusion at dose of 5-10 microgram/min. once
pain has resolved Oral Isosorbide Dinitrate 10 • Acute Heart failure.
mg BD can be given. • Rupture of papillary muscle.
• Aspirin initial dose of – 325 mg followed by • Embolism leading to stroke.
150 mg/day lifelong.
• Ventricular remodelling.
• Clopidogrel - Loading dose of 300 mg followed
by 75 mg/ day for 2 years. • Ventricular aneurysm.
• Tab Atorvastatin 40 mg / day lifelong.

• Intravenous beta blocker – Metoprolol 5-15 mg
4.4. Treatment
over 5 mins followed by tab Metoprolol 50-100 • Bed rest.
mg/day in divided doses with BP check. • Oxygen therapy - 2-4 L/min.
• Unfractionated Heparin (UFH) bolus 60–70 • Sublingually Nitroglycerin .3-.6 mg stat can
U/kg (maximum 5000 U) IV followed by repeat after 5 min - 3 Doses if symptoms persist,
infusion of 12–15 U/kg per hour (initial intravenous Nitroglycerin infusion at dose of 5-
maximum 1000 U/h) titrated to A PTT 50–70 s. 10 microgram/min. once pain has resolved Oral
or Isosorbide Dinitrate 10 mg b.i.d can be given.
• Enoxaparin 1 mg/kg SC every 12 hr. • Aspirin 325 mg and then 150 mg once a day.
• Clopidogrel 300 mg and then 75 mg BD.
Page 35
• Atorvastatin 80 mg and then 40 mg HS. • Stool softeners – Bisacodyl (Dulcolax) 10 mg at
night.
• Reperfusion therapy: If presenting within 12
hours of chest pain with ECG showing ST Message
elevation > 1 mm then give Inj. Streptokinase
Acute myocardial infarction is an emergency
1.5 million units over 1 hour (contraindications-
whatever treatment possible should be started at the
a history of cerebrovascular haemorrhage at any
center and patient should be transferred to District
time, a non-haemorrhagic stroke or other
Hospital or any hospital where ICU facility is
cerebrovascular event within the past year,
available in a cardiac ambulance. Patient should not
marked hypertension at any time during the
be allowed to walk for even short distances and
acute presentation, suspicion of aortic
absolute Bed Rest is important. Treatment of
dissection, and active internal bleeding).
complications like Heart failure, Arrhythmias may
• Beta blockers: Metoprolol 25 to 50 mg b.i.d, need expert opinion.
Atenolol 25 to 100 mg one a day (if pulse rate > Coronary Angiography and revascularisation therapy
60/mm, BP > 90/60 mm Hg, lung fields clear). should be advised.
• ACE inhibitors – Enalapril 2.5 – 20 mg / day in
divided doses twice a day.
Bibliography
Further Reading:
1. India. Ministry of Health and Family Welfare. Guidelines for Acute Myocardial Infarction. [cited 2016
Jul 5]
Available from: http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/acute-myocardial-
infarction.pdf
2. Vamadevan S. Ajay and Dorairaj Prabhakaran. Coronary heart diseases in Indians: Implications of
INTERHEART Study. Indian J Med Res.[Internet]. 2010 Nov; 132(5): 561–566. [cited 2016 Jul 5]
3. WHO. Clinical management guidelines for CAD. SEARO: World Health Organization. [cited 2016 Jul
5]
Available from:
http://www.searo.who.int/india/topics/cardiovascular_diseases/NCD_Resources_CLINICAL_MANA
GEMENT_GUIDELINES_FOR_CAD.pdf?ua=1

Page 36
14. ACUTE RHEUMATIC FEVER (ARF)
Acute rheumatic fever (ARF) is a multisystem

1. Introduction disease resulting from an autoimmune reaction to
infection with group A streptococcus.
2. Criteria for diagnosis of ARF

Major manifestations Carditis (Pancarditis)
Polyarthritis (Migratory)
Chorea
Erythema marginatum
Subcutaneous nodules
Minor manifestations Clinical: fever, polyarthralgia
Laboratory: elevated erythrocyte sedimentation rate or leukocyte
count
Electrocardiogram: prolonged P-R interval
Supporting evidence of a preceding Elevated or rising anti-streptolysin O or another streptococcal
streptococcal infection within the last 45 days antibody, or
A positive throat culture, or
Rapid antigen test for group A. streptococcus, or
Recent scarlet fever
Two major or one major and two minor Penicillin is the drug of choice and can be given
manifestations plus evidence of preceding group A orally [as Phenoxymethyl Penicillin, 500 mg
streptococcal infection. (250 mg for children 27 kg) PO twice daily, or
Amoxicillin 50 mg/kg (max 1 g) daily, for 10
3. Investigations days] or as a single dose of 1.2 million units
White blood cell count, Erythrocyte sedimentation (600,000 units for children 27 kg) IM
rate, C-reactive protein, Blood cultures if Benzathine Penicillin G.
febrile, Electrocardiogram, Chest x-ray if clinical or
• Aspirin in initial dose of 80–100 mg/kg per day
echocardiographic evidence of
in children (4–8 g/d in adults) in 4–5 divided
carditis, Echocardiogram (consider repeating after 1
doses is used for the treatment of arthritis,
month if negative). Throat swab (preferably before
arthralgia, and fever for 4 weeks.
giving antibiotics)–culture for group A.
streptococcus. • Inj. Benzathine Penicillin G 1.2 IU (6 lakhs
units for children 27 kg) IM every 3 weeks as
Anti-streptococcal serology: both anti-streptolysin O
prophylactic dose up to the age of 25 years.
and Anti-DNase B titres, if available.
4. Treatment 5. When to refer

Evidence of Congestive cardiac failure, Arrhythmia.
• All patients with Acute Rheumatic Fever (ARF)
should receive antibiotics sufficient to treat the
precipitating group A. streptococcal infection.

Page 37
Bibliography
Further reading
1. Kumar RK, Tandan R. Rheumatic fever and rheumatic heart disease: Last 50 years, Indian J Med Res
[Internet]. 2013 Apr; 137(4): 643–658. [cited 2016 Jul 5]

Page 38
15. INFECTIVE ENDOCARDITIS
1. Definition Streptococci, Pneumococci Enterococci,

Staphylococcus Aureus, Coagulase-negative
Infective endocarditis is a form of endocarditis, or Staphylococci. Fastidious Gram-negative
inflammation, of the inner tissue of the heart (such as coccobacilli (HACEK group i.e.
its valves) caused by infectious agents. The agents Haemophilus species, Aggregatibacter Aphrophilus,
are usually bacterial, but other organisms can also be Cardiobacterium, Eikenella, Kingella), Gram-
responsible. negative bacilli, Candida spp.
Infection most commonly involves heart valves either
native or prosthetic.
3. Clinical Manifestations
2. Organisms Causing Major (Symptoms and signs)
Clinical Forms of Symptoms- Fever, chills, arthralgia, fatigue.
Endocarditis
Figure 15.1: Signs of Infective Endocarditis
Page 39
iv. Immunological
4. Diagnosis phenomenon;(glomerulonephritis; Osler
nodes; Roth's spots; rheumatoid factor)
Modified Dukes Criteria v. Microbiological evidence positive blood
cultures but not meeting major criteria or
4.1 Major Criteria serological evidence of active infection with
organism consistent with infective
i. Positive blood culture – endocarditis.
Two separate positive blood cultures with
microorganism(s) typical for infective Documentation of 2 major / one major and 3 minor /5
endocarditis: Viridians streptococci, minor criteria allow a diagnosis Infective
streptococcus bovis, HACEK group, endocarditis.
Staphylococcus aureus, community acquired
enterococci
5. Investigations
or
Persistently positive blood culture defined as
presence of microorganism consistent with • CBC-Anaemia, Leucocytosis.
infective endocarditis from blood cultures • Urine-Microscopic haematuria.
drawn >12 hours apart. • Elevated ESR, Elevated CRP.
or • Blood culture 3 sets of two bottle blood. Culture
Single positive blood culture for Coxiella from different venepuncture site separated from
burnetii or phase one IgG antibody titre of >1: one another by at least one hour over 24 hours.
800. • Echocardiography.
ii. Echocardiographic evidence of endocardial 6. Complications

involvement typical Valvular lesions;
vegetations, abscess, or new partial dehiscence • Blood clots or emboli that travel to brain,
of a prosthetic valve New Valvular kidneys, lungs, or abdomen.
regurgitation. • Brain abscess.
• Congestive heart failure.
4.2 Minor Criteria • Glomerulonephritis.
• Jaundice.
i. Predisposition; predisposing heart condition or • Neurological changes.
intravenous drug use. • Rapid or irregular heartbeats, including atrial
ii. Temperature greater than 38.0 C. fibrillation.
iii. Vascular phenomenon; major arterial emboli, • Severe valve damage.
septic pulmonary infarcts, mycotic aneurisms, • Stroke.
intracranial haemorrhages, conjunctival
haemorrhages, Janeway lesion
Page 40
7. Treatment
Table 1: Antimicrobial Therapy
Organism Drug (Dose, Duration)

Penicillin-susceptible streptococci Inj. Penicillin G (2–3 MU IV q4h for 4 weeks) or
Inj. Ceftriaxone (2 g/d IV as a single dose for 4 weeks) plus
Inj. Vancomycin (15 mg/kg IV q12h for 4 weeks)
Moderately penicillin-resistant streptococci Inj. Penicillin G (4–5 MU IV q4h) or Ceftriaxone (2 g IV

q.d.) for 6-weeks plus
Inj. Gentamicin (3 mg/kg q.d. IV or IM as a single dose or
divided into equal doses q8h for 6 weeks) Plus
Inj. Vancomycin (15 mg/kg 12 hourly) as noted above for 4
weeks
Enterococci Inj. Penicillin G (4–5 mU IV q4h) plus
Inj. Gentamicin (1 mg/kg IV q8h), both for 4–6 weeks
Staphylococci (native valve) Inj. Vancomycin (15 mg/kg IV q12h for 4–6 weeks)
Staphylococci (prosthetic valves) Inj. Vancomycin (15 mg/kg IV q12h for 6–8 weeks) plus
Inj. Gentamicin (1 mg/kg IM or IV q8h for 2 weeks) plus
Rifampin (300 mg PO q8h for 6–8 weeks)
8. Prevention
High Risk cardiac lesions where antibiotic
prophylaxis is needed.
1. Prosthetic heart valve.

2. Prior endocarditis.
3. Unrepaired cyanotic congenital heart disease.
4. Completely repaired cyanotic heart disease
within 6 months.
5. Incompletely repaired cyanotic heart disease
with residual defects.
Page 41
Table: 2: Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk
Cardiac Lesion
A. Standard oral regimen
1. Amoxicillin: 2 g PO 1 h before procedure
B. Inability to take oral medication
1. Ampicillin: 2 g IV or IM within 1 h before procedure
C. Penicillin allergy
1. Clarithromycin or azithromycin: 500 mg PO 1 hour before procedure
2. Cephalexin: 2 g PO 1 h before procedure
3. Clindamycin: 600 mg PO 1 h before procedure
D. Penicillin allergy, inability to take oral medication
1. Cefazolin or Ceftriaxone: 1 g IV or IM 30 min before procedure
2. Clindamycin: 600 mg IV or IM 1 h before procedure
Message- If any valvular heart disease or prosthetic valve patient develops fever, infective
endocarditis should be thought of apart from other normal causes of fever.
Bibliography
Further reading
1. Ashish Gupta, Anu Gupta et el. Infective endocarditis in an Indian setup, Indian J Crit Care Med
[Internet]. 2013 May-Jun; 17(3): 140–147. [cited 2016 Jul 5]

Page 42
16. DIABETES MELLITUS
• Diseases of exocrine pancreas – Trauma,
1. Introduction Pancreatitis, Pancreatectomy, Cystic fibrosis,
Diabetes mellitus is a clinical syndrome characterized Fibro-calculous Pancreatic diabetes,
by hyperglycaemia due to absolute or relative Haemochromatosis.
deficiency of insulin.
• Gestational Diabetes Mellitus (GDM) Onset /
Recognition of glucose intolerance in
2.Classification of Diabetes pregnancy.
Mellitus 3. Diagnosis of Diabetes

2.1. Type 1 Diabetes Mellitus
Autoimmune Pancreatic B cell destruction; absolute Mellitus
insulin deficiency. ● Symptoms of Diabetes Mellitus and Random
Blood Sugar > 200 mg% (mg / dl)
2.2. Type 2 Diabetes Mellitus
Characterized by peripheral tissue Insulin Resistance ● Fasting blood sugar > 126 mg % on more than
/ Relative Insulin deficiency. one occasion.
● 2 hours Plasma glucose > 200 mg% during oral
2.3. Other Specific Types glucose tolerance test with glucose – 75 g
glucose.
• Genetic defects of B cell function – Maturity
Onset Diabetes in Young (MODY).
• Genetic defects of insulin action.
Table 1: Criterion for Diagnosis based on blood glucose levels
Pre-diabetic
Normal Glucose Impaired glucose Diabetes mellitus
tolerance
FPG <100mg/dl 100-125 mg/dl >126 mg/dl
2hr PG <140mg/dl 141-199 mg/dl >200 mg/dl
A1C (Glycosylated <5.6% 5.7-6.4% >6.5 mg/dl

Haemoglobin)
Other symptoms are tiredness, fatigue, pruritus

4. Clinical symptoms vulvae, giddiness, burning over feet and can present
with complications of diabetes.
Common symptoms are
1. Polyuria {increased frequency of micturition),
2. Polydipsia (increased thirst),
3. Polyphagia (increased appetite),
4. Weight loss.
Page 43
5. Management
Table -2: Major differentiating features of Type 1 and Type 2 diabetes are as follows:
5.1 Type 1 Diabetes Mellitus e) α Glucosidase inhibitors - Acarbose, Voglibose,

Miglitol
• Strict meal plan * Carbohydrate: 50 - 60%* f) DPP4 inhibitors- Sitagliptin, Vildagliptin
Protein: 10 – 20% * Fat: 30% (If patient is
dyslipidemic, fat should be 15%) Parenteral agents
*Caloric intakes: 30 Kcal / kg 1. Insulin
2. GLP-1 receptor agonist- Liraglutide, Exenatide
• Physical exercise
• Only Insulin (a) Biguanides
Dose- 500 mg-2000 mg/day.
5.2 Type 2 Diabetes Mellitus: Contra-indications to Biguanides therapy: 1. Renal
failure when creatine clearance < 40 ml / min 2.
• Strict meal plan Arteriography or intravenous urography – as
• Physical exercise intravenous iodinated products may precipitate lactic
• Oral hypoglycaemic agents acidosis on patients with biguanides 3. Advanced
• Insulin liver cell failure 4. Alcoholism 5. Cardiac diseases 6.
Diabetes with significant acute and late
Oral Hypoglycaemic Agents:
complications 7. Pregnancy 8. Old age > 70 years.
a) Biguanides - Metformin
(b) Sulphonylureas
b) Sulphonylureas - Glibenclamide, Glipizide, Mechanism of action- Increases insulin secretion
Glimepiride, Gliclazide from the beta cells through the ATP sensitive K
channels.
c) Glinides (Nonsulphonylurea Secretogouge) -
Repaglinide
d) Thiazolidinediones –Pioglitazone
Page 44
Table-3: Sulphonylurea drugs with dosage and side effects
Drug Dose Side effects

Glibenclamide 1.25-20 mg Hypoglycaemia, weight gain
Glimepiride 1-8 mg Hypoglycaemia
Glipizide 2.5 -25 mg Hypoglycaemia
Gliclazide 30-240 mg Hypoglycaemia
Contraindications for sulphonylurea therapy thereby increasing insulin secretion only with the
intake of food. They do not cause hypoglycaemia.
1. Insulin dependent diabetes mellitus (IDDM)
Dose- Vildagliptin 50 mg BD, Sitagliptin 100 mg
2. Pregnancy
OD.
3. Patients with severe infections
Insulin
4. Allergic reactions
Consider insulin as initial therapy in patients
5. Significant liver and kidney disease with:
6. Patients undergoing surgery • Fasting plasma glucose > 250 - 300 mg/dl since
more rapid glycaemic control will reduce
(c) Glinides - (Nonsulphonylurea) Secretogouge-
glucose toxicity to islet cells, improve insulin
Increase insulin secretion
secretion and possibly make oral hypoglycaemic
Dose-Repaglinide – 0.5-3 mg/day. agents more effective.
(d) Thiazolidinedione - These are insulin sensitizers. • Lean patients or those with severe weight loss.
Pioglitazone is commonly used.
• Underlying renal or hepatic disease.
Dose- 15- 45 mg/day.
• Hospitalized or acutely ill patients.
Side effects- Weight gain, congestive cardiac failure,
fractures, • If response to oral hypoglycaemics is not
adequate. Consider insulin as initial therapy
(e) α Glucosidase inhibitors – Decreases intestinal
glucose absorption and reduce postprandial • Pregnancy
hyperglycaemia. Types of Insulin
Dose- Acarbose - 25 -100 mg/day to be taken with 1. Rapid-acting insulin: Aspart insulin and Lispro
food. insulin
Voglibose - 0.2- 0.3 mg thrice a day 2. Regular or Short-acting insulin
Intermediate-acting insulin: Lente insulin and
(f) DPP 4 Inhibitors NPH insulin
Mechanism of action – They inhibit the enzyme 3. Long-acting insulin: Insulin Detemir and insulin
DPP 4 and increase endogenous GLP-1 action Glargine
Page 45
Figure-15.1: Treatment Protocol for DM – Type II
History & Physical examination RBS>140 mg/dl Suspect
Confirmation of diagnosis by
Fasting blood sugar - >126 mg/dl OR
Post Prandial B.S - >200 mg/dl OR
Random Blood Sugar - > 200 mg/dl
Educate Patient on Diet, physical activity,

de-addiction, foot care and regular follow up.
(Refer to Health Workers Manual)
Other investigation Urine

Take blood for serum Creatinine & Start the albumin & Sugar treatment
Fasting B.S.:> 126-200 or/and Fasting B.S.:>200-300and/or

Post Prandial B.S.: >300-350
Post Prandial B.S.:> 200-300
Start with combination therapy
Start with monotherapy Metformin + Sulphonyl Urea
Tab. Metformin 500mg BD 500 mg BD (Glimepiride or Glipizide)
(1 mg once a day) (2.5mg once a day)
Evaluate after
> 1.5 mg%
15 days with Sr. Creatinine Report
If Sr. Creat is
Cont. Rx Urgent Referral to DH
< 1.5 mg%
Target to be achieved with therapy Fasting 100 – 126 mg/dl
Target achieved with given therapy Target not achieved with given therapy
Continue the Rx and regular follow up after Step wise increase the dose of medicine
15-30 days.
Target achieved Target not achieved
Follow up after 15-30 days. Refer to DH
Page 46
Steps to increase dose in: 3) 1 gm BD + 2 mg BD Or 5 mg BD (If target
not achieved)
A) Monotherapy: Refer the patients to DH.
I. Start with T. Metformin 500 mg BD
(If target not achieved) * The main aim of this protocol is to control raised
II. T. Metformin 750 mg BD Blood sugar however not to complicate by
(If target not achieved) hypoglycaemia.
III. T. Metformin 1 gm BD
(If target not achieved) Instruction: - Don’t allow patients to fast while
Refer the patients to DH. on medication.
- Strict De-addiction state should
B) Combination therapy: be maintained.
Metformin + Glimepiride or Glipizide. - If sudden rise in blood sugar
1) 500mg BD + 1mg one a day or 2.5mg BD observed then  urgent referral
(If target not achieved) to District Hospital.
2) 750mg BD + 1mg once a day or 2.5mg BD
(If target not achieved)
6. Check list
Page 47
o Nephropathy
7. Complications of Diabetes
Mellitus • Macrovascular complications –
7.1Acute complications o Coronary heart disease
o Cerebrovascular disease
• Hypoglycaemia
o Peripheral arterial disease
• Diabetic Ketoacidosis (DKA)
• Diabetes and infections • Other – gastroparesis, sexual dysfunction,
• Hyperosmolar Hyperglycaemic coma dermatologic
(HHNKC).
8. Hypoglycaemia
7.2 Chronic complications Hypoglycaemia is a clinical emergency occurring in
diabetes characterized by either autonomic or
• Microvascular complications – neuroglycopenic symptoms (or) biochemically
random blood sugar < 60 mg, due to antidiabetic
o Eye disease- Retinopathy, Macular oedema. agent, food and activity mismatch.
o Neuropathy- Sensory and motor neuropathy
(mono and poly),
o Autonomic neuropathy
Table-4: Clinical presentation of Hypoglycaemia
Page 48
8.1 Management • Referral: If the patient remains unconscious
even after dextrose administration refer the
• Draw blood sample immediately patient immediately to higher centre for further
• Dextrose supplementation - Conscious: Oral evaluation.
Glucose, Sugar, Fruit Juice, Unconscious: 50% • Important Note Patient Education:
Dextrose 100 ml IV Stat. Followed by 10% • Educate patient and his family members about
Dextrose then by 5% DNS maintenance (or) Inj. low blood sugars and symptoms
Glucagon 1 mg IM if not accessible to • Never miss a meal after insulin / Oral
intravenous route hypoglycaemic agents
• Patient still remains unconscious - To rule out • Be cautious of unaccustomed physical activity
cerebral oedema, If present IV mannitol + Inj. • To carry diabetic identity card
Dexamethasone 8 mg IV • Always carry simple sugar (biscuits and toffee)
• Stop the antidiabetic agents for 3 days in Type 2 to avoid low sugar.
Diabetic mellitus patients and recheck blood
sugars. In Type 1 Diabetic mellitus patients,
9. Diabetic Ketoacidosis (DKA)
recheck blood sugars after 6 hours and adjust Ketoacidosis is a major medical emergency and
insulin dose accordingly. remains a serious cause of morbidity, principally in
• Identify the cause of hypoglycaemia people with type 1 diabetes, which should be treated
• If recurrent hypoglycaemia, rule out - Renal in hospital. Patient should be referred to tertiary
function disorder, Liver function disorder health centre after the primary management.
• Repeat blood sugar value after hypoglycaemia
9.1 Manifestation of DKA
correction and monitor blood sugars
Table 5
Page 49
9.2 Investigations • ABG for pH and bicarbonate
• Urine sugar [positive]
• Blood glucose [usually > 250 mg %] • Urine acetone [positive]
• Blood urea [may or may not be ↑] • Chest X-ray
• Serum creatinine [may or may not be ↑] • ECG
• Serum electrolyte [Na ↑ or ↓, K ↑ or decreased] • Ultra-sonogram abdomen / KUB.
• Serum bicarbonate < 10 mmol / l
9.3 Management of DKA
9.4 Referral
Refer the patient to a higher centre if:
• Anuric
• Patient is comatose • Elevated renal parameters
• Hypotension requiring ionotropic support • Evidence of septicaemia
Page 50
9.5 Complications of Diabetic Ketoacidosis
10. Hyperglycaemic
Hyperosmolar Non-Ketotic 10.2 Symptoms
Coma (HHNKC)
• Polyuria
It is an acute metabolic complication in middle aged • Polydipsia
and elderly diabetics with high morbidity and • Severe hyperglycaemia (Blood sugar > 600
mortality. mg%)
• Profound dehydration
10.1 Causes • Elevated osmolality
• Hemianopia, muscle fasciculation, seizures
Precipitated by • Altered sensorium, coma
• Infection 10.3 Treatment

• Trauma
• Burns • Fluid replacement: ½ normal saline at the rate of
• Infarction 2 litres in 1st 2 hours and 1 litre in another 2
• Hyper-alimentation hours
• Drugs like - Thiazide, Cimetidine, Phenytoin • Low dose insulin.
and parenteral diuretics • Correction of electrolytes and hyper osmolality.
• Low-dose heparin to prevent vascular
thrombosis intravascular coagulation.
Page 51
10.4 Distinguishing features
Table-6: Distinguishing features between DKA and HHNKC
• In obese people - Reduce 500 kcal from the

11. Medical Nutrition Therapy
calculated energy requirement
A non-pharmacological mode of management of • For underweight- Add 500 kcal to the calculated
diabetes. Medical Nutrition therapy is individualized energy requirement of the total kcal, 45 - 65 %
and should be a tailor made regimen. It is used as a kcal from carbohydrate and 10-25 % kcal from
compliment for an oral glucose lowering agent / proteins
insulin therapy.
• Fat recommendation - 500 ml / month of a
Energy Recommendations: blend of oils / individual Gingelly oil and any
• This depends on body weight and physical refined vegetable oil could be used or Rice
activity. 20 kcal/kg Ideal body weight – brand oil and any refined vegetable oil
Sedentary worker 30 kcal/kg Ideal body weight
– Moderate worker 40 kcal/kg Ideal body
weight – For heavy worker
Page 52
• Fibre recommendation – 14 gm/1000 kcal
12. Gestational Diabetes
provided.
Mellitus
• Fluid recommendation - 8 to 10 glasses / day of
water except in LVF, CKD, Cirrhosis etc. Gestational Diabetes mellitus is defined as
carbohydrate intolerance of variable severity with
11.1 MNT in Gestational Diabetes onset or first recognition during the present
pregnancy.
Mellitus
12.1 Risk for gestational diabetes
• 30 kcal / kg Instant Body weight in first
trimester mellitus
• 30 kcal / kg Instant Body weight + 300 kcal/day • Age more than 25 years
in II and III trimester
• Family history of diabetes mellitus
• Protein - 1gm/kg Instant Body weight + 10gm
daily throughout pregnancy • History of unexplained Foetal loss
• Avoid hypocaloric diets in obese GDM • History of baby being large for gestational age
• Provide compulsory bed time and evening snack • History of congenitally malformed infant
to avoid accelerated starvation and nocturnal • Maternal obesity
hypoglycaemia
• History of Polycystic ovarian disease
Gestational Diabetes mellitus:
• Polyhydramnios
• Strict meal plan
• Pre-eclampsia
• Physical exercise
• Unexplained intrauterine death
• Insulin
Other specific types 12.2 Methods of screening
• Strict meal plan ● Spot test: Fasting < 90 mg% [normal 2 hr post-
• Physical exercise prandial < 120 mg%, random < 105 mg% values]
ADA recommendation
• Insulin with or without oral hypoglycaemic
agents
Figure-15.2: Methods of Screening
Page 53
12.3 Diagnostic Criteria Target Glycaemic Level
WHO criteria (with 75 gm of glucose) F - 95 mg % Fasting glucose – 90 mg %
1 hour - 180 mg % 2 hour - 155 mg % If any two 2 hr postprandial – 120 mg %
values equal or crosses normal value, it is termed as Monitoring Glycaemic Control

Gestational Diabetes mellitus. • Blood glucose fasting and postprandial every
Important Note OGTT value should never be treated. three days till euglycaemia is achieved; then
every fortnightly, throughout first and second
12.4 Treatment trimester.
• Medical Nutrition Therapy [refer MNT] • Every week in third trimester.
• Insulin is essential if MNT fails to achieve • Glycaemic profile monitoring once in 1st and
euglycaemia 2nd trimester and then every month.
Bibliography
Further reading
1. India. Ministry of Health and Family Welfare. Guidelines for Diabetes Mellitus. [cited 2016 Jul 5]
Available from: http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/diabetes-mellitus.pdf
2. India. Ministry of Health and Family Welfare. Guidelines for Gestational Diabetes Mellitus. [cited
2016 Jul 5]
Available from:http://nrhm.gov.in/images/pdf/programmes/maternal-
health/guidelines/National_Guidelines_for_Diagnosis_&_Management_of_Gestational_Diabetes_Mel
litus.pdf


Page 54
17. THYROID DISORDERS
* Measure TSH levels after about 6 weeks of
1. Hypothyroidism instituting therapy
1.1. Types * Adjust by 12.5 or 25 mcg increments if TSH is

high; decrement of the same if TSH is
Hypothyroidism may be suppressed.
* When full replacement is achieved then follow up
1.1.2. Primary measurement at annual intervals and later by a 2 -
Common causes of which are autoimmune, iatrogenic 3 yearly interval
due to Iodine131, anti-thyroid or lithium treatment * Ensure ongoing compliance.
and thyroidectomy
1.1.2. Secondary 1.5. Special treatment considerations
i. Pituitary disease • A hypothyroid woman should be euthyroid prior
ii. Hypothalamic disease. to conception and during early pregnancy
(effect on foetal neuronal development).
1.2. Symptoms Thyroid profile should be immediately done
after confirmation of pregnancy and in second
• Coarse dry skin and third trimester.
• Hoarseness of voice ✓ Dose of Thyroxine should be increased by 50%
during pregnancy and return to previous level
• Facial puffiness, weight gain
after delivery
• Cardiac enlargement and / or pericardial ✓ Elderly require less Thyroxine (less by up to
effusion, 20%) especially those with coronary artery
disease, starting dose 12.5 mcg/day with similar
• Goitre with or without prolonged relaxation increments every 2 - 3 months until TSH level is
phase of deep tendon reflexes. normalized.
• Myxoedema coma is a rare complication of ✓ In Hypothyroidism due to low TSH (supra-
severe hypothyroidism with hypothermia, thyroid cause is suspected) detailed
hypoventilation, hyponatremia, hypoxia, investigations are required and patient should be
hypercapnia and hypotension. referred to a tertiary care level
✓ Asses the response clinically and by serum TSH
1.3. Diagnosis is confirmed by (serum T3 in suprathyroid type) at 8 weekly
intervals
• Low serum free T3 and T4 ✓ Once euthyroid state is restored, follow-up at 6 -
12 monthly intervals.
• Serum TSH raised
Other investigation – blood sugar level and lipid 1.6. Treatment of Myxoedema coma
profile
✓ Warm blankets, mechanical ventilation for
1.4. Treatment respiratory failure.
✓ Correction of metabolic disturbances and treat
• Pharmacological precipitating factors.
✓ Drugs
* Tab. L - Thyroxine- 1.6 mcg per kg body o L-Thyroxine 500 mcg IV bolus, then 50-
weight or Start with 50 – 100 mcg/day 100mcg IV daily
* Dose to be adjusted based on TSH levels o If intravenous preparation not available, the
same dose is administered through Ryle’s
* Goal is normal TSH (lower half of reference tube.
range o Once acute phase is over, maintain L-
Thyroxine as above.
Page 55
o Inj. Hydrocortisone 100 mg IV stat, 25-50 • Explain to the patient that the treatment is
mg 8 hourly. lifelong. Do not modify dose or stop treatment
✓ Caution: Avoid sedatives without consultation.
1.7. Patient Education • Over treatment may lead to decreased bone

mineral density and adverse cardiac
• L-Thyroxine should be taken as a single daily complications.
dose, ideally on awakening, at least 30 minutes
before breakfast. 2. Hyperthyroidism
• Fibre and bran products (e.g., Isaphghul husk) Thyrotoxicosis is defined as the state of thyroid
may impair absorption, as also Cholestyramine, hormone excess and is not synonymous with
Colestipol, Iron Sulphate, Sucralfate, hyperthyroidism, which is the result of excessive
Aluminium hydroxide thyroid function. However, the major aetiologies of
• Metabolism of L-Thyroxine is increased by thyrotoxicosis are hyperthyroidism caused by Graves'
Phenytoin, Rifampicin and carbamazepine. disease, toxic MNG, and toxic adenomas
2.1. Symptoms
Grave’s disease is characterized by diffuse goitre, tachycardia. Tab. Propranolol 40 – 120 mg a

Ophthalmopathy and Dermopathy in varying day or Tab. Atenolol 25 mg to 50 mg a day
combinations. • Anti-thyroid drug-
Ophthalmopathy in Graves' disease; lid retraction, • Tab. Propylthiouracil 100 – 150 mg every 6
periorbital oedema, conjunctival injection, and – 8 hours or Tab. Carbimazole 10 – 20 mg
proptosis are marked every 8 – 12 hours;
• After euthyroid state is achieved in 6 – 8 weeks
2.2. Diagnosis once daily dosage. Review with serum TSH and
FT3 after 3 – 4 weeks’ treatment has been
Diagnosis is confirmed by low to undetectable serum
initiated.
TSH and increased Serum free (FT3) and free (FT4)
• Once controlled reduce to the smallest effective
Ultra-sonography of neck dose or continue initial dose combined with L-
Thyroxine
Thyroid scan (if available)
• Drugs are given for an average of 2 years.
2.3. Treatment • Definitive treatment is surgery/ablation of
thyroid tissue
Pharmacological • Subtotal thyroidectomy in younger patients
(<30 years) in whom anti-thyroid therapy has
• Adjunctive treatment * For adrenergic been unsuccessful and in very large goitres.
symptoms such as sweating, tremor and
Page 56
• Radioactive iodine (I131): Method of choice in • Treatment with anti-thyroid drugs given till
Elderly Younger patients who have completed patient is euthyroid.
family with recurrent thyrotoxicosis following • Propranolol may be useful before and after
surgery or when surgery is refused or radioactive iodine administration.
contraindicated. Caution Radioactive iodine
should never be given in pregnancy. In woman 2.6. Thyrotoxic crisis or thyroid
of childbearing age if radioactive iodine is
planned, a pregnancy test should always be
storm
carried out.
• Refer to a tertiary care centre.
2.4. Pregnancy • Life threatening hyperthyroidism with fever,
vomiting, diarrhoea, jaundice, delirium and
• In pregnant woman, surgery should not be coma.
performed in 1st or 3rd trimesters • Usually precipitated by acute illness such as
• Anti-thyroid drugs are less risky but may induce stroke, infection, diabetic ketoacidosis, trauma,
hypothyroidism in the foetus and should be used patients undergoing surgery or radioactive
in the smallest necessary dose to keep serum iodine treatment in a poorly prepared patient:
TSH and FT4 in normal range. • Tab. Propylthiouracil 600 mg loading dose, then
• Propylthiouracil is preferred – usual 200 – 300 mg every 6 hours orally or through
maintenance is 200 mg/day. If > 300 mg/day Ryle’s tube. (or) Tab. Carbimazole 15 – 25 mg
required during 1st trimester, Subtotal 6 hourly.
thyroidectomy is indicated in 2nd trimester • 1 hour after the 1st dose of anti-thyroid drug,
• Propranolol should be avoided as it can cause saturated solution of Potassium iodide (SSKI) 5
foetal growth retardation and neonatal drops every 5 hours (or) Lugol’s iodine 10
respiratory depression. drops 3 times a day (or) Sodium iodide 1 g IV
slowly.
Ophthalmopathy: Refer to ophthalmologist. Initiate • Tab. Propranolol 40 – 60 mg 4 hourly or 0.5 – 2
therapy in mild cases with elevation of head at night, mg IV every 4 hours.
diuretics to decrease oedema, use of tinted sun • Inj. Dexamethasone 2 mg IV 6 hourly
glasses and 1 % methyl cellulose eye drops to prevent • Continue iodides and dexamethasone until
drying and refer patients with severe and progressive normal metabolic stage is achieved and give
exophthalmos to an ophthalmologist. supportive treatment such as cooling,
antipyretics, antibiotics for infection,
2.5. Toxic multinodular goitre intravenous fluids, etc.
• Once euthyroid status is achieved, manage as
• Radioactive iodine is the treatment of choice. already outlined.
• Large doses are usually required.
Bibliography
Further reading
1. Ambika Gopalakrishnan Unnikrishnan and Usha V. Menon. Thyroid disorders in India: An
epidemiological perspective, Indian J Endocrinal Metab [Internet]. 2011 Jul; 15(Suppl2): S78–S81.
[cited 2016 Jul 5]

18. Cerebrovascular Accidents
Page 57
side in 90% of right handed people).
1. Definition • Transient or permanent loss of central vision
A stroke, or cerebrovascular accident, is defined by due to involvement of ophthalmic artery a
the abrupt onset of a neurologic deficit that is branch of internal carotid artery.
attributable to a focal vascular cause. • Difficulty in swallowing, speaking due to bulbar
involvement could be a presentation. In cases
Thus, the definition of stroke is clinical, and
where patient has previously had
laboratory studies including brain imaging are used to
cerebrovascular accident, fresh infarct now
support the diagnosis.
causing bilateral cortical involvement may lead
The clinical manifestations of stroke are highly to dysphagia and dysarthria causing what is
variable because of the complex anatomy of the brain known as pseudobulbar palsy. On examination,
and its vasculature. TIA (Transient Ischemic Attack) in these patients, jaw jerk is brisk.
is a brief episode of neurological dysfunction lasting • Midbrain lesions have ocular involvement.
1 hour to 24 hours without residual deficit. Stroke in • Sensory involvement occurs in stroke involving
evaluation means when deficit worsens after patient thalamus or medulla.
first presents. • The neurological deficit may be preceded by
Cerebral ischemia is caused by a reduction in blood tingling numbness.
flow that lasts longer than several seconds. If the • TIA - Transient Ischaemic Attack is a
cessation of flow lasts for more than a few minutes, neurological deficit that recovers completely
infarction or death of brain tissue results. When within 24 hours.
blood flow is quickly restored, brain tissue can • A focal deficit progressing over a period of
recover fully and the patient's symptoms are only hours and is characteristic of thrombotic. stroke.
transient. • Any focal deficit preceded by a prolonged
headache could be due to infarct with
Focal ischemia or infarction, conversely, is usually haemorrhagic conversion secondary to cerebral
caused by thrombosis of the cerebral vessels venous sinuous thrombosis.
themselves or by emboli from a proximal arterial • Focal deficit could be accompanied by
source or the heart. convulsions.
Intracranial haemorrhage is caused by bleeding
directly into or around the brain; it produces 3. Examination
neurologic symptoms by producing a mass effect on
• Patient may have bradycardia if he is on beta
neural structures, from the toxic effects of blood
blockers or due to raised intracranial pressure
itself, or by increasing intracranial pressure.
secondary to cerebral oedema.
2. Clinical features • Blood pressure should be recorded and
monitored.
• Most of the patients are elderly. • The power of all 4 limbs should be graded and
• There could be a history of Hypertension, any improvement or deterioration in the power
Diabetes, Ischaemic heart disease should be recorded.
• History of cerebrovascular accident may be • Reflexes on the involved side are brisk and
present. plantar reflex is extensor on the involved side.
• Hemiplegia or hemiparesis: Paralysis or • History of headache, altered sensorium, fever,
weakness of right or left half of the body with vomiting.
deviation of one side of the face seen.
• Lower limb monoparesis or monoplegia. 4. Investigations
• Faciobrachial stroke: involving right or left
• Non-contrast CT scan brain to differentiate
upper limb along with ipsilateral facial
between infarct and haemorrhage and site of
weakness.
lesion.
• Rarely bilateral lower limb weakness in
• Routine investigations like HB, CBC, ESR,
unpaired anterior cerebral artery thrombosis.
liver function test, renal function test, serum
• Hemiplegia or hemiparesis may be accompanied electrolytes, fasting and post prandial glucose,
by motor aphasia (patient unable to speak) or complete lipid profile.
sensory aphasia (inability to comprehend) if
• ECG, X- ray chest, 2D echo especially in young
there is cortical involvement of dominant
patients to rule out cardiac source of embolism.
hemisphere (right side in left handed people, left
Page 58
• Ideally MR angiography in cases of infarction to • Tab Atorvastatin 40mg Once a day H.S.
look for the stenosis in intracranial vessels. • Antiepileptics (Inj. Phenytoin 100 mg t.d.s) if
• SOS MR venography if any doubt of cerebral convulsions are present. But in case the bleed is
venous thrombosis. large and if the patient is going to be shifted to a
higher centre it may be advisable to give anti-
5. Complications epileptics as the patient’s general condition
might worsen if he gets a convulsion.
• Aspiration pneumonia • Half an hour before Ryle’s tube feeding
• Deep vein thrombosis in lower limb Domperidone should be administered. Ryle’s
complicating further as pulmonary embolism. tube feeding in strict propped up position.
• Bed sore • Inj. Heparin (5000 IU IV bolus and then once a
day to keep PT (INR) 2 to 3 times of normal
6. Treatment value) for prophylaxis of deep vein thrombosis
• Blood pressure, blood glucose and temperature in cases of cerebral infarction (not in
of patients of acute cerebral infarction should be intracranial bleed) in patient of hemiplegia.
controlled. • Physiotherapy.
• Anti-hypertensive medication. A blood pressure • Early detection and treatment of complications.
of 150/90 mm of Hg can be maintained initially
to prevent Cerebral Ischaemia due to hypo 7. When to refer
perfusion. • All young patients of stroke, intracranial bleed
• IV Mannitol 100 cc 8 hourly in cases of or infarction.
IntraCerebral Bleed, in large infarcts, brainstem • Patients diagnosed with cerebral venous
infarction, Cerebellar lesions and all patient thrombosis.
having altered Sensorium. Serum electrolytes • Subarachnoid haemorrhage if seen on the CT.
and urine output should be monitored (on
• Patient suspected to have AV malformation.
mannitol.)
• Large intracerebral bleeds who might require
• Tab Aspirin 75-150 mg Once a day after lunch
evacuation to be transferred after stabilizing
should be started in cases of Cerebral Infarction.
blood pressure.
As Intracranial Bleed is ruled out.
Bibliography
Further reading
1. Pandian JD, Sudhan P. Stroke Epidemiology and Stroke Care Services in India, J Stroke [Internet].
2013 Sep; 15(3): 128–134. [cited 2016 Jul 5]

19. SUBARACHNOID HEMORRHAGE (SAH)
Page 59
Excluding head trauma, the most common cause of A detailed history should be sought for use of oral
SAH is rupture of a saccular aneurysm. Other causes contraceptive pills in young females to rule out SAH
include bleeding from a vascular malformation secondary to cerebral venous thrombosis as could
(arteriovenous malformation or dural arterial-venous occur in any procoagulant state.
fistula) and extension into the subarachnoid space
from a primary intracerebral haemorrhage. 2. Investigations
1. Clinical features CT brain, MRI angiography and MRI venography to
rule out cerebral venous thrombosis which could
Most unruptured intracranial aneurysms are present as subarachnoid haemorrhage.
completely asymptomatic. Symptoms are usually due
to rupture and resultant SAH, although some 3. Treatment: Subarachnoid
unruptured aneurysms present with mass effect on
cranial nerves or brain parenchyma. At the moment Haemorrhage
of aneurysmal rupture with major SAH, the ICP i. Protecting the airway.
suddenly rises. This may account for the sudden
transient loss of consciousness that occurs in nearly ii. Managing blood pressure before and after
half of patients. Sudden loss of consciousness may be aneurysm treatment, with antihypertensive
preceded by a brief moment of excruciating agent. Preventing re-bleeding prior to
headache. treatment.
The most important characteristic is sudden onset or iii. Managing vasospasm, treating hydrocephalus.
as a change in the patient's usual headache pattern. iv. Maintaining electrolyte balance and hydration
The headache is usually generalized, often with neck
stiffness and vomiting is common. v. IV Mannitol 100cc 8 Hourly to treat raised
Intra cranial pressure.
Although sudden headache in the absence of focal
neurologic symptoms is the hallmark of aneurysmal vi. Treatment with the calcium channel
rupture, focal neurologic deficits may occur. The antagonist Nimodipine (60 mg PO every 4 h)
deficits that result can include hemiparesis, aphasia, improves outcome, perhaps by preventing
and abulia. ischemic injury rather than reducing the risk
of vasospasm.
Occasionally, prodromal symptoms suggest the
location of a progressively enlarging unruptured vii. Volume expansion helps prevent hypotension,
aneurysm. augments cardiac output, and reduces blood
viscosity by reducing the haematocrit. This
A third cranial nerve palsy, particularly when method is called "Triple-H" (Hypertension,
associated with pupillary dilation, loss of ipsilateral Haemodilution, and Hypervolemic) therapy.
(but retained contralateral) light reflex, and focal pain
above or behind the eye, may occur with an viii. Acute hydrocephalus can cause stupor or
expanding aneurysm at the junction of the posterior coma. It may clear spontaneously or require
communicating artery and the internal carotid artery. temporary ventricular drainage. When chronic
Visual field defects can occur with an expanding hydrocephalus develops, ventricular
supraclinoid carotid or anterior cerebral artery shunting is the treatment of choice.
aneurysm.
Aneurysms can undergo small ruptures and leaks of
4. When to refer
blood into the subarachnoid space, so-called sentinel A patient diagnosed to be having SAH should be
bleeds. Sudden unexplained severe headache at any transferred to a higher centre at the earliest after
location should raise suspicion of SAH and be stabilizing blood pressure for further management.
investigated, because a major haemorrhage may be
imminent.
Bibliography
Page 60
Further reading
1. Sodhi HBS, Savardekar AR, Mohindra S, et al. The clinical profile, management and overall outcome
of aneurysmal subarachnoid haemorrhage at the neurosurgical unit of tertiary care center in India, J
Neurosci Rural Pract. [Internet]. 2014 Apr-Jun; 5(2): 118–126. [cited 2016 Jul 5]

Page 61
20. PYOGENIC MENINGITIS
Meningitis is a serious disease in which there is Meningeal signs (Can be found in any type of
inflammation of the meninges that cover the brain meningitis)
and spinal cord.
i. Neck stiffness: Stiffness of neck & resistance to
Bacterial meningitis can be deadly and contagious passive movements, with pain & spasm on
among people in close contact. attempted motion. The chin cannot be placed
upon the chest.
Viral meningitis tends to be less severe and most
people recover completely. ii. Kernig’s sign:
Fungal meningitis is a rare form of meningitis and With the hip flexed, the knee is extended.
generally occurs only in people with weakened Normally it can be done up to 135 degrees. In
immune system. meningitis it is restricted due to spasm of
hamstrings.
1. Clinical Presentation iii. Brudzinski’s sign:
• Meningitis can present as either an acute Neck sign- on flexing the neck, there is flexion
fulminant illness that progresses rapidly in a of hips & knees.
few hours or as a subacute infection that
progressively worsens over several days. Leg sign- on flexing one leg, other leg also
flexes.
• The classic clinical triad of meningitis is fever,
headache, and nuchal rigidity. Nausea, iv. Straight leg raising test (SLR):
vomiting, and photophobia are also common With the patient supine & both legs extended, one
complaints. leg is passively flexed at the hip keeping the knee
• Seizures occur as part of the initial presentation extended. Normally it can be lifted to 90 degrees.
of bacterial meningitis or during the course of It is restricted in meningitis.
the illness in 20–40% of patients. Generalized
seizure activity and status epilepticus may be 2. Diagnosis
due to hyponatremia, cerebral anoxia. CSF Studies
• Raised Intracranial Pressure (ICP) is an The classic CSF abnormalities in bacterial meningitis
expected complication of bacterial meningitis are (1) Polymorphonuclear (PMN) leucocytosis
and the major cause of obtundation and coma in (>100 cells/L in 90%), (2) decreased glucose
this disease. concentration [<2.2 mmol/L (<40 mg/dL) and/or
• Signs of increased ICP include a deteriorating CSF/serum glucose ratio of <0.4 in 60%, hence it is
or reduced level of consciousness, mandatory that a blood glucose levels be estimated
papilledema, dilated poorly reactive pupils, simultaneously with the CSF study], (3) increased
sixth nerve palsy, decerebrate posturing. protein concentration [>0.45 g/L (>45 mg/dL) in
90%], and (4) increased opening pressure (>180
• Cushing reflex (bradycardia, hypertension, mmH2O in 90%). CSF bacterial cultures are positive
and irregular respirations). in >80% of patients, and CSF Gram's stain
demonstrates organisms in >60%
• The rash of meningococcemia for
meningococcal meningitis, which begins as a
diffuse erythematous maculopapular rash 3. Treatment
resembling a viral exanthema; however, the skin i. Intravenous fluids.
lesions of meningococcemia rapidly become ii. Inj Mannitol 100mg 8 hourly to 6 hourly.
petechial. Petechiae are found on the trunk and iii. Inj Dexamethasone 4mg 8 hourly but first dose
lower extremities, in the mucous membranes to be given 20 minutes before first dose of
and conjunctiva, and occasionally on the palms antibiotics.
and soles. iv. Antimicrobial therapy of
• On examination meningeal signs are positive.
Page 62
• (Ceftriaxone – 2 g twice a day intravenously, • For gram-negative bacillary meningitis, the
cefotaxime, or Cefepime) A 2-week course of third-generation Cephalosporins - Cefotaxime
intravenous antimicrobial therapy is (2 gm 4 hourly i.e. total 12 gm per day),
recommended for Pneumococcal meningitis. Ceftriaxone (2 gm 12 hourly), and
Ceftazidime (2 gm 8 hourly) - are efficacious
• Or Ampicillin IV 2 gm 4 hourly (total 12 gm
for the treatment of, with the exception of
per day) for at least 3 weeks. Gentamicin is
meningitis due to P. aeruginosa, which should
added in critically ill patients (2 mg/kg
be treated with Ceftazidime, Cefepime, or
loading dose, then 7.5 mg/kg per day given
Meropenem. (2 gm 8 hourly). A 3-week
every 8 hours and adjusted for serum levels
course of intravenous antibiotic therapy is
and renal function). The combination of
recommended for meningitis due to gram-
Trimethoprim (10–20 mg/kg per day) and
negative bacilli.
Sulfamethoxazole (50–100 mg/kg per day)
given every 6 hours may provide an
alternative in penicillin-allergic patients.
4. When to refer
i. Lumbar puncture requires to be done and facility
• Vancomycin 2 g 12 hourly is the drug of
not available.
choice for methicillin-resistant staphylococci
and for patients allergic to penicillin (3 ii. Presence of any focal deficit.
weeks).
Note: If meningitis is suspected empirical antibiotic
treatment has to be started immediately.
Bibliography
Further reading

Page 63
21. TUBERCULOUS MENINGITIS
1. Clinical Manifestations 3. Treatment

• The disease often presents subtly as headache • IV fluids
and slight mental changes after a prodrome of • Inj. Mannitol 100 cc thrice a day to four times a
weeks of low-grade fever, malaise, anorexia, day, should be tapered and stopped to be
and irritability. overlapped with oral glycerol 1oz three times a
• If not recognized, tuberculous meningitis may day. Patient may have worsening of headache or
evolve acutely with severe headache, confusion, get signs of raised ICT, mannitol should be
lethargy, altered sensorium, and neck rigidity. reinstituted and tapered again.
• Typically, the disease evolves over 1–2 weeks, a • For treatment of tubercular meningitis, first-line
course longer than that of bacterial meningitis. drugs are Isoniazid (5 mg/kg) along with
• Since meningeal involvement is pronounced at Pyridoxine 50mg, Rifampin (10 mg/kg) given
the base of the brain, paresis of cranial nerves before breakfast, Pyrazinamide (25 mg/kg), and
(ocular nerves in particular) is a frequent Ethambutol (15 mg/kg).
finding, and the involvement of cerebral arteries • Duration of treatment is up to 9 months to 1
may produce focal ischemia. year.
• The ultimate evolution is toward coma, with • Steroids are given as Inj. Dexamethasone 4 mg
hydrocephalus and intracranial hypertension. three times a day for 3 weeks to be continued as
Tab Prednisolone 1mg/kg and tapered and
2. Diagnosis omitted over one-and-a-half-month duration.
CSF Studies 4. Complications
In adults, the mean white blood cell (WBC) count
• Hydrocephalous.
(range, 0-4000 cells/µL) with lymphocytic
predominance. The mean protein level in adults • Vasculitis induced stroke.
averages 224 mg/dL (range, 20-1000 mg/dl). The • Drug induced hepatitis.
proportion with depressed glucose levels (< 45
mg/dL or 40% of serum glucose).
5. When to refer
• Patient having any focal deficit.
• Diminution of vision.
• Patient not improving on treatment.

Bibliography
Further reading


Page 64
22. VIRAL MENINGITIS
• Constitutional signs can include malaise,
1. Clinical features myalgia, anorexia, nausea and vomiting,
Immuno-compromised adult patients with viral abdominal pain and/or diarrhoea.
meningitis usually present with. • Patients often have mild lethargy or drowsiness;
however, profound alterations in consciousness,
• Headache, fever, and signs of meningeal such as stupor, coma, or marked confusion do
irritation coupled with an inflammatory CSF not occur in viral meningitis and suggest the
profile. presence of encephalitis or other alternative
• Headache is almost invariably present and often diagnoses.
characterized as frontal or retro-orbital and
frequently associated with photophobia and pain
on moving the eyes.
2. Etiology
Acute Meningitis
Common Less Common
Enteroviruses (Coxsackie viruses, echoviruses, and human Lymphocytic Choriomeningitis virus

enteroviruses 68–71)
Varicella zoster virus Cytomegalovirus
Epstein-Barr virus
Herpes simplex virus 2
Arthropod-borne viruses
HIV
Acute Encephalitis
Common Less Common
Herpesviruses Rabies
Herpes simplex virus 1 Powassan virus
Varicella zoster virus (VZV) Enteroviruses
Epstein-Barr virus (EBV) Mumps
Arthropod-borne viruses
Cytomegalovirus
Table No.1- Aetiology
Page 65
• Fluid and electrolyte status should be monitored.
3. Diagnosis IV fluids should be administered.
The most important laboratory test in the diagnosis of • Oral or intravenous Acyclovir may be of benefit
viral meningitis is examination of the CSF. The in patients with meningitis caused by Herpes
typical profile is a lymphocytic pleocytosis (25–500 simplex virus-1 or -2 and in cases of severe
cells/L), a normal or slightly elevated protein Epstein-Barr virus or Varicella zoster virus
concentration [0.2–0.8 g/L (20–80 mg/dL)], a normal infection. Seriously ill patients should receive
glucose concentration, and a normal or mildly intravenous Acyclovir (15–30 mg/kg per day in
elevated opening pressure (100–350 mm H2O). three divided doses for 7-10 days i.e. which can
be followed by an oral drug such as Acyclovir
4. Treatment: Acute Viral (800 mg, five times daily. Patients with HIV,
meningitis should receive highly active
Meningitis antiretroviral therapy).
• Treatment of almost all cases of viral meningitis
is primarily symptomatic and includes use of
analgesics, antipyretics, and antiemetics.
Bibliography
Further reading

Page 66
23. VIRAL ENCEPHALITIS
• In rare cases, a pleocytosis may be absent on the
1. Definition initial LP but present on subsequent LPs.
In contrast to viral meningitis, where the infectious
Patients who are severely immunocompromised
process and associated inflammatory response are
by HIV infection, glucocorticoid or other
limited largely to the meninges, in encephalitis the
immunosuppressant drugs, chemotherapy, or
brain parenchyma is also involved. Many patients
lymphoreticular malignancies may fail to mount
with encephalitis also have evidence of associated
a CSF inflammatory response.
meningitis (meningoencephalitis) and, in some cases,
involvement of the spinal cord or nerve roots • CSF cell counts exceed 500/L in only about
(encephalomyelitis, encephalomyeloradiculitis). 10% of patients with encephalitis. Infections
with certain arboviruses (e.g., EEE virus or
2. Clinical Manifestations California encephalitis virus), mumps, and
In addition to the acute febrile illness with evidence LCMV may occasionally result in cell counts
of meningeal involvement characteristic of >1000/L, but this degree of pleocytosis should
meningitis, the patient with encephalitis commonly suggest the possibility of non-viral infections or
has an altered level of consciousness (confusion, other inflammatory processes.
behavioural abnormalities), or a depressed level of
• Atypical lymphocytes in the CSF may be seen
consciousness ranging from mild lethargy to coma,
in EBV infection and less commonly with other
and evidence of either focal or diffuse neurologic
viruses, including CMV, HSV, and
signs and symptoms.
enteroviruses.
Patients with encephalitis may have hallucinations,
agitation, personality change, behavioural disorders, • However, persisting CSF neutrophilia should
and, at times, a frankly psychotic state. Focal or prompt consideration of bacterial infection,
generalized seizures occur in many patients with leptospirosis, amoebic infection, and non-
infectious processes such as acute haemorrhagic
encephalitis.
leukoencephalitis. About 20% of patients with
Virtually every possible type of focal neurologic encephalitis will have a significant number of
disturbance has been reported in viral encephalitis; red blood cells (>500/L) in the CSF in a non-
the signs and symptoms reflect the sites of infection traumatic tap. The pathologic correlate of this
and inflammation. finding may be a haemorrhagic encephalitis of
the type seen with HSV; however, CSF red
The most commonly encountered focal findings are
blood cells occur with similar frequency and in
aphasia, ataxia, upper or lower motor neuron patterns
similar numbers in patients with non-herpetic
of weakness, involuntary movements (e.g.,
focal encephalitis.
myoclonic jerks, tremor), and cranial nerve deficits
(e.g., ocular palsies, facial weakness). • A decreased CSF glucose concentration is
distinctly unusual in viral encephalitis and
3. Laboratory Diagnosis should suggest the possibility of bacterial,
3.1. CSF Examination fungal, tuberculous, parasitic, leptospiral,
• CSF examination should be performed in all syphilitic, sarcoid, or neoplastic meningitis.
patients with suspected viral encephalitis unless
contraindicated by the presence of severely
3.2. MRI, CT, EEG
increased intracranial pressure (ICP). • Patients with suspected encephalitis almost
invariably undergo neuroimaging studies and
• The characteristic CSF profile is often EEG. These tests help identify or exclude
indistinguishable from that of viral meningitis alternative diagnoses and assist in the
and typically consists of a lymphocytic differentiation between a focal, as opposed to a
pleocytosis, a mildly elevated protein diffuse, encephalitic process.
concentration, and a normal glucose
concentration. A CSF pleocytosis (>5 cells/L) • Focal findings on MRI in a patient with
occurs in >95% of immunocompetent patients encephalitis should always raise the possibility
with documented viral encephalitis. of HSV encephalitis. Approximately 10% of
patients with PCR-documented HSV
Page 67
encephalitis will have a normal MRI, although Prior to intravenous administration, acyclovir
nearly 80% will have abnormalities in the should be diluted to a concentration 7 mg/ml. (A
temporal lobe, and an additional 10% in extra 70-kg person would receive a dose of 700 mg.
temporal regions. which would be diluted in a volume of 100 ml.)
Each dose should be infused slowly over 1 hour,
4. Treatment rather than by rapid or bolus infusion, to
Vital functions, including respiration and blood minimize the risk of renal dysfunction. Care
pressure, should be monitored continuously and should be taken to avoid extravasation
supported as required. In the initial stages of intramuscular or subcutaneous administration.
encephalitis, many patients will require care in an The alkaline pH of Acyclovir can cause local
intensive care unit. inflammation and phlebitis (9%). Dose
adjustment is required in patients with impaired
i. Intravenous fluids. renal glomerular filtration. Penetration into CSF
ii. IV Mannitol 100 cc 12 hourly for 3 days is excellent, with average drug levels 50% of
serum levels. Complications of therapy include
Seizures should be treated with standard elevations in blood urea nitrogen and creatinine
anticonvulsant regimens (Inj. Diazepam 10 levels (5%), thrombocytopenia (6%),
mg, IV or Inj. Midazolam 2 mg), and gastrointestinal toxicity (nausea, vomiting,
prophylactic therapy should be considered in diarrhoea) (7%), and neurotoxicity (lethargy or
view of the high frequency of seizures in obtundation, disorientation, confusion, agitation,
severe cases of encephalitis. hallucinations, tremors, seizures) (1%).
iii. Acyclovir is of benefit in the treatment of iv. Antipyretics for fever
HSV and should be started empirically in
patients with suspected viral encephalitis,
especially if focal features are present, while
5. Complications
Aspiration pneumonia, stasis ulcers and decubitus
awaiting viral diagnostic studies. ulcer, contractures, deep venous thrombosis and its
Adults should receive a dose of 10 mg/kg of complications and infections of indwelling lines and
Acyclovir intravenously every 8 hours (30 catheters.
mg/kg per day total dose) for 14–21 days.
CSF PCR can be repeated at the completion of
6. When to refer
Ideally all suspected patients of viral encephalitis
this course, with PCR-positive patients
after starting therapy as mentioned above and patients
receiving additional treatment, followed by a
of viral meningitis not improving over or worsening
repeat CSF PCR test.
over 48 hours should be referred to a higher centre.
Bibliography
Further reading

Page 68
24. EPILEPSY
1. Definition 3. Investigations
This is a condition characterized by recurrent
Apart from routine laboratory investigations, patients
episodes of seizures which are paroxysmal abnormal
of epilepsy can be further investigated with an EEG
discharges at high frequency from an aggregate of
and MRI. from routine laboratory investigations.
neurons in cerebral cortex.
4. Treatment
2. Types of epilepsy
• Correct any metabolic cause (hypo or
• Grand mal epilepsy or Tonic-Clonic Seizures hyperglycaemia, hypo or hypernatremia).
Aura, epileptic cry, sudden fall due to tonic • Stop drugs like Theophylline (CNS Stimulant)
convulsions followed by clonic convulsions and which may cause seizures.
then prolonged sleep and depression. The attack • Look for any structural CNS lesions like Brain
lasts for 1-2 min. Tongue bite; urinary tumour, Vascular lesions, Meningitis, CVST or
incontinence may occur. abscess and treat them.
• Petit mal epilepsy or Absence seizures - No • Avoid precipitating factors like sleep
aura, no loss of consciousness. Prevalent in deprivation, fasting, video games.
children and episode lasts for few seconds.
There is momentary loss of consciousness 4.1 Antiepileptic should be started
hardly for 5 seconds without loss of postural when
control. Presence of freezing or staring in one
direction. • A history suggestive of recurrent epileptic
• Partial seizures - Most common seizure types seizure is established.
occurring in 80% of epileptic patients. Seizure • An abnormal neurological examination.
activity is restricted to a discrete area belonging • Presenting as Status Epilephcy.
to one cerebral hemisphere only. • Abnormal EEG suggestive of general seizure.
• Other types of seizures: Myoclonic seizures, • Family history of epilepsy.
atonic seizures, tonic seizures.
• Febrile seizures- Young children develop To start anti epileptics in single isolated seizure is not
seizures during high fever. yet established. Monotherapy should be the mantra of
treatment.
4.2 Anti-epileptic drugs

Table No.1: Antiepileptic Drugs & their Doses with type of seizure
Seizure Drug Dose
Generalized onset tonic clonic Valproic acid 750-2000 mg/day
convulsions (20-60 mg/kg/day)
In divided doses
Phenytoin 300-400 mg/day
(3-6 mg/kg/day for adult, 4-8 mg/kg/day for
Children) BD doses
Levetiracetam 1 gm – 3 gm per day
Lamotrigine 1000-3000 mg/day BD doses
Topiramate 150-500 mg/day, BD doses
Focal onset tonic clonic Carbamazepine 600-1800 mg/day (15-35 mg/kg, child) in
convulsions Lamotrigine BD doses
Page 69
Levetiracetam Same as Above
Oxcarbazepine Same as Above
900-2400 mg/day (30-45 mg/kg, child) BD
doses
Typical Absence Valproic acid Same as Above
Ethosuximide 750-1250 mg/day in BD doses, 20 – 40 mg
per kg divided in BD doses
Atypical Absence, myoclonic, Valproic Acid, Same as Above
Atonic Seizures
Lamotrigine, Same as Above
Topiramate
dextrose solution) Put it in a normal saline

5. Status Epilepticus solution to minimize the risk of crystal
Status Epilepticus refers to continuous seizures or precipitation or Fosphenytoin 20 mg/kg iv to
repetitive discrete seizures with impaired maximum 150 mg/minute.
consciousness in the interictal period for duration of • Correct any metabolic imbalances. Control
15-30 minutes traditionally but practically for hyperthermia.
generalized convulsive Status Epilepticus the duration • If seizures continue after 20 minutes, give
is 5 minutes. maximum rate 50 mg/minute or Fosphenytoin 7
to 10 mg/kg to maximum rate of 150 mg/minute.
• It is a medical emergency and must be treated
• If seizures continue after 20 minutes, give
immediately.
Phenobarbital (20 mg/kg IV at 60 mg/min)
• Monitor vital signs. Maintain airway, breathing,
• Other Antiepileptic Drugs which can be given IV
and circulation. Administer supplementary
are - Valproate sodium 30 mg/kg IV bolus or IV
Oxygen by mask.
Levetiracetam 10-50 mg/kg
• Laboratory analysis-glucose, electrolytes,
• If seizures continue, consider administering
calcium, magnesium, creatinine, CBC and urine
general anaesthesia with medications such as
analysis.
Propofol, Midazolam, or Pentobarbital.
• Establish intravenous access.
• All the Patients after initial IV Antiepileptic Drug
• Lorazepam (0.1 mg/kg) IV over 1-2 min, Repeat should be followed by maintenance doses with
if no response after 5 minutes. the oral antiepileptic drugs regularly.
• Phenytoin 15-20 mg/kg, at a rate not to exceed 50
mg/min (Never mix Phenytoin with a 5%
Figure-24.1: Management of Status Epilepticus algorithm
Page 70
Figure 24.2: Pharmacological treatment algorithm of Non-Convulsive Status Epilepticus
Lorazepam (0.1, 0.15 mg/IV) (repeat once if no Admit to ICU and EEG monitoring
seizure suppression
Seizures continuing
Phenytoin (7-10 mg/kg Iv) or Fosphenytoin Consider valproate in absence SE (30

(Phenytoin equivalent dose) mg/kg IV)
Seizures continuing
Phenytoin (7-10 mg/kg Iv) or Fosphenytoin (Phenytoin equivalent Consider valproate in absence SE (30
dose) mg/kg IV)
Refractory NCSE
Intravenous anaesthetic agents

Midazolam/Propofol/Pentobarbital
Seizures continuing
Newer AEDs – Topiramate / Levetiracetam
or
Inhalational anaesthetics - Isoflurane/Desflurane
Page 71
Bibliography
Further reading
1. Santhosh NS, Sinha S, Satishchandra P. Epilepsy: Indian Perspective, Ann Indian Acad Neurol. 2014
Mar; 17(Suppl 1): S3–S11. [cited 2016 Jul 5]

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Page 72
25. GUILLAIN-BARRE SYNDROME (GBS)
Poliomyelitis–fever and meningismus is common.
1. Definition
Guillain-Barre syndrome (GBS) is an acute,
4. Investigations
frequently severe, and fulminant polyradiculopathy CSF analysis by lumbar puncture by the end of first
that is autoimmune in nature. week – Elevated CSF protein 100-1000 mg/dl
without pleocytosis called as albuminocytological
2. Clinical Features dissociation.
GBS manifests as rapidly evolving areflexic motor Can refer for electro-diagnosis- Demyelination or
paralysis with or without sensory disturbance. Usual axonal involvement seen, according to the variant
pattern is an ascending paralysis. Weakness typically type
evolves over hours to a few days and frequently
accompany by tingling dysesthesias in extremities. 5. Treatment
Legs are usually more affected than arms. Facial
Treatment should be initiated at the earliest. Each day
diparesis is present in 50% of affected individuals.
counts. >2 weeks after the first motor symptoms,
The lower cranial nerves are also frequently
immunotherapy is no longer effective. Either high
involved, causing bulbar weakness with difficulty
dose intra-venous immune globulin (IVIg) or
handling secretions and maintaining airway. Pain in
plasmapheresis can be initiated, as they are equally
the neck, shoulder or back is also common in the
effective.
early stages.
Fever and constitutional symptoms are absent at the • Intra-venous Immuneglobulin (IVIg): Total
onset, and if present cast a doubt on the diagnosis. dose of 2 g/kg body weight divided into 5 doses
Deep tendon reflexes disappear within the first few given over 5 consecutive days.
days of onset. Bladder dysfunction may occur in • Plasmapheresis: 40-50 ml/kg plasma exchange
severe cases but is usually transient. Autonomic four times over a week.
involvement is common, usually presenting as wide In the worsening phase of GBS, most patients require
fluctuation in blood pressure, postural hypotension & monitoring in a critical care setting, with particular
cardiac dysrhythmias. attention to vital capacity, heart rhythm, blood
pressure, nutrition, DVT prophylaxis and chest
Approximately 70% of cases of GBS occur 1-3 physiotherapy. Nearly 30% of patients with GBS
weeks after an acute infectious process, usually require ventilator assistance.
respiratory or gastro-intestinal.
6. When to refer: Any of the
3. Differential diagnosis
following
The diagnosis is made by recognizing the pattern of
rapidly evolving paralysis with areflexia, absence of • Single breath count ≤ 12/min
fever or other systemic symptoms, and characteristic • Respiratory failure.
antecedent events. Other disorders that may enter into • Fulminant quadriparesis.
the differential diagnosis include: • Poor Gag reflex with risk of aspiration.
• Autonomic dysfunction
Acute myelopathies – prolonged back pain and
sphincter disturbances. • Recurrent GBS.
Botulism – pupillary reactivity lost early.
Bibliography
Page 73
Further reading
1. Meena K, Khadilkar SV, Murthy JMK. Treatment guidelines for Guillain Barre Syndrome, Ann Indian
Acad Neurol.[Internet] 2011 Jul; 14(Suppl1): S73–S81. [cited 2016 Jul 5]

Page 74
26. APTHOUS ULCERS
• Fever, adenopathy, gastrointestinal symptoms
1. Introduction are typically absent.
Recurrent Aphthous stomatitis (RAS) is a common
Important note –Repeated ulcers at the same site or
condition, restricted to the mouth, that typically starts
slow healing ulcers with systemic symptoms e.g.,
in childhood or adolescence as recurrent small,
uveitis, arthritis and fever adenopathy are worrisome.
round, or ovoid ulcers with circumscribed margins,
Malignancy should be excluded.
erythematous haloes, and yellow or grey floors. A
positive family history of similar ulcers is common,
and the natural history is typically of resolution in the
4. Treatment
third decade of life.
4.1 Topical and systemic antibiotics
Tetracycline 250 mg dissolved in 180 ml of water
2. Causes and used as swish and spit 4 times a day for several
• Some RAS cases involve a familial and genetic days. Avoid in children and pregnancy.
basis; approximately 40% of patients with RAS
have a familial history, but inheritance may be
4.2 Probiotics in powder form
polygenic with penetrance dependent on other placed in oral cavity and
factors. swallowed 3 -4 times a day
• Most relevant studies have found hematinic
(e.g. iron, folic acid, vitamin B-12) deficiencies 4.3 Anti-inflammatory
in as many as 20% of patients with recurrent
ulcers. In addition, deficiencies of vitamins B-1, Hydrocortisone pellets 5 mg kept at ulcer base and
B-2, and B-6 have been noted in some patient swallowed every 4 hours for 3-4 days. Triamcinolone
cohorts. 0.1 % applied to ulcers 2-4 times a day.
Betamethasone (Betnesol) mouthwash - 0.5 mg tab
dissolved in 5-10 ml of water for mouth wash 6
3. Symptoms hourly during attack.
• Significant pain while chewing food. Minor 4.4 Immune modulators Levamisole
aphthae are recurrent, painful, single or
multiple, shallow surrounded by erythematous 50 mg twice a day for three consecutive days for 4
mucosa anywhere in the oral cavity. Small weeks, no medication for 2 weeks; then Levamisole 150
ulcers heal without scar, while larger and deep mg tab, half tab twice daily for 3 days for 2 weeks.
ulcers leave a scar.
Bibliography
Further reading
1. Patil S, Reddy SN, Maheshwari S. Prevalence of Recurrent Aphthous ulceration in the Indian
Population, J Clin Exp Dent. [Internet]. 2014 Feb; 6(1): e36–e40. [cited 2016 Jul 5]

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Page 75
27. OESOPHAGEAL CANDIDIASIS
1. Introduction
Oesophageal candidiasis is an opportunistic infection chemotherapy, uncontrolled Diabetes Mellitus,
of the oesophagus by Candida albicans. Occurs in Chronic steroid therapy.
immune compromised patients like AIDS, Post-
Figure 27.1: Endoscopic view of Oesophageal Candidiasis
2.Signs and symptoms 4. Treatment

Oral lesions are painless but oesophageal lesions • Nystatin suspension local application in mouth.
produce painful dysphagia. Discrete or confluent
curdy plaques on the oesophageal mucosa. • Clotrimazole oral lozenges 10 mg dissolve 1
lozenge 5 times a day.
3. Investigations • Tab Fluconazole 100 mg/day for 10-14 days.
Demonstration of pseudo hyphae on wet smears and

culture.
Bibliography
Further reading
1. America. Centers for Disease Control and Prevention (CDC) Information web-page. [cited 2016 Jul 5]
Available from: https://www.cdc.gov/fungal/diseases/candidiasis/thrush/

Page 76
28. DYSPEPSIA
1. Introduction 5. Treatment
Nonspecific group of symptoms related to upper GI • Cap Omeprazole 20 mg once a day taken 45
Tract. Also referred to as non-ulcer dyspepsia, min before breakfast for 4 weeks or Tab
functional dyspepsia, GERD. Ranitidine 150 mg twice a day before food 45
mins for 4-6 weeks.
2. Symptoms • For those with dysmotility symptoms - Tab
Domperidone 10 mg three times a day 30 mins
Upper abdominal symptoms simulating an ulcer
before food.
disease or heart burn with or without regurgitation,
heaviness, post-prandial fullness or early satiety. • Antacids 2-3 teaspoon when symptomatic.
Symptoms of gas in abdomen is common.
• Anti H. Pylori treatment is recommended for –
those on long term NSAIDS, those with
3. Red flag signs duodenal/gastric ulcers.
Anorexia, weight loss, anaemia, dysphagia and mass Treatment of H Pylori- Combination of
in abdomen.
• Cap. Omeprazole 20 mg twice a day plus
4. Investigations • Cap. Amoxicillin 1gm BD or Tab.
Metronidazole 500 mg BD for 14-days plus
History and upper GI-scopy.
• Tab Clarithromycin 500mg BD for 14 days
Bibliography
Further reading
1. Ghoshal UC, Singh R. Functional dyspepsia: The Indian Scenario. Supplement to JAPI. [Internet]
March 2012, Vol 60. [cited 2016 Jul 5]
Available from:
http://www.japi.org/march_2012_special_issue_dyspepsia/02_functional_dyspepsia_the.pdf

Page 77
29. GASTROOESOPHAGEAL REFLUX
GERD is a common disorder caused by retrograde • Antacid with or without alginate acid liquid or
flow of gastric contents through an incompetent tab 2-3 chewed - 4-6 times a day 1/2-1 hour
gastroesophageal junction. There are two groups- after a meal.
erosive GERD and non-erosive GERD. Untreated
may result in to oesophagitis, ulceration, stricture, • Cap. Omeprazole 20 mg Once a day/BD OR
and rarely adenocarcinoma. Rabeprazole 20 mg Once a day or Pantoprazole
40 mg Once a day.
2. Symptoms • Esomeprazole 40 mg Once a day, OR
Retrosternal pain, heart burn, regurgitation mostly • Lansoprazole 30 mg Once a day.

after meals. Rarely present with chronic cough, • All taken 45 mins before meals for 4-6 weeks.
laryngitis, bronchospasm, recurrent pulmonary
infections, otitis media etc. • Add Prokinetic Domperidone 10 mg thrice a
day 30 mins before meals if regurgitation is
significant.
Bibliography
Further reading
1. Poddar U. Diagnosis and management of gastroesophageal disease: An Indian perspective, Indian
Pediatr. [Internet] 2013 Jan 8;50(1):119-26. [cited 2016 Jul 5]
Available from: http://www.ncbi.nlm.nih.gov/pubmed/23396785
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30. PEPTIC ULCER DISEASE
radiation to the back is suggestive of a posterior

1. Introduction penetrating gastric ulcer complicated by
Peptic ulcer is an important organic gastrointestinal pancreatitis.
disease.
4. Alarm features that warrant
2. Aetiology prompt gastroenterology
Peptic ulcer disease (PUD) may be due to any of the
following: referral include the
following
• H. pylori infection
• Drugs • Bleeding or anaemia
• Lifestyle factors • Early satiety
• Severe physiologic stress • Unexplained weight loss
• Hypersecretory states (uncommon) • Progressive dysphagia or odynophagia
• Genetic factors • Recurrent vomiting
There is ulceration of the gastric and duodenal • Family history of GI cancer
mucosa due to acid and pepsin.
5. Physical Examination
3. Clinical features
In uncomplicated PUD, the clinical findings are few
• Obtaining a medical history, especially for and nonspecific and include the following:
peptic ulcer disease, H. pylori infection,
ingestion of NSAIDs, or smoking, is essential in • Epigastric tenderness (usually mild)
making the correct diagnosis. Gastric and • Right upper quadrant tenderness may suggest a
duodenal ulcers usually cannot be differentiated biliary aetiology or, less frequently, PUD.
based on history alone, although some findings
• Guaiac-positive stool resulting from occult
may be suggestive.
blood loss
• Epigastric pain is the most common symptom of
both gastric and duodenal ulcers. It is • Malena resulting from acute or subacute
gastrointestinal bleeding
characterized by a gnawing or burning sensation
and occurs after meals—classically, shortly 6. Differential Diagnosis
after meals with gastric ulcer and 2-3 hours
afterward with duodenal ulcer. Food or antacids
• Acute Coronary Syndrome
relieve the pain of duodenal ulcers but provide
minimal relief of gastric ulcer pain. • Aneurysm, Abdominal
• Duodenal ulcer pain often awakens the patient • Cholangitis
at night. About 50-80% of patients with
duodenal ulcers experience nightly pain, as • Cholecystitis
opposed to only 30-40% of patients with gastric • Cholecystitis and Biliary Colic in Emergency
ulcers and 20-40% of patients with non-ulcer Medicine
dyspepsia (NUD). Pain typically follows a daily • Cholelithiasis
pattern specific to the patient. Pain with
• Diverticular Disease
Page 79
• Oesophageal Perforation, Rupture and Tears 7.1 H. pylori Testing
• Oesophagitis
• Testing for H. pylori infection is essential in all
• Gastritis, Acute
patients with peptic ulcers.
• Gastritis, Chronic
• Endoscopic or invasive tests for H. pylori
• Gastroenteritis include a rapid urease test, histopathology, and
culture. Rapid urease tests are considered the
• Gastroesophageal Reflux Disease endoscopic diagnostic test of choice. The
• Inflammatory Bowel Disease presence of H. pylori in gastric mucosal biopsy
specimens is detected by testing for the bacterial
• Viral Hepatitis product urease
7. Approach Considerations 7.2 Endoscopy

Upper GI endoscopy is the preferred diagnostic test
• Testing for H. pylori infection is essential in all
in the evaluation of patients with suspected PUD. It is
patients with peptic ulcers. In most patients with
highly sensitive for the diagnosis of gastric and
uncomplicated peptic ulcer disease (PUD),
duodenal ulcers, allows for biopsies and cytological
routine laboratory tests usually are not helpful.
brushings in the setting of a gastric ulcer to
Documentation of PUD depends on
differentiate a benign ulcer from a malignant lesion,
radiographic and endoscopic confirmation.
and allows for the detection of H. pylori infection
• If the diagnosis of PUD is suspected, obtaining with antral biopsies for a rapid urease test and/or
CBC count, liver function tests (LFTs), histopathology in patients with PUD. (See the images
amylase, and lipase may be useful. CBC count below.)
and iron studies can help detect anaemia, which
is an alarm signal that mandates early
endoscopy to rule out other sources of chronic
GI blood loss.
Figure-30.1: Endoscopic view of Peptic Ulcer
Page 80
8. Treatment
Anti H. pylori treatment is recommended for patients
on long term NSAIDS, bleeding peptic ulcer.
H. pylori treatment
Drugs Dose(mg) Frequency Duration

Proton Pump Inhibitors (PPI) 20 mg BD 14 days
Clarithromycin 500 mg BD
Metronidazole 400 mg BD
PPI 20mg BD 14 days
Amoxicillin 1gm BD
Metronidazole 400 mg TDS
PPI 20 mg BD 14 days
Amoxicillin 1 gm BD
Clarithromycin 500 mg BD
• Tab Ranitidine (150 mg) BD, 9. Do’s and don’ts

• Famotidine (40 mg) once a day equally
• Avoid alcohol
efficacious, but takes longer time.
• Stop smoking
• Maintenance dose of PPI for patients on
NSAIDS, IHD patients. • Avoid NSAIDs
• Prefer paracetamol, avoid foods that aggravate
symptoms
• No role of bland diet
• Excess milk, meals at regular intervals.
Bibliography
Further reading
1. Fashner J, Gitu AC et al. Am Fam Physician. [Internet] 2015 Feb 15;91(4):236-242. [cited 2016 Jul 5]
Available from: http://www.aafp.org/afp/2015/0215/p236.html

Page 81
31. VOMITING
Vomiting is the forceful expulsion of the gastric • Intravenous fluids if dehydrated. Start oral
contents due to contraction of abdominal musculature fluids as soon as patient tolerates.
and simultaneous relaxation of gastric fundus and
lower oesophageal sphincter. • Rule out gastric outlet obstruction then
• Inj. Metoclopramide 10 mg IM repeat after 6

2. Causes hours if needed or
i. Central (stimulation of vomiting centre)
neurological disease raised intracranial • Tab Mosapride 5 mg thrice a day, or
pressure.
• Tab Domperidone 10 mg thrice a day or
ii. Vestibular system disorders
iii. Drugs and toxins
• Tab Metoclopramide 10 mg thrice a day or
iv. Toxic and metabolic disorders such as
ketoacidosis • Tab Prochlorperazine 5 mg thrice a day repeat
v. Systemic infections after 4- 6 hrs if needed, or
vi. Pregnancy
vii. Psychogenic vomiting • Tab/Inj. Ondansetron 8 mg stat dose and
viii. Obstructive diseases of GIT repeated 8 hourly
ix. Acute gastritis, gastroenteritis
x. Radiation exposure. • In Pregnancy Tab/Inj. Promethazine 25 mg is
safe in the first trimester.
3. Investigations
• For motion sickness Tab Cyclizine 50 mg thrice
Evaluation should exclude CNS causes and upper GI a day.
endoscopy to rule out upper GI pathology. Barium
meal is recommended if upper GI scopy is normal. • If vomiting is part of suspected acute abdomen,
Psychogenic vomiting is considered after excluding acute MI, refer for further evaluation.
organic cause.
Bibliography
Further reading

Page 82
32. CONSTIPATION
Bisacodyl, oral, Adults 10-20 mg at night
Common causes of constipation are Diet deficient in
roughage Ignoring the urge to defecate e.g. due to Or
immobility, lack of exercise. Psyllium (Isaphghul husk), oral, Adults 5-10 ml
Other causes are neurological, Myxoedema, drugs once or twice a day
like Atropine, Codeine, etc and Malignancy Or
2. Symptoms Liquid Paraffin, oral - 10-30 ml at night Or

Glycerol Suppositories Adults 4 mg at night; 1 mg
Constipation itself is a symptom. When associated at night Or Lactulose liquid, oral, Adults 15-30 ml
with inability to pass flatus, severe abdominal pain, orally daily until response then 10-20 ml daily
or vomiting there may be the need for urgent referral
to a surgeon.
• Alternative treatment - Magnesium Sulphate,
oral, Adults 5-10 g in a glass of water, once or
3. Signs twice daily
Constipation, if associated with frequent high pitched
bowel sounds or absent bowel sounds 6. Do’s and Don’ts
• Advice patients to take plenty of fluids, high
4. Investigations fibre diet – green leafy vegetables, fruits, avoid
caffeinated drinks.
• Stool routine examination
• Regular walk and exercise ½ to 1 hour daily,
• Stool for occult blood abdominal exercise.
• Sigmoidoscopy/Colonoscopy • To use Indian closet as far as possible (this will
straighten the anorectal angle).
A rectal examination with a short length colonoscopy
is a must for all patients with recent onset of • Avoiding suppression of urge to defecate,
constipation irrespective of bleeding per rectum. (making a regular habit).
When acute, the constipation may be a part of a
• Avoid purgative frequently to treat constipation,
serious illness such as acute bowel obstruction. These
as it may be habit forming.
patients present with abdominal pain, vomiting and
distension and non-passage of flatus. These patients Suppository or simple enema is preferred in IHD
should be referred immediately to a higher center
after rectal examination, passage of rectal tube (for
passage of flatus) and a plain X-ray abdomen.
Bibliography
Further reading
1. Longstreth GF. Approach to adult with nausea and vomiting. Uptodate.com. Last updated May 12 th,
2016. [cited 2016 Jul 5]
Available from: http://www.uptodate.com/contents/approach-to-the-adult-with-nausea-and-
vomiting?source=outline_link&view=text&anchor=H23#H23

Page 83
33. IRRITABLE BOWEL SYNDROME
• Antidiarrheals – Tab Loperamide 2 to 4 mg
1. Definition daily for several days
A constellation of gastrointestinal symptoms • Anti-depressants
associated with lower bowel symptoms that occur in
absence of an organic disease. o IBD Diarrhoeal type –TCA (Imipramine)
o IBD constipation type – SSRI (paroxetine)
2. Symptoms • Calcium channel activators – Lubiprostone

8 micrograms for 3 months
Clinically the diagnosis is made when continuous or
• Any IBS patient with change in presentation e.g.
recurrent symptoms of abdominal pain are associated
change in bowel habit requires re-evaluation.
with any of the three features viz. Relief by
defecation and / or onset with change in stool
frequency or consistency for at least 3 months.
Supportive symptoms of IBS include passage of 4. Do’s and Don’ts
mucous, abnormal stool passage (straining, urgency,
• Diet should contain high fibre and
and feeling of incomplete evacuation) and feeling of
supplemented with bulk forming agents such as
abdominal fullness. Exclude IBS if individual has
Isaphghul husk
alarm symptoms such as fever, weight loss, bleeding
per rectum or anaemia • Avoid caffeine and alcohol
• Avoid milk and other dietary constituents,
3. Treatment which worsens the symptoms
• Psychotherapy may be helpful in selected cases
• Stool bulking agents – High fibre diet
• Antispasmodics – Anticholinergic drugs
(Dicyclomine)
Bibliography
Further reading
1. Spiller R, Aziz Q, Creed F, Emmanuel A, et al. Guidelines on the irritable bowel syndrome:
mechanisms and practical management, Gut. [Internet] 2007; 56:1770–1798. [cited 2016 Jul 5]
Available from: http://www.bsg.org.uk/pdf_word_docs/ibs.pdf

Page 84
34. ULCERATIVE COLITIS
• Sulphasalazine has a higher incidence of side
1. Introduction
effects compared with newer 5-ASA drugs.
Ulcerative colitis is a chronic inflammatory bowel
Selected patients, such as those with a reactive
disease of unknown aetiology.
arthropathy, may benefit.
2. Symptoms • Prednisolone 40 mg daily is appropriate for
During the first attack the patient often presents with patients in whom a prompt response is required,
bloody diarrhoea, with systemic symptoms of low to or those with mild to moderate active disease, in
moderate fever, backache, arthralgia. The first attack whom Mesalazine in appropriate dose has been
is a close mimicker of acute infective diarrhoea. A unsuccessful. It should be reduced gradually
stool examination followed by sigmoidoscopy is according to severity of the patient.
mandatory, especially if the bloody diarrhoea persists
• Long-term treatment with steroids is
for more than a month. It is important to exclude
undesirable. Patients with chronic active steroid
amoebic infection prior to institution of steroids.
dependent disease should be treated with
Rectum is uniformly involved in these patients.
Azathioprine 1.5–2.5 mg/kg/day
Frequency of stool can provide information on
severity of the disease: mild (2 - 4 stools/day), • Topical agents (either Steroids or Mesalazine)
moderate (4 – 6 stools/day) or severe (>6 stools/day). may be added to the above agents. Although
During remission, patient may be asymptomatic or they are unlikely to be effective alone, they may
may have extra-intestinal symptoms. benefit some patients with troublesome rectal
symptoms.
3. Treatment • Severe UC: close monitoring at a tertiary centre.
These patients require a referral to a tertiary unit.
Aim is induction of remission in acute stage and then 3.2 Maintenance of remission
maintenance of remission. • Lifelong maintenance therapy is generally
Therapeutic decisions depend on disease activity and recommended for all patients, especially those
extent. Patients with severe disease require hospital with left sided or extensive disease, and those
admission, whereas those with mild/moderate disease with distal disease who relapse more than once
can generally be managed as outpatients. a year.
• Disease extent can broadly be divided into • Discontinuation of medication may be

distal and more extensive disease. reasonable for those with distal disease who
have been in remission for 2 years and are
o Distal disease (Proctitis/Proctosigmoiditis):
averse to such medication. However, there is
Topical management is appropriate. some evidence that maintenance therapy
o Extensive disease: Oral or parenteral therapy
reduces the risk of colo-rectal cancer.
is the mainstay of treatment.
For the maintenance of remission in UC:
3.1 Choice of drugs
• Most patients require lifelong therapy, although
Mesalamine preparations and Steroid preparations
some patients with very infrequent relapses
Treatment of active left sided, or extensive UC: (especially if with limited extent of disease)
may remain in remission without maintenance
• Mesalazine 2 – 4 g daily or Balsalazide 6.75 g
therapy.
daily are effective first line therapy for mild to
moderate active disease.
Page 85
• Oral Mesalazine 1 – 2 g daily or Balsalazide 2.5 azathioprine, but limited evidences that this is
g daily should be considered as first line necessary.
therapy.
Important Note
• Sulphasalazine 2–4 g daily has a higher
• Regular surveillance is necessary for UC lasting
incidence of side effects compared with newer
for more than 10 years.
5-ASA drugs.
• Explain to the patient the chronic nature of the
• Topical Mesalazine 1 g daily may be used
disease and continuation of maintenance
• Steroids are ineffective at maintaining
• Treatment for life with regular follow-up. Risk
remission.
of colonic cancer after 10 years of disease onset
• Azathioprine 1.5 – 2.5 mg/kg/day or must be explained
Mercaptopurine 0.75 – 1.5 mg/kg/day are
effective at maintaining remission in UC. 3.3 Do’s and Don’ts
However, in view of toxicity they should be Milk is preferably avoided during the acute phase of
reserved for patients who frequently relapse illness.
despite adequate doses of amino-salicylates, or
are intolerant of 5-ASA therapy. It is a common
practice to continue amino-salicylates with
Bibliography
Further reading
1. Kornbluth A, Sachar DB. Ulcerative colitis in adults. Am J Gastroenterol. [Internet] 2010; 105:500;
doi:10.1038 / ajg.2010.52; published online 23 February 2010. [cited 2016 Jul 5]
Available from: http://gi.org/guideline/ulcerative-colitis-in-adults/

Page 86
35. AMOEBIC LIVER ABSCESS
1. Introduction 3.2. Imaging Studies
Liver abscess is the commonest extra-intestinal form • Ultrasonography is the preferable initial
of amoebiasis, caused by E. histolytica infection but diagnostic test. It is rapid, inexpensive, and is
occurs in only less than 1% of E. histolytica only slightly less sensitive than CT scan (75-
infections. The disease usually affects young males, 80% sensitivity vs 88-95% for CT scan).
particularly chronic alcoholics, in endemic areas.
Patients commonly affected are between 20 to 40 4. Treatment
years of age with residence in or recent travel to or
emigration from an endemic region. 4.1 Medical Management
• Tab. Metronidazole 800 mg three times orally
2. Clinical Manifestations (or IV, if necessary) daily for 5-10 days or Tab.
Tinidazole 600 mg 2 times a day for 7-10 days
2.1. History • If the patient is very toxic, Inj. Metronidazole
500 mg given 8 hourly until patient improves.
The signs and symptoms of amoebic liver abscess Switch over to oral therapy whenever possible.
often are nonspecific, resembling those of pyogenic Followed by Diloxanide Furoate (luminal agent
liver abscess or other febrile diseases. for cysts) 500 mg three times a day for 10 days
• Abdominal pain • Chloroquine 600 mg orally daily 2 days,
followed by 300 mg daily for 2 weeks; dose is
• Weight loss
calculated as chloroquine base. Drug is active
• Fever with rigors against E. histolytica trophozoites
• Diarrhoea/Dysentery
2.2. Physical Examination 4.2 Indications for drainage of an

• Fever is the most common sign and is found in
abscess
as many as 99% of cases.
• If pyogenic abscess cannot be excluded
• Hepatomegaly is present in some cases. • No improvement with medical therapy in 72
hours
• Signs of complications • Impending rupture of abscess (severe pain,
pleuritic pain, hiccups) - one very close to the
• Signs of peritoneal irritation, such as rebound surface of the liver
tenderness, guarding, and absence of bowel
• Large left lobe abscess, to prevent rupture in to
sounds, are present when the abscess ruptures in
the pericardium
the peritoneal cavity. Peritonitis occurs in 2-7%
of cases. 4.3 Follow-up
• Pericardial friction rub can be audible when the • Monitor the patient for resolution of symptoms
abscess extends into the pericardium. This sign with medical treatment and aspirate if there is
is associated with very high mortality. any indication.
• Signs of pleural effusion are present when the • Abscess cavity may persist for several weeks
abscess ruptures in the pleural cavity even after cure of infection. Frequent US scan is
unnecessary unless patient develops fever etc.
3. Investigations Scan may be repeated after 4 - 6 weeks, after
the patient becomes asymptomatic.
3.1. Laboratory Studies
Examination of the stool for hematophagous
trophozoites of E histolytica must be made on at least 5. Do’s and Don’ts
3 fresh specimens because the trophozoites are very
sensitive and may be excreted intermittently
Page 87
• Avoid taking alcohol, specifically if on • Maintain good hygiene during food intake to
treatment with Metronidazole prevent enteric infections
• Avoid contaminated food and drinking water.
Vegetables should be cooked or washed well.
6. Refer
• Use boiled water (kills the cyst) or bottled water Patients with abscesses that are large or not
from a known source. responding to treatment will need to be referred to a
physician or surgical specialist.
Bibliography
Further reading
1. Brailita DM, Anand BS. Amebic Hepatic Abscesses. Medscape.com. Last updated April 15, 2015.
[cited 2016 Jul 5]
Available from: http://emedicine.medscape.com/article/183920-overview

Page 88
36. PYOGENIC LIVER ABSCESS
Gentamicin: 2 mg/kg load, then adjust for renal
1. Introduction function
Liver abscess constitutes about 48% of all visceral
abscesses. Pyogenic liver abscess is usually caused Ciprofloxacin: 400 mg I/V 12 hourly for 10
by spread of infection from peritoneum, abdominal days
viscera such as appendicitis / diverticulitis / portal or
Pyaemia or diseases of biliary tract. It is most
commonly caused by coliform organisms. Inj. Ceftriaxone 1-2 g IV every 12 hours 2 times
a day
2. Clinical Manifestation or
Fever, abdominal pain, toxaemia, features of Inj. Cefotaxime 2 g 8-hourly for 10 days
associated problems such as appendicular pain/ mass
etc. Mostly abscesses are small and multiple. • Combination of Amoxicillin + Ciprofloxacin
+Metronidazole is also a recommended
3. Investigations schedule
Diagnostic investigations include total counts, USG • In the elderly or those with renal impairment: A
scan of the abdomen, blood culture, and pus culture. Penicillin (such as Amoxicillin) plus an
CECT and MRI is seldom indicated. injectable Cephalosporin (such as Cefotaxime or
Cefuroxime) plus Metronidazole is
4. Treatment recommended
4.1. Drainage • Inj. Penicillin – allergic patients: Ciprofloxacin

plus Clindamycin
Percutaneous catheter or open surgical- remains the
mainstay of treatment for a large abscess • Once the sensitivity is known, antibiotic therapy
is amended accordingly. Duration of therapy is
Patient should be kept nil by mouth and given IV usually from 2–4 weeks or longer depending on
fluids if toxic and sick. number of abscesses and the clinical response.
4.2 Recommended antibiotics 5. Follow-up

Metronidazole plus Ampicillin and Gentamicin, • Monitor for clinical improvement and modify
Ciprofloxacin, or a third-generation Cephalosporin the therapy based on culture sensitivity report.
• Abscess should always be drained.
Standard dosage
• Surgery is considered if no improvement with
• Ceftriaxone 2 g intravenously every 24 hours, or medical treatment and percutaneous drainage in
Cefotaxime 2 g intravenously every 8 hours. 4-7 days.
• Initial empirical treatment should include broad Important Note
spectrum antibiotics.
1. Avoid taking alcohol, specifically if on
• Various combinations recommended are: treatment with Metronidazole.
2. Maintain good hygiene regarding food intake to
Metronidazole: 500 mg I/V three times daily prevent enteric infections.
Ampicillin: 2 g I/V 6 hourly
Page 89
Figure-36.1: Approach to Pyogenic Liver Abscess
Bibliography
Further reading
1. Dutta A, Bandyopadhyay S. Management of Liver abscess, Medicine Update. [Internet] 2012, Vol.
22. [Cited 2016 Jul 5]
Available from: http://www.apiindia.org/pdf/medicine_update_2012/hepatology_04.pdf

Page 90
37. INTESTINAL PROTOZOAL INFECTION
giardiasis may contribute to protein-energy
1. Amoebiasis malnutrition in children.
Entamoeba Histolytica is the most prevalent Protein-losing enteropathy has also been described.
intestinal protozoa in India.
1.1 Clinical Features 2.2. Investigations

Diagnosis is made by stool examination and looking
Intestinal Amoebiasis / Amoebic Dysentery: for cysts and trophozoites.
Patient with acute amoebic dysentery present with a
1-2-week history of abdominal pain, tenesmus, and Parasites are best seen in fresh watery stools.
frequent loose stools containing blood and mucus.
Duodenal aspirate is better for isolation but invasive.
Fever may or may not be present.
1.2 Investigations 2.3. Treatment

Treatment is Metronidazole 400 mg TID for 5 days
Despite the presence of ulcerations and occult blood
orally or Tinidazole 2 gm PO once is equally
in stools, leucocytes may not be present in stools.
effective.
A definite diagnosis is made by the demonstration of
E. Histolytica cysts/ trophozoites in stools by a WET Furazolidone 6 mg/kg q.i.d for 7-10 days is effective
MOUNT PREPARATION. and well tolerated in children.
1.3 Treatment 3. Spore forming protozoa

The drug of choice for amoebic colitis is These include:
Tinidazole/Metronidazole
Doses are: • Cryptosporidium parvum
• Tinidazole: 2 g/day with food for 3 days or • Isospora belli
• Metronidazole: 750 mg TDS orally / IV for 5-10 • Cyclospora cayetanensis
days. • Microsporidia
Treatment of intraluminal Amoebiasis is Diloxanide The spectrum of diseases caused by these is as
Furoate 500 mg PO-TID for 20 days or Paromomycin follows:
30 mg/kg qd in 3 divided doses for 5-10 days.
3.1 Asymptomatic infection
2. Giardiasis This can be seen in immunocompetent as well as
immunocompromised patients.
It is a parasitic infection caused by Giardia Lamblia a
single celled organism. 3.2 Acute infectious diarrhoea in
immunocompetent hosts
2.1 Clinical Features Acute watery diarrhoea with abdominal pain, with
2.1.1 Acute symptoms include: malaise with or without fever can be seen in all
except microsporidia. (generally pathogenic only for
• Crampy abdominal pain immunocompromised patients)
• Watery diarrhoea, vomiting and fever which last
for few days.
3.3 Infections in immune
2.1.2 In the chronic stage: compromised hosts
Patients have bloating, nausea, abdominal fullness, All spore-forming protozoa have a predisposition for
epigastric or substernal burning, malaise and fatigue. more frequent and prolonged infections in patients
who are immunodeficient.
Although severe forms of chronic giardiasis may Patients with HIV especially with low CD4 count
occur in otherwise healthy individuals, they are (<50-100) are more prone.
common in patients with Hypoglobulinemia,
particularly IgA deficiency in association with
lymphoid hyperplasia of the bowel. Chronic
Page 91
Severe life-threatening watery diarrhoea, dehydration Stool examination with a wet mount preparation is
and chronic malabsorption leading to lethargy, failure required for isolation of the parasites.
to thrive, and malnutrition may occur. Modified acid fast staining is used to identify
3.4. Investigations Cryptosporidium, Isospora and Cyclospora as these
are acid fast.
3.5. Treatment
PATHOGEN TREATMENT
Cryptosporidium Nitazoxanide 500 mg b.i.d for 3 days
Paromomycin 30 mg/kg per day divided
Isospora Cotrimoxazole (TMP/SMX,160/800 MG) four times a day for 10
days and then 3 times a day for 21 days
Microsporidia No definite drug but Albendazole 400- 800 mg/day divided in b.i.d
can be given
Cyclospora Cotrimoxazole (TMP/SMX, 160/800 MG) twice daily for 7 days
Supportive treatment with ORS or iv fluids for fluid • Eosinophilia

and electrolyte supplementation is necessary.
• Urticaria
4. Intestinal helminthic • Asthma
(nematodes) infections • Angioneurotic oedema

Nematodes are round worms infesting the intestines. Intestinal invasion:
The infective forms are the eggs/larvae transmitted
by the feco-oral route. • May be asymptomatic (small number).
Generally seen in low socio economic states with • Abdominal pain (usually vague).
poor sanitation and hygiene.
Their life cycle is complex with stage of passage • Abdominal cramps/colic.
through lungs in some worms (ascaris, hookworm,
• Diarrhoea.
strongyloides) leading to various manifestations like
LOEFFLER’S SYNDROME. • Vomiting (rarely).
Several clinical signs and symptoms can occur as • Constipation (occasionally).

follows: • Intestinal obstruction due to worm mass.
The common nematode infections are described
Lung invasion - Loeffler's or Loeffler's like below:
syndrome (ascariasis, hookworm infections,
strongyloidiasis) 4.1 Ascariasis
Ascaris lumbricoides is the largest of the intestinal
• Fever nematodes. Symptoms can be divided into 2
• Cough categories: early larvae migration and late
mechanical effects.
• Blood-tinged sputum
In the early phase (4-16 hours after eggs ingestion),
• Wheezing respiratory symptoms occur because of migration of
larvae through the lungs with symptoms of
• Rales eosinophilic pneumonia (Loffler Syndrome). Patient
• Dyspnoea may have fever, non-productive cough, dyspnoea or
wheezing.
• Substernal pain
• Pulmonary consolidations
Page 92
In the late phase (6-8 weeks after egg ingestion) Chronic hookworm infection:
gastrointestinal symptoms may occur. Patient may
Generally, presents with Iron deficiency anaemia,
vomit out worms from mouth, nose.
Hypoproteinaemia.
Diffuse abdominal pain, nausea, vomiting, biliary and
intestinal obstruction, appendicitis and pancreatitis. 4.2.2 Diagnosis
Ascaris worms invade the biliary duct and cause Demonstration of eggs in stool examination.
pancreatic-biliary ascariasis. The most common Sensitivity improved with stool concentration.
presenting feature is abdominal pain, observed in Microcytic hypochromic anaemia with proteinemia
98% of patients. Less common features include may be seen in chronic cases. Eosinophilia may be
ascending cholangitis, acute pancreatitis, and, rarely, present.
obstructive jaundice.
4.2.3 Treatment
4.1.1 Diagnosis
i. In early infection (larval migration): Albendazole 400 mg once / Mebendazole 500 mg
CBC may show peripheral eosinophilia once / Pyrantel Pamoate 11 mg/kg for 3 days.
Sputum may show Charcot laden crystals. Treat anaemia with iron supplements.
Chest X Ray may show patchy infiltrates of
eosinophilic pneumonia. 4.3 Enterobiasis
ii. In the late stage (adult worm): Enterobius vermicularis / pinworm is prevalent in
• Stool microscopic examination shows most tropical countries.
eggs. The adult worms migrate to perianal area at night and
• USG may be used for ascariasis related release up to 10,000 eggs which after hatching are
biliary disease. transmitted by hand to mouth passage.
• CT abdomen may show adult worms or
obstruction due to worm mass. 4.3.1 Clinical features
The infection is generally asymptomatic.
4.1.2 Treatment:
The primary symptoms of pinworm infestation occur
Albendazole 400mg one dose orally is the drug of
at night which include pruritus in the perianal region.
choice OR Mebendazole 100 mg twice daily for 3
days. It is contraindicated in pregnancy. Heavy infection can cause abdominal pain and
weight loss.
4.2 Ancylostoma Duodenale:
4.3.2 Diagnosis
(Hookworm)
Since pinworm eggs are not released in faeces, stool
Many patients may be asymptomatic carriers. examination is not informative.
4.2.1 Clinical features Detection of worms / eggs in perianal cellophane
The symptoms are classified into 2 phases: swab / cellophane tape applied in the early morning
establishes diagnosis.
In the migratory phase:
4.3.3 Treatment
Pruritus and erythema and Vesiculation will occur
once the filariform larvae have penetrated the skin of Single dose Mebendazole 100 mg once / Albendazole
the feet and hands. This is called as “ground/dermal 400 mg once.
itch” in people who goes bare feet.
4.4 Strongyloidiasis
The pulmonary symptoms may develop with A.
Duodenale during the phase of lung migration like Strongyloides stercoralis is the only intestinal
mild transient pneumonitis. nematode with the ability to replicate inside humans,
In the intestinal phase: thus leading to repeated auto infection.
Patients may present with abdominal pain (often In immunocompromised hosts it can lead to invasive
epigastric). and disseminated infection which can be fatal.
Inflammatory diarrhoea, with eosinophilia. 4.4.1 Clinical features

• Many patients are asymptomatic.
Page 93
• Cutaneous manifestations include recurrent 4.4.3 Treatment
Urticaria involving buttocks and wrists. Ivermectin (200 mcg/kg daily for 2 days) is most
• “Larva currens”: Cutaneous migration of effective. In cases with disseminated infection extend
larvae results in serpiginous eruption which is the duration for 5 to 7 days or up to clearance of
pruritic, erythematous. parasites. Albendazole (400 mg daily for 3 days.) is
• Burning or colicky abdominal pain, often also effective.
epigastric, occurs and is associated with 4.5 Trichuris Trichiura
diarrhoea and the passage of mucus. Pain is • Also called as whip worm.
aggravated by food. • Most infections are asymptomatic. Heavy
• Some patients with strongyloidiasis report infections can cause gastro intestinal symptoms.
nausea, vomiting, and weight loss, with • Common in low socio economic status with
evidence of malabsorption or of protein-losing children especially affected.
enteropathy. 4.5.1 Clinical features
• Massive larval invasion of the lungs and other
tissues may occur with hyper infection, usually • Usually mild symptoms with abdominal pain,
in immunocompromised hosts. anorexia, diarrhoea which can be
• Disseminated infection in immunocompromised bloody/mucoid.
hosts severe generalized abdominal pain, diffuse • Rectal prolapse may occur in massive infections
pulmonary infiltrates, ileus, shock, and in children.
meningitis or sepsis due to gram-negative bacilli 4.5.2 Diagnosis
may occur.
• Stool examination for eggs.
4.4.2 Diagnosis • Proctoscopy for adult worms.
• Stool examination for rhabditiform larvae is
diagnostic. 4.5.3 Treatment
• Duodenal aspirate may reveal the larvae if stool Mebendazole 500 mg / Albendazole 400 mg daily for
is persistently negative. 3 days.
• In disseminated infections filariform larvae
should be sought in stool, sputum, broncho-
alveolar lavage etc.
Bibliography
Further reading
1. Wright SG. Protozoan infections of the gastrointestinal tract, Infect Dis Clin North Am.[Internet] 2012
Jun;26(2):323-39. [cited 2016 Jul 5]
Available from: http://www.ncbi.nlm.nih.gov/pubmed/22632642

Page 94
38. ASCITES
1. Causes Lab tests
Cirrhosis is the common cause of ascites. Other • In general, start with cell count and differential,
causes are malignancy, cardiac failure, tuberculous TP and albumin when uncomplicated ascites
ascites, pancreatitis, nephrotic syndrome, alcoholic due to cirrhosis is suspected. Culture is also
hepatitis, acute liver cell failure etc. usually sent.
• In patients with PMN >250, only 50% of
2. Physical Exam cultures grow bacteria if sent down to lab in a
• Almost all patients with cirrhosis severe enough syringe or plain tube. 80% grow bacteria if
to cause ascites will have stigmata of cirrhosis – inoculated into blood culture vials at bedside
spider angiomata, palmar erythema, and caput (prior to antibiotics).
medusae. • Glucose < 50, LDH > upper limit of normal for
• Elevated JVP should raise suspicion of heart serum, TP >1 and culture results can help
failure or constrictive pericarditis as a cause, differentiate secondary from spontaneous
although cirrhosis with tense ascites or peritonitis.
pulmonary HTN may cause this. • SAAG (serum albumin and ascitic albumin
• Sister Mary Joseph nodule with ascites may be gradient) > or = 1.1 has ~97% accuracy for
caused by gastric or colon CA, HCC, or portal hypertension.
lymphoma. If found, FNAC can provide a rapid • TP > or = 2.5 can help differentiate cardiac from
tissue diagnosis. cirrhosis ascites.
• When PMN > or = 250, but less than 50% of
3. Investigations WBC, consider peritoneal carcinomatosis and
• Ultra-sonography of abdomen is useful to tuberculous ascites.
confirm/refute presence of ascites, cirrhosis,
splenomegaly, biliary obstruction, vessel 4. Management
patency, signs of portal hypertension, and • Goal is to minimize ascitic fluid volume and
cancer. peripheral oedema without intravascular volume
• CT-abdomen, tumour markers, HBsAg Anti depletion.
HCV, serum amylase are other investigations. • First line treatment includes 2 grams per day
• Abdominal paracentesis sodium restricted diet and oral diuretics
(Spironolactone / Lasix).
Along with history and physical exam, ascitic fluid
• The usual diuretic regimen is single morning
analysis helps in the diagnosis of aetiology. It is a
doses of 100 mg Spironolactone and 40 mg
safe procedure ascitic fluid analysis.
Frusemide (Lasix).
Appearance • The ratio of 100:40 generally maintains
normokalemia. Usual max dose is 400 mg and
• Turbid/cloudy – 98% sensitive but only 23%
160 mg per day.
specific for SBP.
• Other specific management as per the cause of
• Milky – Chylous ascites, TG level usually
ascites.
greater than serum TG level and >200 mg/dl.
• Bloody/ink – Usually a traumatic tap, but seen
in 50% of patients with HCC and 22% with
5. When to Refer
malignancy overall. Acute ascites, bleeding tendency, refractory ascites,
hepatic encephalopathy.
• Dark brown – If bilirubin level is higher than in
serum, worry about ruptured gallbladder or
perforated duodenal ulcer.
Bibliography
Page 95
Further reading
1. Shah R, Katz J. Ascites. Medscape.com. Last updated: January 3rd, 2016. [cited 2016 Jul 5]

Page 96
39. HEPATITIS
hypertension and end stage liver disease
1. Introduction develops.
• Onset is gradual or sometimes rapid.
• There is fever, fatigue and nausea for a few days 4. Obstructive jaundice
followed by jaundice accompanied by dark
• Sometimes jaundice is due to obstruction to
urine and sometimes clay - coloured stools.
flow of bile and not due to a virus.
• The severity of jaundice varies.
• On such cases the yellowing of eyes is very
• On examination liver may be mildly enlarged marked and may even be greenish.
with mild tenderness.
• There is much itching and the stools are always
• This being the most common cause one must whitish in colour.
always make this clinical diagnosis after the
• Usually the liver is enlarged.
exclusion of obstructive or haemolytic jaundice.
In most cases this can be done on clinical • Ultrasound of the liver confirms obstruction
grounds alone. best and the patients should be referred to a
centre with ultrasonography facilities.
• There are five viruses that are commonly
associated with hepatitis, called Hepatitis A, B, • Refer to higher centre as these cases need
C, D and E virus. Of these two, Hepatitis A and surgery.
E spread through faecal contamination of water.
When there is an outbreak of jaundice in a 5. Haemolytic jaundice
village, it is probably this virus. Almost always
this jaundice becomes alright on its own. Except • Sometimes jaundice is due to increased
in pregnant women where it can be life breakdown of haemoglobin secondary to
threatening. Three other types of viruses spread destruction of RBCs in a haemolytic anaemia.
through the blood and through unprotected • Jaundice is invariable light coloured, and urine
sexual contact (hepatitis B, C, D). These types is also normal in colour.
are more severe, tend to worsen and have more
long term complications. • Diagnosis needs to be established by blood
smear examination, by ruling out hepatitis by
2. Acute fulminant hepatitis liver function tests and by specific tests for
• Sometimes, especially with hepatitis B and D haemolytic anaemia.
hepatitis turns severe due to cell necrosis.
• Patient develops confusion, stupor and then 6. Alcoholic hepatitis
coma and it is difficult to save the life.
Excessive alcohol consumption is a significant cause
• Pregnant women are prone to develop this of hepatitis and liver damage (cirrhosis). Alcoholic
picture with all viruses but commonly with hepatitis usually develops over years-long exposure
hepatitis E. to alcohol. Alcohol intake in excess of 80 grams of
alcohol a day in men and 40 grams a day in women is
3. Chronic hepatitis associated with development of alcoholic hepatitis.
• Sometimes the liver disease goes on for years Alcoholic hepatitis can vary from mild asymptomatic
without becoming well. disease to severe liver inflammation and liver failure.
Symptoms and physical exam findings are similar to
• Such patients have frequent intermittent other causes of hepatitis. Laboratory findings are
episodes of jaundice. significant for elevated transaminases, usually with
elevation of Aspartate Transaminase (AST) in a 2:1
• Elevated liver enzymes over 6 months is enough
ratio to Alanine Transaminase (ALT).
to make this diagnosis.
Alcoholic hepatitis may lead to cirrhosis and is more
• Eventually it can become well but more often common in patients with long-term alcohol
leads to cirrhosis of the liver and portal consumption and those infected with Hepatitis C.
Page 97
Patients who drink alcohol to excess are also more 8.1. Treatment for Acute fulminant
often than others found to have Hepatitis C. The
combination of Hepatitis C and alcohol consumption hepatitis
accelerates the development of cirrhosis. • Patient needs hospitalization.
• Treatment is supportive & consists of
maintaining parenteral fluids.
7. Investigations for jaundice
• Care is taken to treat infections or other
These tests are needed to establish diagnosis & precipitating factors like hematemesis.
monitor improvement.
• Urine examination for bile salts & pigments. • Gut sterilization with capsule amoxicillin and/or
metronidazole may help.
• Serum bilirubin & Serum liver enzymes level.
8.2. Treatment for obstructive
8. Treatment for hepatitis jaundice
• Refer for Surgery.
• Only supportive: Rest, hydration, correct but not
specific diet. 8.3. Treatment for Haemolytic
• Avoid oily spicy foods that are ill tolerated. anaemia
• Referral for further work up in higher centre
• Avoid Corticotherapy. NEVER give steroids. with tests for type of haemolysis.
• There are no specific drugs to cure jaundice.
Fortunately, most persons become well on their 9. Vaccine
own. • Vaccine against hepatitis B is available.
• Remember many drugs commonly used are • Hepatitis-B Vaccine is included in National
harmful when given to a person with jaundice. Immunization Schedule.
Bibliography
Further reading
1. America. Center for Disease Control and Prevention (CDC). Sexually transmitted diseases treatment
guidelines: Hepatitis A. [cited 2016 Jul 5]
Available from: http://www.cdc.gov/std/tg2015/hepatitis.htm
2. Kahn A and Higuera A. Hepatitis. Healthline.com. October 14, 2015. [cited 2016 Jul 5]
Available from: http://www.healthline.com/health/hepatitis#Overview1
 
Page 98
40. HEPATIC COMA
1. Introduction Search for precipitating factors – every advanced
Hepatic Encephalopathy is a term used to describe a cirrhotic patient displaying a change in mental status
spectrum of neuropsychiatric abnormalities occurring is septic until proven otherwise. Common
in patients with significant liver disease and/or precipitating factors are GI bleeding, sepsis,
portosystemic shunting of blood. hypokalaemia, high protein load, constipation,
hyponatremia, Other causes include sedative
2. Diagnosis drugs, superimposed liver injury.
There are 2 major components of HE, altered mental
status and generalized motor disturbance. 3. Grade / Stage the severity of
Disturbances in awareness and mentation from
forgetfulness and confusion to stupor and finally disease
coma. Asterixis / flapping tremors is also commonly
seen.
Table-1: West-Haven Criteria for Hepatic Encephalopathy (HE)
Stage Consciousness Intellect and Behaviour Neurologic Findings

0 Normal Normal Normal examination; if impaired psychomotor
testing, consider MHE*
1 Mild lack of awareness Shortened attention span Impaired addition or subtraction; mild Asterixis
or tremor
2 Lethargic Disoriented; Inappropriate Obvious Asterixis; Slurred speech

behaviour
3 Somnolent but Arousable Gross disorientation; Muscular rigidity and clonus;
Bizarre behaviour Hyperreflexia
4 Coma Coma Decerebrate posturing
*MHE, minimal hepatic encephalopathy.
ii. Rifaximin 400 mg PO t.i.d marginally better

4. Treatment than lower doses (400 mg-550 mg b.i.d) or
A. 4-pronged approach to treatment Neomycin 1 gm PO 6 hourly for up to 6 days
Supportive care. (if used chronically, 1-2 gm/day).
Search for and correct precipitating factors iii. Dietary protein restriction – No longer
Exclude and treat other causes of altered mental recommended.
status. iv. L-ornithine-aspartate promotes waste nitrogen
Start empiric therapy for HE excretion.
i. Lactulose: 30 cc b.i.d- q.i.d titrated to goal 2-4 v. Antibiotics if sepsis suspected.
soft BMs/day or retention enema 300 cc
lactulose + 700 cc tap water retained for 1
hour reduces the ammonia production and 5. When to refer
absorption. Deteriorating sensorium, haematemesis, melena,
bleeding tendencies.
Page 99
Bibliography
Further reading
1. Vilstrup H et al, Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the
American Association for the Study of Liver Diseases and the European Association for the Study of
the Liver, Hepatology. Volume 60, Issue 2. [Internet]. August 2014, Pages 715–735. [cited 2016 Jul 5]
Available from: http://onlinelibrary.wiley.com/doi/10.1002/hep.27210/abstract
2. Hepatic Coma. Nmihi.com. [cited 2016 Jul 5]
Available from: http://www.nmihi.com/h/hepatic-coma.htm
3. Mohamad R, Brendan MM. Current trends in the treatment of hepatic encephalopathy. Ther Clin Risk
Manag. [Internet] 2009; 5: 617–626. Published online 2009 Aug 3. [cited 2016 Jul 5]

Page 100
41. NEPHROTIC SYNDROME
• Renal Function Test: Blood Urea Level and
1. Definition Serum Creatinine Level
Nephrotic Syndrome is a clinical complex
• Renal Biopsy: In Adult patients for a)
characterized by a number of renal and extra renal
Establishing a Definitive Diagnosis b) Guiding
features, the most prominent of which are
Therapy & c) Assessing Prognosis.
• Proteinuria of 3-3.5 gm / 24 hour,
• Hypoalbuminemia,
• Oedema, 5. Treatment
• Hyperlipidaemia, Lipiduria • Steroid: Minimal change disease accounts for
about 80% of Nephrotic Syndrome in children
younger than 16 years and 20% of adult.
2. Symptoms and Signs Adult: Tab Prednisolone 1-1.5 mg/kg body
Puffiness of face, increase in morning weight per day for 4 week followed by 1
Ankle pitting oedema with increasing severity to mg/kg/day on alternate day for 4 weeks.
generalized anasarca Ascites, Pleural Effusion Check for urine protein after four weeks if nil
no treatment needed and if present start with
3. Complications Prednisolone 1.5 mg for 2 weeks
Recurrent Infections, hypocalcaemia, anaemia, • HMG-Co-A Reductase Inhibitor:
Thrombotic Tendencies Tab Atorvastatin 10 mg Once a day
• Loop Diuretic
• Salt Restriction 1-2 Gram per Day.
4. Investigation • High Protein Diet
• Urine Analysis for Proteinuria, Protein / • Vitamin D Supplementation.
Creatinine ratio
• Urine Microscopy for Deposit
• 24 Hour Urinary Protein 6. When to Refer
• Serum albumin i. For Renal Biopsy
• Ultra-sonography abdomen and pelvis ii. When Dialysis is required.
Bibliography
Further Reading:
1. KDIGO. Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl. [Internet] 2012; 2:209.
[cited 2016 Jul 5]
Available from: http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO-GN-Guideline.

Page 101
42. ACUTE NEPHRITIC SYNDROME
It is Clinical Correlate of Acute Glomerular • Blood Urea and Serum Creatinine elevations.
Inflammation Which May Be a Primary Disease OR • Decrease C3 Level, Normal C4 Level
Secondary to Systemic Process. • ASO Titre
• Ultra-sonography renal
1. Definition • Renal Biopsy
It is characterized by sudden onset (over days to
weeks) of acute renal failure and Oliguria (400 4. Treatment
ml/day of urine) renal blood flow and GFR fall as a
result of obstruction of the glomerular capillary 4.1 General Management
lumen.
• Bed Rest
2. Clinical Features • Adequate Fluid Intake to ensure 400 ml Urine
Tetrad of per Day
• Salt restriction especially if oedema present
• Oedema
• Hypertension mild 4.2 Management of Renal Failure
• Haematuria [macroscopic]
• Proteinuria (Sub-nephrotic Range < 3g/24 • Tab Frusemide if volume overload hypertension
Hours) • Not to be given if no evidence of fluid excess
Symptom: • Rarely require Dialysis
• Puffiness of Face 4.3 Antihypertensive Drug

• Oedema of Feet
• Cola Coloured Urine 4.4 Control of Infection
• Dyspnoea If Pulmonary Oedema
• Hypertension 4.5 Renal Biopsy
• Generalized Symptoms- Anorexia, Nausea,
Vomiting, Malaise, Flank OR Back Pain. If features not suggestive of Post Streptococcal
Glomerulonephritis.
3. Investigation
• Urine Microscopy: Dysmorphic RBCs and RBC 5. When to Refer
Cast, Leucocytes i. For Renal Biopsy
• Urine- Gross Haematuria (Red or Smoky Urine) ii. When Dialysis is required.
• Sub-nephrotic range Proteinuria
Bibliography
Further Reading:
1. KDIGO Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl. [Internet] 2012; 2:209.
[cited 2016 Jul 5]
Available from: http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO-GN-Guideline.

Page 102
43. ACUTE RENAL FAILURE / ACUTE KIDNEY
INJURY
1. Definition
c. Acute tubular necrosis
AKI is a syndrome characterized by rapid decline in
glomerular filtration rate (hours to days), retention of Ischemia, Exogenous toxins: radiocontrast,
nitrogenous waste products and perturbation of chemotherapy, acetaminophen, Endogenous toxins:
extracellular fluid volume and electrolyte and acid rhabdomyolysis, haemolysis, myeloma.
base homeostasis.
d. Interstitial nephritis
AKI is defined as any of the following (Not Graded):
• Increase in Sr. Creatinine by X 0.3 mg/dl Antibiotic, NSAID, Sulphonamide, Beta lactam
(X26.5 lmol/l) within 48 hours; or antibiotics
• Increase in Sr. Creatinine to X 1.5 times
baseline, which is known or presumed to have 2.3. Post renal:
occurred within the prior 7 days; or
a. Ureter:
• Urine volume 0.5 ml/kg/h for 6 hours
Calculi, blood clot, carcinoma
2. Classification b. Bladder neck:
2.1. Prerenal: Prostatic hypertrophy, calculi, carcinoma
a. Hypovolemia: c. Urethra:
Haemorrhage, burns, dehydration, vomiting, Stricture, phimosis.

diarrhoea, pancreatitis, peritonitis.
3. Symptoms
b. Low cardiac output:
CCF, Disease of myocardium, valves and 3.1. Prerenal
pericardium,
• Evidence of true volume depletion- Thirst,
Pulmonary Hypertension, Pulmonary emboli. postural or absolute hypotension and
c. Altered renal systemic vascular resistance ratio; tachycardia, dry mucous membrane.
• Urine- Low volume, low sodium and high
Systemic vasodilatation- Sepsis, Antihypertensive osmolality.
drug
Renal vasoconstriction: Hypercalcemia 3.2. Renal
Cirrhosis with ascites- Hepatorenal syndrome. Symptom and sign of underlying disease affecting
glomeruli or tubule.
2.2. Intrinsic renal
a. Renovascular obstruction:
3.3. Post renal
Renal artery obstruction: atherosclerosis, thrombi, Abdominal or flank pain, palpable bladder.
emboli, Renal vein obstruction: thrombi, compression
b. Disease of glomeruli: 3.4. Symptoms of uraemia
Glomerulonephritis and vasculitis, Haemolytic Anorexia, nausea, vomiting, Mental status changes,
uremic syndrome, DIC, Toxaemia of pregnancy, Pruritus, shortness of breath
Accelerated Hypertension.
Page 103
• Routine blood chemistry: BUN, creatinine,
4. Signs electrolyte, Ca, PO4
Asterixis, Pericardial rub, Pedal oedema, Pulmonary • Complete Haemogram
oedema, Raised JVP • Special test: Bence Jones protein
• Serology: ANA, ANCA, anti GBM,
5. Investigation complement, ASO
• Imaging: Renal ultrasound, Plain radiograph of
• Urine analysis: Routine microscopy abdomen.
• Renal biopsy.
6. Staging of AKI
STAGE Serum creatinine criteria Urine output criteria

I 1.5 to 2-fold increase <0.5 ml/kg/hr for > 6 hours
II 2 to 3-fold increase <0.5 ml/kg/hr for >12 hours
III >3-fold increase, absolute value > 4 mg/dl < 0.3 ml/kg/hr for 24 hours or
anuria for 24 hours.
•
7. Treatment alcium gluconate (10ml 10% solution)
7.1. Prerenal • Inhaled β2 agonist- Salbutamol
Restore blood volume (with isotonic saline 0.9%, or • IV glucose insulin infusion (100ml 25%
blood, plasma) dextrose with 10 unit of human Actrapid in
Treat underlying cause. 1 hour)
• Dialysis.
7.2 Renal
Eliminate toxins, Nephrology consultation 7.5. Treatment of metabolic
acidosis
7.3. Post-renal Inj. Sodium bicarbonate IV as per Base deficit
Relieve obstruction, Urology consultation
7.6. Dialysis: indication
7.4. Hyperkalaemia Metabolic acidosis, Hyperkalaemia, Encephalopathy,
Volume overload, Pericarditis
8. Complication
COMPLICATION MANIFESTATION
1. Metabolic Hyperkalaemia, hypocalcaemia, hyperphosphatemia, hypermagnesemia,
hyperuricemia, metabolic acidosis.
2. Cardiovascular Cardiac arrhythmia, pulmonary oedema, pericardial effusion, pericarditis
3. Gastrointestinal Gastrointestinal haemorrhage
4. Neurological Altered sensorium, seizures
5. Hematological Anaemia, bleeding.
• Management and prevention of sepsis

9. Prevention
• Appropriate and adequate fluid management
• Optimization of hemodynamic
Page 104
• Nephrotoxic drug should be stopped if patient is at risk of developing AKI.
Bibliography
Further Reading:
1. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. [Internet] 2012; vol 2.
[cited 2016 Jul 5]
Available from:
http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf


Page 105
44. CHRONIC KIDNEY DISEASE
iii. Nondiabetic glomerular disease- Nephritic and
1. Definition nephrotic presentation
iv. Cystic kidney disease
A. Presence of marker of kidney damage more than v. Tubulo-interstitial disease.
3 months as defined by structural or functional
abnormality of the kidney with or without decrease 3. Staging
GFR manifested by either pathological abnormality According to GFR (glomerular filtration rate)
or other marker of kidney damage. Cockcroft-Gault equation for calculation of
B. GFR < 60 ml/min/1.73 m2 for more than 3 creatinine clearance:
months with or without sign of kidney damage.
(140- Age) × Body weight (kg)
2. Causes 72 × plasma creatinine (mg/dl)
i. Diabetes Multiply by 0.85 for women.
ii. Hypertension
Table-1: Staging of CKD
STAGE DESCRIPTION GFR (ml/min/1.73 m2)

1 At increased risk of kidney damage with normal or raised 90
GFR
2 Kidney damage with mildly decreased GFR 60-89
3 Moderately decreased GFR 30-59
4 Severely decreased GFR 15-29
5 Renal failure <15
4. Symptoms and signs 6. Evaluation and management

Hypertension, proteinuria, anaemia, deep respiration
(Kussmaul’s respiration), tiredness, breathlessness,
of patient of CKD
pruritus, anorexia, nausea, vomiting. 6.1. History and physical
5. Risk factors examination
• Age > 65 years H/O HTN, DM, use of analgesic Measure blood
• Diabetes pressure
• Family H/O renal disease
• Autoimmune disease 6.2. Laboratory investigation
• Systemic infection
• Haemoglobin level.
• UTI, stone, urinary tract obstruction,
• HTN • Urine for proteinuria and haematuria
• Blood urea, serum creatinine
Page 106
• Blood sugar level 6.3. Imaging study
• Serum electrolyte
USG abdomen for the renal size and Cortico-
• Serum calcium, phosphorus level medullary differentiation.
Table-2: To Delay Progression to Next Stage:
MEASURES GOAL
1. ACE inhibitors / ARB Proteinuria <0.5 g/day and GFR decline <2ml/min/yr.
2. Additional antihypertensive drug as needed BP<130/80 if proteinuria <1 gm/day
BP<125/75 if proteinuria >1gm/day
3. Dietary protein restriction 0.6 to 0.8 gm/kg/day
4. Glycaemic control HbA1C <7 %
5. Anaemia correction Target Hb 10 to 12 gm/dl
6. Cholesterol lowering agent LDL <100 mg/dl
7. Dietary salt restriction 3 to 5 gm/day
6.4. Treatment osteodystrophy: Target Ca 8.8 – 9.7, phosphorus 3.5

– 5.5, Use of calcium carbonate, phosphorus
a. Slowing the progression of CRF:
restriction – avoid dairy product, meat, colas, oral
Protein restriction 0.6 gm/kg/day calcitriol.
b. Slowing diabetic renal disease: d. Renal replacement therapy:
Glucose control – target HbA1c <7%

Dialysis: refer to higher center, A-V fistula; if GFR
c. Managing complications of CRF: <25ml/min Serum creatinine > 4 mEq/L.
Cardiovascular complication- Yearly screening of

cardiovascular diseases, Anaemia: target Hb 11
gm/dl, use of iron and erythropoietin injection, Renal
Bibliography
Further Reading:
1. Varma PP. Prevalence of Kidney disease in India – where are we heading? Indian J Nephrol.[Internet].
2015 May-Jun; 25(3): 133–135. [cited 2016 Jul 5]

Page 107
45. MALARIA
Fever comes down with profuse sweating. The
1. Introduction temperature drops rapidly to normal and skin is cool
Malaria is a protozoal disease caused by infection and moist. The pulse rate becomes slower; patient
with parasites of the genus plasmodium and feels relieved and often falls asleep. This stage lasts
transmitted to man by female Anopheles mosquito. It for 2-4 hours.
is a very important public health problem in India The febrile paroxysms occur with definite
particularly due to Plasmodium falciparum which is intermittent periodicity repeating every third or
prone to various complications. fourth day depending upon the species of the parasite
involved. The classical 3 stages (cold, hot and
2. Agent sweating) may not always be observed due to
Malaria in man is caused by Plasmodium vivax, maturation of generations of parasite at different
Plasmodium falciparum, Plasmodium Ovale and times. The disease has a tendency to relapse and is
Plasmodium malaria. Out of these, Plasmodium vivax characterized by enlargement of the spleen and
and Plasmodium falciparum are very common in secondary anaemia.
India including Maharashtra. In patients with P. falciparum infection, the primary
fever in its first few days is usually irregular or even
3. Mode of transmission continuous and then the classical 48-hour periodicity
Direct – through blood or plasma. becomes established or the fever may continue to be
irregular and the hot and cold stages, so typical of
Vectors – bite of female Anopheles mosquito. other malarial infections are less clearly separated
from one another, in persons with poor immunity.
4. Incubation Period The paroxysms are associated with marked
prostration. Headache, nausea and vomiting are
The duration varies with species of parasite.
usually more severe, and there is greater tendency
• 12 (9-14) days for falciparum malaria. towards the development of delirium, haemolytic
• 14 (8-17) days for vivax malaria. jaundice and anaemia. The mortality is much greater
than in other forms of malaria.
5. When to suspect With P. vivax infection, symptoms are same but are
usually milder and more regularly divided into “hot”
The typical attack comprises three distinct stages viz.
and “cold” stages than in P. falciparum infections.
cold stage, hot stage and sweating stage.
Cold Stage:
6. Complications
The onset is with lassitude, headache, nausea and
chilly sensation followed in an hour or so by rigors. The complications of P. falciparum malaria are
The temperature rises rapidly to 39-41°C. Headache cerebral malaria, acute renal failure, liver damage,
is often severe and commonly there is vomiting. In gastro-intestinal symptoms, dehydration, collapse,
early part of this stage, skin feels cold; later it anaemia, black water fever etc. The complications of
becomes hot. Parasites are usually demonstrable in P. vivax, infection are anaemia, splenomegaly,
the blood. The pulse is rapid and may be weak. This enlargement of liver, herpes, renal complications,
stage lasts for ¼-1 hour. ARDS etc.
Hot Stage:
7. Investigations
The patient feels burning hot and casts off his
clothes. The skin is hot and dry to touch. Headache is
intense but nausea commonly diminishes. The pulse • Diagnosis of Malaria: One of the above clinical
is full and respiration rapid. This stage lasts for 2 to 6 features, supported by blood smear examination
hours. for malarial parasites.
• Fever with splenomegaly in a patient with the
Sweating Stage: above mentioned clinical features make
diagnosis of malaria more likely.
Page 108
• Confirmation of diagnosis always depends on ensure treatment with full therapeutic dose with
seeing the parasite in the blood. In all cases, appropriate drug to all confirmed cases. Presumptive
thick and thin smears should be examined. treatment of malaria with a single dose of
• Blood smears may be negative in severe and chloroquine has been stopped.
chronic forms and this would need repeated All fever cases diagnosed as malaria by either RDT
smears. or microscopy should be promptly given effective
treatment. The medicine chosen will depend upon
8. Diagnosis of Malaria whether the patient has vivax malaria or falciparum
It is stressed that all fever cases should be suspected malaria as diagnosed by the blood test. The flow
of malaria after ruling out other common causes and charts in different settings for diagnosis and drug
should be investigated for confirmation of malaria by selection for the treatment of malaria are mentioned
Microscopy or Rapid Diagnostic Kit (RDK) so as to below.
Where microscopy result available within 24 hours
Suspected malaria case
Take slide and send for microscopic examination
Result?
Positive for Positive for Positive for Negative

P. vivax P. falciparum Mixed infection No anti-malarial
Treat with: Treat with: SP-ACT 3 days Treatment.
CQ 3 days + ACT-SP + Treat as per
PQ 0.25 mg for 3 days + PQ 0.75mg Primaquine clinical
per kg body per kg body 0.25 mg per kg diagnosis
weight daily for weight body weight
14 days Single dose on daily for
second day 14 days.
Figure-45.1: Management chart for suspected Malaria case
Page 109
ACT-SP- Artemisinin-based Combination Therapy Where microscopy result is not available within 24
(Artesunate + Sulfadoxine-Pyrimethamine) hours and Monovalent RDT is used
CQ – Chloroquine PQ –Primaquine TfR= Test falciparum rate
Where TfR ≥ 1%, and In other areas, if

Pf %> 30% in any of Patient not
last 3 years at high risk of Pf*
Do RDT for detection Wait for slide result. Give

of Malaria & CQ 25 mg/kg over 3 days
Prepare slide only if high suspicion of
malaria
Positive for Positive for

Positive for RDT Negative:
P. vivax P. falciparum
P. falciparum Wait for slide result.
CQ if not In other states:
Treat with: ACTSP Give CQ 25 mg/kg
already Treat with: ACTSP
for 3 days + over 3 days, if
given + for 3 days
PQ Single dose high suspicion of
PQ 0.25 + PQ Single
on second day malaria
mg/kg single dose on PQ 0.75 mg
dose for 14 per kg body
If confirmed as days over 3 weight
P.vivax days, if high Single dose on
CQ if not already suspicion of second day
Given PQ 0.25 malaria
mg/kg/day over
14 days
Figure-45.2: Management of suspected Malaria
Note: if a patient has severe symptoms at any stage, ACT-SP- Artemisinin-based Combination Therapy
then immediately refer to a facility with indoor (Artesunate + Sulfadoxine-Pyrimethamine)
patient management. CQ –Chloroquine PQ – Primaquine.
Note: PQ is contra-indicated in pregnancy and in Where microscopy result is not available within 24
children under 1 year (Infant). hours and Bivalent RDT is used
Page 110
Do blood test with RDT
Positive for Positive for Positive for Negative

P. falciparum P. vivax Mixed infection No anti-
Treat with: ACTSP Treat with: SP-ACT 3 days + malarial
for 3 days + CQ 3 days Primaquine 0.25 mg per Treatment
PQ Single dose on second + PQ 14 days kg body weight daily for
day malaria case 14 days.
Figure-45.3: Suspected Malaria management based on RDT results

ACT-SP- Artemisinin-based Combination Therapy Drug schedule for treatment of P vivax malaria:
(Artesunate + Sulfadoxine-Pyrimethamine).
i. Chloroquine:
CQ –Chloroquine PQ - Primaquine
25 mg/kg body weight divided over three days i.e.
Differential Diagnosis:
10 mg/kg on day 1,
Other causes of fever like – Dengue, UTI, URTI. All
10 mg/kg on day 2 and
D/D can be excluded by using lab investigation
(microscopy/RDT). 5 mg/kg on day 3.
ii. Primaquine:
9. Treatment 0.25 mg/kg body weight daily for 14 days.
9.1. Treatment of Vivax Malaria
Primaquine is contraindicated in infants, pregnant
Diagnosis of vivax malaria may be made by the use
women and individuals with G6PD deficiency.
of RDT (Bivalent) or microscopic examination of the
blood smear. On confirmation following treatment is 14-day regimen of Primaquine should be given under
to be given: supervision.
Table-1: Dosage Chart for Treatment of Vivax Malaria
Day 4 to 14
Day 1 Day 2 Day 3
Age
CQ (150 PQ (2.5 CQ (150 mg PQ (2.5 CQ (150 mg PQ (2.5 mg) PQ (0.25
mg base) mg) base) mg) base) mg)
Less than
½ 0 ½ 0 ¼ 0 0
1 year
1-4 years 1 1 1 1 ½ 1 1
5-8 years 2 2 2 2 1 2 2
9-14 years 3 4 3 4 1½ 4 4
15 years
4 6 4 6 2 6 6
or more*
Pregnancy 4 0 4 0 2 0 0
Note: Chloroquine 250 mg tablet is having 150 mg base
Page 111
9.2. Treatment of Falciparum Treatment of uncomplicated P. falciparum cases
in pregnancy:
Malaria • 1st Trimester: Quinine salt 10 mg/kg 3 times
Diagnosis of falciparum malaria may be made by the daily for 7 days. Quinine may induce
use of RDT (Monovalent or Bivalent) or microscopic hypoglycaemia; pregnant women should not take
examination of the blood smear. It is imperative to quinine on empty stomach and should eat
start the treatment for falciparum malaria regularly, while on quinine treatment.
immediately on diagnosis. The treatment for • 2nd and 3rd trimester: ACT as per dosage
falciparum malaria is as follows: schedule given above.
Dose schedule for Treatment of uncomplicated P.
falciparum cases:
i. Artemisinin based Combination Therapy (ACT- 9.3. Treatment of mixed infections
SP) * (P. vivax + P. falciparum) cases
Artesunate 4 mg/kg body weight daily for 3 days Plus All mixed infections should be treated with full
Sulfadoxine (25 mg/kg body weight) – course of ACT and Primaquine 0.25 mg per kg body
Pyrimethamine (1.25 mg/kg body weight) on first weight daily for 14 days.
day. SP-ACT 3 days + Primaquine 0.25 mg per kg body
* ACT is not to be given in 1st trimester of wt. daily for 14 days.
pregnancy.
ii. Primaquine: 0.75 mg/kg body weight on day 2.
Table-2: Treatment of mixed infections
Day 4to
Day 1 Day 2 Day 3
14
Age As tablet SP tablet PQ (2.5 As tablet PQ (2.5 As tablet PQ (2.5 PQ (0.25
(50 mg) mg) (50 mg) mg) (50 mg) mg) mg)
Less than
1 year ½ ½ 0 ½ 0 ½ 0 0
1-4 years 1 1 1 1 1 1 1 1
5-8 years 2 1½ 2 2 2 2 2 2
9-14 years 3 2 4 3 4 3 4 4
15 years
or more 4 3 6 4 6 4 6 6
All cases of mixed infection are to be treated as Pf (Did the patient get the drug from an authentic,
plus Primaquine for 14 days. designated provider? Did the patient get the
right amount of the drug? Was all of it
When a patient fails to respond to treatment swallowed as prescribed? Was the drug vomited
(symptoms fail to disappear, or they reappear), one out? How many days has it been since drug
should think of the possibility of drug resistance in treatment was begun (if it is not yet 72 hours,
such case refer patient to FRU. In the absence of any one can wait)? Can you see the packing to check
of these conditions, if a patient has completed full the expiry date? Are there symptoms of other
treatment and is still having symptoms after 72 hours, obvious causes of fever? If the symptoms had
treatment failure may be suspected. disappeared and then reappeared, how long was
the interval (if more than 15 days, it could be a
The course of action when a patient has persistent fresh infection)?)
symptoms is: • If it appears that the drug was not adequately
• Ask the patient and the family a series of taken or retained, a fresh course may be given
questions to help rule out some of the causes unless the patient has symptoms of severe
Page 112
malaria. Take a fresh blood smear (take two, for Febrile convulsions, repeated vomiting and
checking in different laboratories, if need be), dehydration are common if the temperature is
and ask the nearest health care provider to keep high due to any cause. Therefore, these
an eye on the patient. symptoms are not necessarily indicative of
• Refer any patient who has symptoms despite severe malaria. However, children with such
taking and retaining a full course of treatment, symptoms should be managed as severe malaria
or who has developed symptoms of severe in routine program situations, and a diagnosis of
malaria. malaria should be confirmed at the earliest.
10.3. In pregnancy
10. Severe and complicated
Malaria, especially P. falciparum is a serious
malaria disease because with each bout of malaria, there
10.1. Clinical Features is a reduction in haemoglobin and profound
Severe manifestations can develop in P. falciparum anaemia may develop rapidly. They are also at
infection over a span of time as short as 12-24 hours high risk of abortions or intrauterine growth
and may lead to death, if not treated promptly and retardation because sequestration of parasites in
adequately. Severe malaria is clinically characterized placenta restricts oxygen and nutrients flow to
by confusion or drowsiness with extreme weakness the foetus.
(prostration) along with one or more of the following The management of severe malaria is possible in
features: health facilities which are equipped with the
• Impaired consciousness/coma following:
• Repeated generalized convulsions • Parenteral anti-malarials, antibiotics,
• Renal failure (Serum Creatinine>3 mg/dl) anticonvulsants, antipyretics.
• Jaundice (Serum Bilirubin >3 mg/dl) • Intravenous infusion equipment and fluids.
• Severe anaemia (Hb<5 mg/dl) • Special nursing for patients in coma.
• Pulmonary oedema/acute respiratory distress • Facilities for blood transfusion.
syndrome • Well-equipped laboratory.
• Hypoglycaemia (Plasma glucose <40 mg/dl) • Oxygen respirator.
• Metabolic acidosis Often these items are not available at the PHC
• Circulatory collapse/shock (Systolic BP<80 mm level. Under such circumstances, the Medical
Hg, <50 mm Hg in children). Officer, PHC and paramedical staff should be able
• Abnormal bleeding and disseminated to administer emergency treatment and refer the
intravascular coagulation. case without delay to other institutions where such
• Haemoglobinuria. facilities are available.
• Hyperthermia (Temperature >106°F or 42°C).
• Hyperparasitemia (<5% parasitized RBCs in 10.4. Treatment of severe malaria
low endemic and >10% in hyper endemic cases
areas). Severe malaria is an emergency and treatment should
• Circulatory collapse/shock. be given as per severity and associated complications
• Spontaneous bleeding and laboratory evidence which can be best decided by the treating physicians.
of DIC. The guidelines for specific antimalarial therapy is as
• Macroscopic haemoglobinuria. follows:
Parenteral artemisinin derivatives or Quinine should
Foetal and maternal complications are more common be used irrespective of Chloroquine resistance status
in pregnancy with severe malaria; therefore, they of the area with one of the following options:
need prompt attention.
10.2. In children
Page 113
Table 3: Chemotherapy of severe and complicated malaria
Initial parenteral treatment for at least 48 hours: Follow-up treatment, when patient can take oral
CHOOSE ONE of following four options medication following parenteral treatment
Artesunate: 2.4 mg/kg IV or IM given on admission Full oral course of Area-specific ACT:
(time=0), then at 12 hours and 24 hours, then once a day.
In other states: Treat with: ACT-SP for 3 days + PQ
Single dose on second day
Quinine: 20mg quinine salt/kg body weight on Quinine 10 mg/kg three times a day
admission (IV infusion or divided IM injection)
with:
followed by maintenance dose of 10 mg/kg 8 hourly;
Doxycycline 100 mg once a day or
Infusion rate should not exceed 5 mg/kg per hour in
normal saline. Loading dose of 20mg/kg should not be Clindamycin in pregnant women and children under 8
given, if the patient has already received quinine. years of age, - to Complete 7 days of treatment.
Note: The parenteral treatment in severe malaria • Renal function should be checked daily,
cases should be given for minimum of 24 hours once institute early haemodialysis if necessary.
started (irrespective of the patient’s ability to tolerate • Fluid management should be carefully done.
oral medication earlier than 24 hours). • Treat convulsions with IV Diazepam and shift
the patient to an Intensive Care Unit with
Note: facilities for ventilator support.
• The parenteral treatment should be given for
minimum of 48 hours.
• Once the patient can take oral therapy, give:
10.5. Some don’ts in severe malaria
Quinine 10 mg/kg three times a day with case management
Doxycycline 100 mg once a day or Clindamycin Do not use corticosteroids, give intravenous
in pregnant women and children under 8 years Mannitol, use Heparin as anticoagulant, administer
of age, to complete 7 days of treatment, in Adrenaline or over-hydrate.
patients started on parenteral quinine.
• Full course of ACT to patients started on In recent years, increased attention has been drawn to
artemisinin derivatives. severe malaria caused by P. vivax, especially in
• Use of Mefloquine should be avoided in Indonesia and Papua New Guinea, where this parasite
cerebral malaria due to neuro psychiatric has become chloroquine resistant. Some cases have
complications associated with it. been found in India, and there is reason to fear that
this problem will become more common in the
Supplementary treatment – coming years. Historically, P. vivax has been an
In unconscious patient, monitor blood glucose level important cause of death in India and in Europe, and
every 4 to 6 hours and treat hypoglycaemia with IV this parasite can no longer be considered as “benign”.
dextrose. If blood sugar estimation is not available,
one can presume hypoglycaemia in all cases of 10.6. When to refer: Any of the
severe and complicated malaria especially cerebral following
malaria and treat with intravenous glucose – 100 ml
of 25% glucose before giving quinine. i. Platelet count ≤ 20,000/cu.mm.
• All unconscious patients on quinine should ii. Pregnancy with malaria.
receive a continuous infusion of 5 to 10% iii. Any feature of complicated malaria.
dextrose. iv. Renal failure.
• Parasite count and haematocrit level should be v. ARDS.
measured every 6 to 12 hourly. vi. Malaria with sepsis.
• Transfuse whole blood or packed cell vii. Malaria with shock.
concentrate when haematocrit drops to <20%.
Page 114
Bibliography
Further Reading:
1. India. Directorate of National Vector Borne Disease Control Programme. Diagnosis and
treatment of Malaria 2013. Ministry of Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://nvbdcp.gov.in/Doc/Diagnosis-Treatment-Malaria-2013.pdf

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46. DENGUE
Infection with any one serotype confers lifelong
1. Introduction immunity to the virus serotype, but no cross
In Maharashtra State, cases of Dengue Fever / protection for other serotypes. It is caused due to bite
Dengue Haemorrhagic Fever occur either in post- of an infected female Aedes Aegypti mosquito.
monsoon period when breeding of mosquitoes is
highest due to accumulation of rainwater in discarded Mode of Transmission It is transmitted through
materials or during scarcity season due to Aedes bite of Aedes Aegypti mosquito.
breeding in stored water in cement tanks and earthen
Incubation period: Varies from 5-10 days.
pots which are not emptied regularly.
2. Etiologic agent 3. Diagnosis

(Table 1)
DF/DHF is caused by a group B arbovirus
(Flavivirus) and includes serotypes 1, 2, 3 and 4
(Den-1, Den-2, Den-3 and Den-4).
Table-1: Recommended diagnostic tool according to laboratory service level
Primary health District health Reference

care centres centres centres
Genome Detection Yes
NS1 Ag detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgM detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgG detection ELISA Yes
IHA Yes
Neutralization assay Yes
ELISA = Enzyme-linked immunosorbent assay; IgG = Immunoglobulin G; IgM = Immunoglobulin M; IHA =

Indirect Haemagglutination; NS1 Ag = Non- Structural protein 1 antigen.
4. Clinical spectrum
Following is the spectrum of dengue viral
infection.
Figure-46.1: Dengue Clinical Spectrum
Dengue Viral infection
Asymptomatic Symptomatic
MILD MODERATE SEVERE
Undifferentiated fever Dengue fever Dengue Haemorrhagic fever
Without Bleeding With bleeding DHF DSS
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precedes rise in hematocrit. A rise of more
5. Clinical management than 20% indicates need for intravenous fluid
Depending upon severity of infection, management therapy.
of the cases differs. Early diagnosis & admission of • If hematocrit determination is not possible,
DHF patients is important in order to reduce case hemoglobin estimation may be carried out as
fatality rates. an alternative.
• Hematocrit should be determined daily from
5.1. Dengue fever the third day until the temperature remains
normal for one or two days.
Management of Dengue fever is symptomatic and
supportive. • Paracetamol is recommended to keep
temperature below 400c. Dosages of
• Bed rest is advisable during acute febrile
paracetamol recommended are: 1 - 2 years: 60-
phase.
120 mg/dose, 3 - 6 years: 120 mg/dose & 7 -
• Antipyretics and sponging is essential to keep
12 years: 240 mg/dose.
body temperature of patient below 370C. Do
• Plenty of fluids like ORS & or fruit juices
not prescribe Salicylates (Aspirin) to suspected
should be given orally, to the extent patient
DF patient. Paracetamol is preferred.
tolerates.
• Analgesic or a mild sedative may be
Management of Grade II DF/DHF
prescribed for severe pain.
• ORS solution is recommended for patients • Any person who has DF with
with excessive sweating, nausea, vomiting or thrombocytopenia & haemoconcentration &
diarrhoea to prevent dehydration. presents with abdominal pain, black tarry
• Patients should be monitored in DHF area stools, epistaxis, bleeding from gums etc.
until they become afebrile & after platelet & needs to be hospitalized. Such patient should
hematocrit determinations are normal. be observed for signs of shock.
• The critical period for development of shock is
5.2 Dengue Haemorrhagic Fever transition from febrile to afebrile. phase of
illness, which usually occurs after third day of
Management of Grade I DF/DHF
illness.
• Management during febrile phase is similar to
that of DF. • A rise of hematocrit of 20% or more reflects
need for IV fluid therapy.
• Patient should be monitored closely. Critical
period for monitoring is transition from febrile • If despite of treatment, patient develops
to afebrile stage, which usually occurs after features of shock, management of grade III &
third day of illness. IV should be started.
• Platelet count & hematocrit estimation is • Blood transfusion may be indicated in patients
essential. with severe shock, massive bleeding and DIC.
• Drop in platelet count to <1,00,000/cu.mm i.e.
1-2 platelets per oil immersion field usually
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Figure-46.2: Management of grade I & II DHF - Volume replacement flow chart
Haemorrhagic tendencies, Thrombocytopenia, haematocrit rise, pulse

pressure low
Initiate IV therapy 6 ml/kg/hour with crystalloid solution for 1 - 2 hours
Improvement No Improvement
Reduce IV 3 ml/kg/hr Increase IV 10 ml/kg/hour

crystalloid solution, 6-12 hours crystalloid solution, 2
hours
Further Improvement
Discontinue IV after 24
hours No Improvement
Improvement
Unstable vital signs
Hematocrit rises Hematocrit falls

Reduce IV 6 ml/kg/hour
Try solution, with further
reduction to 3 ml/kg/hour,
discontinue after 24-48 IV colloid Dextran (40) 10 Blood transfusion
hours ml/kg/hour, duration 1 hour 10ml/kg/hour,
duration 1 hour
Improvement
IV therapy by crystalloid. Successively reduce the flow from 10 to 6 & 6 to 3

ml/kg/hr. Discontinue after 24 - 48 hours
• Improvement: Haematocrit falls, pulse rate & BP stable, urine output rises
• No improvement: Haematocrit, pulse rate rises, pulse pressure falls below 20 mm Hg, urine output
falls
• Unstable vital signs: Urine output falls, signs of shock
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Figure-46.3: Management of grade III & IV DHF - Volume replacement flow chart
Unstable vital signs

Urine output falls, signs of shock
Immediate, rapid volume replacement: Initiate IV therapy 10-20

ml/kg/hour crystalloid solution for 1 hour
Improvement No improvement
IV therapy by crystalloid. Oxygen

Successively reduce the flow from 20 to 10,
10 to 6 & 6 to 3ml/kg/hour
Hematocrit Rises Hematocrit falls
Further
Improvement
IV colloid (Dextran 40) or plasma 10 Blood transfusion 10 ml/kg/hour
ml/kg/hour as IV bolus (repeat if if, hematocrit is still more than
necessary) 35%
Discontinue IV after
24 hours
Improvement
IV therapy by crystalloid.
Successively reduce the flow from 10 to 6 & 6 to

3ml/kg/hr. Discontinue after 24 - 48 hours
Page 119
Bibliography
Further Reading:
1. India. Standard Treatment Guidelines for Dengue. Ministry of Health and Family Welfare. [cited 2016
Jul 5]
Available from: http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/dengue.pdf
2. India. Directorate of National Vector Borne Diseases and Control Programme. Guidelines for Clinical
Management of Dengue 2008. Ministry of Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://www.nvbdcp.gov.in/Doc/Clinical%20Guidelines.pdf

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47. LEPTOSPIROSIS
• Hypotension & circulatory collapse.
1. Introduction
• Jaundice – Important clinical feature.
Leptospira is an infectious disease caused by
spirochetes Leptospira interrogans Mild to severe.
Leptospira enter the host through abrasions in the Starts after 4 to 7 days of illness.
skin or through intact mucosa, especially the Hepatomegaly liver tenderness usually present.
conjunctiva and the lining of oro- and nasopharynx,
when host come in contact with water contaminated • Almost invariably present is renal involvement.
with Leptospira. • ATN and interstitial nephritis are pathologic
features.
2. High risk group
• Haematuria and cola coloured urine with RBC
• Agricultural workers. casts.
• Fisherman, sewer workers. • Oliguria and anuria.
• Lorry drivers and masons. • Oedema, facial puffiness, breathlessness,
Usually starts at the onset of rainy season and convulsions.
declines as the rains recede. • Renal impairment worsens in 1st to 2nd week,
recovers by the end of 4th week with treatment.
3. Anicteric leptospirosis
• Lung - Haemorrhagic pneumonitis with
Accounts for 90% cases, usually recover completely interstitial and alveolar haemorrhages.
with proper treatment.
• High mortality.
• Fever with chills. Moderate to severe.
• Death occurs within few hrs to 2 days.
• Myalgia – Very characteristic finding. Calf,
abdominal & lumbosacral muscles are very • Mild cases- Cough, chest pain and haemoptysis.
painful & severely tender. Increase in serum
• Severe cases - Breathlessness increases and
Creatinine Phosphokinase.
patient goes into respiratory failure.
• Conjunctival Suffusion – Reddish colouration.
• Pancreatitis and acalculous cholecystitis can
Headache – commonly in frontal region.
occur.
• Renal involvement is invariable. Asymptomatic
• Cardiac involvement
in the form of mild proteinuria with few casts in
urine. • Hypotension shock- Cold clammy skin,
tachycardia and hypotension due to dehydration
• Cough chest pain & in few cases haemoptysis.
and peripheral vasodilation.
• Bleeding tendency in few cases. • Arrhythmias- palpitations, syncope and irregular
• All cases of fever with myalgia & conjunctival pulse, AV blocks and ST and T wave changes.
suffusion should be considered as a suspect case
• CNS Meningitis usually present. Headache,
of leptospirosis.
irritability, restlessness, seizures and late stage
is coma.
4. Icteric leptospirosis
• Maculopapular erythematous skin lesions over
Weil’s disease. face, trunk and extremities.
• Fever, Myalgia, Headache, Conjunctival • Bleeding in leptospirosis is not directly related
suffusion. to the level of thrombocytopenia.
• Oliguria, anuria, proteinuria.
• Nausea, vomiting, diarrhoea, abdominal pain.
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• Rise in enzyme level is not very high as
5. Investigations compared to that in viral or alcoholic hepatitis.
• CBC Thrombocytopenia is characteristic. • Raised CPK helps to differentiate from viral and
• LFT – Direct hyperbilirubinemia., raised alcoholic hepatitis.
Alk.PO4, rise in bilirubin is very fast & reaches • Raised serum creatinine levels.
high level. • Urine albuminuria.
Table 1: Lab Investigations for Leptospirosis
CULTURE MICROSCOPY IMMUNOLOGICAL MOLECULAR
Blood (10 days) Dark Field MAT PCR

Urine (10-30 days) Silver impregnation ELISA
CSF (5-10 days) Latex agglutination tests
Laboratory diagnosis for current leptospirosis • AVOID NEPHROTOXIC DRUGS in cases

with renal involvement
• Culture –positive
• Severe cases- meticulous correction of
• MAT- seroconversion/four-fold rise in the titre
hypovolemia and electrolyte imbalance, fluid
• High titre management as per CVP.
• ELISA/Latex agglutination positive. • Patient with renal failure may require
haemodialysis.
6. Treatment
6.1 Mild Case 7. Complications
• Tab. Doxycycline 100 mg BD for 7 days Fluid overload, hyperkalaemia, acidosis
• Cap. Ampicillin and Cap. Amoxicillin 30-50
LUNG INVOLVEMENT - Continue O2 therapy
mg/kg 5-7 days.
• Inj. Crystal Penicillin 20 lac units 6 hourly AST • In patients with alveolar haemorrhages with
for 5-7 days or ARDS, they require mechanical ventilation with
• Inj. Ampicillin 500 mg-1 gm 6 hourly 5-7 days low tidal volume and high PEEP.
• Mortality is very high.
6.2 Severe case • Supportive treatment with Platelet concentrate,
FFP, Vitamin K.
• Inj. Ceftriaxone / Cefotaxime or Erythromycin
Bibliography
Further Reading:
1. India. National Center for Disease Control (NCDC). Program for prevention and management of
leptospirosis, National Guidelines, 2015. Ministry of Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://www.ncdc.gov.in/writereaddata/mainlinkfile/File558.pdf

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48. INFLUENZA A- H1N1 (SWINE FLU)
We have faced pandemic of this Communicable air

borne disease in 2009. This is commonly known as
5. Mode of transmission
swine flu. Influenza spreads form person to person by droplet
infection created by sneezing, coughing or talking.
1. Epidemiological factors The portal of entry is the respiratory tract.
Pandemic Influenza A (H1N1) 2009, currently the

most common circulating strain of influenza virus
6. Incubation period
globally, first caused illness in Mexico and the It could range from one to seven days, and most
United States in March and April, 2009. likely from one to four days.
2. Agent factors 7. Signs and symptoms

The causative agent is Influenza virus. It is an An acute Respiratory Tract Infection (RTI), caused
enveloped RNA virus and belongs to the family by Influenza virus, characterised by sudden onset of:
Fever/chills, Headache, myalgia, Sore throat, Cough,
Orthomyxoviridae. The size of the virus is 80-200 nm
Coryza, and Prostration.
/0.08 -0.12 micron in diameter. There are three types Range of symptoms differs by age. Vomiting &
of influenza viruses, namely A, B & C which are diarrhoea in children/elderly. Fever alone in infants
characteristically distinct and bear no cross may be atypical in elderly. Serious complications can
immunity. The virus contains two surface antigens H occur among high risk groups.
(hemagglutinin) and N (neuraminidase).
8. Diagnosis
3. Host factors The recommended test to confirm the diagnosis of
H1N1 influenza A virus is real-time Polymerase
The disease can occur in all ages and both sexes. Chain Reaction (RT-PCR) in designated laboratories.
Also viral culture and four-fold rise in new influenza
4. High Risk Groups A (H1N1) virus-specific neutralizing antibodies can
be done.
These risk groups include:
8.1. What sample to be collected?
• Children younger than 5 years old;
• Nasopharyngeal/oropharyngeal swabs.
• Adults 65 years of age and older;
• Bronchoalveolar lavage.
• Chronic pulmonary condition (including
• Tracheal aspirates.
asthma), cardiovascular (except hypertension),
renal, hepatic, haematological (including sickle
• Nasopharyngeal / oropharyngeal aspirates as
washes.
cell disease), neurologic, neuromuscular, or
metabolic disorders (including diabetes • Samples should be collected in VTM.
mellitus);
8.2. Transportation of samples:
• Immunosuppression, including that caused by
medications or by HIV; • All samples should be kept at 2-8 degree
• Pregnant women; Celsius until they can be placed at -700C.
• Residents of nursing homes and other chronic- • Samples transported on dry ice in triple
care facilities; packaging.
• Obesity. • Clear labels with patient’s complete
information.
• Samples should be sent within 24 hrs.
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disorders, diabetes, neurological disorders,
9. Treatment cancer and HIV/AIDS;
Treatment with Oseltamivir or Zanamivir is • Patients on long term cortisone therapy.
recommended for all people with suspected or
• Obese persons.
confirmed influenza who require hospitalization. It is
given in a dose of 75 mg Bid in adults. No tests for H1N1 is required for Category-B
(1) and (2).
All individuals seeking consultations for flu like
symptoms should be screened at healthcare facilities All patients of Category-B (1) & (2) should confine
both Government and private or examined by a themselves at home and avoid mixing with public
doctor and these will be categorized as under: and high risk members in the family.
Broad Spectrum antibiotics as per the Guideline for
9.1. Category- A Community-acquired pneumonia (CAP) may be
prescribed.
• Patients with mild fever plus cough / sore
throat with or without body ache, headache,
diarrhoea and vomiting will be categorized as 9.3. Category-C
Category-A. They do not require Oseltamivir
and should be treated for the symptoms In addition to the above signs and symptoms of
mentioned above. The patients should be Category-A and B, if the patient has one or more of
the following:
monitored for their progress and reassessed at
24 to 48 hours by the doctor. • Breathlessness, chest pain, drowsiness, fall in
• No testing of the patient for H1N1 is blood pressure, sputum mixed with blood,
required. bluish discolouration of nails;
• Patients should confine themselves at home and • Children with influenza like illness who had a
avoid mixing up with public and high risk severe disease as manifested by the red flag
members in the family. signs (Somnolence, high and persistent fever,
inability to feed well, convulsions, shortness of
breath, difficulty in breathing, etc.).
9.2. Category-B • Worsening of underlying chronic conditions.
1. In addition to all the signs and symptoms
mentioned under Category-A, if the patient has All these patients mentioned above in Category-C
high grade fever and severe sore throat, may require testing, immediate hospitalization and
require home isolation and Oseltamivir; treatment.
2. In addition to all the signs and symptoms
mentioned under Category-A, individuals 9.4. Oseltamivir Medication -Doses
having one or more of the following high risk
conditions shall be treated with Oseltamivir: Details
• Children with mild illness but with
Oseltamivir is the recommended drug for treatment.
predisposing risk factors.
• Pregnant women; In the current phase, if a person confirms to the case
• Persons aged 65 years or older; definition of suspect case, should be provided
• Patients with lung diseases, heart disease, Oseltamivir.
liver disease, kidney disease, blood
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Dose for treatment is as follows:
By Weight:
‐ For weight <15 kg 30 mg BD for 5 days
‐ 15-23 kg 45 mg BD for 5 days
‐ 24-<40 kg 60 mg BD for 5 days
‐ >40 kg 75 mg BD for 5 days
mothers, high risk persons (DM, HT, Obese,

10. Vaccine Respiratory diseases, Immunocompromised).
A Vaccine is available for swine flu. It gives
immunity for one year. It is given to pregnant
Bibliography
Further Reading:
1. India. Ministry of Health and Family Welfare. H1N1 Guidelines. [cited 2016 Jul 5]
Available from: http://mohfw.gov.in/index4.php?lang=1&level=0&linkid=372&lid=3066

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49. DIARRHOEAL DISEASES
Diarrhoeal diseases include acute diarrhoea, • Acute diarrhoea – Cholera, Rota virus, food
persistent diarrhoea (diarrhoea duration two weeks poisoning, gastrointestinal disorders and
or more) and dysentery (blood stained stools with medications (rare).
fever). Diarrhoeal diseases are one of the most
common causes of epidemic in our State. Most of • Persistent diarrhoea – Chronic bacterial
the deaths in diarrhoeal diseases are due to infections, inflammatory bowel disorders,
dehydration which is preventable by timely and malabsorption syndrome.
adequate replacement of fluids. • Dysentery – Amoebiasis, Giardiasis,
Shigellosis.
1. Following are important
causes of diarrhoeal
diseases in rural areas
Table-1: Diagnosis of diarrhoea

Sign/symptom Acute diarrhoea Persistent diarrhoea Dysentery
Frequency of stools/day Three or more Three or more Three or more
Consistency of stools Watery Variable Variable
Duration of diarrhea Less than 2 weeks Two or more weeks Less than 2 weeks
H/o fever No Variable Yes
H/o blood stained mucus No Variable Yes
Effect on appetite No Loss of appetite Loss of appetite
Dehydration Important, may lead to Patient may have Patient may have
severe dehydration if not some dehydration. some dehydration
treated in time.
Treatment principle Management of Start management of Start management of
dehydration is priority dehydration. dehydration.
Simultaneously find Simultaneously start
cause of persistent appropriate
diarrhoea and treat antibiotics.
accordingly.
Long term effects No long term effect for If not treated Repeated attacks may
occasional episodes. correctly, child may lead to Protein
Repeated attacks may get severe Protein Energy Malnutrition
lead to PEM. Energy Malnutrition
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Table-2: Dehydration Diagnosis Chart
Severity of symptoms and signs (Encircle the finding)
Sign/Symptom
No dehydration Some dehydration Severe dehydration
General condition of Patient Patient well alert Restless and irritable Lethargic, unconscious,
floppy
Presence of thirst Normal/not thirsty Thirsty, drinks water Not able to drink
immediately when
offered
Dryness of mouth and Moist mouth and Mouth and tongue dry Mouth and tongue very
tongue tongue dry
Condition of eyes Normal Sunken Very sunken, patient’s
face looks like old
man's face.
Condition of tears Tears appear while Tears appear while No tears, dry eyes even
crying crying in crying child
Skin turgor Normal. Pinch to Pinch slowly goes back Pinch remains as it is
skin immediately and takes some time to for 2-3 seconds and then
goes back to normal. become flat. slowly goes back.
Classification of No dehydration Some dehydration Severe dehydration
dehydration
Treatment of dehydration Plan – A Plan – B Plan – C
Symptoms and signs of cholera are entirely due to loss

2. Important diseases causing of large volume of isotonic fluid and resultant
diarrhoea or dysentery in depletion of intravascular and extra vascular fluid
leading to severe dehydration, metabolic acidosis and
adults hypokalaemia. Patient develops thirst, cramps, and
anxiety due to depleting isotonic fluid.
2.1. Cholera
Diagnosis
Cholera is the most important diarrhoeal disease which
leads to rapid dehydration. Suspect cholera when patient has severe watery
diarrhoea and vomiting. Collect stool sample of
Etiologic agent suspected cases in Cary Blair media and transport to
Cholera is caused by bacteria Vibrio cholerae which District Public Health Laboratory. However, treatment
exists in two biotypes, Classical and El tor. Each and control measures should be started immediately on
biotype is further divided into two subgroups Inaba and the basis of clinical symptomatology without waiting
Ogawa. for laboratory confirmation.
Clinical manifestations Treatment
Cholera is an acute infection of small intestine Carefully examine patient for signs of dehydration and
manifested as watery diarrhoea and vomiting. Clinical treat as per dehydration status. Most important
spectrum of cholera is broad, ranging from in apparent treatment of cholera is rehydration of patient with ORS
infection to cholera gravis, which may be fatal in few and Ringer’s Lactate. In addition to this, start one of
hours. Incubation period of 24 to 48 hours is followed the following antibiotics to patient -
by abrupt onset of painless, profuse and watery • Cap Doxycycline 6 mg/kg/ day as a single dose
diarrhoea associated with vomiting. for 3 days OR
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• Cap Tetracycline 50 mg/kg/day in 4 divided doses a. Home available fluids
for 3 days OR
• Advise to give Home Available Fluids (HAF)
• Tab Erythromycin 30mg/kg/day in 3 divided e.g. sorbet, lassi, vegetable soup, kheer,
doses for 3 days. buttermilk, tea, coconut water, etc. i.e. any liquid
available at home to patient as much he/she can
3. Diagnosis of dehydration drink.
Although number of organisms are responsible for • Continue breast feeding and feeding – If child is
causing diarrhoea, clinical presentation is same i.e. being breastfed, then breast-feeding should be
passage of watery stools leading to dehydration in all continued. Regular feeding of non-breast fed
these cases. Therefore, assessment of dehydration child should also be continued.
status and correct management of dehydration by ORT b. ORS to prevent dehydration
is mainstay of diarrhoeal disease control programme.
• If frequency and amount of diarrhoea is not
4. Management of dehydration declining or amount of stool is large, then start
ORS.
Most important aspect in management of diarrhoeal
diseases is correction of dehydration. • Contents of WHO ORS are as follows – (New
low osmolarity ORS).
Treatment of dehydration is divided into three plans as
follows - Sodium chloride - 2.6 grams
• Plan-A: For patients with no dehydration – Potassium Chloride - 1.5 grams
Principle is to prevent dehydration. Trisodium Citrate - 2.9 grams
• Plan-B: For patients with some dehydration – Glucose - 13.5 grams
Principle is treatment of some dehydration and
preventing patient from going into severe Dissolve the packet in one liter of water to prepare ORS.
dehydration. • Show caretaker how to prepare ORS.
• Plan-C: For patients with severe dehydration - Following steps should be carried out for preparation
This is lifesaving plan. Rehydrate patient as early of ORS -
as possible and prevent from going again into
severe dehydration. • Take clean pot of one and half liter capacity and
one clean spoon.
Description of treatment plans in details is as follows.
• Pour 1 liter of clean drinking water in the pot.
4.1. Plan-A (No need to boil water).
Plan-A is for patients who are having diarrhoea but no • Add whole packet of ORS into one-liter of water
signs of dehydration. and stir till all powder is dissolved. Now ORS is
ready for use.
4.1.1 Principle of treatment
As diarrhoea is continuing, there is continuous loss of • Give ORS by cup or spoon to small children and
water and electrolytes from body of patient which may by glass to older children and to adults as per
lead to dehydration. Therefore, principle of Plan-A indicated dose.
schedule is correction of whatever loss of water and • If patient has vomiting, wait for 5 minutes and
electrolytes before the patient develops signs of start again.
dehydration. Plan-A can be advised at home to
caretaker of patient. However, make sure that care • Keep ORS covered. Once prepared ORS should
taker has understood danger signs of dehydration (like be used within 24 hours. Do not use ORS beyond
thirst). Following steps are recommended in Plan-A. 24 hours, as there are chances of contamination.
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• If child develops swelling on eyelids, stop ORS as 4.2. Plan -B
it indicates overhydration.
Start Plan-B treatment to patients showing signs and
• Ask her to give ORS in following doses after symptoms of some dehydration as per dehydration
passage of each liquid stool. diagnosis chart. Aim of this plan is to correct
Less than 6 months - 50 ml dehydration and prevent patient from going into severe
dehydration.
6 months to 2 years - 50 - 100 ml
4.2.1 Principle of treatment
2 to 5 years - 100 - 200 ml
Patient with some dehydration should be given ORS
for correction of dehydration.
Dose of ORS: Dose of ORS is calculated, preferably according to weight of patient. Give ORS in a dose of 100
ml/kg in 4 hours. If weighing is not possible, calculate age wise ORS requirement for four hours as follows –
Table -3: Age wise ORS requirement for four hours
Age < 4 months 4–11 months 12–23 months 2 – 4 years 5 – 14 years 15 + years
Dose 200-400 ml 400 – 600 ml 600 – 800 ml 800 – 1200 ml 1200 – 2200 ml 2200-4000 ml
Continue breast feeding and feeding – If child is being 4.2.2 Re-examination of patient
breastfed, then breast-feeding should be continued.
Re-examine patient after every four hours for status of
Regular feeding of non-breast fed child should also be
dehydration with the help of Dehydration. (Table 4)
continued.
Table-4: Management advice based on re-examination findings
Condition of patient on re-examination Management advise
Patient improves, no signs of dehydration on Keep patient under observation for 24 hours. Continue
examination and diarrhoea stops HAF. Observe if diarrhoea and/or vomiting start again.
Patient improves, no signs of dehydration on Continue giving ORS in doses suggested in Plan-A, re-
examination but diarrhoea continues examine after four hours.
Dehydration status same Continue with Plan-B. Check whether ORS is being
given in correct dose. Re-examine after four hours.
Signs of severe dehydration appear Switch on to Plan - C (start IV fluids). Continue to give
ORS as much as possible.
4.3. Plan – C 4.3.1 Principles of management

If signs and symptoms of patient are suggestive of Principle of management of severe dehydration is
severe dehydration, start Plan – C. This is replacing fluid loss by giving rapid IV infusion.
emergency plan. Incorrect or incomplete Only Ringer's lactate should be used as IV fluid and
management of severely dehydrated patient may the dose is 100 ml/kg body weight.
lead to death of patient. Medical Officer must
personally examine patient and treat for severe
dehydration.
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Table -4: Details of Ringer’s Lactate administration
Duration of
Age group Intensive phase Maintenance phase Remarks
treatment
Infants (0-1 30 ml/kg body wt. 70 ml/kg body wt. Assess patient after
6 hours
year) during first 1 hour. in next 5 hours. every 6 hours
Older children 30 ml/kg body wt. 70 ml/kg body wt. Assess patient after
3 hours
and adults in first half hour. in next 21/2 hours. every 3 hours
4.3.2 Re-examination of patient dehydration with the help of dehydration diagnosis

Re-examine patient after every six hours in infants chart and decide management plan as follows -
and three hours in adults for status of
Table-5: Treatment advice based on condition of patient
Condition of patient Treatment advise
Patient improves, no signs of dehydration on Keep patient under observation for 24 hours as patient
examination and diarrhoea stops may start diarrhoea/vomiting again
Patient improves, no signs of dehydration on Continue giving ORS (Plan-A)
examination but diarrhoea continues
Patient improves, signs of some dehydration Stop IV fluids after required dose is administered.
on examination. Continue giving ORS (Plan-B)
Dehydration status same Continue with Plan-C. Check for any complications
like anuria. If yes, carefully examine the patient and
decide for referral. Continue giving IV during
transportation of patient.
ORS or Oral rehydration therapy (in case ORS is
not available), irrespective of type of dehydration.
5. Use of antibiotics and
Zinc administration as per age of child:
other drugs a) Children from 2-6 months:
Antibiotics are recommended only to suspected
Children aged between 2-6 months should be given
patients of cholera and dysentery. Other drugs like
10 mg of elemental zinc per day for a total period of
anti motility drugs, binding agents, anti-secretary
14 days from the day of onset of diarrhoea. A tablet
agents and steroids are not of any use in
of zinc contains 20 mg of elemental zinc. Therefore,
management of diarrhea. They are harmful to
half tablet should be given to the children in this age
patients and therefore not at all recommended for
group.
treatment. Judicious use of antibiotics is appropriate
in selected patients. Severely ill patients with febrile Zinc when supplied in the form of dispersible
dysentery can be treated with Ciprofloxacin 500mg tablets, easily dissolves in breast milk or water.
BD for 3-5 days. Therefore, in infants below 6 months of age, the
tablet should be given by dissolving in breast milk
Use of Zinc Tablets
and in infants above 6 months of age, it should be
Zinc Dosage Recommendation: given by dissolving in breast milk or water.
Zinc is very safe drug and has a very large window b) Children above 6 months:
of safety. Zinc dispersible tablets are to be given in
One full tablet (20mg) should be given to all
each diarrhoeal episode along with low osmolality
children with diarrhoea above 6 months of age. It
should start from the day of onset of diarrhoea and
continued for a total period of 14 days.
Page 130
Bibliography
Further Reading:
1. World Health Organization (WHO) Factsheet. April 2013. [cited 2016 Jul 5]
Available from: http://www.who.int/mediacentre/factsheets/fs330/en/
2. Keusch GT, Fontaine O, Bhargava A, Pinto CB, Bhutta ZA, Gotuzzo E et el. Diarrheal Diseases,
Disease Control Priorities in Developing countries. 2nd Edition. Chapter 19. New York: Oxford
University Press 2006. [cited 2016 Jul 5]
Available from: http://www.ncbi.nlm.nih.gov/books/NBK11764/
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50. RHEUMATOID ARTHRITIS
vi. Oral - Xerostomia, periodontitis.
1.Introduction vii. Pulmonary – Pleural effusion, pulmonary nodules,
Rheumatoid arthritis (RA) is a chronic inflammatory interstitial lung disease, pulmonary vasculitis,
disease of unknown aetiology marked by a symmetric, organizing pneumonia.
peripheral polyarthritis. It is the most common form of viii. Cardiac- Pericarditis, IHD, myocarditis,
chronic inflammatory arthritis and often results in joint cardiomyopathy, mitral regurgitation.
damage and physical disability. ix. Renal – Membranous nephropathy.
x. Skin – Rheumatoid nodules, pyoderma
gangrenosum.
2. When to suspect
3. Investigations
• The incidence of RA peaks between 25 and 55
years of age. The clinical diagnosis of RA is largely based on signs
• Early morning joint stiffness lasting more than 1 and symptoms of a chronic inflammatory arthritis, with
hour and easing with physical activity. laboratory and radiographic results providing important
• Earliest involved joints typically the small joints of supplemental information.
the hands and feet.
• The wrists, metacarpophalangeal (MCP), and
3.1 Rheumatoid factor
proximal interphalangeal (PIP) joints stand out as Serum IgM RF found in 75-80% of RA patients;
the most frequently involved joints. therefore, the negative result does not exclude RA.
• Flexor tendon tenosynovitis is a frequent hallmark
Found in other connective diseases as well.
of RA.
Deformities are Swan-neck deformity, Boutonnière 3.2 Anti –CCP antibodies
deformity, Z-line deformity. Highly specific 95%
So, useful for distinguishing RA from other forms of
arthritis.
3.3 Synovial fluid analysis-

Inflammatory state.
Synovial fluid WBC count ranges from 5000 to 50000
WBC/mm3.
Useful for confirming inflammatory arthritis, excluding
infection or crystal induced arthritis.
3.4 X ray hands

Juxta articular osteopenia,
Other findings include soft tissue swelling, symmetric
Figure-50.1: Hand changes in RA joint space loss, subchondral erosions.
Extra-articular features – 3.5 MRI

i. Neurologic-atlanto-axial dislocation, cervical Offers greatest sensitivity for detecting synovitis, joint
myelopathy. effusions as well as early bone and bone marrow
ii. Haematological- Anaemia of chronic disease, changes.
neutropenia, splenomegaly, Felty’s syndrome.
iii. GI-vasculitis.
iv. Skeletal- osteoporosis.
v. Ocular- Episcleritis, Scleritis,
Keratoconjunctivitis sicca.
Page 132
4. Treatment
Table-1: Treatment of RA
Non-pharmacologic treatment Pharmacologic treatment

Counselling, physiotherapy, diet NSAIDS
Stress reduction, exercise Glucocorticoids
DMARDS
4.1 NSAIDs 4.3 DMARDS

Tab. Ibuprofen (200 mg BD or TDS) / Tab. Hydroxychloroquine, Methotrexate, Leflunomide,
Diclofenac (50 mg BD) - Now considered to be Sulfasalazine, Biologicals, anti TNF agents,
adjunctive therapy for management of symptoms Rituximab.
uncontrolled by other measures.
5. When to refer
4.2 Glucocorticoids Severe case of rheumatoid arthritis not responding to
first line therapy (Hydroxychloroquine,
May be administered in low-to-moderate doses to Methotrexate, NSAIDS), with extra articular
achieve rapid disease Control before the onset of manifestations should be referred to Higher institute
fully effective DMARD therapy, which often takes for further work up.
several weeks or even months.
Bibliography
Further Reading:
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Page 133
51. SNAKE BITE
approach, stressing the need for Reassurance,
1. Introduction Immobilization of the part, getting to hospital
Envenoming by poisonous animals (Snakes, without delay and telling the doctor of any
Scorpions, Wasps, Ants and Spiders) is an symptoms that develops.
occupational hazard often faced by farmers, farm
labourers. Poisoning by venomous snakebite is a
common acute life-threatening time-limiting medical 2. Common Poisonous snakes
emergency. The majority of current first aid methods
adopted by the victims such as tourniquet, cutting and in India
suction and herbal remedies are completely
ineffective and dangerous. It is now recommended to (1) Cobra (2) Krait (3) Russell’s Viper (4) Saw
adopt what has been called the ‘Do it R.I.G.H.T.’ Scaled Viper (5) Indian Pit Viper (6) Sea snake
HISTORY OF SNAKE BITE
ABSENT LOCAL EDEMA PRESENT
Floor bed • BLEED

Neuro-paralysis • DIC Bleeding
• SHOCK
Abdominal colic • RF
Pain
Neuro-paralysis
RUSSELL’S ECHIS
KRAIT COBRA VIPER CARINATUS
ASV, Ventilator ASV, N + A, ASV, Dialysis, ASV, Dialysis,

N+A Ventilator Blood transfusion Blood transfusion
Figure 51.1. Snake Bite: Diagnostic Algorithm and Treatment

(ASV- Anti-snake venom, N- Neostigmine, A- Atropine, RF- renal failure, DIC- Disseminated intravascular
coagulation)
Local Names- Kala gandait, Kala taro, Kandar,

3. Clinical manifestations Manyar, Chitti, Kattu Viriyan and Valla Pamboo.
The common krait is regarded as the most dangerous
3.1. Common Indian Krait (Bungarus species of venomous snakes in the Indian
Caeruleus)
Page 134
subcontinent. Majority of krait bite cases are reported ACh receptors of Acetyl choline. If there is slight
between 11 pm – 5 am. improvement in ptosis, you can try AChEI.
Neostigmine 50 µg/kg over first hour & then 25
3.1.1 Symptoms µg/kg in the next hour preceded by Atropine
• Mild pain at the site
• Paraesthesia or numbness 3.2. Cobra Bite
• Abdominal pain/vomiting/chest pain Cobra bite tends to occur during day time.
• Difficulty in bringing tongue beyond teeth
margin 3.2.1. Symptoms
• Slurred speech • Pain at site
• Difficulty in breathing • Progressive swelling / ecchymosis
3.1.2 Signs • Blurred vision
• Bradycardia, hypotension 3.2.2 Signs

• Bilateral ptosis, external ophthalmoplegia, • Sinus bradycardia, hypotension
dysphagia • Ptosis, bulbar palsy
• Paralysis, coma • Respiratory depression
3.1.3 Management 3.2.3 Management
(a) First aid at home or place where bite happens: Victim should not be allowed to walk or run and the
If one succeeds in locating the bite site on the bitten part should be kept below heart level.
victim’s body, clean the surface where venom is On arrival 100 ml (10 vial) ASV to be added to 200
deposited by clean cloth or cotton. Keep the bitten cc of normal saline run over 30-50 minutes.
part below heart level.
Maximum dose 200-250 ml (20-25 vials).
Neostigmine 50 µg/kg over first hr. & then 25 µg/kg
(b) At hospital: in the next hr preceded by Atropine
Thorough clinical examination including If patient develop respiratory paralysis intubate the
neurological exam patient and refer to higher centre
Haemogram, urine exam, ECG, serum electrolytes, Local wound care is done by intravenous antibiotic,
renal profile sterile dressing and skin grafting of all victims with
Anti-snake venom (ASV): non-healing wound.
- On arrival 100ml (10 vials) ASV to be added to 3.3. Sea snakes

200 cc of normal saline run over 30-50 minutes. Sea snake bite cases are reported from coastal region.
- Repeat dose of 100 ml (10 vials) after 30 min if Fishermen accidentally handle sea snake resulting in
no improvement in neurological manifestation. envenoming. Its venom is neurotoxin, myotoxic and
haematotoxic.
- Maximum dose 200 ml (20 vials).
3.3.1 Symptoms
Ventilation
Indicated if victim has pooling of saliva, unable to lift • Headache
the neck from pillow, reduction in oxygen saturation, • Nausea
respiratory failure, abdominal-thoracic respiration, • Vomiting
suffocation and signs of cerebral hypoxia. • Tingling numbness
Refer the patient to higher centre with intubation and • Foreign body sensation in throat
Ambu bag ventilation • Swelling of tongue
• Severe muscle pain
Acetylcholine esterase inhibitor (AChEI): • Brown coloured urine
Indian common krait venom contains both pre and
3.3.2 Signs
post synaptic blocker. Whether victim responds to
AChEI or not can be confirmed by putting ice-filled • Trismus
glove finger over eyelid. Hypothermia sensitizes the • Muscular paralysis
Page 135
• Respiratory arrest • No tourniquet
• Myoglobinuria • Bitten part should be kept below heart level
• No intramuscular injection unless 20 MWBCT
3.3.3 Management is done and blood clots within 20 minutes.
On arrival 100 ml (10 vial) ASV to be added to 200
20-minutes whole blood clotting test (20 MWBCT)
cc of normal saline run over 30-50 minutes.
Before injection of ASV take 2-3 ml of blood in a
Ventilator for respiratory failure. Refer to higher
new dry glass test tube which is not irrigated by any
centre with intubation.
detergents. Keep the tube undisturbed for 20 minutes
Correction of hyperkalaemia - Calcium gluconate, and then tip it off. If blood does not clot, it confirms
insulin glucose drip (10% dextrose 100 ml add 12- hypofibrinogenemia. ASV – 100 ml (10 Vials) ASV
unit insulin for 6 hours), salbutamol nebulization or diluted in 200 ml of 5% dextrose run over 30 minute
dialysis. by intravenous route. If external bleeding does not
stop within 20-30 minutes one can repeat 50 ml of
3.4. Russell’s viper ASV. Thrombocytopenic, abnormal fragmented
RBC’s are a diagnosis of DIC. In addition, if victim
It is found in South Asian Countries. In Pakistan, is too late in such situation in addition to ASV one
India, Sri Lanka, Bangladesh, Burma and Thailand it has to try plasma products and whole blood
ranks amongst the most important causes of snakebite transfusion which is rarely required if ASV is
mortality. With protecting the paddy, wheat by administered in time with adequate dose.
containing rodents (rats), the Russell’s viper kills Hypotension is to be managed with fluid and
many farmers unlucky enough to treat on it during inotropic agents. Severe hypotension due to bleed in
harvesting. adrenal and pituitary glands and abdominal bleed and
endothelial dysfunction with capillary leak needs
3.4.1 Symptoms
heavy doses of intravenous methyl-prednisolone and
• Severe local pain at the site of bite. correction of electrolytes.
• Rapid swelling progresses to whole limb within Renal failure
six to eight hours.
One should keep in mind and look for renal failure
3.4.2 Signs from the time of admission. Risk factors such as
• Regional lymphangitis with ecchymosed skin. hypotension, hypovolemia can be corrected.
• Development of compartment syndrome Intravenous frusemide 80-100 mg and oral acetyl
characterized by swelling, hypotension and cysteine 600 mg three times a day may help to arrest
shock. the renal damage.
Refer to higher centres for haemodialysis, if needed.
Renal dysfunction
3.5. Saw scaled viper or Carpet
20-40% cases subsequently develop anuria, oliguria, viper or Echis carinatus
acute renal failure. Renal angle tenderness is most Farmers, hunters, labourers and persons walking bare
important clinical sign for early diagnosis of renal foot or in jungle and rocky areas are often bitten by
failure. There is serial rise in blood urea and serum
this snake.
creatinine with acidosis and hyperkalaemia.
Generalized anasarca, renal failure is due to tubular 3.5.1 Clinical manifestations
damage by venom itself.
Haemoglobinuria, hypotension and micro thrombi in Soon after the bite within one hour there is
the kidney contribute to the acute tubular necrosis development of swelling over the bitten part.
which is the most common cause of death. Ptosis, Swelling progresses in more than one segment. The
bulbar palsy, internuclear ophthalmoplegia and victim experiences a painful lymphadenopathy at the
respiratory paralysis due to presynaptic drainage area of the bitten part.
neuromuscular block in a Russell’s viper bite
poisoning are often seen and reported from Kerala At times if the patient remains untreated, bleeding
(South India) and Sri Lanka. persists for 1-2 weeks in the form of blood stain
sputum, haematuria and disappears on its own. Such
3.4.3 Management patients are markedly anaemic and report to hospital
Page 136
for weakness or non-healing cellulitis with The approximate serum half-life of anti-venom in
uncontrolled bleeding from cellulitis. envenomed victims ranges from 26 to 95 hours.
Before discharge envenomed victims should be
3.5.2 Management closely observed daily for minimum 3 to 4 days.
Local wound care ASV doses and repeat doses
ASV required is 30-50 ml The recommended initial dose of ASV is 8 to 10 vials

administered over 1 hour.
3.6. Green pit viper and bamboo
Repeat doses for neurotoxic species is based on 1 to
pit (Trimeresurus) 2-hour rule.
Pit viper victims report during the monsoon season. Repeat doses for haematotoxic species is based on
the 6-hour rule.
3.6.1 Clinical manifestation
The maximum recommended dose for neurotoxic bite
It shows up in sudden rapid development of massive is 20 vials of ASV.
oedema without regional involvement. Rarely the
victim manifests external bleeding or renal failure. The maximum recommended dose for haematotoxic
bite is 30 vials of ASV.
3.6.2 Management
Anti-venom should be administered as soon as signs ASV Reactions
of systemic or severe local swelling are noted.
No ASV test doses are to be administered.
The mean times between envenoming and death are At the first sign of an adverse reaction the ASV is
halted
• 8 hours (12 minutes to 120 hours) in Cobras,
• 18 minutes (3-63 hours) in Bungarus Caeruleus, Adrenaline 0.5 ml is given SC
• 3 days (15 minutes to 264 hours in Russell’s Steroid and antihistamine perform a secondary
viper supportive function to Adrenaline.
• 5 days (25 to 41 days) for Echis-Carinatus.
(National Snakebite Management Protocol 2008)
Bibliography:
1. India. Directorate General of Health Services. National Snakebite Management Protocol 2009.
Ministry of Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://164.100.130.11:8091/nationalsnakebitemanagementprotocol.pdf
Further Reading:
1. Warrell DA. Guidelines for the management of snake bites. World Health Organization. [cited 2016
Jul 5]
Available from: http://apps.searo.who.int/PDS_DOCS/B4508.pdf?ua=1
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Page 137
52. SCORPION STING
1. Introduction Grade 1: Severe excruciating local pain at the

sting site radiating along with corresponding
• Scorpion envenomation is an occupational dermatomes, mild local oedema with sweating at the
hazard for farmers, farm labourers, migrating sting site, without systemic involvement.
population and hunters.
Grade 2: Pain, paraesthesia remote from the site
• The endemic areas are western Maharashtra, of sting, in addition to local findings.
Karnataka and Konkan Region.
• Severe Scorpion stings are due to Mesobuthus Grade 3: Either cranial nerve / autonomic
Tamulus species of scorpion. dysfunction.
Cold extremities, tachycardia, hypotension
2. Clinical features (Respiratory rate > 24 per minute, basal rales or
• The venoms of genera Hadrurus, Vaejovis and crackles in lungs).
Uroctonus has local effects only including sharp Grade 4: Combined cranial nerve / autonomic
burning, swelling and discoloration at the bite dysfunction and somatic nerve dysfunction.
site.
• The second type of venom produced by the 4. Investigations
genera of the poisonous varieties of ECG- Tall T waves is a common finding. Others are
Centruroides and Mesobuthus contain atrial arrhythmias, non-sustained ventricular
neurotoxins which block sodium channels. This tachycardia, and various conduction defects seen.
leads to spontaneous depolarization of Chest X-ray - shows pulmonary oedema.
parasympathetic and sympathetic nerves which
results in stimulation. 5. Management
• In adults, the first time is rarely dangerous. But If it is for the first time in adult, do the following:
if the second time, the person may die if not
treated soon. The body becomes allergic after • Give Paracetamol if possible, put ice on sting.
• Infiltration of site with local anaesthetic may
the first sting. So it is important to find out if he
relieve pain and anxiety.
had an earlier scorpion sting. • Anti-histaminic tablets can be given
• Severe pain, redness and swelling at the site of • If the sting is for the second time in adult, or is
the sting. in children under 5, do the following
o IV Fluid management
• Clinically “autonomic storm” evoked due to
o Inj. Scorpion anti-venom 30 ml in 200 ml of
venomous envenoming is characterized by normal saline neutralises circulating venom.
transient parasympathetic stimulation- vomiting, o If evidence of myocarditis and pulmonary
profuse sweating, ropy salivation, bradycardia, oedema, strict bed rest and management of
ventricular premature contraction, priapism in heart failure is indicated.
male, hypotension and prolonged sympathetic o Prazosin 0.5 mg 3 hourly orally for first 2
stimulation - cold extremities, hypertension, days (or 0.25 mg in children and for adults) is
acceptable therapy
tachycardia, pulmonary oedema and shock.
o Injection Frusemide 20 to 60 mg IV to control
Pulmonary oedema
3. Gradation o Inj. Dobutamine 5-20 microgram/kg/min IV
On basis of clinical manifestations at the time of given in heart failure, tachycardia, pulmonary
arrival to hospital and according to severity they are oedema with warm extremities
graded in 4 grades. o Patients in Pulmonary oedema may need Inj
NTG drip 5 microgram/kg
Page 138
o At times with severe respiratory distress may ventilation.
need non-invasive ventilation or mechanical
Stage- 1 - Stage- 2 Stage-3 - Stage-4 - Stage-5 -

(0-4 hours) (4-6 (6-10 hours) (10-12 hours) (>12 hours)
hours)
- - - - - - - - - -
Sweating Hypertension - Tachycardia - Massive - Warm -
Salivation Tachycardia Hypotension pulmonary extremities
Mydriasis Cold extremities Pulmonary oedema Tachycardia
Priapism oedema Hypotension
Hypertension Cold extremities Pulmonary
Hypotension oedema
Cold Grey pallor
extremities (warm shock)
- - - - - - - - - -
ASV + Prazosin ASV + Prazosin - ASV +Prazosin - ASV - Dobutamine -
+ +
Dobutamine SNP or NTG
+
NIV/MV
Figure 52.1 Scorpion sting: stages, clinical presentation and treatment
(ASV – Anti Scorpion Venom, SNP- Sodium Nitro Prusside, NTG- Nitroglycerine, NIV-Non-invasive ventilation,
MV – Mechanical Ventilation)
Bibliography:
Further Reading:
1. Bawaskar HS, Bawaskar PH, Scorpion Sting: Update. January 2012, Vol 60. [Internet] [cited 2016 Jul
5]
Available from: http://www.silae.it/files/08_scorpion_sting_update.pdf
2. Chippaux JP, Emerging options for management of scorpion sting, Drug Des Devel Ther. 2012; 6:
165–173. [Internet] [cited 2016 Jul 5]
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Page 139
53. DOG BITE (RABIES)
Rabies can be transmitted by dog bites or licks of Treatment (post-exposure prophylaxis)
rabid animals on abraded skin and intact mucosa.
Other animals which can transmit rabies are cat, 2. Categories of dog bite
monkey, horse, sheep, goat, mongoose, jackal, fox,
• Category I – Touching or feeding animals, licks
hyena and bat. Exposure to rodents, rabbits and hares
on the intact skin
seldom requires specific anti-rabies treatment.
• Category II – Nibbling of uncovered skin, minor
1. Clinical features scratches or abrasions without bleeding, licks on
Prodromal symptoms- such as headache, malaise, broken skin
sore throat and fever last about 3-4 days. Pain and • Category III – Single or multiple transdermal
tingling at the bitten site. bites or scratches, contamination of mucous
Stage of excitation- Patient is intolerant to noise; membrane with saliva from licks; exposure to
bright light or a cold draught. Aerophobia may be bat bites or scratches
present. Hydrophobia is a characteristic symptom of The WHO recommended classification of animal bite
rabies. Examination shows increased reflexes, for post-exposure treatment should be followed.
dilatation of pupils, increased sweating, lacrimation Every instance of human exposure to a suspected
and salivation. Mental changes include fear of death, rabid or wild animal must be treated as a category III.
anger, irritability and depression. Convulsions may The post-exposure treatment is a three-pronged
occur resulting in death. The last stage is that of approach. All three carry equal importance and
paralysis and coma. The total duration of illness lasts should be done simultaneously:
for 2-3 days.
Table-1: WHO Guide for post-exposure treatment against rabies
Category
Type of contact with a suspect or confirmed rabid Recommended treatment.
domestic or wild animal or animal unavailable for
observation
I. Touching or feeding of animals Licks on None, if reliable case history is available
intact skin
II. Nibbling of uncovered skin Minor scratches Administer vaccine immediately. Stop treatment if
or abrasions without bleeding Licks on animal remains healthy throughout an observation
broken skin period of 10 days or if animal is killed humanely and
found to be negative for rabies by appropriate
laboratory techniques
III. Single or multiple transdermal bites or Administer rabies immunoglobulin and vaccine
scratches Contamination of mucous immediately. Stop treatment if animal remains healthy
membrane with saliva (i.e. licks) throughout an observation period of 10 days or if
animal is killed humanely and found to be negative
for rabies by appropriate laboratory techniques.
A. Exposure to rodents, rabbits and hares seldom, if ever, requires specific anti-rabies treatment
B. If an apparently healthy dog or cat in or from a low-risk area is placed under observation, the situation
Page 140
may warrant delaying initiation of treatment.
C. This observation period applies only to dogs and cats. Except in the case of threatened or endangered
species, other domestic and wild animals suspected as rabid should be killed humanely and their tissues
examined using appropriate laboratory techniques.
Equine Anti-Rabies Serum (ERIG) 40 IU/kg (max

3. Treatment of dog bite 3000 IU), available in concentration of 300 IU/ml,
3.1. Management of wound given after prior skin sensitivity testing, single dose
on day 0. Half the dose is infiltrated around the bitten
Immediate washing of the wound is a priority. wound and the rest is given I.M.
Wound toilet must be done even if several hours or (Caution: A negative skin test must never reassure
days have elapsed. The wound is immediately the physician that no anaphylactic reaction will
flushed and washed with plenty of soap and water occur. Avoid alcohol, glucocorticoids and
(avoid direct touching of wounds with bare hands). chloroquine during vaccination; avoid multiple
Punctured wounds should be irrigated with the help needle injections into the wound. Must not exceed the
of catheters followed by 70% alcohol or povidone total recommended dose of IG as it may reduce the
iodine application. The application of irritants (like efficacy of the vaccine).
chillies, oil, turmeric, lime, salt etc.) is unnecessary
If the calculated dose of IG is insufficient to cover
and damaging.
infiltration in all wounds, sterile saline can be used to
Do not suture bite wounds immediately. If suturing is dilute 2 or 3 fold to permit thorough infiltration.
required, hold it for 24-48 hours, applying minimum
RIG is not indicated beyond the seventh day after
number of stitches under the cover of anti-rabies
administration of the first dose of vaccine.
Immunoglobulin locally. Anti-tetanus treatment can
be given after local wound treatment.
3.2. Passive immunization with 3.3. Active immunization with anti-

rabies immunoglobulin (RIG) rabies vaccine:
Local infiltration of RIG in category III rabies-RIG Anti-rabies vaccine (ARV)
should be infiltrated in the depth and around the • Intramuscular schedule.
wound even if the lesion has begun to heal followed The course for post-exposure prophylaxis
by administration of anti-rabies vaccine. consists of five injections (days 0, 3, 7, 14 and
(Caution: RIG should never be administered in the 28) irrespective of severity of exposure. The 6 th
same syringe or at the same anatomical site as injection (day 90) is optional for
vaccine). immunologically deficient and extremes of age
and on steroid therapy. The dose of vaccine per
Doses of rabies immunoglobulin (IG) injection is 2.5 IU/dose/ml for HDCV.
Human rabies immunoglobulin (HRIG) 20 IU/kg (max Preferable site is deltoid; anterolateral thigh in
1500 IU), available in concentration of 150 IU/ml, it children (Caution: Must NOT be given into
does not require any prior sensitivity testing. SHOULD gluteal muscle).
NEVER BE INJECTED INTRAVENOUSLY. The anti- • Intradermal (ID) schedule.
rabies sera should always be brought to room
temperature (20-25°C) before use. (i) The 2 site ID TRC schedule (2-2-2-0-1-1) to
be administered: One ID injection of 0.1 ml per
Or ID site over each right and left deltoid on days
0, 3, 7 and 0.1 ml at a single site on days 28 and
Page 141
90 or as per updated TRC schedule (2-2-2-0-2) vaccine should be given only two booster doses,
on days 0, 3, 7 and 28. intramuscular (0.5 ml/1 ml) / intradermal (0.1 ml at 1
site) on days 0 and 3, but no rabies immunoglobulin.
Note: Correct ID injection should result in a
Proper wound toilet should be done.
raised papule with an orange peel appearance. If
a papule is not observed, the needle should be
withdrawn and vaccine re-administered
4. Pre-exposure prophylaxis
correctly nearby. Indications: Laboratory staff working with rabies
virus, veterinarians, animal handlers and wildlife
(ii) The 8-site ID method (8-0-4-0-1-1) for use
officers. Three full IM or ID doses of tissue culture
with HDC/PCECV in emergency, when no RIG
vaccine given on days 0, 7, and 28. Laboratory staff
is available.
and others at high continuing risk of exposure should
The intradermal route is preferred as it reduces have their neutralizing antibody titre checked every 6
cost but must not be used in case of months. If it is less than 0.5 IU/ml, a booster dose of
immunocompromised patients, individuals vaccine should be given. Such individuals on getting
receiving long-term corticosteroids or other exposed to rabies virus after successful pre-exposure
immunosuppressive therapy or chloroquine. immunization require only two booster injections of
Anti-rabies vaccine should be kept and transported at vaccine given on days 0 and 3 without any anti-rabies
a temperature range of +2°C to 8°C. The serum/RIGs.
reconstituted vaccine should be used immediately or
within 6-8 hours of reconstitution.
5. Patient education
Dog bite (category II and III) is an emergency and as
3.4. Post-exposure treatment of a general rule rabies post exposure treatment should
persons previously vaccinated not be delayed or deferred.
Managing re-exposure following post-exposure Immediate washing with plenty of water and
treatment with tissue culture vaccine (TCV) disinfecting with alcohol/iodine.
If re-exposed, persons who have previously received
full post-exposure treatment with a potent cell-culture
Bibliography
Further Reading:
1. India. National Institute of Communicable Diseases. National Guidelines for Rabies Prophylaxis 2007.
Ministry of Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://www.ncdc.gov.in/Rabies_Guidelines.pdf
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54. POISONING
• Anilides
1. Introduction
Poisoning due to the pesticides is increased due to the 3. Stepwise Case Approach
accessibility to the pesticides used in agriculture. Of
the total burden of acute pesticide poisoning the • Diagnosis - Suspect and identify poison, if
majority of deaths are from self-poisoning with possible.
organophosphorus pesticides, aluminium phosphides • Management includes basic principles,
and Paraquat. antidotes, symptomatic and supportive
treatment.
2. Classification of Pesticides • Anticipate complications, preserve evidence and
prevent sequelae as well as recurrence
2.1. Insecticides
• Acetylcholinesterase inhibitors 4. Organophosphorus
• Organophosphates
• Carbamates
Compounds
• Organochlorines Broadly OP compounds can be divided in to
• Pyrethrins 1] Dimethyl compounds - Dichlorvos, Fenthion,
• Pyrethroids Malathion, Methamidophos, Dimethoate
2.2. Herbicides 2] Diethyl compounds – Chlorpyrifos, Diazinon,
Parathion-ethyl, Quinalphos
• Dipyridyl pesticides
• Paraquat and diquat 4.1. Mechanism of toxicity
• Dichlorophenoxyacetate weed killers
• Bromoxynil, 2,4-D Organophosphorus compounds inactivate
acetylcholinesterase by phosphorylation leading to
2.3. Fungicides accumulation of acetylcholine at cholinergic
synapses.
• Substituted benzene
• Chloroneb The rate of spontaneous reactivation of AChE is very
• Chlorothalonil slow with diethyl OPs while it is relatively fast with
• Thiocarbamates dimethyl OPs. Further, there is ageing of the
• Organomercurials phosphorylated enzyme after which the enzyme
• Methylmercury cannot be reactivated by oximes. The half-life of
• Phenyl mercuric acetate ageing of dimethyl phosphorylated and diethyl
phosphorylated AChE in vitro is 3.7 hours and 33
• Molluscicides – Metaldehyde
hours, respectively, and the therapeutic windows
2.4. Rodenticides therefore are 13 and 132 hours, respectively (4 times
the half-life).
• Aluminium phosphide
• Zinc phosphide 4.2. Organophosphorus intoxication
• Warfarin and super warfarin compounds
• Yellow phosphorus results in triphasic illness
• Heavy metal: Thallium – containing pesticides including
2.5. Insect repellents (a) Acute cholinergic syndrome
• Diethyltoluamide (DEET) (b) Intermediate syndrome
2.6. Miscellaneous (c) Organophosphate-induced delayed
polyneuropathy
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4.2.1 Acute cholinergic syndrome ii. Further contamination is prevented by removal
from the site of exposure and of contaminated
• Acute cholinergic syndrome may occur within clothing. Skin should be cleaned thoroughly
minutes with water.
• Pathognomonic features via muscarinic and
nicotinic receptors- iii. The airway is cleared and high-flow oxygen is
administered.
Muscarinic effects– Include meiosis,
bronchorrhea, salivation, lacrimation, pain in iv. Direct mouth to mouth and nose resuscitation
abdomen, bradycardia, urination, defecation must be avoided.
Nicotinic effects– Muscle fasciculation, muscle v. Following ingestion, gastric lavage must be
cramps, flaccid muscle weakness with reduced done within an hour of intake, followed by
tendon reflexes, tachycardia, hypertension activated charcoal via nasogastric tube after
establishing intravenous and airway protection.
Central nervous system effects– Headache,
dizziness, confusion, convulsions, central Sample should be collected from the gastric
respiratory depression, coma lavage, sealed and handed over to the police
registering the medicolegal case.
4.2.2 Intermediate syndrome
vi. Convulsions are treated with intravenous
• This begins 48 hours after poisoning in diazepam 10 mg or midazolam 2 mg.
approximately 20% of patients but may be
delayed for 72-96 hours. vii. Monitoring of ECG, blood gases, temperature,
• The onset is often rapid with progression of blood urea and serum electrolytes, amylase and
muscular weakness from ocular muscles to neck glucose is mandatory.
and proximal limbs to respiratory muscles over
24 hours. • For muscarinic effects
• Endotracheal intubation and ventilation are to be
done, if not instituted early, cyanosis, coma and Injection Atropine 1.8-3mg bolus immediately –
death may follow rapidly. double the dose every 5minutes until
atropinized. Once patient is atropinized give
4.2.3 Organophosphate induced delayed 20%- 30% dose required for atropinisation as
polyneuropathy infusion/hour [5 mg/hour]. The best guide to
adequate atropinisation is to monitor features of
• This occurs 1-3 weeks after acute exposure and cholinergic poisoning (Bradycardia, Sweating,
uncertain period following chronic exposure due meiosis, bronchorrhea and hypotension). A
to degeneration of long myelinated nerve fibres. confused, agitated, febrile patient with no bowel
• Cramping muscle pain in the legs are followed sounds and a full bladder with urinary retention
by numbness and paraesthesia in distal upper certainly has atropine toxicity, indicating the
and lower limbs. need to reduce or stop atropine temporarily.
• Symmetrical flaccid paralysis in distal muscles
especially in the legs. The dominant hand may
be more affected. • For nicotinic effects
4.3. Investigations Pralidoxime chloride- Cholinesterase reactivator

which reverses the nicotinic effects and some
Plasma cholinesterase (pseudo cholinesterase) is less CNS effects. It is given 1 gm bolus in 30
reliable. Red cell cholinesterase level falls to 20% of minutes then infusion at 0.5 gm/hour. (Loading
normal when symptoms appear. dose of 30mg/kg and 10 mg/kg/hour infusion).
4.4. Treatment of
• Treatment of the intermediate syndrome
Organophosphorus Poisoning
Early institution of ventilatory support, which
i. Airway, breathing and circulation should be may be required for a prolonged duration, is
ensured and monitored. essential for management. Close monitoring of
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respiratory function such as chest expansion, suggesting hyperkalaemia. Besides the features
arterial blood gas monitoring and oxygen related to OCs, associated solvents may produce
saturation is essential to identify the onset and aspiration pneumonitis.
monitor the progress of the intermediate
syndrome. Some patients develop an offensive
and profuse diarrhoea and it is important to 5.4. Management
maintain a close watch and a positive fluid
balance. Recovery usually occurs without • Nasogastric aspirate may be useful if liquid
residual deficit. preparation has been taken and should be kept
and handed over to medical official for
medicolegal purposes.
5. Organochloride • Activated charcoal is given within 1hour of
Compounds (OC) ingestion.
• Seizures should be treated with
Benzodiazepines. (Diazepam 10 mg or
The commonly used OC insecticides are Endrin,
Midazolam 2 mg I.V.)
Aldrin, Benzene Hexachloride (BHC), Endosulphan,
• Patients should be kept on cardiac monitor. Use
Dieldrin, Toxaphene, DDT, Heptachlor, Kepone,
Dopamine instead of Epinephrine if patient has
Dicofol, Methoxychlor, etc. DDT, the most toxic OC,
hypotension, as OC compounds sensitise the
is available in dry powder form or as a mixture with
myocardium.
other pesticides in powder or liquid form.
6. Carbamate Poisoning
5.1. Mechanism of toxicity
OC compounds impair nervous system function by Carbamate insecticides- Aldicarb, Carbofuran
depolarization of the nerve membranes they also Methomyl inhibit a number of tissue esterases-AchE.
cause sensitization of the myocardium to both Aldicarb, Benomyl, Carbaryl, Carbendazim,
endogenous as well as exogenous catecholamine and Carbofuran, Propoxur, Triallate, etc. are the
predispose to arrhythmias. commonly used carbamates.
5.2. Clinical effects within minutes

6.1. Clinical features
to hours
• Nausea Clinical features are similar and less severe compared
• Vomiting to organophosphorus poisoning.
• Agitation
• Fasciculation 6.2. Complications
• Paraesthesia of face and extremities
Pancreatitis and death.
• Seizures dizziness
• Tremors
• Myoclonus
6.3. Treatment
• Coma Nasogastric aspirate may be useful if liquid
• Respiratory depression and death preparation has been taken and should be kept and
handed over to medical official for medico-legal
5.3. Complications purposes.
Hyperthermia, Rhabdomyolysis, Pulmonary oedema
and Disseminated intravascular coagulation. Lindane Injection Atropine 0.5-1mg I.V. in small doses for an
is particularly toxic to the central nervous system. It adult till atropinisation occurs.
can also produce alterations in the ECG including
rhythm abnormalities and changes in ST–T waves Role of PAM is unclear.
Bibliography:
Page 145
Further Reading:
1. Eddleston M, Buckly NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide
poisoning. Lancet. [Internet] 2008 Feb 16; 371(9612): 597–607. [cited 2016 Jul 5]
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55. ALCOHOL INTOXICATION /ALCOHOL
WITHDRAWL
• CBC, LFT, obtaining toxicology screens for
1. When to Suspect opioids or other CNS depressants
Alcohol has CNS depressant effect; hence person • Neuroimaging
intoxicated with alcohol will present with depressed
level of consciousness, sometimes with respiratory 3. Treatment
depression, cardiac arrhythmia, or blood pressure • Adequate nutrition and oral or I.V. Vitamin B
instability. complex, including 50–100 mg of Thiamine
If the patient agrees to stop drinking, sudden daily for a week
decreases in alcohol intake can produce withdrawal • Inj. Dextrose 25% in patients of altered
symptoms, many of which are the opposite of those sensorium (dose 100 cc 25% dextrose)
produced by intoxication. Features include tremor of
the hands (shakes); agitation and anxiety; autonomic • Administering any depressant in doses that
nervous system over activity including an increase in decrease the agitation- 25–50mg of
pulse, respiratory rate, and body temperature; and Chlordiazepoxide or 10 mg of Diazepam given
insomnia. These symptoms usually begin within 5–10 PO every 4–6 hour on the first day, with doses
hours of decreasing ethanol intake, peak on day 2 or then decreased to zero over the next 5 days.
3, and improve by day 4 or 5. About 2–5% of • Rehabilitation
alcoholics experience a withdrawal seizure.
2. Investigation 4. Whom to Refer

Those with poor Glasgow coma scale, Recurrent
• History of Alcoholism Seizure, Focal neurological deficits or with delirium
• Blood ethanol level (Avoid cleaning with spirit tremens / Korsakoff psychosis.
while collecting Sample)
Bibliography:
Further Reading:
1. India. National Health mission. Standard Treatment Guidelines; Alcohol and Substance use. Ministry
of Health and Family Welfare. [cited 2016 Jul 5]
Available from:
http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/alcohol-sustance-use-disorders.pdf
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56. ANAEMIA
vii. H/O chronic diarrhoea, malabsorption
1. Introduction viii. H/O chronic illness e.g. chronic renal failure,
Anaemia is one of the most common disease a TB or any other causing anaemia of chronic
physician can come across in the community. It can disease
be defined as HB < 13 g/dL for male and < 12 g/dL ix. H/O blood transfusion in the past
for females as per WHO. x. H/O similar complaints in the past
xi. H/O pure vegetarian diet causing Vit. B12
Anaemia can be due to nutritional deficiency, blood
deficiency causing Megaloblastic Anaemia
loss, and increase in destruction of RBCs or due to
disturbance in formation of RBCs in bone marrow.
Detailed history and clinical examination is must to
4. Signs
reach the diagnosis. Patients especially females don’t i. Pallor– Conjunctiva, mucous membranes, skin
report to clinics until they have severe anaemia. ii. Nails – Platonychia (flat) or koilonychias
Chronic anaemia patients are usually well adjusted to (spoon shaped) nails in iron deficiency
HB as low as 5 g/dL. anaemia (IDA)
iii. Severe anaemia signs of hyper dynamic
2. When to suspect circulation e.g. tachycardia, flow murmurs
(ejection systolic loudest at apex),
Symptoms cardiomegaly
i. Easy fatigability iv. Congestive Heart failure – with oedema feet,
ii. Breathlessness right hypochondriac tenderness, raised JVP
iii. Swelling of feet and basal crepitation
iv. Hypo menorrhea, amenorrhea v. Other signs of aetiology may be found e.g.
v. Stunted growth in adolescent icterus, Lymphadenopathy, stigmata of TB
3. History to be inquired for

aetiology of anaemia 5. How to Investigate
3.1. Acute 5.1. Complete blood count
The most important investigation gives maximum
i. H/O blood loss –hematemesis, haemoptysis or information regarding diagnosis.
any other Mean Cell Volume (MCV) -Normal 76 -96
ii. H/O Fever or jaundice – acute blood loss due
to either haemolysis or blood loss due to Low MCV (microcytic anaemia)
coagulopathy
• Iron deficiency anaemia (IDA) most common
iii. H/O petechiae, ecchymosis or
• Hereditary haemolytic anaemia e.g.
lymphadenopathy with fever – Acute
Thalassemia
Leukaemia
iv. Recovering from recent surgery Normal MCV (normocytic anaemia)
• Acute blood loss
3.2. Chronic • Haemolyses
i. Antenatal or postnatal female • Anaemia of chronic disease
ii. H/O passage of worms in stool causing • Chronic renal failure
chronic blood loss • Pregnancy
iii. H/O Chronic blood loss– Haemorrhoids,
• Bone marrow failure e.g. Aplastic anaemia
Melena, Menorrhagia
• Hypothyroidism
iv. H/O Chronic Alcoholism leading to Vitamin
B12 deficiency High MCV (Macrocytic anaemia)
v. H/O Anorexia or any GI complaints leading to
malnutrition • Vitamin B12 or folate deficiency (strict
vi. Poor socioeconomic status leading to vegetarian diet, Pernicious anaemia)
malnutrition • Alcoholism
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• Myelodysplastic syndromes (MDS) - Elemental Iron – 100 mg once daily can be
• Drug induced e.g. Phenytoin increase up to 300 mg OD
5.2. Stool examination Repeat HB at the end of 1 month to confirm
Parasites, occult blood, malabsorption response to treatment, if HB is increasing then
repeat after 3 months.
5.3. Other Baseline investigations ii. Megaloblastic anaemia-
FBS, Creatinine, Liver enzymes, reticulocyte count, Oral supplements–Vitamin B12 (7.5 mcg)
LDH +Folate (0.75 mg) BD for 1 month.
iii. Deworming - All Patients Tab Albendazole
5.4. Iron studies, serum folic / (400 mg) 1 stat, can be repeated after 2 weeks
iv. Treat aetiology if possible
Vitamin B 12 levels v. Packed cell transfusion if haemoglobin is less
than 7
5.5. Bone marrow biopsy if malignancy
suspected 7. When to refer
• Severe anaemia (HB < 4g /dL) requiring blood
transfusion
6. Treatment • Signs of Heart failure
• No response to oral supplements of Iron or B12
i. IDA – and folate at the end of 2 months
Oral iron – Ferrous Sulphate (200 mg) thrice a • Any suspicion of Leukaemia, Lymphoma, MDS
day for 3 months. or Aplastic anaemia
• No apparent cause found
Or (300 mg) BD Ferrous fumarate, Ferrous
ascorbate can also be used
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Bibliography:
Further Reading:
1. India. National Health Portal. Anaemia. National Institute of Health and Family Welfare. [cited 2016
Jul 5]
Available from: http://www.nhp.gov.in/disease/blood-lymphatic/anaemia
2. India. National Health Mission. Iron Deficiency Anaemia. Ministry of Health and Family Welfare.
[cited 2016 Jul 5]
Available from: http://nrhm.gov.in/images/pdf/guidelines/nrhm-guidelines/stg/anaemia.pdf
3. India. Ministry of Health and Family Welfare. Guidelines for control of iron deficiency anaemia.
National Iron Plus Initiative. 2013. [cited 2016 Jul 5]
Available from: https://groups.google.com/forum/#!topic/hrh-pediatrics/JIIMPXkEJmY
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57. HEAT STROKE
central nervous system (CNS) depression, core
1. Definition temperatures usually above 40°C (105oF), and typical
Heat Stroke is a syndrome of acute thermoregulatory biochemical and physiologic abnormalities.
failure in warm environments characterized by
Figure 57.1: Effects of Heat Exhaustion and Stroke
• Hyperthermia: Hypothalamic set point is

unchanged; does not respond to antipyretics.
3. When to Suspect Heat
Distinct from fever (pyrogens change Stroke
Hypothalamic temperature set point). i. In any patient exercising in hot weather or in
susceptible individuals; mainly elderly
• Uncontrolled increase in body temperature that population.
exceeds the body's ability to lose heat due to ii. Coma or profound stupor is nearly always
failed thermoregulation. present.
iii. Diagnostic criteria for Heat Stroke should
• Life-threatening medical emergency. include
a. A core temperature above 40°C
• Core temperature >40 °C (105 °F) & CNS b. Severely depressed mental status or
disturbances in patients with a history of heat Coma on Central Nervous System
exposure. examination
2. Clinical spectrum of heat c. Elevated Serum Creatinine and Serum

Electrolyte levels (Hyperkalaemia)
illness d. Compatible historical setting.
• Heat Oedema
• Heat Rash (Miliaria) 4. Causes
• Heat Cramps i. Increased Heat production- Exercise,
• Heat Tetany Fever, Thyrotoxicosis, Amphetamines, Atropine
• Heat Exhaustion toxicity.
• Heat Stroke ii. Impaired Heat loss- High ambient temperature
or humidity, Ineffective voluntary control, Lack
Page 150
of acclimatization, Dehydration, Cardiovascular • Exertional: Typically seen in healthy young
diseases. adults who over exert themselves in high
iii. Drugs- Anticholinergics, Phenothiazines, ambient (Surrounding) temperatures or in a hot
Butyrophenones, Thiothixene, Barbiturates, environment to which they are not acclimatized
Anti-Parkinson's agent, Alcohol. (To adapt). Sudden inability to dissipate / Lose
iv. Debilitating conditions- Skin diseases, Cystic body heat through perspiration (evaporation) or
fibrosis, Central nervous system lesion, older cutaneous vasodilatation (convection),
age. especially after strenuous physical activity in hot
weather. (Increased heat production).
5. Clinical examination of • Non-exertional (classic): Usually affects
patient with Heat Stroke elderly and debilitated patients with chronic
underlying disease. Result of impaired
• Anhidrosis often present (but is no longer thermoregulation combined with high ambient
criteria for diagnosis) temperatures. Often due to impaired sweating.
• (Hot, dry skin)
7. Management
• Altered mental State.
Primary therapy includes cooling and decreasing
• Often missed in physically inactive patients. thermogenesis.
• Baseline body temperature increased (core i. Evaporative cooling methods involve placing a
temperature). nude patient in a cool room, wetting the skin
Non-glass medical thermometer. with water and encouraging evaporation by the
use of fans.
Rectum –preferred site
ii. Direct external cooling involves immersing the
Axillary and inguinal sites are unreliable patient in water. Close monitoring of
haemodynamics i.e. Pulse, Blood pressure,
6. Types respiration and urine output is mandatory.
Figure 57.2: Primary therapy of hyperthermia
• Seek medical attention immediately-continue • It is not advisable to give the victim anything by
first aid to lower temperature until medical help mouth (even water) until the condition has been
takes over. stabilized.
• DO NOT give any medication to lower fever- It • Body cooling methods
will not be effective and may cause further
harm. • Body immersion in iced water
• DO NOT use an alcohol rub • Evaporative cooling: Spraying water and the use
of fans over the patient facilitates evaporation
and convection
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• Gastric lavage with cold water / ice, bladder, or • Take time out to find a cool place.
peritoneal lavage
• Immersion method of body cooling
9. Complications
Aggressive ice water immersion is gold standard • Acute renal failure
for life threatening heat stroke • Rhabdomyolysis
• Liver failure
• Advantages: Cools patients faster; cooling rate
of 0.20°C/min for iced water • Disseminated intravascular coagulation(DIC)
• Acute respiratory distress syndrome (ARDS)
• Disadvantages
• CNS: Altered Mental state, confusion, delirium
o May cause peripheral vasoconstriction (not
clinically relevant in RCT) • Seizure, decorticate posture
o Difficult in patients with reduced level of • Coma and Death
consciousness • Dehydration
o For alert - It is uncomfortable and often • Caution – Over hydration
intolerable
• Electrolyte Imbalance
o Shivering leads to worsening
• Other cooling methods • Hypernatremia
• Hyperkalaemia
(a) Placement of ice packs in the axillae, groin,
and neck • Hypokalaemia
• Localized muscle pain on active/passive flexion
- Easy method, slower cooling
of limbs
(b) Gastric, peritoneal, and bladder lavage with • Urine- Haemoglobinuria, Myoglobinuria
cold water 1)
- Used in resistant cases 10. Management of
(c) Cooling gloves
complications
• Supportive treatment i. Benzodiazepines- Lorazepam (2 to 4 mg I.V.
slowly) or Midazolam (2 to 5 mg I.V. slowly)
o Treated in ICU settings
Indicated in patients with agitation & shivering
o IV Fluids, treat electrolyte disturbance to prevent heat production. Also, given in
patients with convulsions.
o Mechanical Ventilation
ii. Rhabdomyolysis- Common in Exertional heat
8. Preventing heat- related stroke & in patients with hypotension.
illness
Signs & symptoms
• Wear loose, lightweight, light-coloured • Dark urine
clothing. Light colours will reflect away some • Acute renal failure
of the sun’s energy. • Treatment
• Wear hats or to use an umbrella. • I.V. fluids
• Alkalinisation of urine – sodium
• Drink water- Carry water or juice with you and
drink continuously even if you do not feel Bicarbonate
thirsty.
iii. Metabolic support- Correcting the electrolyte
• Avoid alcohol and caffeine, which dehydrate the disturbances like hyponatremia, hypercalcemia,
body. hypocalcaemia, hyperphosphatemia
• Avoid foods that are high in protein, which iv. Hepatic injury
increase metabolic heat. • Monitor liver function tests
• Avoid hypoglycaemia
• Stay indoors when possible.
• Early recognition & treatment of DIC
• Take regular breaks when engaged in physical • Respiratory support
activity on warm days.
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v. Pulmonary injury- Pulmonary oedema is
11. When to Refer
common complication. • Evaporative and direct external cooling methods
ARDS- Patient should be referred for fail to reduce the temperature.
mechanical Ventilation. • Arrhythmias, metabolic acidosis and
cardiogenic failure complicate the early
vi. Renal injury- ARF may develop due to many management of hyperthermia crisis.
reasons. These patients may need haemodialysis • Those with evidence of renal failure,
& so referred to higher centre. disseminated intravascular coagulation or
superadded infections.
Bibliography:
Further Reading:
1. India. National Disaster Management Authority. Guidelines for preparation of Action Plan –
Prevention and Management of Heat Wave 2016. Government of India. [cited 2016 Jul 5]
Available from: http://ndma.gov.in/images/guidelines/guidelines-heat-wave.pdf
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58. TUBERCULOSIS (RNTCP)
with evening rise, night sweats, chest pain,
1. Introduction shortness of breath, anorexia and haemoptysis.
Tuberculosis is an infectious disease caused a. Pulmonary TB Suspects
predominantly by Mycobacterium tuberculosis.
Pulmonary tuberculosis is the most common form of A pulmonary TB suspect is defined as:
TB (more than 85% of all TB cases), while extra
pulmonary tuberculosis can affect almost any organ • An individual having cough of 2 weeks or
in the body. Transmission occurs by the airborne more.
spread of infectious droplets and droplet nuclei • Contacts of smear-positive TB patients
containing the tubercle bacilli. The source of having cough of any duration.
infection is a person with sputum smear-positive • Suspected/confirmed extra-pulmonary TB
pulmonary TB. Transmission often occurs indoors, having cough of any duration.
where droplets and droplet nuclei can stay in the air • HIV positive client having cough of any
for a long time. duration.
b. Extra-Pulmonary TB Suspects
2. Epidemiology of
Tuberculosis A patient with extra-pulmonary TB (EP TB) may
have general symptoms like weight loss, fever
• TB is a bacterial disease caused by with evening rise and night sweats. Other
Mycobacterium tuberculosis. These organisms symptoms depend on the organ affected.
are also known as tubercle bacilli or as acid-fast
bacilli. Examples of these symptoms are, swelling of a
lymph node in TB lymphadenitis, pain and
• Transmission of tuberculosis occurs by airborne swelling of a joint in TB arthritis, neck stiffness
spread of infectious droplets and droplet nuclei. and disorientation in a case of TB meningitis.
Source of infection is patient of tuberculosis Patients with EP TB, who also have cough of any
who spreads tuberculosis bacilli during duration, should have sputum samples examined.
coughing, sneezing, etc. If the smear result is positive, the patient is
classified as pulmonary TB and his/her treatment
• Most common symptom of pulmonary TB is
regimen will be that of a case of smear-positive
persistent cough for two weeks or more, usually
pulmonary TB.
with expectoration. Persistent cough for 2
weeks or more may be accompanied by one or
more symptoms such as weight loss, loss of
4. Screening for TB among
appetite, tiredness, evening rise fever, chest high risk groups
pain, shortness of breath and haemoptysis.
a) Contact investigation among the diagnosed
• Incidence of tuberculosis is usually similar in smear-positive cases is to be systematically
both sexes below 15 years of age, thereafter implemented and monitored, and it offers a
incidence is higher in males than females and major opportunity for early case detection.
difference is greatest in old people. b) HIV care centres: Intensified TB case finding
should be implemented in all facilities providing
• Early detection of sputum positive tuberculosis
HIV care, like ICTCs, ART Centres, Care and
case and conversion into sputum negative by
support centres etc. Involve NGOs working with
effective treatment are most important measures
HIV programmes in TB case finding activities.
for tuberculosis control.
c) Diabetic patient: regularly screening for TB in
all diabetic patients at each visit.
3. Diagnosis of TB d) Elderly patients.
• Identification of Tuberculosis Suspects e) Smokers.
f) Other High risk groups: Malnutrition, patients
The most common symptom of pulmonary TB with silicosis, patients on corticosteroids and
is persistent cough, usually with expectoration. other chronic diseases need to be screened for
Persistent cough may be accompanied by other TB regularly.
symptoms such as weight loss, tiredness, fever
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5. Tools for diagnosis of TB 7. Management of Patient after
Following are RNTCP recommended diagnostics receiving the sputum results
tests for TB
7.1 Smear positive pulmonary TB.
• Sputum smear microscopy.
• Histopathology/cytology/radiology. Patients with at least one sputum positive smear
• Solid/liquid culture and DST for diagnosis TB result out of two samples are diagnosed by the
and Drug Resistant TB. physician as having smear-positive pulmonary TB.
• PCR based newer rapid diagnostic tools for They are further classified as a new or re-treatment
diagnosis of TB/drug resistant TB e.g. case based on their previous treatment history and
Line probe assay (LPA), CBNAAT. appropriate regimen is prescribed.
6. Guidelines for collecting 7.2 Follow up of the sputum

sputum negative symptomatic
• The patient is given the sputum container with Patients, who are negative for AFB in both the
Laboratory Serial Number written on its side. samples, will be prescribed a course of antibiotics for
The patient is instructed to inhale deeply 2– duration of 10-14 days. In such cases antibiotics such
3times with mouth open, cough out deeply from as fluoroquinolones (Ciprofloxacin, Ofloxacin,
the chest, open the container and spit out the Levofloxacin, and Moxifloxacin etc.), Clavulanate
sputum into it. Sample should be at least 2 ml. If Macrolides, Rifampicin or Streptomycin, which are
the quantity is less, then the procedure can be active against tuberculosis, are not to be used.
repeated. Once adequate quantity of sample is Antibiotics of choice include Cotrimoxazole,
collected, the container should be closed. This is Amoxicillin, & Doxycycline. Most patients are likely
the first spot specimen (A). to improve with antibiotics if they are not suffering
• The patient is given a labelled container with from TB. If the symptoms persist after a course of
instructions to cough out sputum in to the broad spectrum antibiotics, repeat sputum smear
container early in the morning after rinsing the examination (2 samples) must be done for such
mouth, before breakfast. This is the early patients.
morning specimen (B). However, if repeat sputum examination turns to be
The person collecting the sputum specimens should negative, they are subjected for chest x-ray
follow the guidelines specified below: examination. If chest x-ray is suggestive of
pulmonary TB, they will be diagnosed as smear
• If the sputum specimens are to be sent negative pulmonary TB and treated accordingly. If
immediately to the laboratory, the person should chest x-ray is not suggestive of TB, then they should
put the container into a special box meant for be evaluated for other respiratory diseases.
transport.
For patients infected with HIV, antibiotic trial is not
• If the sputum specimens are not being sent indicated and Chest X-ray needs to be taken to avoid
immediately to the laboratory, these should be delay in diagnosis of smear negative TB.
stored in a cool and shady place in the referring
Patients with suspected EP TB should be referred to a
health facility.
competent medical practitioner / doctor / specialist
• The person should wash hands thoroughly with for expert opinion. Diagnosis of such patients may be
soap and water every time when the material is made using appropriate diagnostic procedures (such
handled. as FNAC/Biopsy/Radiology) as well as clinical
methods.
• Patients should be told to come back to receive
the results of sputum examination. Diagnosis of TB by chest X-ray alone is unreliable
because no radiological pattern is pathognomonic of
Alternatively, sputum results may be sent to the pulmonary TB. Unless the prescribed algorithm is
referring health facility by hand. Laboratory followed, a large number of patients who do not have
serial number (and/or specimen identification TB will be falsely diagnosed and treated.
number) should be clearly written on the side of
the sputum container.
Page 155
its duration, and the need for prompt evaluation of
8. Diagnostic Algorithm children under six years or contacts with cough of
any duration living in the household. The patient
When the referring doctor receives the results of
should also be informed that his address would be
sputum examination, and it is decided to put the
verified by a competent person prior to the start of
patient on chemotherapy, health education must be
treatment.
imparted to the patient. The patient is told about TB,
how it spreads, precautions to be taken to prevent the
spread, importance of directly observed treatment and
Figure-58.1: Diagnostic Algorithms for Pulmonary Tuberculosis
9. Treatment of TB
MO must undertake detailed clinical examination and V. Culture / Drug Susceptibility Test (DST) report
history before starting the TB treatment. from RNTCP certified laboratory (if available).
The following is required before starting treatment: 9.1. Directly Observed Treatment
I. History of patient, including history of any (DOT)
previous treatment for TB.
II. Sputum smear examination results from an RNTCP Definitions: Case Definitions, Types of
approved DMC. Cases and Treatment outcomes
III. Chest X-ray report if the case warrants
radiographic examination.
IV. Other supporting investigation reports, if any.
Page 156
Table-1: Definitions under RNTCP
9.2. Treatment Regimens alternate days and lasts for 2 months (8 weeks, 24
doses).
For the purpose of treatment regimen to be used, TB This is followed by the continuation phase, which
patients are classified into two groups, namely, consists of 4 months (18 weeks; 54 doses) of
“New” or “Previously Treated”, based on the history isoniazid and rifampicin given thrice a week on
of previous treatment. alternate days with at least the first dose of every
9.2.1. Regimen for New cases week being directly observed. If the sputum smear is
positive after 2 months of treatment, the intensive
This regimen is prescribed to all new pulmonary phase of four drugs (H, R, Z and E) are continued for
(smear-positive and negative), new extra pulmonary another one month (12 doses), and sputa sent for
and new ‘others’ TB patients. culture and drug susceptibility testing (C&DST) to an
The regimen is 2H3R3Z3 E3 / 4 H3R3. accredited RNTCP C&DST laboratory. Treatment
remains continued as per regimen if C&DST report is
Treatment is given in two phases. For “New” Rifampicin-sensitive. Sputum is examined after the
patients, the intensive phase consists of isoniazid (H), completion of the extension of intensive phase.
rifampicin (R), pyrazinamide (Z) and ethambutol (E) Irrespective of the sputum results after this extension
given under direct observation thrice a week on of the intensive phase, the 4 months (18 weeks) of the
continuation phase is started.
Page 157
If the sputum smear is positive after 5 or more Treatment after Default, Failures and Others are
months of treatment, the patient is declared as a treated with this regimen.
“Failure” and is placed on the “Previously Treated”
The regimen is IP: 2S3H3R3Z3 E3+ 1H3R3Z3 E3
treatment regimen afresh. If patient remains smear
CP: 5 H3R3 E3.
positive in any follow-up sputum examination, then
sputum samples are sent for culture and drug Treatment is given in two phases. For “Previously
susceptibility testing (C&DST) to a certified RNTCP Treated” cases, the intensive phase consists of two
C&DST laboratory. If the report indicates Rifampicin months (24 doses, 8 weeks) of isoniazid (H),
resistant, then the Cat I regimen is stopped and rifampicin (R), pyrazinamide(Z), ethambutol (E) and
patient is counselled and referred to District / Drug streptomycin (S), followed by one month (12 doses, 4
Resistance TB centre for pre-treatment evaluation weeks) of isoniazid, rifampicin, pyrazinamide and
and treatment initiation. While treating TB ethambutol, all given under direct observation thrice
meningitis(TBM) in “New” patients, streptomycin is a week on alternate days. Patient is subjected for
to be used in place of ethambutol during the intensive follow-up sputum examination at the end of three
phase (H3R3Z3S3 instead of H3R3Z3E3). The months. If the sputum smear is positive at the end of
continuation phase of treatment for patients with 3 months of treatment, the intensive phase drugs (H,
TBM or spinal TB is for 7 months. Hence, the total R, Z and E) are extended for another one month (12
duration of treatment will be for 9 months. doses,4 weeks). Irrespective of the sputum results at
the end extended intensive phase, 5 months (22
9.2.2. Regimen for Previously Treated cases weeks) of continuation phase is started. If the sputum
This regimen is prescribed for TB patients who have remains positive at the end of the extended intensive
had more than one-month anti-tuberculosis treatment phase, sputum is sent to an accredited RNTCP
previously. These patients are at a higher risk of C&DST laboratory for culture and drug susceptibility
having drug resistance. Hence all such patients are testing. The continuation phase consists of 5 months
also subjected to C&DST for identification of (22 weeks; 66 doses) of isoniazid, rifampicin and
MDRTB. If C&DST report is expected beyond 7 ethambutol given thrice a week on alternate days,
days, then patients are initiated on Cat II regimen with at least the first dose of every week being
with 5 drugs in the intensive phase, and the total directly observed.
duration of treatment is 8 months. Relapses,
Table-2: Treatment regimen under RNTCP
Regimen1
Treatment groups
Type of patient Intensive phase (IP) Continuation phase
(category)
(CP)
New Sputum smear-positive 2H3R3Z3E3 4H3R3
(Cat I: Red Box) Sputum smear-negative
Extra-pulmonary
Others
Previously Smear-positive relapse 2H3R3Z3E3S3 5H3R3E3
Treated** Smear-positive failure / 1H3R3Z3E3
/Retreatment case Smear-positive treatment after
(Cat II: Blue Box) default
Others2
i. The number before the letters refers to the number • Patients who weigh 60 kg or more receive
of months of treatment. The subscript after the letters additional rifampicin 150 mg.
refers to the number of doses per week. • Patients who are more than 50 years old receive
streptomycin 500 mg. Patients who weigh less
The dosage strengths are as follows: Isoniazid (H) than 30 kg, receive drugs as per Paediatric
600 mg, Rifampicin (R) 450 mg, Pyrazinamide (Z) weight band boxes according to body weight.
1500 mg, Ethambutol (E) 1200 mg, Streptomycin (S)
750 mg. ii. In rare and exceptional cases, patients who are
sputum smear-negative or who have extra-pulmonary
Page 158
disease can have recurrence or nonresponse. This Paediatric cases are to be treated under RNTCP with
diagnosis in all such cases should always be made by the same thrice weekly short course chemotherapy
an MO and should be supported by culture or regimens (“New” or “Previously Treated”) given
histological evidence of current, active TB. In these under DOT as for adult patients. They are to be
cases, the patient should be typed as ‘Others’ and registered in the respective RNTCP TB Register.
given treatment regimen for previously treated. Paediatric patient-wise boxes are available with
different dosages as two product codes to be used
Note: - All doses in Intensive phase and at least first under four weight bands for children weighing 6 to
dose in Continuation phase should be directly 10 kg, 11 to 17 kg, 18 to 25 kg and 26 to 30 kg.
observed by DOT provider.
9.3. Paediatric TB
Table-3: Paediatric patient wise boxes for new cases according to weight band
INH Chemoprophylaxis 9.4. Monitoring of Treatment

All children aged < 6 years in contact with smear- Follow up of patient
positive pulmonary TB case are screened by MO to
rule out TB. If suffering from TB, should be treated
appropriately. Children not having TB are to be
administered preventive chemotherapy with INH,
10mg/kg body weight for 6 months.
Table-4: Follow up of DOTS patients
If smear + at the end of IP

CAT Follow up sputum Remarks
Follow up
Action
sputum
If sputum +ve at 5 months,

At 2,4,6 months of Extend IP for another one 3,5,7 months
CAT-I declare patient as failure
treatment month of treatment
and put on CAT-II
If +ve at 3 months then

At 3,5,8 months of 4,6,9 months
CAT-II extend IP, 4 drugs for one -
treatment of treatment
more month
Page 159
Default retrieval action is resistant in-vitro to isoniazid and rifampicin with
or without other anti-tubercular drugs based on DST
In spite of counselling and health education at the
results from an RNTCP-certified Culture & DST
time of diagnosis and follow up by health workers,
Laboratory.
some patients remain irregular for treatment.
Defaulter retrieval action is action taken to bring XDR TB case: An MDR TB case whose recovered
back patients for treatments who do not take M. tuberculosis isolate is resistant to at least
medicines regularly. DOT provider should take isoniazid, rifampicin, a fluoroquinolone (Ofloxacin,
defaulter action. Following actions are suggested Levofloxacin, or Moxifloxacin) and a second-line
under RNTCP for defaulter patients- injectable anti-TB drug (Kanamycin, Amikacin, or
• If patient does not come as scheduled during
Capreomycin) at a RNTCP-certified Culture & DST
Laboratory.
Intensive Phase (IP) then health worker / DOT
provider makes home visit immediately same Diagnosis of MDR-TB
day or next day and brings patient for regular
treatment. Presently, 3 technologies are available for diagnosis
of MDR TB viz. the conventional solid Egg-based
• If patient is in Continuation Phase (CP) home Lowenstein-Jensen (LJ) media, the liquid culture
visit should be made and patient should be (MGIT), and the rapid molecular assays such as Line
retrieved within a period of a week after missed Probe Assay (LPA) and similar Nucleic Acid
dose. Amplification Tests like Xpert MTB/Rif (CBNAAT).
In case of community DOT provider / ASHA / Molecular/genotypic tests are much faster than
Anganwadi, the respective ANM/MPW of that areas phenotypic tests, as molecular tests don’t require
should supervise the DOT provider fortnightly for growth of the organism, and M. tuberculosis is
ensuring DOT implementation and assist in ensuring notoriously slow growing. The turnaround time for
patient adherence, timely follow-up. C-DST results by Solid LJ media is around 84 days,
by Liquid Culture (MGIT) is around 42 days, by LPA
9.5. Programmatic Management of is around 72 hours and by CBNAAT is around 2
hours. Currently LPA does the DST of INH and
Drug Resistant TB (PMDT) Rifampicin and CBNAAT gives the DST of
MDR-TB Suspects Rifampicin. Liquid culture DST is used to do the
DST of second line drugs – Ofloxacin / Kanamycin.
The following are the criteria to label a patient as
MDR-TB suspect. RNTCP MDR/XDR-TB Treatment
• All previously treated pulmonary TB cases at As per PMDT guidelines, a specialized centres
diagnosis. named “Drug Resistant TB Centres” are been
• Any smear positive follow-up result in new or established at tertiary care hospitals like medical
previously TB cases. college/ TB hospitals/civil hospital for admission of
• HIV TB co-infected cases at diagnosis. MDR TB patients for pre-treatment evaluation and to
• All pulmonary TB cases who are contacts of initiate treatment.Patients should receive counselling
known MDR TB case at every level on 1) the nature and duration of
Once the districts will have adequate laboratory treatment, 2) need for regular treatment, 3) possible
capacity for DST, all TB patients will be provided side effects of these drugs and 4) the consequences of
DST at the time of diagnosis. Two fresh sputum irregular treatment or pre-mature cessation of
samples (Spot and early morning) are to be collected treatment.
from MDR TB suspects and transported from
Regimen for MDR-TB
DMC/PHI to the RNTCP certified C & DST
laboratory in cold chain by using transport This regimen comprises of 6 drugs - Kanamycin,
mechanism (courier/post/human carrier) within 72 Levofloxacin, Ethionamide, Pyrazinamide,
hrs. Ethambutol and Cycloserine during 6-9 months of the
Intensive Phase and 4 Drugs-Levofloxacin,
Definitions
Ethionamide, Ethambutol and Cycloserine during the
MDR-TB case: A TB patient whose sputum is 18 months of the Continuation Phase.
culture positive for Mycobacterium tuberculosis and
Page 160
All drugs should be given in a single daily dosage Follow-up monitoring in XDR TB
under directly observed treatment (DOT) by a DOT
Provider. All patients will receive drugs under direct XDR TB requires more intensive monitoring during
observation on 6 days of the week. On Sunday, the follow-up.
oral drugs will be administered unsupervised whereas
injection Kanamycin will be omitted. If intolerance • Complete Blood Count with Platelets Count:
occurs to the drugs, Ethionamide, Cycloserine and, weekly in first month, then monthly to rule out
bone marrow suppression and anaemia as a side
PAS may be split into two dosages and the morning effect of Linezolid.
dose administered under DOT. The evening dose will • Kidney Function Test- monthly creatinine and
be self-administered. The empty blister packs of the addition of monthly serum electrolytes to the
self-administered doses will be checked the next monthly creatinine during the period that Inj
morning during DOT. Pyridoxine should be Capreomycin is being administered.
administered to all patients on Regimen for MDR • Liver Function Tests: Every month in IP and for
TB. Drugs are provided to the DOT provider in every 3 months during CP.
monthly patient wise boxes (PWB). PWBs are • CXR every 6 months.
prepared at State Drug store as per the five weight No difference to follow-up Culture for patients on
bands- <16kg, 16-25Kg, 26-45kg, 46 -70kg and > regimen for MDR TB and XDR TB.
70kg.
M/XDR TB Treatment Outcome definitions
If patient gains or loses >5 kg weight during
treatment and crosses the weight band range, Standardised treatment outcome definitions are to be
Committee may consider moving the patient in higher used following treatment of an MDRTB case. These
or lower weight band in next supply of drugs. definitions apply to patients with rifampicin
resistance (who are taken to be MDR TB for
Follow-up investigations during MDR TB management purposes), and XDR TB cases as well:
treatment
• Cure: A patient who has completed treatment
• One specimen for follow up culture at the end of and has been consistently culture negative (with
3,4,5,6,7,9,12,15,18,21,24 months of treatment. at least 5 consecutive negative results in the last
• Monthly weight. 12 to 15 months). If one follow-up positive
• Chest X-ray during pre-treatment evaluation, culture is reported during the last three quarters,
end of IP, end of treatment and whenever patient will still be considered cured provided
indicated. this positive culture is followed by at least 3
• Physician evaluation every month for 6 months consecutive negative cultures, taken at least 30
and then every 3months for 2 years. days apart, provided that there is clinical
• Serum Creatinine monthly for first 3 months evidence of improvement.
and then every 3 months till inj. Kanamycin is • Treatment completed: A patient who has
given. completed treatment according to guidelines but
• TSH during pre-treatment evaluation and when does not meet the definition for cure or
indicated. treatment failure due to lack of bacteriological
• Patients will be considered culture converted results.
after having two consecutive negative cultures • Treatment failure: Treatment will be
taken at least one month apart. Based on culture considered to have failed if two or more of the
conversion patient is shifted from IP to CP. five cultures recorded in the final 12-15 months
are positive, or if any of the final three cultures
Regimen for XDR TB are positive.
• Death: A patient who dies for any reason
The Intensive Phase will consist of 7 drugs – during the course of M/XDR-TB treatment.
Capreomycin (Cm), PAS, Moxifloxacin (Mfx), High • Treatment default: A patient whose treatment
dose-INH, Clofazimine, Linezolid, and Amoxiclav. was interrupted for two or more
Consecutive months for any reasons.
The Continuation Phase will consist of 6 drugs – • Transfer out: A patient who has been
PAS, Moxifloxacin (Mfx), High dose-INH, transferred to another reporting unit (DR-TB
Clofazimine, Linezolid, and Amoxiclav. Centre in this case) and for whom the treatment
outcome is not known.
Page 161
• Switched to Regimen for XDR TB: A MDR- By an RNTCP certified C-DST laboratory, who
TB patient who is found to have XDR-TB. subsequently switched to a regimen for XDR TB
treatment initiated.
Bibliography
Further Reading:
1. India. Central Tuberculosis division. Revised National Tuberculosis Control Programme. Ministry of
Health and Family Welfare. 2016 [cited 2016 Jul 5]
Available from: http://tbcindia.nic.in/
http://tbcindia.nic.in/index1.php?lang=1&level=2&sublinkid=4573&lid=3177
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Page 162
59. LEPROSY (NLEP)
ii. Thick and/or Tender nerve
1. Cardinal signs of leprosy Selection of Leprosy case on clinical sign &
i. Hypo-pigmented / Erythematous anaesthetic symptoms.
patch/s.
Figure-59.1: Algorithm for Confirmation
Treatment for 6
PB case months (6 BCP
Confirmation of
in 9 Month)
Suspect Case cases at
PHC/RH
MB case Treatment for 12
months (12 BCP
in 18 Month)
Table-1: Cardinal signs for classification of Leprosy Case
Clinical aspects PB (Paucibacillary) MB (Multibacillary)

Skin lesions 1 to 5 skin Patches with definite sensory 6 & 6 + skin Patches with definite
deficit sensory deficit
Nerve involvement And/or one definite thicken or tender And/or More than one definite
peripheral nerve involvement thicken or tender peripheral nerve
If any one or both signs present in suspected case, then it is diagnosed as leprosy.
2. Management
Table-2: Management of Leprosy case as per classification2
Multi Drug Treatment for PB leprosy
Drug Adult Children Children below 10 years Frequency

10-14 years
Rifampicin 600 mg 450 mg 300 mg
Once a month
Dapsone 100 mg 50 mg 25 mg
25 mg daily or 50 mg alternate day Daily/ alternate
Dapsone 100 mg 50 mg
day
Page 163
Multi Drug Treatment for MB leprosy.
Drug Adult Children 10-14 years Children below 10 years Frequency

Rifampicin 600 mg 450 mg 300 mg
Dapsone 100 mg 50 mg 25 mg Once a month
Clofazimine 300 mg 150 mg 100 mg
Dapsone 100 mg 50 mg 25 mg Daily
50 mg 50 mg 50 mg
Clofazimine weekly twice
(Daily) (Alternate day)
The appropriate dose for children under 10 • Dapsone: 2 mg per kilogram body weight daily.
years of age can be decided on the basis of
MDT Multi drug Treatment is safe and well tolerated
body weight.
by most of the patients.
• Rifampicin: 10 mg per kilogram.
3. Management of Reaction
• Clofazimine: 6 mg per kilogram monthly and 1
mg per kilogram per body weight daily.
Table-3: Features of Lepra Reaction

Features Type – I Type-II
Skin Existing lesions suddenly become red, Red, painful, tender, subcutaneous (deep)
swollen, warn and tender. New lesions nodules (ENL) appear commonly on face,
may appear arms and legs. They appear in groups and
subside within a few days.
Lesions when subsiding, may show scales
on surface
Nerves Nerves close to skin become enlarged, Nerves may be affected but not as common as
tender and painful with loss of nerve in Type-I reaction
function.
Other organs Not common Fever, joint pains fatigue
10 mg once a day for first 9-10 weeks.
Treatment of Lepra Reaction (Type-I and Type II)
• Assurance to the patient & family (The total duration should not exceed 12 weeks
even in type 2).
• Early diagnosis & prompt treatment to prevent Cap Clofazimine 100mg T.D.S. in type 2 reaction
deformity. for 12 weeks, followed by 100 mg once a day for
• Removal of precipitating factor wherever possible. 12 weeks & 100 mg od for 12-24 weeks.
• Rest: Adequate rest to the affected nerve until
Tab. Prednisolone symptoms clear, by applying a padded splint or
40 mg once a day for first 2 weeks. any other suitable material to immobilize the joints
30 mg once a day for first 3-4 weeks. near the affected nerve.
Page 164
• Continuation of Anti Leprosy Treatment only if appearance of reactions with new development of
not completed. the disease.
• It has been observed that many medical officers
become panicky and start MDT again equating the
Figure-59.2: MDT Blister Packs
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Bibliography
Further Reading:
1. India. Directorate General of Health Services. National Leprosy Eradication Programme. Ministry of
Health and Family Welfare. [cited 2016 Jul 5]
Available from: http://nlep.nic.in/about.html
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
Page 165
Paediatrics
2. Paediatrics
1 Emergency Management in Paediatrics 166
2 Neonatal Resuscitation Guidelines 177
3 Guidelines for Management of Normal Newborn 179
4 Care of at Risk Neonates 187
5 Care of Sick Neonates 190
6 Management of Low Birth Weight Babies 194
7 Neonatal Sepsis 199
8 Treatment of Respiratory Distress in Newborn 203
9 Meconium Aspiration Syndrome 205
10 Bleeding Neonate 207
11 Jaundice in the Newborn 209
12 Management of Surgical Neonate 213
13 Vitamin A Deficiency 214
14 Rickets 215
15 Management of Children with SAM 217
16 Mumps 220
17 Case Management of Children with Sever Acute Malnutrition (SAM) 222
18 Fever with Rash 227
19 Enteric fever / Typhoid 230
20 Acute Meningoencephalitis 232
21 Tuberculous Meningitis 234
22 Acute Respiratory Infection 236
23 Bronchial Asthma 241
24 Breath holding spell 244
25 Bronchiolitis 245
26 Empyema 247
27 Approach to Fever 249
28 Acute Flaccid Paralysis (AFP) 250
29 Febrile seizures 254

30 Acute Nephritis 256
31 Nephrotic Syndrome 258
32 Congestive Heart Failure (CHF) 260
33 PICA 262
34 Nocturnal Enuresis 263
35 Thrush / Candidiasis 265
36 Congenital Hypothyroidism 266
37 Urinary Tract Infection (UTI) 268

1. Emergency Management in Pediatrics
In children under five years of age, Pneumonia, Efforts should be made to maintain euglycemia and
Diarrhea, Birth asphyxia, Low birth weight and euthermia while managing ABCD. Thus Blood sugars
neonatal infections are the most important causes of should be done for every sick Newborn, Infant and
death. Many children suffer from more than one illness older child.
at a time and also many different diseases present with
similar symptoms. This chapter describes a sequential 3. How to Keep baby warm
process for managing sick young infants and children
as soon as they arrive in the facility. Only the key • Keep the infant dry and well wrapped.
• Cap, gloves and stockings are helpful to reduce
protocols from Integrated Management of Childhood
heat loss.
Illness (IMNCI) and Facility Based IMNCI are re- • Keep the room warm (at least 25ºC) making sure
emphasized. that there is no heat source directed straight at the
newborn.
1. Emergency Management • Keep the baby under a radiant warmer and re-
warm so as to bring the child’s temperature to
process of the sick child (0- 5 36.5ºC. Pay special attention to avoid chilling the
years) infant during examination or investigation.
• Monitor temperature every half hourly for first 2
The first step in assessing children referred to a hospital hrs and then every 2 hourly.
should be triage – The process of rapid screening to
decide to which of the following group(s) a sick child 4. How to Treat Hypoglycemia
belongs: • Check for blood glucose in all children presenting
with emergency sign, those with severe acute
• First assess every child for emergency signs.
malnutrition and all sick young infants (0-2
Those with emergency signs require immediate
emergency treatment. months):
• If emergency signs are not present, look for
priority signs. Those with priority signs should • If hypoglycemia detected defined as: < 45 mg/dl
alert you to a patient who is seriously ill and for young infants and < 54 mg/dl in older sick
needs immediate assessment and treatment. children beyond 2 months), give I/V bolus dose of
• Children with no emergency or priority signs are 10% dextrose, in the dose of 2 ml/kg for young
treated as non-urgent cases. infants, and 5 ml/kg for older children.
2. Triage • If you cannot measure blood glucose, give bolus

All sick children are assessed for Airway, Breathing, dose as above. Refer the case to higher center.
Circulation, Coma, Convulsions and severe
Dehydration (ABCD). Table 1
Table-1: Assessment of Airway and Breathing
Not breathing or • Manage airway

gasping or • Provide basic life
ASSESS
Central cyanosis support
AIRWAY
or (Not breathing/gasping)
AND
Severe respiratory ANY SIGN POSITIVE • Give oxygen
BREATHING
distress • Make sure child is
warm
Page 166
a) Positioning to improve the Airway when neck
5. Airway and Breathing: trauma suspected
To limit the risk of aggravating a potential cervical
5.1. Signs of severe respiratory spine injury, open the airway with a jaw thrust
distress while you immobilize the cervical spine. It is safe to
use in cases of trauma for children of all ages.
• Respiratory rate in
✓ 0 -2 months > 60,
b) Neck trauma suspected (possible cervical spine
✓ 2 months – 1 year > 50 & injury)
✓ >1 year – 5 years > 40. • Stabilize the neck, as shown in Figure 1.2.
• Severe lower chest in-drawing • Inspect mouth and remove foreign body, if present
• Head nodding • Clear secretions from throat by suction catheter
• Grunting • Check the airway by looking for chest
• Apnoeic spells movements, listening for breath sounds, and
• Unable to feed due to respiratory distress feeling for breath
• Stridor in a calm child.
5.2.2 Jaw thrust maneuver
5.2. Management of airway in a child The jaw thrust is achieved by placing two or three
with gasping or who has just fingers under the angle of the jaw on both sides, and
stopped breathing. lifting the jaw upwards and outward. The jaw thrust
maneuver is also used to open the airway when bag-
Table-2: Positioning to Improve the Airway when no mask ventilation is performed.
neck trauma suspected.
Child Conscious Child Unconscious

• Inspect mouth and • Open the airway by
remove foreign body, Head tilt and Chin
if present. lift method.
• Clear secretions from • Inspect mouth and
throat using suction remove foreign
catheter. body, if present Figure-1.2: Using Jaw thrust without head tilt
• Let child assume • Clear secretions
position of maximal from throat • If after any of these maneuvers the child starts
comfort. • Check the airway by
breathing, an oropharyngeal airway should be put
• Give Oxygen. looking for chest
and start oxygen.
• Continue with further movements,
assessment. listening for breath
sounds and feeling • If the child is not breathing even after the above
for breath. maneuvers or spontaneous ventilation is
inadequate (as judged by insufficient chest
5.2.1 Head tilt-chin lift maneuver (Figure 1.1) movements and inadequate breath sounds),
The neck is slightly extended and the head is tilted by ventilate with a self-inflating bag and mask
placing one hand on to the child’s forehead. Lift the
mandible up and outward by placing the finger tips of 5.3. Ventilation with Bag and mask
other hand under the chin.
• Positioning (Figure 1.3)
Infant Older Children • A “sniffing” position (padding under the shoulder
to prevent excessive flexion of the neck that
occurs when their prominent occiput rests on the
surface on which the child lies without hyper-
extension of the neck) is usually appropriate for
children less than 2 years old.
Figure-1.1: Position for opening airway
Page 167
In correct sniffing position, the opening of the • Reservoir and oxygen (5-6 L/min) should be
external ear canal should be in line with or in front connected to the self-inflating bag during
of (anterior to) the anterior aspect of the shoulder. resuscitation.
Extreme hyperextension of the infant neck can • After two effective ventilations, check the pulse
produce airway obstruction. (femoral, brachial or carotid) for no more than
• In children older than 2 years you may need to give ten seconds. If pulse is absent, the second
padding under the occiput to obtain optimal airway person should start chest compression.
position. 5.3. Chest compressions:
The techniques for chest compression vary for a
child under 1 year and those between 1-8 years and
are detailed below:
5.3.1 Chest compression in the infant (less

than 1 year of age)
There are two techniques for performing chest
compression. These techniques are:
• Thumb technique, where the 2 thumbs are used

to depress the sternum, while the hands encircle
the torso and the fingers support the spine
Figure-1.3: Difference in padding for an infant and

older child
• Bags and masks should be available in sizes for the

entire pediatric range (size 0, 1 and 2).
• It is important for the mask to be the correct size for
the child; it must completely cover the mouth and Figure-1.6: Thumb technique
nose without covering the eyes or overlapping the
chin. The correct size and position are shown in the • 2-finger technique, where the tips of the middle
Figure 1.4 & 1.5. finger and either the index finger or ring finger
of one hand are used to compress the sternum,
while the other hand is used to support the
baby’s back (unless the baby is on a very firm
surface).
• Using either method to give chest compressions,
compress the lower half of the sternum but do
not compress over the xiphoid. After each
compression allow the chest to recoil fully
Figure-1.4: Bag and mask ventilation because complete chest re-expansion improves
blood flow into the heart.
• “Push hard”: push with sufficient force to
depress the chest approximately one third to one
half the anterior-posterior diameter of the chest.
• “Push fast”: push at a rate of approximately 100
compressions per minute.
Figure 1.5: Choosing the correct mask size
• Self-inflating bags of minimum volume 450-500ml

should be used. Use force and tidal volume just
enough to cause the chest to rise visibly.
Page 168
• Release completely to allow a complete recoil of
7. Giving Oxygen to a child
the chest by completely releasing the pressure but
maintaining contact with the compression site. with respiratory distress
• Minimize interruptions in chest compressions.
• With a Head box (8-10 L/min) or a Face mask
• During cardiopulmonary resuscitation, chest
(5-6 L/min).
compressions must always be accompanied by
• Should be allowed to take a comfortable
positive-pressure ventilation.
position of his choice and should be given
• Avoid giving a compression and ventilation
oxygen.
simultaneously, because one will decrease the
• Continue giving oxygen continuously until the
efficacy of the other.
child is able to maintain a SaO2 > 92% in room
• Therefore, the 2 activities must be coordinated,
air. When the child is stable and improving, take
with one ventilation interposed after every third
the child off oxygen for a few minutes. If the
compression (3 compressions followed by one
SaO2 remains above 92%, discontinue oxygen,
ventilation), for a total of 30 breaths and 90
but check again ½ hour later, and 3 hourly
compressions per minute
thereafter on the first day off oxygen to ensure
5.3.2 Chest compressions for the child (1 to 8 the child is stable. Where pulse oximetry is not
years of age) available, the duration of oxygen therapy is
• Place the heel of one hand over the lower half of guided by clinical signs, which are less reliable.
the sternum. Lift your fingers to avoid pressing on • Any child who has been successfully
the ribs. resuscitated or any unconscious child who is
breathing and keeping the airway open should
be placed in the recovery position. This position
helps to reduce the risk of vomit entering the
child’s lungs. It should only be used in children
who have not been subjected to trauma. A child
with cyanosis or severe respiratory distress
should be allowed to take a comfortable position
of his choice.
• Organize Urgent transfer to higher centers in
ambulance and ensure doctor accompanies the
Figure-1.7: Chest compression for the child sick child.
• Depress the sternum 1/3 to 1/2 of the depth of the

chest. This corresponds to a 1 to 1-½ inches.
8. Circulation:
• Compress at the rate of approximately 100 times • After the Airway has opened, assess if a child
per minute. has a circulation problem you need to know:
• The ratio of chest compressions and ventilation The letter C in “ABCD” stands for Circulation,
should be 15:2, (Fifteen compressions followed by Coma and Convulsions.
two ventilation). • Assess the circulation for signs of shock
• Bag and mask ventilation is a very effective way of The most common cause of shock in children is
ventilation if done correctly. due to loss of fluid from circulation, either
• Setup an intravenous or an intraosseous line for use through loss from the body as in severe
of any drugs, where needed. diarrhoea or when the child is bleeding, or
through capillary leak in a disease such as
6. Use of Adrenaline severe Dengue fever. In all cases, it is important
to replace this fluid quickly. An intravenous line
Adrenaline 0.1 ml /kg (1: 10,000) intravenous can be must be inserted and fluids given rapidly in
used in a child who does not respond to initial children with shock without severe malnutrition.
ventilation and chest compressions and his pulses are
absent. Two such doses can be used 3-5 minutes apart.
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• Capillary Refill Time: To assess the circulation, 9.1. Young Infants:
take the child’s hand and feet in your own hand. If • Fluid bolus of 20ml/kg of normal saline over 20-
it feels warm, the child has no circulation problem 30 minutes. E.g. in a baby weighing 3 kg, 60 ml of
and you do not need to assess capillary refill or normal saline should be infused over 20-30
pulse. If the child’s hands and feet feel cold, you minutes. If no or partial improvement (i.e.
need to assess the capillary refill. tachycardia and CRT still prolonged), repeat a
bolus of 20 ml/kg of normal saline.
• If the signs of poor perfusion persist despite 2
fluid boluses, start vasopressor support, except in
infants with severe dehydration who should be
treated as per Plan C of diarrhea management.
9.2. Children above 2 months of age:

The recommended volumes of fluids to treat shock
Figure-1.8: Capillary refill time depending on the age/weight of child. If the child has
severe malnutrition, you must use of different fluid
a. Applying pressure to the nail bed for 3 seconds
and a different rate of administration and monitor the
b. Check the time to the return of the pink colour
child very closely. Therefore, a different regime is
after releasing the pressure
used for these children.
c. The capillary refill time is the time from release
of pressure to complete return of the pink color.
If it is more than 3 seconds, the child may be in 10. Coma and Convulsion
shock. Lift the limb slightly above heart level to
• C also represents “Coma and Convulsion”.
assess arteriolar capillary refill and not venous
• Assess the child for coma and convulsion
stasis.
• Weak & Fast Pulse: Evaluation of pulses is 10.1 Coma
critical to the assessment of systemic perfusion. For assessment of the conscious level of a child is, a
The radial pulse should be felt. If it is strong and simple scale (AVPU) is used.
not obviously fast the pulse is adequate; no further • A - Is the child Alert? If not,
assessment is needed.
• V - Is the child responding to Voice? If not,
• Weak and fast pulse is defined as:
In Infants - >160/min • P - Is the child responding to Pain?
In Children - > 140/min. • U - The child who is Unresponsive to voice (or
Thus if the child has cold extremities, a capillary refill being shaken) AND to pain is Unconscious.
time more than 3 seconds, and a fast weak pulse, then • A child who is not alert, but responds to voice, is
he or she is in shock. lethargic.
• An unconscious child may or may not respond to
9. Treatment of Shock: pain.
• If the child has any bleeding, apply pressure to • A child with a coma scale of “P” or “U” will
stop the bleeding. Do not use a tourniquet. receive emergency treatment for coma as
• Give oxygen. described below.
• Give fluids and other treatment for shock. 10.2. Convulsions
• The child must be seen to have a convulsion
during the triage process for emergency treatment
for convulsion.
Page 170
• Convulsion are recognized by the sudden loss of
consciousness associated with uncontrolled jerky
movements of the limbs and/or the face. There is
stiffening of the child’s arms and legs and
uncontrolled movements of the limbs. The child
may lose control of the bladder, and is
unconscious during and after the convulsion.
Figure-1.9: Position of Unconscious child (no trauma
suspected)
• Sometimes, in infants, the jerky movements may
be absent, but there may be twitching (abnormal
• If trauma is suspected
facial movements) and abnormal movements of
the eyes, hands or feet. - Stabilize the child while lying on the back.
- When the patient is not being moved, a sandbag
10.3. Treatment of Coma & placed on each side or a cervical collar can
Convulsions are similar and is splint the neck.
as follows: - Use bottles or rolled towels in case sandbags are
10.3.1. Manage the Airway not available as shown in the figure 1. 10 below.
a) Coma
Managing the airway is done in the same way
as treating any child with an airway or
breathing problem. This has been discussed
earlier. Give oxygen for the emergency setting.
b) Convulsion
To manage the airway of a convulsing child
gentle suction of oropharyngeal secretions Figure 1.10 Position of unconscious child (trauma
should be done & child put in recovery position suspected)
and oxygen started.
• Use the “log roll” technique to turn the child on the
Do not try to insert anything in the mouth to keep it side if the child is vomiting.
open.
10.3.2. Put the child in Recovery Position

Any unconscious child who is breathing and
keeping the airway open should be placed in the
recovery position.
This position helps to reduce the risk of vomit

entering the child’s lungs. Figure 1.11 “Log roll” technique
• If neck trauma is not suspected • Insertion of an oropharyngeal (Guedel) airway

- Turn the child on the side to reduce risk of - The oropharyngeal or Guedel airway can be
aspiration used in an unconscious patient to improve
- Keep the neck slightly extended and stabilize airway opening.
by placing the cheek on one hand
- Bend one leg to stabilize the body position
Page 171
- It may not be tolerated in a patient who is Table 4: Dose of Phenobarbitone for young infants
awake and may induce choking or vomiting.
- Guedel airways come in different sizes Inj. Phenobarbitone intravenous dose (200mg/ml)
(Guedel size 000 to 4). An appropriate sized Weight of Infant Initial dose Repeat dose
airway goes from the centre of the teeth
(incisors) to the angle of the jaw when laid on 2 kg or less 0.2 ml 0.1 ml
the face with the convex side up. 2 to 4 kg 0.3 ml 0.15 ml
• Caution: Do not use Diazepam for control of

convulsions in Neonates < 2 weeks
10.3.4. Management of Convulsions in infant more

than 2 weeks of age:
• Diazepam is the first drug used to stop convulsions

(anticonvulsant), if the child is convulsing in front of
Figure 1.12 Inserting an oropharyngeal airway you. No drug should be given if the convulsion has
in an infant: convex side up stopped.
• Diazepam can be given by the rectal or intravenous
- Select an appropriate sized airway
route.
- Position the child to open the airway as
• Rectal diazepam dose is 0.5mg/kg (0.1ml/kg) by
described above, taking care not to move the
tuberculin syringe or a catheter acts within 2 to 4
neck if trauma suspected.
minutes. Hold the buttocks together for a few
- Using a tongue depressor, insert the
minutes.
oropharyngeal airway the convex side up.
• Intravenous dose is 0.25mg/kg (0.05 ml/kg) over 1
- Re-check airway opening.
minute. Diazepam can affect the child’s breathing, so
- Use a different sized airway or reposition if
it is important to reassess the airway and breathing
necessary.
regularly.
- Give oxygen
Table 5: Dose of Diazepam
10.3.3. Management of Convulsions in infant
Diazepam given Diazepam given
up to 2 weeks of age: rectally IV
Age / weight 10 mg / 2 ml 10 mg / 2 ml
1. Secure IV access
solution solution
2. If blood sugar < 45 mg/dl, give 2 ml/kg 10%
dextrose Dose 0.1 ml/kg Dose 0.05 ml/kg
3. If seizures continue: IV 10% Calcium gluconate 2 weeks to 2
2ml/kg to be diluted in distilled water in months 0.3 ml 0.15 ml
proportion 1:1 over 10 minutes to be diluted in (<4 kg)
while monitoring heart rate (in young infants). 2 - <4 months
0.5 ml 0.25 ml
4. If seizures still continue: IV Phenobarbitone 20 (4 - <6 kg)
mg/kg in 5ml of 5% dextrose or saline over 20 4 - <12
min (Table 4) months (6 - 1.0 ml 0.5 ml
5. If no control: Repeat Phenobarbitone 10 mg/kg <10 kg)
till a total of 40 mg/kg 1 - <3 years
1.25 ml 0.6ml
6. If seizures continue: Give phenytoin 20 mg/kg (10 - <14 kg)
in 5 ml of normal saline over 20 min 3 - <5 years
1.5 ml 0.7ml
(14 – 19 kg)
Page 172
• If convulsions do not stop after 10 minutes of Table 6: IV fluids for severe dehydration
second dose of diazepam.
• Inj. Phenytoin can be given intravenously if access First give 30 Then give 70
AGE
has been achieved. 15 - 20 mg/kg Phenytoin is ml/kg in ml/kg in
diluted in about 20 ml of saline and given slowly
Infants (Under 12
(Not more than 1 mg/kg Phenytoin per minute). 1 hour* 5 hours
months)
• Alternatively, Phenobarbitone can be used in a
dose of 15- 20mg/kg IV (in 20 ml 5% dextrose or Children (12
saline) or IM. months up to 5 30 minutes* 2 ½ hours
• At this stage, seek help of a senior or more years)
experienced person, if available
* Repeat once if radial pulse is still very weak or
not detectable.
11. If there is high fever:
• Sponge the child with room-temperature water to • Reassess the child every 15-30 minutes. If
reduce the fever. hydration status is not improving, give the IV
drip more rapidly.
• Do not give oral medication until the convulsion
has been controlled (danger of aspiration) • Also give ORS (about 5 ml/kg/hour) as soon as
the child can drink: usually after 3-4 hours
(infants) or 1-2 hours (children).
12. Dehydration
Table 7: Volume of ORS per hour
The letter D in the ABCD formula stands for
Weight Volume of ORS
Dehydration.
solution per hour
Assess for severe dehydration. To assess if the child is
< 4 kg 15 ml
severely dehydrated ask for:
• Lethargic
4 - <6 kg 25 ml
• Child have sunken eyes
• Skin pinch take longer than 2 seconds to go back 6 - <10 kg 40 ml
If child has diarrhea with any two of the above signs
he is classified to have severe dehydration. 10 - <14 kg 60 ml
14 – 19 kg 85 ml
If IV treatment not possible, give ORS 20

ml/kg/hour for 6 hours (120 ml/kg/day) by NG tube
• Reassess an infant after 6 hours and a child
after 3 hours. Classify dehydration. Then
choose the appropriate plan (A, B, or C) to
continue treatment as you have learned in
IMNCI / F-IMNCI.
Figure 1.13 Skin pinch • Give oral antibiotic for cholera if child 2 is
years or older.
12.1 Treatment of severe dehydration • If possible, observe the child for at least 6
in an emergency setting hours after rehydration to be sure that the
mother can maintain hydration by giving the
12.1.1 Severe dehydration (without severe acute child ORS solution by mouth.
malnutrition)
• Start IV fluid immediately. If the child can drink,
give ORS by mouth while the drip is set up. Give
100 ml/kg Ringer’s lactate solution (or, if not
available, normal saline), divided as follows:
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• BEFORE Starting any rehydration
12.1.2. Severe dehydration with severe acute
treatment:
malnutrition
It is difficult to determine dehydration status in a - WEIGH the child (The weight should be
severely malnourished child, as the usual signs of taken on admission)
dehydration (Such as lethargy, Sunken eyes) may - MARK the edge of the liver and the
be present in these children all of the time, whether costal margin on the skin
or not they are dehydrated. - RECORD the respiration rate.
Signs of Dehydration • In addition, the following should be
• Lethargy recorded:
• Restless, irritable - Pulse rate.
- The capillary refill time
• Sunken eyes
• In malnourished child look out for:
• Thirsty
- Clinical signs of improvement and
• Skin pinch goes back slowly
- Clinical signs of over-hydration.
13. Management of Shock in

children with SAM
Give this treatment only if the child has signs of
shock and is lethargic or has lost consciousness
Figure 1.14 Severe dehydration with severe 13.1 Weight the child Estimate
acute malnutrition the weight if child cannot
Treatment of dehydration in the children with
be weighed or weight not
SAM without shock known
• If the child has had watery diarrhea or 13.2 Give oxygen
vomiting, assume dehydration and give ORS. 13.3 Make sure child is warm
WHO recommends use of ReSoMal, which is 13.4 Insert an IV line and draw
not available commercially. Use either WHO-
low Osmolarity ORS with potassium
blood for emergency
supplements (15 ml of potassium chloride laboratory
syrup added to one litre ORS) as mentioned in 13.5 Broad spectrum antibiotic
step 4 or ReSoMal prepared from WHO-low should be administered
Osmolarity ORS
Immediately to all SAM with septic shock
• Calculate amount of ORS to give
packed RBCs 10ml/kg should be given over
4-6 Hours if HB is less than 4 gm/dl or
Table-8: Give ORS as follows in amounts based
active bleeding. If there is no improvement
on the child’s weight
with fluid bolus start dopamine at
10pg/kg/min if there is no improvement in
How often to give ORS Amount to give next 24-48 hours upgrade antibiotics.
Every 30 minutes for the 5 ml/kg body weight
first 2 hours
Alternate hours for up to 5-10 ml/kg
10 hours
The amount offered in this range should be based
on the child’s willingness to drink and the amount
of ongoing losses in the stool. Starter (diet is
given in alternate hours during this period until the
child is rehydrated.
Page 174
Investigations
Give IV 10% Glucose (5ml/kg)
Give IV fluid 15 ml/kg over 1 hour of either ringer’s lactate in 5%
Dextrose or half-normal saline with 5% glucose
Measure the pulse and breathing rate at the start and every 5-10 minutes
If the child fails to

Improve after the first If the child deteriorates
15ml/kg IV During the IV
(RR increases by 5/min or PR
by 15 beats per min)
Repeat same fluid IV

15ml/kg over 1 hour more;
then
Stop the infusion and reassess
Give maintenance IV fluid

(4 ml/kg/hr) Assume
The child has septic shock
Start dopamine
Sign of improvement
(PR and RR fall)
Rehydration
Review antibiotic treatment
• Switch to oral or nasogastric rehydration

• With ORS 10ml/kg/hr up to 10hours Initiate re-feeding as soon as
• Initiate feeding with starter formula Possible
Figure-1.15: The management of shock in child with severe acute malnutrition is given
Page 175
13.6 How to give Dopamine (By • Add this amount of dopamine (ml) to make 10
ml of total fluid.
infusion pump)
• 0.1 ml/hour of this fluid gives 1 mcg/kg/minute
• Amount of dopamine (mcg) to be added = • To give 10 mcg/kg/minute gives infusion at the
weight in kgX6 rate on 1ml /hr
• To convert this dose into amount to ml of
dopamine divided by 40 (1 ml of dopamine=
40mg of dopamine)
Bibliography:
1. Kliegman R, Stanton B, Geme JS, Schor N. Nelson’s Textbook of Pediatrics. 20th Edition. Elsevier;
April 2015
2. Singh M. Care of Newborn. 8th Edition. CBS Publishers; 2015
3. Paul VK, Bagga A. Ghai Essential Pediatrics. 8th Edition. CBS Publishers; 2013
4. Cloherty JP. Manual of Neonatal Care (SAE). 7th Edition. Wolter Kluwer; 2012
5. India. Navjaat Shishu Suraksha Karykram, Basic Newborn Care and Resuscitation Program Training
Manual. Ministry of Health and Family Welfare. [cited 18 July 2016]
Available from: http://www.nihfw.org/pdf/NCHRC-Publications/NavjaatShishuTrgMan.pdf
Further reading:
1. Hashim, Muhammad. Et al. Common issues in the care of sick neonates. American family physician.
2002; 66 (9): p.1685.
2. Bhimani, Salima. Et al. Streamlining Pediatric Emergency Medicine at a Tertiary-care Hospital of a
Low- to Middle-income Country. Indian pediatrics. 2015; 52: 1021-1024.

Page 176
2. NEONATAL RESUSCITATION GUIDELINES
1. What is Neonatal
Resuscitation?
• Neonatal resuscitation means to revive or restore
life to a baby from the state of asphyxia.
• The following guidelines are intended to neonates
undergoing transition from intrauterine to extra
uterine life.
2. A rapid assessment of the

following 4 characteristics:
• Was the infant born full-term gestation
• Is the amniotic fluid clear of meconium and
evidence of infection
• Is the infant crying or breathing, colour of
baby?
• Does the infant have good muscle tone?
If the answer is to all 4 of these question is yes, the
infant does not need resuscitation and should not be
separated from mother.
Observation of breathing, activity, and colour should be
ongoing.
Figure-2.1: Neonatal Resuscitation Protocol
Page 177
Table-1: Immediate Newborn Care
Immediate Newborn Care
Assess by checking
 Is the baby term gestation?
 Is the amniotic fluid clear?
 Is the baby Breathing or crying?
 Does the baby have Good muscle tone?
If yes, provide Routine Care If no
 Place the baby on the mother's abdomen. Dry the baby with a warm clean sheet.
Do not wipe off vernix. Proceed for
 Wipe the, mouth and nose with a clean cloth. resuscitation
 Clamp the cord after 1-3 min and cut with a sterile instrument. Tie the cord with a
sterile tie.
 Examine the baby quickly for malformations/birth injury.
 Leave the baby between the mother's breasts to start skin-to –skin care.
 Support initiation of breastfeeding.
 Cover the baby's head with a cloth. Cover the mother and baby with a warm cloth.
 Place an identity label on the baby.
 Give Inj Vit K 1 mg IM (0.5mg for preterm).
 Record the baby's weight
 Refer if birth weight <1500g or has major congenital malformations or has severe
respiratory distress
Bibliography:
April 2015
5. India. Navjaat Shishu Suraksha Karykram, Basic Newborn Care and Resuscitation Program Training
Manual. Ministry of Health and Family Welfare [cited Jul 18 th 2016]
Available from: http://www.nihfw.org/pdf/NCHRC-Publications/NavjaatShishuTrgMan.pdf
Further reading:
1. American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and
Emergency Cardiovascular Care (ECC) of Pediatric and Neonatal Patients: Pediatric Basic Life
Support. 2006; volume 117: Issue 5.

Page 178
3. GUIDELINES FOR MANAGEMENT OF
NORMAL NEWBORN
• Most babies would require routine care; 5-10%
1. Care at Birth:
The four basic needs of ALL newborns at the time of may need assistance to establish adequate
birth and for the first few weeks of life are: breathing and therefore will need resuscitation.
i. To be warm • Deliver the baby onto a warm, clean and dry
ii. To breathe normally towel or cloth and keep on mother's abdomen or
iii. To be protected (prevent infection) chest (between the breasts).
iv. To be fed • Dry the Baby with a warm clean sheet. Do not
wipe off vernix
• Wipe both the eyes separately with sterile swab.
2. Newborn Care Corner • Clamp and cut the umbilical cord after 1 to 3
This is a space within the delivery room for minute, if baby is breathing well.
facilitating immediate care of the newborn. This
• Assess the baby's breathing while drying.
area is mandatory for all health facilities where
deliveries take place. • Examine the baby quickly for Malformation and
birth injury.
2.1 Equipment and supplies that • Leave the baby between the mother's breasts to
should be available in the corner: start skin-to-skin care for at least an hour.
• Cover the baby's head with a cap. Cover the
2.1.1 Equipment:
 Radiant warmer with bassinet mother and baby with a warm cloth.
 Suction equipment • Place an identity label/band/tag on the baby and
 Weighing machine mother
 Self-inflating resuscitation bag (500 ml) with • Encourage mother to initiate breastfeeding
masks (size 0,1) (within half an hour of birth).
 Oxygen source
 Laryngoscope (straight blade, size 0,1) 4. Ensuring 'WARM CHAIN'
 Wall Clock
 Room thermometer
4.1. At delivery
2.1.2 Supplies: • Ensure the delivery room is warm (25-28° C),
 Clean baby sheets with no draughts of air
 Sterile cord ties • Dry the baby immediately; remove the wet
 Sterile Gloves
cloth.
 Sterile blade/scissors
• Put the baby on the mother’s abdomen.
 Mucus extractors
• Cover the baby and mother with clean dry cloth
 Suction catheters (10F, 12F)
• Keep the baby in skin to skin contact with
 Feeding tube (6F, 8F)
mother on chest or abdomen
 Endotracheal tubes (3, 3.5 mm)
• Postpone bathing/sponging for at least 12 hours
 IV cannula (24G)
or next day
 Drugs (Inj. Epinephrine, Normal saline, Inj.
Vitamin K1) 4.2. After delivery
• Keep the baby clothed and wrapped with the
3. Immediate Newborn Care of
head covered.
a Normal Newborn at the • Avoid bathing especially in cool weather or for
time of Birth: small babies.
Page 179
• Keep the baby close to the mother 5.3. Immediate Cord Care
• Use kangaroo care for stable LBW babies and • Clamp the cord after 1-3 min of delivery and cut
for re-warming stable bigger babies with a sterile instrument
• Show the mother how to avoid hypothermia, • Tie the cord between 2 to 3 cms from the base
how to recognize it, and how to re-warm a cold and cut the remaining cord.
baby.
• Observe for oozing blood. If blood oozes, place
• The mother should aim to ensure that the baby's a second tie between the skin and first tie.
feet are warm to touch
• Do not apply any medication/substance on the
stump.
4.3 If mother and baby’s separation • Leave stump uncovered and dry.
is necessary, do the following
• Wrap the baby in a clean dry warm cloth and 5.4. Care of the eyes
place under a radiant warmer. If warmer is not • No routine eye care is required
available, ensure warmth by wrapping the baby • Do not instill any medicine in the eyes
in a clean dry warm cloth and cover with a
blanket. Ensure baby’s head, hands and feet are
covered.
6. Weighing the baby
• Weigh all babies before transfer from the
• Re-start Skin-to-skin contact as soon as mother
delivery room
and baby can be roomed-in
• Initiate breastfeeding within 1 hour
- Support mother to initiate breast feeding
5. Prevention of infections: within the first hour.
‘CLEAN CHAIN' - The baby’s first feed of colostrum is very
important because it helps to protect against
infections.
5.1. Clean delivery (WHO’s six - The baby can feed from its mother whether
cleans) she is lying down or sitting; baby and mother
must be comfortable
• Clean attendant's hands (washed with soap) • Do not give artificial teats or pre-lacteal feeds to
• Clean delivery surface the newborn e.g. sugar water or local foods or
• Clean cord- cutting instrument (i.e. razor, blade) even water.
• Clean string to tie cord
• Clean cloth to cover the baby
• Clean cloth to cover the mother 7. Examine the baby
7.1 A complete examination
5.2. After delivery should be performed within
• All caregivers should wash hands before
about 60 minutes after birth
handling the baby
• Count the number of breaths during one minute.
• Feed only breast milk
• Observe the movement of the limbs when
• Keep the cord clean and dry; do not apply
awake, their position when not moving and their
anything
tone.
• Use a clean absorbent cloth as a diaper/napkin
• Observe the skin color.
• Wash your hands after changing diaper/napkin.
• Inspect the following body areas for
Keep the baby clothed and wrapped with the
abnormalities: head, face, mouth and palate,
head covered
chest, abdomen, genitalia, anus, limbs and skin
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7.2 A Healthy baby should have • A mother who has had an epidural (spinal)
anesthesia may be able to start skin-to- skin
• Normal temperature, warm to touch, pink with
contact very soon after surgery
Weight > 2.5 kg
• These mothers will need additional assistance in
• Breathe easily at 40-60 breathes/minute
positioning and attaching the baby comfortably.
• Move arms and legs equally when active and
Breastfeeding in lying down position may be
rest with limbs flexed
more comfortable in the first few days
• Explain to mother the examination findings to
allay her concern.
• Document in case record and ask her to inform 10.2 HIV and newborn care at birth
you, in case any other concerns develop • Care of a baby born to HIV +ve mother at
subsequently. delivery should be no different from the care
already described.
8. Give Vitamin K • Standard safety precautions must be followed as
• Vitamin K will protect babies from serious
with any other delivery.
bleeding.
• Baby can have immediate skin-to-skin contact
• Give Vitamin K by intramuscular (IM) injection
as any other mother and baby.
1.0 mg for every newborn (0.5 mg for newborn
• Exclusive breast feeding is the recommended
<1000 gm).
feeding choice in their first 6 months,
• Encourage mothers to breastfeed their baby
irrespective of the fact that the mother is on
during the injection for comfort.
ART early (or) infant is provided with
9. Monitoring the Baby prophylaxis for 6 weeks.
Table-1: Monitoring the baby in the first hour after • If mother chooses replacement feeding, prepare
birth formula for the first few feeds. Ensure it is safe,
Parameter What to look for? affordable and sustainable for family.
Breathing Listen for grunting; • All other care (including cord care and eye care)
Look for chest in-drawing and fast remains the same.
breathing • Give oral dose of Nevirapine for six weeks to
Warmth Check to see if baby's feet are cold to the neonate as per national policy
touch (by using dorsum of your • Mother should be counseled regarding the mode
hands) of feeding before delivery and dangers of mixed
Color Evaluate the color of the trunk and feeding.
extremities 11 Postnatal Care of Normal
10. Special Situations Baby
10.1 Difficult delivery: Ideally, all pregnant women should be counseled
• Encourage Skin-to-skin contact and regarding the care of the baby during the antenatal
breastfeeding in difficult deliveries (caesarean period itself. This would help them to be mentally
section, instrumental and breech delivery) prepared to take care of their babies after birth.
• Breastfeeding can begin as soon as the mother is
comfortable and able to respond to her baby. It 11.1 Postnatal environment
does not have to be delayed • Ensure that the room is warm without air
• A mother who was given a general anaesthetic currents
agent should begin skin-to-skin contact as soon • Keep mother and baby close together in
as she is able to respond to her baby. This may same room and same bed
be initiated within one hour of birth • Provide bed nets to sleep
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11.2 The key areas of everyday care It is important to teach the mothers that the
umbilical stump should be left dry; they SHOULD
of a newborn baby include: NOT APPLY ANYTHING on the stump.
11.2.1 Breastfeeding 11.2.3 Ensuring hygiene
• Support exclusive breastfeeding on demand day • Wash the face, neck, and underarms of the baby
and night. daily.
• Ask the mother to get help if there is a • Do not bathe the baby before 24 hours of age or
breastfeeding difficulty. postponed it till the cord falls to avoid infections
• Assess breastfeeding in every baby before • In case of small babies, bathe only after the
planning for discharge. baby reaches a weight of 2000g.
• If the mother reports a breastfeeding difficulty, • If bath is given ensure room is warm and there
assess breastfeeding and help her with is no draught while changing clothes, washing
attachment and positioning. and bathing
• DO NOT discharge the baby if breastfeeding is • Use warm water for bathing
not established. • Thoroughly dry the baby, dress and cover after
bath
• Take extra precautions if the baby is small
• Wash the buttocks when soiled. Dry thoroughly.
• Use cloth diaper on baby's bottom to collect
stool. Dispose-off the stool as for woman's pads.
Wash hands after disposing.
• Do not apply ‘Kajal’ on eyes
11.2.4 Looking for danger signs and giving

treatment
Figure 3.1 Attachment • It is important that mothers, care givers and
health workers are able to recognize the signs
11.2.2 Keeping the cord healthy
and symptoms which indicate that the baby is
• Wash hands before and after cord care.
not well ('DANGER SIGNS').
• Put NOTHING on the stump.
• Early recognition of the danger signs will help
• Fold nappy (diaper) below the level of the
in identifying those babies who need urgent care
stump.
and treatment.
• Keep cord stump loosely covered with clean
clothes.
Danger Signs are -
• If stump is soiled, wash it with clean water and
• Not feeding well
soap.
• No movement
• Dry it thoroughly with clean cloth.
• Fast breathing (more than 60 breaths per
• Look for signs of infection (daily)
minute)
- Pus discharge from the cord stump
• Moderate or severe chest in-drawing
- Redness around the cord especially if there is
• Jaundice on day 1 or palms or sole stained
swelling
yellow (any age)
- High temperature (more than 37.5°C) or other
• Abnormal movements.
signs of infection
• Fever (temperature >37.5°C)
• Explain to the mother that she should seek care
• Temperature <35.5ºC or not rising after re-
if the umbilicus is red or draining pus or blood.
warming
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head Keep the room warm avoid direct draught
12. Ensure immunization of air
All babies should receive the following vaccines
immediately after birth before discharge from the • Keep next to mother for warmth; it promotes
health facility: lactation and mother-baby bonding
- BCG, • Encourage Kangaroo Mother Care (KMC) for
- OPV-0 Low birth weight babies
- Hepatitis B (Hep B-0)
13. Criteria for discharge from

a health facility
• Feeding well (suckling effectively) at least 8
times in 24 hours
• Baby has passed urine and stool.
• No danger signs
• Mother is confident to take care of baby
• Understands the need for follow up and danger
signs when to report early
Figure 3.2 Kangaroo Mother Care (KMC)
• For small baby below 2500gms: feeding well
and gaining weight adequately
14.4. Counsel and educate the
14. Advise on essential care for mother and family
• Build confidence of the family in taking care of
neonate at discharge baby at home
14.1. Feed breast milk • Ensure that the family understands importance
• Breast milk is the best and is the only food baby of administering prescribed medicines for the
needs for first six months Mother needs to whole duration.
breastfeed day and night, at least eight times in • Educate mother when to report for follow up
24 hours Mothers need to take nutritious meals after discharge
and should drink lots of clean water • Educate mother when to report early if there is
• For a small baby who finds difficult to suckle, worsening of condition at any time after
express breast milk and collect in a clean cup to discharge
feed the baby with a paladai, cup or spoon • Educate mother for signs of well-baby feeds on
breast, active behavior, pink extremities and
14.2. Keep clean trunk & extremities are warm to touch.
• Wash your hands with clean water and soap • Ensure baby is gaining weight on follow up.
before every feed and after visiting toilet and • Advise for timely immunization
handling baby's faeces / urine.
• Keep the surroundings clean
15. Management of Common
• Keep the cord stump clean, do not apply
anything on cord Clinical Conditions in
Newborns
14.3. Keep warm • There are several phenomena after birth that are
• Keep the baby well wrapped in a clean dry cloth normal and mothers only need reassurance.
or blanket (in cold season) Cover baby's head These include:
with part of cloth / blanket or put a cap on the
Page 183
- Developmental variations & Physiological • Weight loss of 6-8% (10-12% in preterm
conditions infants) in the first few days of life is normal
- Knowledge of developmental variations, and most infants regain their birth weight by 10-
physiological conditions and their evolution in
newborns is important for advising and assuring
the mother. Mothers observe their babies very
carefully and are often worried by minor
physical peculiarities, which may be of no
consequence and do not warrant any therapy.
15.1. Mastitis neonatorum

• Engorgement of breasts occurs in term babies of
both sexes on the third or fourth day and may
last for days or even weeks which is due to
persistence of maternal hormones for some 14 days.
time. Figure 3.3: Erythema neonatorum
• Local massage, fomentation and expression of
milk should not be done as it may lead to 15.5. Bowel disorders.
infection. Mother should be reassured that this
• No medication should be prescribed for passage
regresses on its own.
of stools after each feed (exaggerated
gastrocolic reflex) as this is normal in some
15.2. Vaginal bleeding babies. From 3rd to 14 days many exclusively
• Vaginal bleeding may occur in female babies breastfeed babies pass loose stools (10-15
about three to five days after birth which is times/day) without illness/dehydration. These
because of withdrawal of maternal hormones. are transitional stools and require no
The bleeding is mild and lasts for two to four medication.
days.
• Additional Vitamin K is unnecessary.
15.6. Delayed passage of urine.
• Non-passage of urine by 48 hours after birth
15.3. Mucoid vaginal secretions may suggest urinary tract anomalies. Such
• Most female babies have a thin, grayish,
babies need to be investigated. Crying before
mucoid, vaginal secretion, which should not be
passing urine is normal.
mistaken for purulent discharge
• Jitteriness is abnormal only when it is excessive
or persists even during feeding and then it may
15.4. Toxic erythema or Erythema suggest hypoglycemia or hypocalcaemia.
neonatorum:
• This is an erythematous rash with a central 15.7. Dehydration fever.
pallor appearing on the second or third day in
• Transitory moderate fever (up to 38.50C)
term neonates which begins on the face and
usually during the second or third day of life in
spreads down to the trunk and extremities in
summer months in an active baby, who sucks
about 24 hours. This should be differentiated
well, is normal and responds to lowering the
from pustules which need treatment.
environmental temperature.
• It disappears spontaneously after two to three
days without any specific treatment. The exact
cause is not known.
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15.8. Excessive crying. • Subconjunctival hemorrhage: Semilunar arcs
of sub-conjunctival hemorrhage is a common
• Most baby cry when either they are hungry
finding in normal babies. The blood gets
or are having discomfort such as due to full
reabsorbed after a few days without leaving any
bladder before passing urine, wet napkin,
pigmentation.
nose block, etc. Excessive inconsolable
crying or high-pitched crying is indicative of Figure 3.5: Subconjunctival hemorrhage
meningitis or any other painful
inflammatory conditions.
15.9. Umbilical granuloma.

• A red flesh-like nodule at the base of
umbilical cord can be managed by cautery
with Silver Nitrate or application of
common salt for 3 to 4 days.
16. Normal phenomena in new • Epstein Pearls: These are white spots,
usually one on either side of the median
born raphe of the hard palate. Similar lesions may
• Peeling skin: Dry skin with peeling and
be seen on the prepuce. They are of no
exaggerated transverse sole creases is seen in all
significance.
post-term and some term babies.
• Sucking callosities: The presence of these
• Milia: Yellow –white spots on the nose or face
button like, cornified plaques over the centre
due to retention of sebum, are present in
of upper lip has no significance.
practically all babies and disappear
• Tongue Tie: It may be in the form of a
spontaneously.
fibrous frenulum with a notch at the tip of
• Stork bites (Salmon patches or nevus
the tongue. This does not interfere with
simplex): These are discrete, pinkish- gray,
sucking or later speech development.
sparse, capillary hemangiomata commonly seen
• Non retractable prepuce: The prepuce is
at the nape of neck, upper eyelids, forehead and
normally non-retractable in all male
root of the nose. They invariably disappear after
newborn babies and should not be diagnosed
a few months.
as phimosis. The urethral opening is often
• Mongolian blue spots: In babies of Asiatic
pinpoint and is visualized with difficulty.
origin irregular blue areas of skin pigmentation
The mother should be advised against
are often present over the sacral area and
forcibly retracting the foreskin.
buttocks, though extremities and rest of the
• Hymenal tags: Mucosal tags at the margin
trunk may also be affected. These spots
of hymen are seen in two-third of female
disappear by the age of six months.
infants.
• Umbilical hernia: Umbilical hernia may
manifest after the age of two weeks or later.
Most of these disappear spontaneously by
one or two years of age.
Figure 3.4: Mongolian blue spots
Page 185
Bibliography:
April 2015
Further reading:
1. Vora S, Chandran S, Rajadurai VS, Hussain K. Hyperinsulinemic Hypoglycemia in Infancy: Current
Concepts in Diagnosis and Management. Indian Pediatr. 2015 Dec; 52 (12): 1051-9.
2. Edmond KM et al. Delayed Breast feeding Initiation Increases Risk of Neonatal Mortality. Pediatrics.
2006 Mar; 117 (3): e380-6.
3. Government of India, Ministry of Health and Family Welfare. INAP: India Newborn Action Plan.
September 2014. [Last Accessed on 9 October 2016].
Available from: http://www.newbornwhocc.org/INAP_Final.pdf

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Page 186
4. CARE OF AT-RISK NEONATES
initial improvement, further care can be provided at
1. An 'at-risk' neonate has one home
or more of the following
features: 2. The care of at-risk babies is
• Weight 1500-2499g
outlined below:
• Temperature (axillary) 36.0°C-36.4°C 2.1. Warmth:
• Babies with moderate or severe hypothermia Grading of hypothermia
who respond to warming • Normal temperature : 35.5-36.5°C
• Cried late (>1min) but within 5 minutes of birth • Cold stress : 36.4-36.0°C
• Sucking poor, but not absent sucking reflex • Moderate hypothermia : 35.5-32°C
• Depressed sensorium, but is arousable • Severe hypothermia : <32°C
• Respiratory rate of over 60 per minute, but no
chest retractions
• Jaundice present, but no staining of palms/soles
• Presence of any one of the following:
• Diarrhea or vomiting or abdominal distension
• Umbilicus draining pus or pustules on skin
• Fever
The care of 'at-risk' neonate should be initiated at the
health facility itself under direct supervision. After
Table 1: The steps are dependent up on the current temperature of the baby:
Temperature Management
Normal - Prevent hypothermia

temperature - Wrap the baby in layers of clothing
- Cover the head and limbs
- Place the baby in direct contact with mother
- In winter months, the room may have to be warmed with heater, etc
Cold stress - Treat hypothermia
(temperature - Wrap the baby with extra layers of clothing
36.0°C and 36.4°C) - Cover the head and limbs
- Place the baby in close contact with the mother, preferably skin-to skin
In winter months, heat the room with a heater , etc.
Hypothermia - Requires immediate exposure to a radiant
(Temperature heat source (such as radiant warmer) or heater
<36.0°C) - Other measures same as for cold stress
Page 187
2.2. Stabilization 2.3. Feeds
Most of these babies do not require stabilization other The baby is started on direct breast feeding. If not
than prevention for hypothermia as above. If there is sucking well, she is provided expressed breast milk
occasional apnea, physical stimulation may be by spoon or paladai. Occasionally, expressed breast
provided. milk may have to be given by gavage feeding.
2.4. Specific therapy

Table 2: Some simple conditions can be readily treated at the health facility and later at home.
Condition Treatment
Umbilical redness - Local application of 1% Gentian Violet
And Discharge - Syrup Amoxicillin 1.25ml TDS x7days
Skin pustules Local application of 1% gentian violet.
Syrup Amoxicillin 1.25ml TDS x7days
Pneumonia (Respiratory
rate >60/min, no chest Syrup Amoxicillin 1.25ml TDSx7days)
retractions)
2.5. Monitoring Communication with the family, especially the

The following signs should be monitored every two mother is very important during the management of
hours: at-risk and sick neonates.
• Signs to be monitored Communication with the family
• Temperature 1. Reassure the mother and family.
2. Prepare a note regarding baby's condition and
• Convulsion
care.
• Sucking
3. If baby improves and is to be sent home, explain
• Bleeding
care of the baby at home.
• Sensorium
4. If baby does not improve or worsens, explain
• Diarrhea
the need for referral and care during transport.
• Respiration
• Vomiting
• Apnea
3. FOLLOW - UP
• Advice about follow-up visits
• Abdominal distension
• Keep the baby warm
• Cyanosis
• Provide exclusive breast milk feeding
• Continue the prescribed treatment
2.6. Re-evaluation • Observe progress of baby
After stabilization and/or specific therapy, the baby
has to be re-evaluated for improvement. The two • Counsel and educate the mother and family
cardinal signs of improvement are: • Follow-up:
- The temperature will become normal (36.5°C - A home visit by the health worker (ASHA) one
37.5°C) and day after evaluation at hospital is desirable.
- The baby will accept feeds well. Thereafter the baby should be seen within 24
hours and than on 3rd,7th,14th,21st,28th and 42nd
day. Child has to visit every 3rd month up to 1yr.
2.7. Communication
Page 188
Bibliography:
Further reading:
1. Hashim, Muhammad. Et al. Common issues in the care of sick neonates. American family physician.
2002; 66 (9): p.1685.
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Page 189
5. CARE OF SICK NEONATES
1. A sick neonate is the one 2.2. Management of severe
who has any of the following hypothermia
• Keep under radiant warmer
features:
• Weight <1500 g • Reduce further heat loss
• Temperature <36°C despite warming for one • Infuse IV 10% Dextrose @ 60ml/kg/day
hour • Inject Vitamin K 1 mg and 0.5 mg for baby
• Cried after 5 minutes of birth weighing less than 1000gm IM.
• Absent sucking • Provide oxygen
• Not arousable • Consider and assess for sepsis
• Respiratory rate more than 60/min with chest
retractions 3. Prevent hypothermia: warm
• Apnea or gasping respiration chain
• Central cyanosis Baby must be kept warm at all times right from birth.
• Jaundice staining palms/soles The "warm chain" is a set of 10 interlinked
• Convulsions procedures carried out at birth and later
• Bleeding • Warm delivery room (>25°C)
• Major malformation • Warm resuscitation
• Presence of two of the following • Immediate drying
- Diarrhea or vomiting or abdominal distension • Skin-to-skin contact between baby and the
- Umbilicus draining pus mother
- Multiple skin pustules • Breast feeding
- Fever • Bathing and weighing postponed
Also remember that if an 'at-risk' neonate does not • Appropriate clothing and bedding
improve while being observed under your care, he is • Mother and baby together
also considered a sick neonate.
• Warm transportation
• Training/ awareness raising of health-care
2. Grading and management of provider
hypothermia
Baby who is cold to touch both centrally and 4. Expression of breast milk
peripherally or temperature is less than 35.5°C Breast milk expression is required for optimal
feeding of newborns for preterm, low birth weight
2.1. Management of hypothermia and sick newborns that cannot breastfeed but can
• Record the actual body temperature tolerate assisted feeding.
• Re-warm a hypothermic baby as quickly as
possible: 4.1. Teach the mother to:
• Severe hypothermia – Radiant warmer • Wash hands with soap and water before
• Mild to moderate hypothermia- Kangaroo expression. Hold, handle or cuddle the baby
mother care or Radiant warmer • Sit comfortably and hold the clean container
• If hypothermia still persists despite taking above near the breast
measures, infection should be suspected • Put thumb and index finger on the breast at the
rim of the areola opposite each other. Support
the breast with other three fingers.
Page 190
• Press thumb and index finger slightly inward • Cover the container of EBM with a clean cloth
towards the chest wall or a lid
• Press the breast between the fore-finger and • EBM can be kept at room temperature for 8
thumb. Press and release, press and release. This hours and in the refrigerator for 24 hours
should not hurt • EBM stays in good condition longer than animal
• Press the areola in the same way from the sides, milk. Do not boil the EBM. For warming, place
this ensures that milk is expressed from all the container in a bowl of warm water
segments of the breast • Before feeding, gently shake the container or
• Avoid rubbing or sliding fingers along the skin use a stirrer to recombine the separated fat
• Express one breast for at least 3-5 minutes until globules with the rest of the milk
the flow slows; then express the other side; and • Feed with cup or spoon or paladai, never feed
then repeat on both sides with bottle
• To express breast milk adequately it may take
20-30 minutes
5. Assisted feeding of low birth
weight neonates
5.1. Newborns that require assisted
feeding:
• Preterm <34 weeks or birth weight <1800 g
• Babies having mild respiratory distress
Figure 5.1: Expression of breast milk • Babies with inability to feed at breast or by
Katori-spoon/paladai
4.2. Storing expressed breast milk • Oro-facial defects/malformation (Cleft lip or
(EBM) palate)
Table 1: Guidelines for the modes of providing fluids and feeding
Birth weight (grams) < 1200 1200-1800 >1800
Gestation (weeks) < 30 30-34 >34
Initial feeding Intravenous fluids try Gavage, try Katori-spoon Breastfeeding, if
gavage feeds, if not sick if not sick unsatisfactory, give
Katori-spoon feeds
After 1-3 days Gavage Katori-spoon Breastfeeding
Later (1-3 weeks) Katori-spoon Breastfeeding Breastfeeding
After some more time Breastfeeding Breastfeeding Breastfeeding
(4-6 weeks)
5.2. Mode for providing fluids and 5.3. Techniques of assisted feeding:
feeds 5.3.1 Gavage feeding
• Breast milk is the ideal feed for low birth • Place an oro-gastric feeding catheter of size
weight babies. 5-6 Fr after measuring the correct insertion
• Those unable to feed directly on the breast length from ala of nose to tragus and from
can be fed Expressed Breast Milk (EBM) by tragus to midway between xiphisternum and
gavage OR Katori-spoon or paladai. umbilicus
Page 191
• Check correct placement by pushing in air with • Allow milk flow into baby's mouth slowly,
10 ml syringe and listening with stethoscope allowing him to actively swallow, avoiding the
over upper abdomen spill
• Attach 10 ml syringe (without plunger) at the • Repeat process till required amount has been fed
outer end of the tube, pour measured amount of • Try gently stimulation if baby does not actively
milk and allow milk to trickle by gravity. Close accept and swallow the feed
outer end of tube after feeding • If unsuccessful, switch back to gavage feeds.
Place baby in left lateral position for 15 to 20
minutes to avoid regurgitation
• Leave oro-gastric tube in situ
6. Intravenous fluid therapy for
• Pinch the oro-gastric tube during withdrawal newborn:
• Measure pre-feed abdominal girth just above the
umbilical stump. Do not attempt pre-feed 6.1 Criteria for starting intravenous
aspirates fluids among newborns
• Evaluate baby for ileus, if abdominal girth
• Neonates with lethargy and refusal to feed
increases by >2cm from baseline
• Moderate to severe breathing difficulty
• Routine refeeding gastric aspirates are not
• Babies with shock
recommended
• Babies with severe asphyxia
• Abdominal distension with bilious or blood
stained vomiting
6.2. Choice of intravenous fluids

• Determine required volume of fluid as per birth
weight and age (Table 2)
• Use 10% Dextrose for initial 48 hours of life
• After 48 hours, if baby is passing urine, use
Figure 5.2: Gavage Feeding commercially available IV fluids such as lsolyte-
P
5.3.2 Katori-spoon/paladai feeds Table 2: Fluid requirements of newborns
• Place the baby in a semi-upright posture Day of Amount of fluids required
• Place the milk filled spoon at the corner of life (ml/kg/day)
mouth Birth weight Birth weight
> 1500 g <1500 g
1 60 80
2 75 95
3 90 110
4 105 125
5 120 140
6 135 150
Day 7 150 150
onwards
• If the premixed solution is not available or baby

Figure 5.3 Paladai feeding
requires higher GIR (Glucose infusion rates)
- Take normal saline (NS) 20 ml/kg body weight
Page 192
- Add remaining fluid volume as 10% Dextrose • If the blood glucose is more than 150 mg/dl on
- Add 1 ml KCL/100 ml of prepared fluid. two consecutive reading: Change to 5%
Dextrose solution-measure blood glucose again
in three hours
6.3. Administration of IV fluid • Weigh the baby daily. If the daily weight loss is
• Use micro-drip infusion set (where 1 ml = 60 more than 5% increase the total volume of fluid
micro drops) by 10 ml/kg body weight for one day
• In this device, ml of fluid per hour is equal to • If there is no weight loss in the initial 3 days of
number of micro-drops per minute life, do not give the daily increment
e.g. 6ml/hr = 6 micro-drops/minute • If there is excessive weight gain (3-5%) decrease
• Calculate rate of administration, monitor to the fluid intake by 15-20 ml/kg/day
ensure that micro-dropper delivers required rate • Check urine output: Normally a baby passes
• Change the IV infusion set and fluid bag every urine 5-6 ml/kg/day
24 hours
• Before infusing IV fluid, carefully check 7.Management of hypoglycemia
• Expiry date of the fluid
• Hypoglycemia in newborns is defined as blood
• Seal of the infusion bottle or bag
glucose levels less than 45 mg/dl
• Fluid is clear and free from any visible particles
• Establish an IV line. Infuse a bolus of 2 ml/kg
body weight of 10% dextrose slowly over 5 min
6.4. Monitoring of babies receiving • If baby had convulsions, give bolus of 4-5 ml/kg
IV fluid: of 10% dextrose
• Inspect infusion site every hour for redness and • If an IV line is not available, administer 2 ml/kg
swelling body weight of 10% dextrose by gastric tube
• If redness and/or swelling is present, stop • Start infusion of dextrose at the daily
infusion, remove cannula, and establish a new IV
maintenance volume to provide at the rate of 6
line in a different vein
• Check the volume of fluid infused, compare to mg/kg/min
the prescribed volume and record all findings • Measure blood glucose after 30 min and then
• Measure blood glucose every nursing shift, i.e. every four to 6 hrs
6-8 hours • If blood glucose < 25 mg/dl:
• If the blood glucose is less than 45 mg/dl, treat - Repeat bolus of dextrose as above
for low blood glucose - Increase to infusion rate of 8 mg/kg/min
Bibliography:
Further reading:
1. Rozance PJ, Hay WW. Hypoglycemia in newborn infants: Features associated with adverse
outcomes. Biol Neonate. 2006;90(2):74-86.
2. Kumar V, Shearer JC, Kumar A, Darmstadt GL. Neonatal hypothermia in low resource
settings: a review. J Perinatol. 2009 Jun;29(6):401-12.

Page 193
6. Management of Low Birth Weight Babies
• Nearly 75 percent neonatal deaths and 50 percent
infant deaths occur among the low birth weight
neonates.
• Even after recovering from neonatal complications,
some LBW babies may remain more prone to
malnutrition, recurrent infections, and
neurodevelopmental handicaps. Figure 6.2: Preterm vs term baby- Breast nodule
• Low birth weight, therefore, is a key risk factor of
adverse outcome in early life. 1.1.4 Breast Nodule: Breast nodule measures less
than 5mm in preterm neonates and 5 mm or more in
1. Low Birth Weight term babies.
• Low birth weight (LBW) baby is the one who
weighs less than 2500 g at birth.
• Low birth weight may result from either
prematurity (gestational age <37 weeks) or
intrauterine growth retardation (IUGR), which is
also called small – for – date baby (SFD).
1.1 Preterm babies:
Preterm babies have distinct physical features that help Figure 6.3: Preterm vs term baby- Sole Creases
in their recognition These are:
1.1.1 Skin: The skin of preterm neonate is thin, 1.1.5 Sole Creases: Anterior one third of the sole
transparent and gelatinous whereas that of a term reveals a deep transverse skin crease in preterm neonates
neonate is thick gelatinous and keratinized. and in term neonates they are present over the anterior
two-thirds.
1.1.2 Hair: The back of the preterm babies has
abundant growth of fine hair called lanugo. 1.1.6 External Genitalia: In males, the scrotum does
not have rugae and testes are not descended into the
scrotum. In female infants, the labia are widely
separated, not covering the labia minora, resulting in the
prominent appearance of the clitoris.
Figure 6.1: Preterm vs term baby- Hair
Figure 6.4:
1.1.3 Ear Cartilage: The external ear or the pinna is
Preterm vs term
soft and devoid of cartilage in preterm neonates and baby- External
hence, it does not recoil back promptly on being folded. Genitalia
In a term baby, there is instant recoil.
Page 194
1.2 Small for date babies/ Small for
gestational age (SFD/SGA) 3. Problems of SGA neonates
The basic underlying problem amongst them is in-
Small-for-dates neonates have an emaciated look
utero undernutrition and hypoxia. They are prone to:
and loose folds of skin because of lack of
subcutaneous tissue. These are particularly • Fetal distress, meconium passage in utero and
prominent over the buttocks and the thighs. They birth asphyxia.
look alert and often plethoric. • Hypothermia.
• Hypoglycemia
• Congenital malformations.
2. Problems of preterm
neonates 4. Treatment:
The basic underlying feature of the preterm LBW Indication for hospitalization are:
infant is immaturity of its organ system. They are
• Birth weight of less than 1800 g;
prone to develop
• Gestational age of less than 34 weeks;
• Asphyxia necessitating resuscitation.
• Neonate who is not able to take feeds from the
• Hypothermia
breast or by cup (Katori) and spoon (irrespective
• Feeding problems - Preterm neonates less than of birth weight and gestation);
34 weeks of gestation cannot coordinate sucking • A sick neonate (irrespective of birth weight and
and swallowing. Therefore, they are unable to
gestation).
feed from the breast.
• Respiratory distress syndrome (RDS): Preterm
4.1. Keeping LBW Babies warm:
• Room temperature should be kept between 28-
babies especially those less than 34 weeks have
300C.
immature lungs, hence they develop RDS
characterized by rapid and labored respiration, • Baby should be provided skin to skin contact
in-drawing of the chest, grunting and cyanosis. care (KMC) in the following ways:
- Provide privacy to the mother. If mother is
• Apneic spells: Because of the immature
not available, skin to skin contact may be
respiratory control mechanisms these babies
provided by the father or any other adult.
also have a tendency for apneic spells. In an
- Request the mother to sit or recline
apneic spell the baby stops breathing; develops
comfortably.
slow heart rate and turns blue.
- Undress the baby gently, except for cap,
• Intra-Ventricular Hemorrhage (IVH): Preterm
nappy and socks.
infants also have immature vascular bed around
- Place the baby prone on mother's chest in an
the brain ventricles. These delicate vessels may
upright and extended posture, between her
rupture and cause intra-ventricular hemorrhage.
breasts, in Skin to Skin contact; turn baby's
• Hypoglycemia - Immature metabolic pathways
head to one side to keep airways clear.
of preterm infants predispose them to develop
- Cover the baby with mother's blouse, 'pallu'
hypoglycemia.
or gown; wrap the baby-mother duo with an
• Hyperbilirubinemia
added blanket or shawl.
• Infection is another major problem among
- Breastfeed the baby frequently.
preterm babies and indeed an important killer
• If possible, warm the room (>250C) with a
because they are immuno-compromised hosts.
heating device.
• Retinopathy of Prematurity (ROP): Preterm
• Skin to Skin contact is the most practical,
infants given excess oxygen may develop
preferred method of warming a hypothermic
blindness because of damage to the immature
infant in a primary health care facility. If not
retina.
possible:
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- Cloth the baby in 3-4 layers, cover head • In order to promote lactation and enable the
with a cap and body with a blanket or a baby to learn sucking, all babies on gavage or
shawl; hold baby close to caregiver's body, Katori-spoon feds should be put on the breasts
OR before each feed for 5 to 10 minutes. This will
- Place the baby under overhead radiant promote lactation and enable the baby to learn
warmer, if available. how to suck.
• Keep the young infant warm on the way to the • When shifting a baby from one mode of feeding
hospital to another, be very careful. Introduce in new
- By Skin to Skin contact OR mode for only some of the feeds to begin with.
- Clothe the baby in 3-4 layers, cover head • The feeding of every baby should be
with a cap and body with a blanket or a individualized. The above recommendations
shawl; hold baby close to caregiver's body. should only serve as broad guidelines.
4.2. Nutrition & Fluids • Ensure use of expressed breast milk & start with
• Neonates weighing less than 1200 g. or those small volume, and gradually build up.
having sickness should receive intravenous fluid • Most LBW babies weighing more than 1800 g
initially. are able to feed directly from the breast. In a
• Enteral feeds should be introduced gradually by stable, growing LBW baby daily intake of feeds
gavage as the baby's acute problem begins to should be gradually built up to 180-200ml/kg.
settle. • LBW babies should be fed every 2-3 hours
• Infants weighing 1200-1800 g and not having starting at 2 hours of age.
significant illness should be put on gavage feeds
initially.
Table 1: Guidelines for the modes of providing fluids and feeding

Age Categories of neonates
Birth weight (gm) < 1200 1200-1800 > 1800
Gestation (weeks) < 30 30-34 > 34
Initial IV fluids Gavage feeds Breast feeds
Triage If unsatisfactory, give
Gavage feeds if not sick cup-spoon feeds
After 1-3 days Gavage feeds Cup-spoon feeds Breast feeds
Later (1-3 wks) Cup-spoon feeds Breast feeds Breast feeds
After some time Breast feeds Breast feeds Breast feeds
(4-6 wks)
Note: baby loses up to 1 to 2 percent weight every day

i. On the first day the fluid requirements range amounting to 10 percent cumulative weight loss
from 60 to 80 ml/kg. during the first week of life. Birth weight is
ii. The daily increment in all the groups is around regained by the 14th day.
15 ml per kg till 150 ml/kg is reached. • SGA-LBW babies who are otherwise healthy
iii. Adequacy of therapy is indicated by weight should not have any appreciable weight loss at
pattern in the expected range. all and they should start gaining weight early.
• It is desirable to weigh all LBW babies at 2
4.2.1 Judging adequacy of nutrition weeks (to check regaining of the birth weight), 4
• The key measure of optimal feeding is the weeks (to ascertain a weight gain of at least
weight pattern of the baby. A preterm LBW 200-300g) and then every month. Hospitalized
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LBW babies should be weighed every day on sick LBW babies however, should receive these
the same weighing machine. vaccines only on recovery.
• Excessive weight loss, or inadequate weight • Vitamin A 1000 IU orally daily – from 1-week
gain indicates inadequate feeding, cold stress, age onwards
excessive insensible water loss or systemic
illness (like anemia, sepsis, late metabolic
5. Immunization in special
acidosis etc). circumstances
5.1. Immunization in preterm
4.3. LBW babies require close
infants:
monitoring and follow up of In general, all vaccines may be administered as per
• Growth monitoring- head circumference and
schedule according to the chronological age
weight
irrespective of birth weight or period of gestation.
• Developmental assessment and early
Very low birth weight / preterm babies can be given
stimulation
immunization, if they are stable otherwise.
• Intraventricular haemorrhage screening by
ultrasound cranium on day 1,3,7& at 4-6 weeks.
• Screening tests for hearing –at discharge
5.2 Children receiving corticosteroids:
• Retinopathy of pre maturity screening at 1 • Children receiving IV immunoglobulin and oral
month of age corticosteroids in high doses (Prednisolone 1-2
• Screening for osteopenia of prematurity mg/kg/day) for more than 14 days should not
receive live virus vaccines until the steroid has
been discontinued for at least one month.
4.4. Vitamin Supplements: • Killed vaccines are safe but may not be
• All LBW Babies should receive intramuscular completely effective in such situations.
Vitamin K at birth. Every new born should • Patients on topical or inhaled steroids should not
receive Injection Vitamin K 1 mg and 0.5 mg, be denied their age appropriate vaccine.
Intramuscular, as per the birth weight > = 1000
gm and < 1000 gm respectively. 5.3 Children awaiting splenectomy:
• All pre-terms < 2000 gm should receive oral Immunization with Pneumococcal, Hib, and
Vitamin and mineral supplement in doses Meningococcal vaccine should be initiated a few
shown below: weeks prior to splenectomy.
• Multivitamin preparation 0.3-0.6 ml (5-10
drops) / day (which usually provides vitamin A
5.4 Vaccination in children with
of 1000 IU/day and vitamin D 400 IU/day)
• Calcium 100-200 mg/kg/day HIV infection:
• Phosphorous 50-100 mg/kg/day. • Immune response may be suboptimal as it
depends on the degree of immunodeficiency at
All these supplements to be given till at least that point of time.
6 months of age. • Re-administration of childhood immunization
may be considered when their immune status
• Iron should be started at a dose of 1mg/kg/day has improved following anti-retroviral therapy.
at 4 weeks of age and provided till 12 months of
age.
5.5 Lapsed immunization:
• Vaccination in LBW Babies
There is no need to restart a vaccine series regardless
• If the LBW baby is not sick, the vaccination
of the time that has elapsed between individual doses.
schedule is the same for as the normal babies. A
In case of unknown or uncertain immunization status,
Page 197
however, it is appropriate to start the schedule as for • Mortality of LBW babies is inversely related to
an unimmunized child. gestation and birth weight and directly to the
severity of complication.
5.6. Minor illnesses • In general, over 90% Low birth weight babies
e.g. fever, diarrhea, respiratory infections and who survive the newborn period have no
malnutrition should not be considered as neurodevelopment handicaps.
contraindications to immunization. • Therefore, essential care of the LBW neonates
is a highly rewarding experience.
6. Prognosis
Bibliography:
Further reading:
1. Saili A. Essential care of Low Birth Weight Neonates. Indian Pediatrics, 2008 Jan;45(1):13-5.
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Page 198
7 Assessment of Neonatal Sepsis
Neonatal sepsis is one of the three major causes of 1.5 CNS:
neonatal mortality. Sepsis is largely preventable.
Fever, seizures, blank look, high pitched cry,
1. Clinical manifestations of excessive crying/irritability, neck retraction, bulging
neonatal sepsis fontanel
1.1 Non-specific: 2. Laboratory diagnosis of a

Lethargy, refusal to suckle, poor cry, not arousable, newborn with sepsis
comatose Sepsis Screening: Any of two tests that come
positive out of the following five tests strongly
1.2 Gastro-intestinal: indicate presence of sepsis:
1. Leukopenia (TLC/ Total leucocyte count
Abdominal distension, diarrhea, vomiting, poor
<5000/cmm)
weight gain
2. Neutropenia (ANC/ Absolute neutrophil count
<1800/cmm)
1.3 Cardiovascular: 3. Immature neutrophil to total neutrophil (I/T)
Hypothermia, poor perfusion, shock, bleeding and ratio (>0.2)
sclerema 4. Micro ESR/Erythrocyte sedimentation rate
(>15mm 1st hour)
1.4 Respiratory: 5. Positive CRP/ C-reactive protein
Cyanosis, tachypnea, chest retractions, grunt,

apnea/gasping
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3. Approach to newborns at- risk of sepsis
Neonate at risk of sepsis
Symptomatic Asymptomatic
High suspicion Low suspicion Do sepsis screen

Blood culture
Blood culture Sepsis Screen Negative Positive

Blood Culture Take blood culture
and start antibiotics
Start antibiotic Negative screen Repeat sepsis screen

after 12 hr after 12 hr
Positive screen
Negative screen Duration - according

to Clinical Course&
culture*
Duration according Monitor clinically Monitor clinically

To clinical course
Culture sterile - 7-10 days Culture Positive - 10-14 days
• In suspected or confirmed meningitis, add

4. Antibiotic therapy for a
Cefotaxime with an aminoglycoside
newborn with sepsis 4.2. Antibiotic therapy of
4.1. Choice of antibiotics neonatal sepsis
• Antibiotic therapy should cover the common Following table provides the antibiotics and dosages
causative bacteria, namely Escherichia coli, of antibiotics for newborn sepsis
Staphylococcus aureus and Klebsiella
pneumoniae
• A combination of Ampicillin and Gentamicin is
recommended for treatment of sepsis and
pneumonia
Page 200
4.2.1 Septicemia of Pneumonia
Table-1: Antibiotic Management for Septicemia of Pneumonia

Antibiotic Each dose Frequency Route Duration
<7 days age >7 days age
Inj Ampicillin or 50 mg/kg /dose 12 hourly 8 hourly IV 7-10 days
Inj Cloxacillin 50 mg/kg /dose 12 hourly 8 hourly IV 7-10 days
and
Inj Gentamicin or 5 mg/kg/dose 24 hourly 24 hourly IV 7-10 days
Inj Amikacin 15 mg/kg/dose 24 hourly 24 hourly IV 7-10 days
4.2.2 Meningitis
Table-2: Antibiotic management of Meningitis

Antibiotic Each dose Frequency Route Duration
<7 days age >7 days age
Inj Ampicillin or 100 mg/kg/dose 12 hourly 8 hourly IV 3 weeks
And
Inj Gentamicin 2.5 mg/kg/dose 12 hourly 8 hourly IV 3 weeks
OR
Inj Gentamicin or 5 mg/kg/dose 12 hourly 8 hourly IV 3 weeks
And
Inj Amikacin 2.5 mg/kg/dose 12 hourly 8 hourly IV 3 weeks
• Start oxygen by hood or mask, if cyanosed or

5. Supportive care of a
grunting
Newborn with sepsis • Provide gentle physical stimulation, if apneic.
• Provide warmth, ensure consistently normal Provide bag and mask ventilation with oxygen if
temperature breathing inadequate
• Start intravenous line • Avoid enteral feed if hemodynamically
• If CFT >3 seconds, infuse normal saline 10 compromised, give maintenance IV fluids
ml/kg over 20-30 minutes, repeat the same 1-2 • Consider use of Dopamine if perfusion is
times, if perfusion continues to be poor persistently poor
• Infuse 10% dextrose 2 ml/kg stat • Consider exchange transfusion if there is
• Inject Vitamin K1 mg intramuscularly sclerema
Page 201
6. Summary of commonly used dosage in Neonates
Drug Dose Route
Ampicillin Age <7 days: 50 mg/kg/dose, q 12 hour IV
Age >7 days: 50 mg/kg/dose, q 8 hour
Gentamycin Sepsis/ pneumonia IV
5 mg/kg/dose, q 24 hour
Meningitis
Age <7 days: 2.5 mg/kg/dose, q 12 hour
Age >7 days: 2.5 mg/kg/dose, q 8 hour
Amikacin <7 days: 15 mg/kg/dose, q 24 hour IV
Cefotaxime <7 days: 50 mg/kg/dose, q 12 hour IV
>7 days: 50 mg/kg/dose, q 8 hour
Chloramphenicol 12 mg/kg/dose, q 12 hour IV
Aminophylline 5 mg/kg loading, IV
then 2 mg/kg/dose q 8-12 hour
Vitamin K 1 mg IM
Phenobarbitone 20 mg/kg loading over 10-15 minutes Loading IV Then IV,
then 3-4 mg/kg q 24 hour IM or oral
Phenytoin 15-20 mg/kg loading over 10-15 minutes IV
then 5 mg/kg q 24 hour
Dopamine/ Dobutamine 5-20 micro g/kg/minute IV continuous
Bibliography:
April 2015
5. Engorn B, Flerlage J. The Harriet Lane Handbook. 20th Edition. Saunders; 2014
Further Reading:
1. Isaacs D. Neonatal Sepsis: The Antibiotic crisis. Indian Pediatrics. 2005 Jan;42(1):9-13.

Page 202
8. Treatment of Respiratory Distress
in Newborn
Dexamethasone => 6mg IM 12 hourly for 2
1. Incidence: Days
Increases as Gestation age decreases
(NOTE: validity of this injection is for one
28 weeks => 60 %
week and do not repeat after that if more delay
28-34 weeks => 30%
in delivery, because it affects brain of newborn).
>34 weeks => 5-10%
2. Prevention: 3. Assessment after delivery:
Can be prevented by giving Antenatal steroid to • Gestational age
mother
• Temperature
• Indicated for those who are at risk for preterm
• Heart rate
delivery in next 8 days
• SaO2
• Treatment for Prevention
• Capillary refill time
Betamethasone 12 mg IM once a day for 2 days
OR
Figure 8.1 Silverman –Anderson score

4 Scoring of distress
Page 203
Interpretation: - Monitor ABG
• SA score=> 3 Oxygen by hood • W/F Apnea
• 3 -7 => CPAP ventilation - Increase CPAP BY 1-2cm up to 8cm water
• >7 Mechanical ventilation pressure
- And FiO2 up to 100%
4.2. Investigation:
- Start Mechanical ventilator: if with FiO2
• X ray chest: PA view
of 100% and CPAP of 8cm
• Septic screening
• Blood culture
• Serum electrolyte
• ABG
• Blood glucose
5. Management: • SA score is > 7

In general: OR
• Maintain temperature =36.5 -37.50C • Baby with persistent Apnea
• Restrict fluid to 2/3 maintenance • Other
• Maintain SaO2 88-95% - watch for diuresis
- watch for clinical improvement
• Antibiotics if septic screen +ve
- give maintenance of fluid
Main management
• If FiO2 requirement is < 30% & SA score <3
Oxygen by hood 5.4 Fluid management
- Watch for diuresis • If CRT is more than 3
- If improvement noticed – give maintenance • Give 10ml/kg NS bolus
- fluid and start feed • Monitor liver size
• If FiO2 Requirement is > 30% & SA score >3 • If require give Dopamine 5-10 micro gr/kg/min
- Start CPAP OR
- CPAP –Begin with 4-6 cm of water pressure Dobutamine 10 micro gr/kg/min
and use FiO2 10 % more than required
Bibliography:
April 2015
Further reading:
1. Prabhakaran P. Acute Respiratory Distress Syndrome. Indian Pediatrics. 2010 Oct;47(10):861-8.
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Page 204
9. MECONIUM ASPIRATION SYNDROME
• Vertex or breech presentation
1. Management in delivery
• Birth Asphyxia
room
1.1 If MAS, watch for – 1.2 Perineal suction – With Dee Lee mucus
• Colour /consistency of meconium Aspirator at delivery of Head of baby
• Gestational Age
Figure-9.1: Indication of Endotracheal intubation

MAS
-----------------> IF baby’s cry is vigorous
If cry is not vigorous No Intubation
ROUTINE CARE
Intubation ------------------ Meconium not retrieved
Under cord suction No suction
Meconium retrieved
Continue suction HR < 100/min
HR > 100 /min IPPR
Continue suction
Page 205
2. Management in NICU
2.1 Assessment of baby: 3. Investigation:
• CBC
• Gestational age
• ABG
• r/o IUGR
• X-ray chest
• r/o Umbilical cord /nail/skin staining
• Blood culture
Downe 0 1 2
score
Respiratory <60 60-80 >80 4. Supportive management
rate • Pass infant feeding tube=> gastric lavage
Grunting NO Audible Audible
• Iv fluid initially if required
with without
• Antibiotic if respiratory distress OR
Stethoscope Stethoscope
• If septic screen is positive
Cyanosis NO In room air With 40%
• Treat complication
oxygen
• Ventilator if required along with surfactant
Air entry good decrease Markedly
decrease
Retraction NO mild severe 5. Complication
• Atelectasis
2.2 Interpretation • Hypoxic Ischaemic encephalopathy
score • Pneumothorax
1 -3 => mild respiratory distress => Oxygen by • PPHN (Persistent primary pulmonary hyper
hood tension) requiring nitrous oxide and sildenafil
4-6 => moderate respiratory distress => CPAP
ventilation
>6 => severe respiratory distress => Ventilator
Bibliography:
Further reading:
1. Wiedemann JR1, Saugstad AM, Barnes-Powell L, Duran K. Meconium Aspiration Syndrome.
Neonatal Network. 2008 Mar-Apr;27(2):81-7.
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Page 206
10. BLEEDING NEONATE
1. Common causes 2.1.1 Antenatal infection
e.g. TORCH Thrombocytopenia
1.1. GI bleeding
• Swallowed maternal blood 2.1.2 Drugs given to mother
• Hemorrhagic disease of New Born Phenytoin
• Sepsis Phenobarbitone Hemorrhagic
• Stress ulcer Aspirin / Anticoagulant disease of NB
• Platelet defect
• Clotting factor deficiency 2.1.3 Bleeding in mother = Thrombocytopenia
e.g. ITP /SLE
1.2. Umbilical cord Birth Asphyxia DIC
Trauma
• Slipped ligature
• Vitamin K deficiency
2.2. Time of Bleeding
1.3. Skin: 2.2.1 < 24 hrs = Swallowed maternal blood
hemorrhagic disease of NB
Petechiae
• Sepsis 2.2.2 > 24 hrs = Classical hemorrhagic
disease of NB
• Platelet disorder
Ecchymosis • Sepsis /DIC
• Sepsis • Platelet abnormality
• Clotting factor deficiency • Trauma
• Liver dysfunction
1.4 Occult blood 2.3. Other clinical features
Cephalohematoma Preterm • Petechiae
Intra Ventricular Hemorrhage Vit..K deficiency • Ecchymosis
Subdural Hemorrhage sick neonate • Pallor
• Jaundice
2. Approach • Hepatosplenomegaly
• Bulging Anterior Fontanelle.
Maternal History INCREASE RISK OF
Page 207
3. Investigation
Figure-10.1: Apt .test:
1 ml gastric aspirate + 5ml distilled water
Centrifuge to form Supernatant
4 ml of Supernatant + 1ml NAOH 1%
Change of colour to Colour remains to pink

Yellow /brown
Maternal blood Fetal blood
Table 1: Differential Diagnosis

Platelet PT PTT
Thrombocytopenia ↓ N N
Hemorrhagic N ↑ ↑
disease of
newborn
Clotting factor N N ↑
deficiency
DIC ↓ ↑ ↑
4. Management
A) If APT test shows –Maternal blood =>parental C) Treat for sepsis / DIC / primary disease
counseling Antibiotics:
B) If APT test shows –fetal blood • Ampicillin 50 to 100 mg/kg in divided doses IV.
a) Injection Vitamin K 1mg IV stat • Gentamycin 5 mg/kg in divided doses iv.
b) If PT/PTT increases OR in sick neonate • If not responding to these then start higher
10-15ml /kg FFP (If required repeat after 12hrs) antibiotics such as Ceftriaxone, Meropenem etc.
c) If Hb<10 gm% = Give fresh blood transfusion • Treatment of DIC.
d) If platelet <50000 in sick Neonate • Treatment of primary disease.
OR <25000 in Healthy Neonate
Platelet transfusion 10-20ml/kg
Bibliography:

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Page 208
11. JAUNDICE IN THE NEWBORN
1. Introduction:
Hyperbilirubinemia is the commonest morbidity in the
neonatal period and 5-10% of all newborns require
intervention for pathological jaundice. Nearly 60% of
term newborn becomes visibly jaundiced in the first
week of life. In most cases, it is benign and no
intervention is required.
2. Physiological jaundice:
Figure 11.1: Levels of Jaundice
Jaundice attributable to physiological immaturity of
neonates to handle increased bilirubin production.
Visible jaundice usually appears between 24-72 hours of
4.2 Clinical determination of
age. Total serum bilirubin (TSB) level usually rises in jaundice by Kramer’s criteria
full-term infants to a peak of 6 to 8 mg/dL by 3 days of
age and then falls. A rise to 12mg/dL is in the Area of body Range of serum
physiologic range. In premature infants, the peak may be bilirubin (mg%)
10 to 12 mg/dL on the fifth day of life, possibly rising Head and neck 4-8
over 15 mg/dL without any specific abnormality of Upper trunk 5-12
bilirubin metabolism. Lower trunk and thigh 8-16
Arms and lower limbs 11-18
3. Pathological jaundice: Palms and soles >15
• TSB concentrations exceeds 5 mg/dl on first day of
life in term neonate, 10 mg/dL on second day, or
12-13 thereafter.
5. Investigations:
• Any TSB elevation exceeding 17 mg/dL. Following investigations must be done in a case of
• Appearance of jaundice within 24 hours, peak TSB neonatal jaundice
levels above the expected normal range, • Serum bilirubin direct and indirect.
• Presence of clinical jaundice beyond 3 weeks and • Blood grouping of mother and child ABO and Rh.
conjugated bilirubin (dark urine staining the clothes • Direct Coomb’s test in infant.
and light colored stool). • Hematocrit and peripheral smear for RBC
morphology and reticulocyte count.
4. Signs & Symptoms: • Indirect Coomb’s test in mother if she is Rh
4.1 Clinical examination of jaundice: negative
• The newborn should be examined in good daylight. 6. Complication:

• The skin should be blanched with digital pressure
6.1 Transient encephalopathy:
and the underlying color of skin and subcutaneous
tissue should be noted. Early bilirubin induced neurologic dysfunction is
• Dermal staining in newborn progresses in a transient and reversible. This is suspected by increasing
cephalo-caudal direction. Newborns detected to lethargy with rising bilirubin levels but recovery
have yellow discoloration of the skin beyond the following or prompt exchange transfusion.
legs should have an urgent laboratory confirmation
for levels of TSB.
Page 209
6.2 Kernicterus.: cortex is generally spared, but 50 % of babies have
extra-neuronal lesions with necrosis of renal tubular
This term has been traditionally used to describe the cells, intestinal mucosa and pancreatic cells. They
pathological findings of bilirubin toxicity within the may manifest as gastrointestinal hemorrhage or
brain. This includes staining and necrosis of neurons hematuria. Clinically, kernicterus is described in
in the basal ganglia, hippocampal cortex, Sub- phases, which may progress over 24 hours to 7 days:
thalamic nuclei and cerebellum followed by gliosis of
these areas, should the baby survive. The cerebral
FIGURE-11.2: DIAGNOSTIC WORKUP FOR HYPERBILIRUBINEMIA IN NEWBORN
Clinical jaundice
Measure bilirubin (Total serum bilirubin-TSB)
Bilirubin >12mg/dl Bilirubin <12mg/dl

Age <24hrs old Age >24hrs old
(Pathological) (Physiological)
Coomb’s test observe
POSITIVE NEGATIVE Follow bilirubin

Rh
ABO Direct bilirubin
Kell
Less than 2mg%
Hct
NORMAL OR LOW HIGH POLYCYTHEMIA
RBC morphology
Reticulocyte count
ABNORMAL NORMAL
Spherocytosis Enclosed hemorrhage
ABO incompatibility Breastmilk jaundice
Red cell enzyme defect Hypothyroidism
Alpha thalassemia Crigler-Najjar syndrome
Gilbert syndrome
Page 210
7. Treatment modalities of
hyperbilirubinemia
• Hydration
• Phototherapy (Do not keep in sunlight).
• Exchange transfusion
• Drugs to increase conjugation.
7.1. HYDRATION
Continued and frequent breast feeding 8-10 times/day
7.2. Phototherapy
• Special blue lights to be used
• 45cm distance between baby and phototherapy
unit, in conventional phototherapy unit and keep
the baby as close as possible around 15-20 cm in
LED phototherapy unit for intensive phototherapy. Figure 11.3 Phototherapy
• Eyes and genitalia should be covered
• Double surface phototherapy is preferred 7.3 Points to remember
• Watch for side effects (diarrhoea, skin rash, • Try to establish diagnosis before instituting
hyper/hypothermia) phototherapy by carrying out necessary
• Healthy, term newborn (>37 weeks) investigations.
TABLE 1- Guidelines for Phototherapy according to • Check blue light functioning; life of these light is
AAP 1500-2000hrs (approx. 3 months). Keep lights at
Age Consider Phototherapy distance of 18’’ from the baby.
(hours) Phototherapy TSB (mg/dl) • When blue lights are not available four pairs of
TSB (mg/dl) white tube light may be used instead.
< 24 • Change the position of baby after every 2 hrs.
25-48 >12 >15 • Babies can be taken out of phototherapy for breast
49-72 >15 >18 feeding
• Monitor baby’s temperature 2 hourly.
>72 >17 >20
• Monitor fluid balance – daily weight and urine
NOTE: TSB-Total serum bilirubin output. Increase fluid as necessary.
7.2.1. Based on birth weight and health of the • Shield the eyes in both sexes to prevent the retinal
newborn damage and genitals in male to prevent mutation
TABLE 2- Phototherapy indications defect in adulthood.
Birth weight Healthy Sick newborn • Monitor rise or fall of bilirubin every 12 hourly.
(grams) Newborn TSB • Do not give phototherapy for direct
TSB (mg/dl) (mg/dl) hyperbilirubinemia.
<1000 5-7 4-6 7.4. Exchange transfusion.
1001-1500 7-10 6-8
1501-2000 10-12 8-10
7.4.1 Choice of blood
2001-2500 12-15 10-12 • If baby and mother is Rh–ve, use only Rh-ve
blood.
TERM
>2500 15-18 12-15 • Always cross match donors blood with both
mothers and baby’s blood.
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7.4.2 Criteria for Exchange Transfusion • In LBW babies, indirect bilirubin> (weight in
• Cord bilirubin more than or equal to 4.5mg% and g)/100
Hb < 11g% • Exchange earlier at level of 2 mg% less for
• Rate of rise of bilirubin >1mg/dl despite following Criteria- Sepsis, RDS, Asphyxia,
phototherapy Acidosis, Hypoglycemia.
Bibliography:
April 2015
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12. MANAGEMENT OF SURGICAL NEONATE
• Chest deformities
1. Neonatal surgical problems
• Congenital Lobar emphysema
1.1. Major • Vascular Ring
• Tracheoesophageal fistula • Orthopedic
• Diaphragmatic hernia
• CTEV (Cong. Talipus Equino Varus)
• Intestinal Obstruction
• Neural tube defect • Developmental dysplasia of hip
• Anorectal malformation • Other
• Clavicle fracture
1.2 Others • Humerus fracture
1.2.1 Orofacial • Femur fracture
• Cleft lip
• Cleft palate
• Choanal Atresia
2. Transporting baby with
• Pierre robin sequel surgical problems
• Laryngeal web • Write specific diagnosis
1.2.2 Gastrointestinal • Write, inform /Delivery details
• Esophageal Atresia • Give radiological, blood or other investigation
• Cong. Hypertophic Pyloric Stenosis (CHPS) report
• Gastrochiasis • Give Inj. Vitamin K to all babies at birth
• Abdominal wall defect • Stabilize and Manage hypoglycemia /
• Omphalocele hypocalcemia / hypothermia or other metabolic
• Omphalitis problems
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Figure 12.1 Gastrochiasis Figure 12.2 Neural tube defect Figure 12.3 Cleft lip
Bibliography:
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13. VITAMIN A DEFICIENCY
6 to 12 months------1,00,000IU Vitamin A orally
1. Introduction >12 months----------2,00,000IU Vitamin A orally
Vitamin A Deficiency Symptoms –
Next day-------------------------Same age specific dose
• Delayed dark adaptation
At least 2 weeks later-------Same age specific dose
• More prone for intestinal, respiratory and
urogenital infections 3.2 Important aspects of Vitamin A
• If the child more than 1 year of age and
2. Classification weighing less than 8 kg., then Vit. A dose is
XN------Night Blindness
1,00,000 IU to avoid Hypervitaminosis A
X1A----Conjunctival Xerosis
• Give oil based preparation
X1B-----Bitot’s Spots
• Bottles have solution strength of 1, 00,000IU
X2-----Corneal Xerosis
Vitamin A/ml
X3A---Corneal Ulceration <1/3
• Cold chain is not required.
X3B---Corneal Ulceration >1/3
• Shelf life of unopened opaque container is 2
XS----Corneal Scarring
years.
XF---Xerophthalmic Fundus
• Opened liquid is to be used in 6 to 8 weeks.
• Capsules are partially protected against loss of
potency.
3.3 Treat
• Night blindness, conjunctival xerosis, Bitot
spots, Corneal xerosis, Corneal ulceration,
Keratomalacia in all except women of
reproductive age group.
• In acute corneal lesion, patient should be
referred to hospital on emergency basis.
• High dosages of Vit A can cause pseudo-tumour
cerebri which will manifest as vomiting
headache and bulging anterior fontanelle
Figure 13.1 Manifestation of Vit A Deficiency 3.4 Corneal Xerophthalmia
i. Topical Antibiotic ointment (Tetracycline 1%,
3. Treatment immediately after eye ointment, Tobramycin eye ointment 3%
diagnosis twice a day)
ii. Eye protection with dark shades
3.1 Age wise doses of Vitamin A
<6 months-----------50,000IU Vitamin A orally
Bibliography:
Further Reading:
1. Arlappa N. et. al. Prevalence of Clinical and Sub-Clinical Vitamin A Deficiency Among Rural
Preschool Children of West Bengal. Indian Pediatrics. 2011 Jan;48(1):47-9.
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14. RICKETS
1. Introduction 3.1 Serology
Metabolic disease of childhood in which the osteoid, • Serum calcium - normal or decreased,
the organic matrix of bone fails to mineralize, due to • Serum phosphorus - decreased,
interference with calcium metabolism. • Alkaline phosphatase - increased,
2. Causes 3.2 Urine Exam
• Vitamin D deficiency Urinary calcium - decreased
• Malabsorption
3.3 X- ray:
• Renal disease
• Celiac disease • Generalized demineralization
• Hepatic osteodystrophy • Loss of transverse trabeculae
• Anti - epileptic drugs
• No sub-periosteal resorption of bone

4 Treatment
• Single oral dose of 6 lakh IU of Vitamin D
• 2nd dose after 3 to 4 weeks (if no sclerotic
Figure 14.1: Clinical features in Rickets change is seen in x-ray)
• If the child responds to above treatment
maintenance dose of 400 IU of vitamin D is
given once Serum alkaline phosphatase is
normal, consider corrective surgery, if any.
• Calcium - 0.5 to 3 gm/day for 3 months
• Vitamin D - 10,000 IU/day once a month
• High protein diet
It is important to note that Rickets is a disease of

Figure 14.2: Swelling in wrist due to Rickets growing bones so it manifests in recovery phase of
Severe Acute Malnutrition (SAM)
3. Investigations
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Bibliography:
Further reading:
1. Cashman KD. Vitamin D in childhood and adolescence. Postgrad Med J. 2007 Apr; 83(978): 230–
235.
2. Pettifor JM. Rickets and vitamin D deficiency in children and adolescents. Endocrinol Metab Clin
North Am. 2005;34(3): 537–553
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15. MANAGEMENT OF CHILDREN WITH
ANAEMIA
Nutritional anaemia results from deficiency of iron,
1. Introduction folic acid and vitamin B12. Children having anaemia
Mild to Moderate anaemia is a common co-morbidity
due to folic acid and/or B12 deficiency
in children attending health facility for various
(megaloblastic anemia) may have hyper pigmentation
conditions. Hence, anemia/pallor should be looked
of knuckles and occasionally bleeding manifestations
for in each patient attending the health facility.
due to thrombocytopenia.
Severe anemia in a child is suggested by the presence
The onset of anaemia in young children is generally
of severe palmar pallor and may be associated with a
after 6 months of age. Before this, iron in breast milk
fast pulse rate, difficulty in breathing, or confusion or
is sufficient to meet the needs of a breastfed child.
restlessness. Nutritional anaemia is the most common
In India, diets for children in the age group 6–23
cause of anaemia in children.
months are predominantly plant-based and provide
insufficient amounts of micronutrients to meet the
recommended nutrient intakes.
Table 1: Clinical assessment of anaemia in children

less than 5 years
Findings on anaemia in children
History Examination
• Duration of symptoms • Severe palmar pallor

• Usual diet (before the • Skin bleeds (petechial
current illness) and/or purpuric spots)
• Family circumstances • Lymphadenopathy
(to understand the • Hepato-Splenomegaly
child’s social • Signs of heart failure
background) (gallop rhythm, raised
• Prolonged fever JVP,
• Worm infestation respiratory distress,
• Bleeding from any site basal crepitations)
•Lymph node
enlargement
• Previous blood
transfusions
• Similar illness in the
family (siblings)
2. Facility level management
Any child reporting to any facility (PHC level and
above) with any illness will be assessed clinically by
the attending Medical Officer for anaemia routinely All children referred from field to health facility due
and should undergo Hb estimation if found to be to palmar pallor will undergo Hb level estimation
anaemic clinically before initiating treatment
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Children will be categorised as having mild, levels and will be managed as per Table below.
moderate and severe anaemia on the basis of Hb
Table 2: Treatment of Anaemia
Level of HB Treatment Follow-up Referral
No Anaemia (>11 20 mg of elemental iron and 100 mcg of folic acid in biweekly regimen
gm/dl)
Mild Anaemia (10–10.9 3 mg of iron/ Kg/ day for 2 Follow-up every 14 In case the child has not
gm/dl) months days by ANM responded to the treatment of
And Hb estimation after anaemia with daily dose of iron
Moderate Anaemia completing 2 months for 2 months, refer the child to
(7–9.9 gm/dl) of treatment to the FRU/DH with F-IMNCI
document Hb>11 trained MO/ Paediatrician /
gm/dl Physician for further
investigation
Severe Anaemia Refer urgently to DH/FRU
(<7 gm/dl)
Note: a known case of haemoglobinopathy and anaemia in

After completion of treatment of anaemia and these cases should be treated as per the standard
attaining Hb level >11.5 gm/dl, the IFA treatment guidelines, by the attending physician, as
supplementation to be resumed. per the merit of the individual case.
Treatment of anaemia with iron should be withheld in
case of acute illness, severe acute malnutrition and in
2.1 Dose of IFA syrup
Table 3: Dose of IFA syrup for anaemic children 6 months–5 years
Age of Child Dose and Frequency
6 months–12 months (6–10 kg) 1 ml of IFA syrup Once a day
1 year–3 years (10–14 kg) 1.5 ml of IFA syrup Once a day
3 years–5 years (14–19 kg) 2 ml of IFA syrup Once a day
2.2 Management of severe anemia at hospital level

2.2.1 History & examination
Table 4: Management of severe anaemia at FRU/DH (as per F-IMNCI) in children 6 months–5 years and 5-
10 years
History to be taken for Examination for
• Duration of symptoms • Severe palmar pallor
• Usual diet (before the current illness) • Skin bleeds (petechial and/or purpuric spots)
• Family circumstances (to understand the child’s • Lymphadenopathy
social background) • Hepato-splenomegaly
• Prolonged fever • Signs of heart failure (gallop rhythm, raised
• Worm infestation • JVP, respiratory distress, basal crepitation)
• Bleeding from any site
• Any lumps in the body
• Previous blood transfusions
• Similar illness in the family (siblings)
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2.2.2 Investigation & blood transfusion indication
Table 5: Investigation & Management
Investigations Indication for Blood Transfusion Blood Transfusion
• Full blood count and • All children with Hb ≤4 gm/dl If packed cells are available, give 10
ml/kg over 3–4 hours preferably. If
• Examination of a thin film • Children with Hb 4–6 gm/dl with not, give whole blood 20 ml/kg over
for cell morphology any of the following: 3–4 hours.
• Blood films for malaria • Dehydration
parasites
• Shock
• Stool examination for ova,
cyst and occult blood • Impaired consciousness
• Heart failure
• Deep and laboured breathing
• Very high parasitaemia
(>10% of RBC)
Bibliography:
Further reading:
1. Zlotkin S. Current Issues for Prevention and Treatment of Iron Deficiency Anemia. Indian
pediatrics. 2002 Feb;39(2):125-9
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16. MUMPS
1. Introduction:
• Orchitis - Occurs in older patients. Occurs one
Mumps is swelling of parotid glands due to infection week following parotitis with painful swelling
of the parotids by mumps virus. Apart from parotids, of testes. Illness lasts for about 4 days.
it affects some other vital organs and systems in the Testicular atrophy may follow in l/3 patients
body and can have serious complications with risk of with rare affection of fertility.
morbidity and mortality. Therefore, it is important to • Oophoritis in females may rarely occur.
know the course of illness, various complications, • Pancreatitis - Epigastric pain, tenderness,
early detection for prompt management, and vomiting, fever are suggestive. Laboratory
preventive measures. evidence of raised amylase confirms the
2. Signs & Symptoms: diagnosis.
• Thyroiditis - May follow after one week in
Un-immunized host gets infected from a case. Patient
adults with development of anti-thyroid
is infective l-2 days before appearance to 2-3 days
antibodies.
after disappearance of parotid swelling. Incubation
• Myocarditis – Mild to moderate myocarditis
period ranges between 2-3 weeks. 30-40% infections
with ST changes on ECG is found in some older
are sub clinical. After entry through air, the virus
patients. Chest pain, bradycardia and fatigue are
multiplies in respiratory tract and reaches all organs
presenting symptoms in a patient with mumps
via blood. Prodromal symptoms are in the form of
fever, muscle pains, neck pain, and malaise. • Deafness - transient or permanent unilateral or
bilateral nerve deafness may follow mumps.
• Arthritis - Migratory poly arthralgia or even
arthritis may be seen. These complications
should be treated symptomatically.
5. Management:
Treatment:
Figure 16.1: Mumps: Parotid Swelling • Mainly symptomatic with paracetamol(10-
15mg/kg) and frequent gargling with warm
3. Investigation: saline.
Diagnosis: is mainly clinical more suggestive with • Orchitis is treated by bed rest and local support.
the history of contact. Typical painful tender bilateral • Watch for evidence of complications. If arthritis
parotid swelling with systemic symptoms is occurs, prednisolone (1 to 2 mg/kg in divided
diagnostic. doses for 5 to 7 days and then tapered).
4. Complication: 6. Prevention:
• CNS- Aseptic meningitis-meningoencephalitis
along with parotitis or 10 days later. Meningitis MMR vaccine - combination of mumps, measles,
is indistinguishable from any other meningitis. and rubella offers above 95% protection. Primary
CSF study shows white blood cell pleocytosis immunization at the age of 15 months, followed by
predominance of lymphocytes. The CSF revaccination at l0 years.
glucose content is normal in most patients, but a Since it is a live viral vaccine, immuno-compromised
moderate hypoglycorrhachia (glucose content hosts should not be vaccinated.
20-40 mg/dl.) may be seen in 10-20% of the Isolation of the affected child is not useful to prevent
patients. The CSF protein content is normal or spread to other children in usual contact. However,
mildly elevated.
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fresh contacts like guest children can be protected if lifelong protection against another, therefore, such
the affected child is isolated from them. children do not benefit from any immunization later.
Children usually recover from mumps in about 10-12
days- First arrack of mumps almost always gives
Bibliography:
April 2015
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17. SEVERE ACUTE MALNUTRITION (SAM)
1. Introduction 3. Assessment of severely
Malnutrition remains one of the most common causes malnourished child
of morbidity and mortality among children. The high
A good history and physical examination is required
case fatality rates among severely malnourished
for deciding the treatment but always start the
children can be reduced by using standardized and
emergency treatment first. The details of history and
easily implementable protocols.
examination can be recorded later.
2. Criteria for hospital
admission
• Weight for height/length <-3 z score of median
of WHO child growth standards or
• Mid-arm circumference < 11.5 cm or
• Presence of nutritional (bipedal) edema.
If weight-for-height or weight-for-length cannot be
measured, use the clinical signs for visible severe
wasting
Table 1: Severe Acute Malnutrition
History Examination
• Recent intake of food and • Anthropometry- weight, height/ length, mid arm circumference
fluids • Oedema
• Usual diet (before the current • Pulse, respiratory rate
illness) • Signs of dehydration
• Breastfeeding • Shock (cold hands, slow capillary refill, weak and rapid pulse)
• Duration and frequency of • Severe palmar pallor
diarrhoea and vomiting • Eye signs of vitamin A deficiency:
• Type of diarrhoea - Dry conjunctiva or cornea,
(watery/bloody) - Bitot’s spots
• Loss of appetite - Corneal ulceration
• Family circumstances (to - Keratomalacia
understand the child’s social • Localizing signs of infection, including ear and throat infections, skin infection or
background) pneumonia·
• Chronic cough • Fever (temperature ≥ 37.5° C or ≥ 99.5° F) or hypothermia (axillary temperature
• Contact with tuberculosis <35.0° C or <95.0° F)
• Recent contact with measles • Mouth ulcers
• Known or suspected HIV • Skin changes of kwashiorkor:
infection. - Hypo or hyperpigmentation
• Immunizations - Desquamation
- Ulceration (spreading over limbs, thighs, genitalia, groin, and behind the ears)
- Exudative lesions (resembling severe burns) often with secondary infection
(including Candida)
• Screening for infections:

4. Laboratory Tests
- Total and differential leukocyte count, blood
• Hemoglobin or packed cell volume in children
culture (If possible)
with severe palmar pallor.
- Urine routine examination
• Blood sugar.
- Urine culture
• Serum electrolytes (sodium, potassium)
- Chest x-ray
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carry out regular feeding during the day and night.
5. Organization of care Accurate weighing machines are needed, and records
On admission, the child with severe malnutrition should should be kept of the feeds given and the child’s weight
be separated from infectious children and kept in a warm so that progress can be monitored.
area (25–30°C, with no draughts), and constantly
monitored. Washing should be kept to a minimum, after 6. Providing general treatment
which the child should be dried immediately. for malnutrition
Facilities and sufficient staff should be available to
There are 10 essential steps in two phases: an initial
ensure correct preparation of appropriate feeds, and to
stabilization phase and a longer rehabilitation phase.
Table-2: Treatment for Malnutrition:
Stabilization Rehabilitation
Days 1-2 Days 3-7 Weeks 2-6
1. Hypoglycemia
2. Hypothermia
3. Dehydration
4. Electrolytes
5. Infection
6. Micronutrients No iron with iron
7. Initiate feeding
8. Catch-up growth
9. Sensory stimulation
10. Prepare for follow-up
with free radical generation and may interfere

6.1 Important things not to do and why?
with the body’s immune mechanisms against
• Do not give I/V fluids routinely. I/V fluids can proliferating bacteria.
easily cause fluid overload and heart failure. Only
give I/V fluids to children with signs of shock. 6.2. Treat hypoglycaemia
• Do not give diuretics to treat oedema. The oedema
will go away with proper feeding. Giving diuretics • If the child is lethargic, unconscious, or
will worsen child’s electrolyte imbalance and may convulsing, give IV 10% glucose 5 ml/kg
cause death. followed by 50 ml of 10% glucose or sucrose
• Do not give high protein formula. Almost all by NG tube. If IV dose cannot be given
severely malnourished children have infections, immediately, give the NG dose first. Give
impaired liver and intestinal function. Because of appropriate antibiotics and start feeding as soon
these problems, they are unable to tolerate the as possible.
usual amount of dietary protein. • If not lethargic, unconscious, or convulsing,
give the first feed of starter formula (75
• Do not give iron during the initial feeding phase. calories/100ml), if it is quickly available and
Add iron only after the child has been on catch-up
then continue with 2 hourly feeds.
formula for 2 days (usually during week 2).
• Giving iron early in treatment has been associated
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• If the first feed is not quickly available give 50 ml 6.3. Infection
of 10% glucose or sugar solution (4 rounded
teaspoon of sugar in 200 ml or one cup of water) 6.3.1 Presume and treat infection
orally or by nasogastric tube, followed by the first Assume all children with severe malnutrition admitted in
feed as soon as possible. a hospital have an infection and give broad spectrum
• Give 2-hourly feeds, day and night, at least for the antibiotics. If a specific infection is identified (such as
first day. Shigella), give specific appropriate antibiotics according
to condition identified. Hypoglycaemia and hypothermia
• Give appropriate antibiotics.
are often signs of severe infection.
• Keep the baby warm and check temperature.
• Prevent hypoglycaemia/Begin Starter Formula
• Feed 2 hourly, starting immediately or, if
necessary, rehydrate first. Continue feeding
throughout the night.
6.3.2 Select antibiotics and prescribe regimen

Select antibiotics as shown in the chart below.
Table 3: Antibiotic Treatment
Status Antibiotic
All admitted cases • Inj. Ampicillin 50 mg/kg/dose 6 hrly and Inj.
Gentamicin 7.5 mg/kg once a day for 7 days
• Add Inj. Cloxacillin 50 mg/kg/dose 6 hrly if
staphylococcal infection is suspected
• Revise therapy based on sensitivity report
For septic shock or worsening/ no • IV Cefotaxime 50 mg/kg/dose 6 hrly or Inj.
improvement in initial ho urs Ceftriaxone 50 mg/kg/dose 12 hrly plus Inj.
Amikacin 15 mg/kg/once a day
Meningitis • IV Cefotaxime 50 mg/kg/dose 6 hrly or Inj.
Ceftriaxone 50 mg/kg/dose 12 hrly plus Inj.
Amikacin 15 mg/kg/once a day
Dysentery • Inj. Ceftriaxone 100 mg/kg once a day for 5 days
6.3.3 Duration of antibiotic therapy depends on • Suspect HIV if he/she has also other problems like
the diagnosis: persistent diarrhoea, oral thrush, pneumonia,
Suspicion of clinical sepsis: at least 7 days Culture parotid swelling or generalized lymphadenopathy
positive sepsis: 10-14 days Meningitis: at least 14-21 • Investigate and follow HIV guidelines.
days • Severe anaemia: Give whole blood or packed cell
Deep seated infections like arthritis and osteomyelitis: at transfusion if Hb is < 4g/dl or Hb is 4-6 g/dl and
least 4 weeks child has respiratory distress. Give 10 ml/kg
slowly over 4-6 hours and give Inj. Frusemide 1
6.4. Treat Associated Conditions
mg/kg at the start of the transfusion. Do not repeat
• Give Anti-malarials, if blood smear positive for blood transfusion within 4 days.
malaria parasites. • If eye problems (Keratomalacia) due to vitamin A
• Start ATT if Tuberculosis is diagnosed or strongly deficiency, in addition to vitamin A doses instill
suspected (Mantoux Test and X-ray chest). Ciprofloxacin eye drops 2-3 hourly and Atropine
eye drops 3 times a day for 7-10 days. Also cover
the eyes with pad and bandage.
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• Skin lesions: Bathe or soak the affected areas for 6.6. Initiate feeding
10 min in 1% potassium permanganate solution
and apply gentian violet or nystatin cream if Essential features of initial feeding are:
available to skin sores and any barrier cream (zinc • Start feeding as early as possible.
cream) to the raw areas. • Feed the child if alert and drinking even during
• Persistent diarrhoea: Diarrhoea is common in rehydration.
severe malnutrition but with cautious refeeding, it • Give frequent and small nutrient rich feeds of low
should subside during the first week. In the osmolarity and low lactose.
rehabilitation phase, the poorly formed loose stools • Offer 130 ml/kg/day of liquids (100 ml/kg/day if
are not a cause for concern, provided the child’s child has severe oedema), 80- 100 Kcal/kg/day and
weight gain is satisfactory. If the child has 1-1.5 g/kg/day of proteins.
persistent diarrhoea, screen for non-intestinal • Use nasogastric feeding till child takes orally 75%
infections and treat appropriately. Continue breast of all feeds.
feeding and try to give feeds with low lactose • If child breastfed, continue breastfeeding but give
initially and subsequently change to lactose free the feed first.
options if diarrhoea persists. • Ensure night feeds.
6.6.1. Starter Formula
6.5. Micronutrients Starter formula is to be used during initial management.
It is started as soon as possible and continued for 2-7
6.5.1 Give oral vitamin A in a single dose.
days until the child is stabilized. Severely malnourished
• Vitamin A orally in single dose as given below:
children cannot tolerate usual amounts of proteins and
- < 6 months: 50,000 IU (if clinical signs of
sodium at this stage, or high amounts of fat. They may
deficiency are present)
die if given too much protein or sodium. Starter formula
- 6-12 months: 1 lakh IU
is specially made to meet the child’s needs without
- Older children: 2 lakh IU
overwhelming the body’s systems in the initial stage of
- Children < 8 kg irrespective of age should receive
treatment which provides 75 calories /100 ml and 0.9 gm
1 lakh IU orally.
of protein/100 ml.
• Give half of the above dose if injectable
6.6.2. Feed the child Starter formula orally, or
(intramuscular) vitamin A needs to be given.
by NG tube if necessary:
• Give same dose on Day 0,1 and 14 if there is
clinical evidence of Vitamin A deficiency. • Oral feeding
It is best to feed the child with a cup and spoon.
6.5.2 Other micronutrients should be given daily
Encourage the child to finish the feed. It takes skill
for at least 2 weeks:
to feed a very weak child, so nursing staff should
• Multivitamin supplement (should contain vitamin
do this task first and mother may help with feeding
A, C, D, E and B12 & not just vitamin B-complex):
later when child becomes stronger. Encourage
Recommended Daily Allowance.
breastfeeding on demand between starter formula
• Folic acid: 5mg on day 1, then 1 mg/day. feeds.
• Zinc: 2mg/kg/day. • Nasogastric feeding
• Copper: 0.3 mg/kg/day (if separate preparation not It may be necessary to use a NG tube if child is
available use Commercial preparation containing very weak. Use a NG tube if the child does not
copper). take 75% of the feed for 2-3 consecutive feeds.
• When weight gain commences and there is no Remove the NG tube when the child takes:
diarrhoea add 3 mg of iron/kg/day. - 75% of the day’s amount orally; or
- Two consecutive feeds fully by mouth.
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6.6.3. Record intake and output on a 24-Hour • After a day on 3-hrly feeds: If there is no
food intake chart vomiting, occasional diarrhoea, and most feeds
Criteria for increasing volume/decreasing frequency are consumed, change to 4-hrly.
of feeds 6.6.4. Monitoring
• If there is vomiting, significant diarrhoea, or Monitor and record
poor appetite, continue 2-hrly feeds. • Amounts of feed offered and left over
• If there is little or no vomiting, diarrhoea is less • Stool frequency and consistency
than before, and most feeds are consumed, • Vomiting
change to 3-hrly feeds. • Daily body weight
Bibliography:
Further reading:
1. Dasgupta R, Sinha D, Yumnam V. Rapid Survey of Wasting and Stunting in Children: What’s New,
What’s Old and What’s the Buzz? Indian Pediatrics. 2016 Jan;53(1):47-9.
2. De Onis M, Weise Prinzo Z. Managing Children with Severe Acute Malnutrition – What’s New? A
health policy perspective. Indian Pediatrics. 2014 Jan;51(1):17-8.
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18. Fever with Rashes
1. Introduction: 2.4. Petechial/purpuric
Fevers associated with generalized skin eruptions/ Epstein Barr virus, Echovirus 9, Cytomegalovirus,
rashes (exanthematous fevers) are common in childhood. Rickettsia, malaria, Pneumococcal, Meningococcal
These are often seen as epidemics in the periods of and Listeria infections.
'season change' like March-April and October-
November when adenoviruses become active. 3. Measles
2. Differential Diagnosis of Measles is a communicable disease manifesting with
fever, cough, coryza, lacrimation and Koplik spots in
Exanthema the pre-eruptive phase and a maculopapular rash
2.1 Macular and/or Papular rash starting on 4th or 5th day of illness. The rash heals
a) Measles, Rubella, Erythema infectiosum, Roseola, leaving brawny pigmentation.
Coxsackie virus, echovirus, CMV, Hepatitis B It is caused by a RNA virus classified as Morbillivirus,
infections. belonging to paramyxovirus family.
b) Erythema multiforme due to Herpesvirus, Epstein Clinical Features: Incubation period is 8-12 days.
Barr Virus, Adenovirus, Chlamydiae, Salmonella, Prodromal Phase: The onset is acute with moderate
Mycobacterium, Histoplasma and Coccidioides. elevation of temperature, dry hacking cough, running
of nose, sneezing, redness of the eyes and excessive
2.2. Nodular lacrimation.
a) Fungal diseases, Atypical mycobacterial and
pseudomonas infections. 3.1. Signs & Symptoms:
b) Erythema nodosum: Due to Streptococcus,
Typical measly look in young babies is due to
Mycobacterium Tuberculosis and Leprae, Yersinia,
conjunctivitis, stomatitis and rhinitis due to viral rash.
Hepatitis C, Sarcoidosis, Drugs and inflammatory bowel The first place for the rash to be seen is around
diseases. opening of parotid ducts in the mouth/inner cheeks
c) Diffuse erythematous with peeling or desquamation: (Koplik's spots). Rash appears on face and progresses
Scarlet fever, Toxic Shock Syndrome, Kawasaki to appear on trunk and limbs over the following three
Disease, Staphylococcal Scalded Skin Syndrome, to four days. Drying of rash and peeling of skin
Steven’s Johnson Syndrome. appears in the same sequence in next 4- 5 days.
2.3. Vesiculo-bullous
Varicella, Herpesvirus, Coxsackie virus, Enterovirus,
Meningococcal, Group A Streptococcal and
Pseudomonas infections.
Figure 18.1: Various types of Rashes
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3.2. Investigation: HB, TLC, DLC, X-Ray It is caused by Varicella Zoster virus belonging to
Herpes Virus family.
Chest, Measles antibody test.
Clinical Features: The incubation period is usually
between 14 to 16 days (with a range of 11 to 21 days)
3.3. Complication: 4.1. Signs & Symptoms:
Acute precipitation of Vitamin A deficiency in a child Symptom of chicken-pox is characteristic rash. The rash
with measles can occur and –hence corneal ulceration is appears in several "crops" of macules (red spots) quickly
a complication to watch out for and to prevent. All turning into watery vesicles and pustules is often more
children with measles should routinely receive vitamin severe in older children and adolescents. over the next 2
A orally – 2 lakh units each on day l, 2 and 14 (for to 3 days and then drying after scab formation over next
infants the dose is half) 5 days.
Due to depressed immunity because of measles, child
can catch infections like diarrhoea, otitis media,
pneumonia and TB. If the child continues to get fever
even after the rash is dry, bacterial pneumonia should be
suspected. Continued low fever and lack of appetite
should make one suspect TB infection.
Extra-feeding during convalescence and when the child
gets well is important to prevent malnutrition after Figure 18.2: Chicken Pox Rash
measles.
Due to multiple 'crops", appearing over a week or so,
one can observe all types of lesions simultaneously on a
3.4. Management: patient's body. The rash is more on covered areas like
Symptomatic treatment should be given Paracetamol 10 trunk of body, and can appear inside mouth.
to 15 mg per kg for fever and Antihistaminic (Cetirizine) Conjunctivae. Vagina leading to irritation symptoms.
Children 6-12 months: 2.5mg once a day, Chicken-pox patient is infective till all scabs are formed.
Children 12-23 months 2.5mg twice a day, Itching is prominent and scratching can lead to super
Children above 6 years to adults: 5-10 mg/day, as a added staphylococcal infection.
single dose or divided into 2 doses, for itching and
rhinitis. Advice continued feeding. Keep baby clean by
sponging or quick clean bath.
Treatment with antibiotics (Amoxicillin 30 mg per kg
per day in 2 to 3 divided doses for 5 days) for
superadded bacterial infections when detected.
3.5. Prevention: Figure 18.3: Vesicles & umbilication in chicken pox

Measles immunization as routine immunization should
be promoted at 9 months and 2nd dose along with DPT 4.2. Investigation: Clinically Diagnosed
Booster at 18-24 months.
Immunization given early to contact of measles case can 4.3. Complication: Aspirin given to a child with
prevent severe disease in the contact. chicken-pox infection may precipitate acute fatty
infiltration of liver. Liver failure and encephalopathy
(Reye's syndrome). Reyes' syndrome is to be suspected
4. Chicken-pox: if there is disproportionate vomiting, rapid breathing (in
Chicken pox is highly contagious disease, presenting the absence of chest signs suggestive of pneumonia) and
with sudden onset of low fever, mild constitutional altered sensorium. The patient should be referred for
symptoms, a centripetal, pleomorphic rash appearing on specialist care, where respirator is available; as this is a
the first day of the illness.
very serious condition with high mortality rate.
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4.4. Management: Acyclovir in the dose of 20mg/kg/dose that is 80
mg/kg/day in 4 divided doses for 5 days start treatment
Symptomatic treatment with paracetamol 10 to 15 mg
within the first 24 hours of rash onset can be given to
per kg per day for 5 days and anti-histaminic (Cetirizine)
immunocompetent patients.
for 5 days is advised. Daily bath is also advised.
Bibliography:
April 2015
Further reading:
1. Hay Jr. WW, Levin MJ, Deterding RR, Abzug MJ, Current Diagnosis and Treatment: Pediatrics, 22nd
Edition, McGraw-Hill Education, 2014


Page 229
19. Enteric Fever / Typhoid
1. Introduction: Although Enteric fever is 3. Investigation:
still a common infection its presentation has changed HB, TLC, DLC, Widal Test (Rising Titers), Blood
partly due to vaccination and partly due to institution of Culture.
antibiotics early in the course of illness. Complication: Shock, enteric perforation, haemorrhage
Diagnosis is problematic since blood cultures may not meningits, myocarditis. Can complicate the illness.
reveal much and Widal test is positive only after 1 week
and has many false positive and false negative results. 4. Management:
Bone marrow culture is more informative, but not
practical. 4.1 Drug Treatment
Hence possibility of enteric fever must be borne in mind Chloramplenicol -75 mg/kg/day x 14 to 21 days
while treating any pyrexia, which shows toxicity, and Or
signs suggestive of enteric like confused sensorium, (no Amoxiycillin 100mg/kg/day (with clavulinic acid) x 14
meningeal focal neurological signs). days
Or
Trimethoprim – Sulphamethaxazole 10& 50 mg/kg/day
2.Clinical Manifestations: are also used with some success.
Classical presentations are becoming rare. Common
specific manifestations are -
4.2 Multi-drug resistance:
Multi-drug resistant typhoid fever has emerged and is
• Relative bradycardia compared to fever.
difficult to treat. Following drugs are found to be useful:
• Tumid tender abdomen (abdomen feels like balloon
Third generation cephalosporins –
filled with water)
Cefixime 20 mg /kg 1 day in 2 divided doses
• Cloudy sensorium. or Ceftriaxone 50 mg/Kg per day
• Maculopapular erythematous rash on abdomen or Ciprofloxacin 20 mgl Kg per day, 10-14 days
blanching on pressure (Rose spots) or Ofloxacin15 mg/Kg 1 day.
• Centrally coated tongue. The antibiotics should be continued at least 5-7 days
• Soft spleen - 1-2 cm tender. after effervescence.
• Continuous fever, not touching the baseline. (If
4.3. Early institution of steroids
antipyretics are not given)
Dexamethasone 3 mg / Kg stat dose followed by 1
• Pea soup diarrhea, nausea, vomiting.
mg/kg 6 hourly for 48 hours improves the survival of
• Headache, myalgia, anorexia, malaise.
patients in shock, myocarditis' CNS complication.
Enteric fever in children.is more severe as compared to
adults. 4.4 Intestinal perforation requires
broad spectrum antibiotics, platelet
transfusions for severe thrombocytopenia with
hemorrhages. This treatment demands referral to higher
level
5. Prevention:
2 types of vaccine are available in commercial market.
• An oral, live- attenuated preparation of the Ty21a
Fig. 19.1: Rose spot in typhoid strain of S. Typhi
• Vi capsular polysaccharide for 2 years and above.
Page 230
Bibliography:
April 2015
Further reading:
1. Hay Jr. WW, Levin MJ, Deterding RR, Abzug MJ, Current Diagnosis and Treatment: Pediatrics, 22 nd
Edition, McGraw-Hill Education, 2014

Page 231
20. ACUTE MENINGOENCEPHALITIS
1. Introduction
Acute meningoencephalitis is an acute inflammatory
process involving meninges and brain tissue, due to
infectious causes. The common etiological agents are
viruses and bacteria. Children of any age may be
affected.
Fever, headache, vomiting, irritability altered state of
consciousness, signs of meningeal irritation and
seizures.
3. Investigations
CSF examination differentiates the viral from bacterial
cause of acute meningoencephalitis
Figure 20.1: Signs of meningitis
Table 1: CSF findings in meningoencephalitis
Pressure Leukocytosis Protein (mg/dl) Glucose
(mmH2O) (mm3) (mg/dl)
Normal 50-80 <5, >75% 20-45 >50 or
lymphocytes 75% serum glucose
Acute bacterial Meningitis Usually 100-10,000 100-500 Decreased

Elevated PMN’s* (<40)
(100-300) predominate
Acute viral Normal or Rarely >1000 50-200 Normal
Meningoencephalitis elevated PMN’s early but rarely decreased
lymphocytes
predominate in
the most of the
course
Tubercular Usually elevated 100-500 PMN’s 100-3000 <50
Meningoencephalitis early but later
lymphocytes
predominate
*PMN’s = Polymorphonuclear leucocytes
c. Increased intracranial tension is treated by proper
4. Treatment positioning of patient with head elevated at 15-30°
4.1 Supportive treatment position, fluid restriction to 2/3rd of maintenance,
Supportive treatment is the mainstay of therapy and is 20% Mannitol 5 ml/kg over 10-15 min followed by
started immediately. 3 ml/kg every 6 hourly for 48 hours and then SOS.
a. Maintain airway, breathing and circulation. Or Acetazolamide 50-75 mg/kg/day in 3
b. Control of seizures with IV injection of Diazepam divided doses through feeding tube Or Glycerine 1
0.2 to 0.4 mg/kg stat followed by Inj. Phenytoin ml/kg/day through feeding tube may be added, if
10-20 mg/kg stat followed by 5 mg/kg/day in increased intracranial tension persists.
divided doses.
Page 232
d. Fever is controlled as given in section on fever. • Inj. Chloramphenicol 100 mg/kg/day in 4 divided
(Caution: Never give aspirin). doses for 10 days
e. The intravenous fluid at two-thirds of the • If Meningococci is suspected/isolated, Inj
maintenance requirement initially. The electrolyte Penicillin G 300,000-400,000 IU/kg/day in 4
concentration of the blood is monitored very divided doses for 7-10 days.
closely. Any imbalance is treated promptly. Fluid 4.2.3. Treatment Viral meningoencephalitis
restriction is not done, if patient is dehydrated or is
• Herpes simplex virus (generally diagnosed by focal
in shock.
encephalitis or CT scan):
f. Feeding: Initially the patient is kept nil orally for
Inj. Acyclovir 30 mg/kg/day in 3 divided doses for
first 24-48 hours. Later on the feeding is guided by
14-21 days.
the level of sensorium. A tube feeding is helpful for
• Non-HSV viral encephalitis is treated by
feeding as well as for giving medicines.
supportive therapy only.
4.2 Specific treatment • Lumbar puncture is repeated at 48 hours to see the
Until a bacterial cause is excluded, parenteral antibiotic response. However, if the patient is improving
therapy should be administered. The choice of well, a repeat lumbar puncture may not be
antibiotics depends upon age of the patient and necessary.
prevalence of organism in the area.
4.2.1Age 0-3 months 5. Advice at discharge
• Regular follow-up for neurological assessment
• Inj. Cefotaxime 200 mg/kg/day IV in 4 divided
including deafness is advised.
doses for 14 days.
• Inj. Ampicillin 300 mg/kg/day IV in 4 divided • Anticonvulsant therapy to be continued, if seizures
doses for 14 days. are recurrent during course of meningitis. Children
4.2.2 Age 3 months-12 years with sequelae would require assessment of
• Inj. Ceftriaxone 100 mg/kg/day IV over 30-60 handicap and multidisciplinary management.
minutes in 2 divided doses for 10 days • Occupational / physiotherapy may be taught during
Or Inj. Cefotaxime 200 mg/kg/day IV in 3 divided hospital stay itself.
doses for 10 days
Or Inj. Ampicillin 300 mg/kg/day IV in 4 divided
doses for 10 days
Bibliography:
April 2015
Further reading:
1. McInerny TK, Adam HM, Campbell D, Kamat DK, Kelleher KJ, eds. American Academy of
Pediatrics (AAP) Textbook of Pediatric Primary Care. 5th Ed. Elk Grove Village; 2009

Page 233
21. TUBERCULOUS MENINGITIS
1. Introduction
Tuberculous meningitis is the inflammation of
meninges due to lymphohaematogenous spread of the
primary infection of tuberculosis to the meninges,
found in about 0.3% of untreated primary infection in
children. It is the most dangerous form of extra-
pulmonary tuberculosis. 70% of the cases are found
in children less than 5 years of age.
The clinical progression of tubercular meningitis
(TBM) may be rapid or gradual. The signs and
symptoms progress slowly over several weeks and
can be divided into three stages.
Figure 21.2: Kernig’s sign & Brudzinski’s Sign
2.1 Stages:
• The 1st stage, which typically lasts 1-2 weeks, • The 3rd stage is marked by coma, hemiplegia
is characterized by non-specific symptoms, such or paraplegia, hypertension, decerebrate
as fever, headache, irritability, drowsiness and posturing, deterioration of vital signs, and
malaise. Focal neurologic signs are absent. eventually, death.
• The 2nd stage usually begins more abruptly.
The most common features are lethargy, neck-
3. Complications: Survivors may have
motor deficits, cranial nerve deficits, mental
rigidity, seizures, positive Kernig or Brudzinski
retardation, learning disabilities, seizures,
signs, Hypertonia, vomiting, cranial nerve hydrocephalus, blindness, deafness and diabetes
palsies and other focal neurologic signs. insipidus.
4. Investigations
• The diagnosis is made by analysis of CSF on
lumbar puncture, which shows lymphocytic
leukocytosis with elevated protein and a low
sugar (for details see Table 1 of Chapter 20.
Acute Meningoencephalitis).
• Demonstration of AFB in CSF confirms the
diagnosis, but the yield is very poor. Culture of
CSF shows growth of M. tuberculosis, takes too
much time.
• Positive tuberculin skin test corroborates the
diagnosis but may be negative in severely
malnourished/disseminated disease.
• 20-50% of children have a normal chest
radiograph others may show primary disease.
• CT scan or MRI of brain may be normal during
early stages of the disease. Later, it can show
exudates in the basal cisterns of brain,
Figure 21.1: Tuberculosis meningitis periventricular ooze and hydrocephalus. Some
may show tuberculomas.
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• Presence of seizures necessitates treatment with
5. Treatment
phenytoin or carbamazepine in appropriate
Treatment consists of proper supportive care,
doses (for details see section on Epilepsy in
including nonpharmacological treatment, specific
Chapter).
anti-tubercular therapy, treatment of increased
• Specific anti-tubercular therapy—as given in
intracranial tension and, if required, surgical
management of tuberculosis (see section on
treatment.
Tuberculosis).
5.1 Nonpharmacological 5.3. Surgical treatment
• Nutrition: After initial stabilization, nutritional
rehabilitation should be done as given in section Ventriculo-peritoneal shunt (VP shunt): TBM
on protein energy malnutrition. shows some degree of hydrocephalus by 4 weeks.
Obstructive hydrocephalus should be shunted
• Skin care and prevention of bedsores.
immediately. Non-obstructive hydrocephalus with
• Care of bowel and bladder.
increased intracranial pressure as shown by
• Physiotherapy and occupational therapy should
ventricular tap or CT scan will also be benefited by
be instituted early to prevent deformities and
VP shunt. An early shunt is preferable.
contractures.
5.2 Pharmacological 5.4. Follow-up
• Patient should be kept under follow-up after
• Appropriate fluid therapy to correct dehydration
discharge from the hospital and assessed for
due to frequent vomiting and decreased oral
neurological deficit and features of increased
intake.
intracranial pressure (ICP). One of the common
• Fluid restriction upto 3/4th or 2/3rd of
causes of increased ICP is untreated
maintenance.
hydrocephalus or blocked shunt.
• Treatment of raised intracranial tension
• Check compliance to drugs and ensure that
- Inj. Dexamethasone: 0.15 mg/kg IV 6 hourly
occupational therapy/physiotherapy is being
for 2 weeks followed by Tab.
continued.
- Prednisolone 1.5 mg/kg/day orally through
• Assess physical, mental, visual and auditory
feeding tube for 4 weeks. This should be
handicap and take expert opinion for
tapered over another 2 weeks. A total of 6 to 8
rehabilitation from other specialists.
weeks of therapy with steroid is
• Patient/parent education
recommended.
- Seriousness of disease must be explained.
- Mannitol (20% solution) 1.5 to 2 g/kg or 8-10
- Contact survey should be done and any other
ml/kg over 30-60 minutes. Repeated every 6-8
member in the family found to have active TB
hours for 7 days. Lower doses (0.25
should be counselled to attend TB clinic for
g/kg/dose) can also be tried. Or Glycerol 1
therapy.
ml/kg/dose every 6-8 hours, diluted in orange
- Need for compliance should be emphasized.
juice or water, given through feeding tube. Or
- Drug toxicity and side effects must be
Tab. Acetazolamide 50 mg/kg/day in 3
explained.
divided doses for 2-3 weeks.
- Neurological deficits may appear even in a
patient on therapy.
Bibliography:
1. Paul VK, Bagga A. Ghai Essential Pediatrics. 8th Edition. CBS Publishers; 2013.

Page 235
22. ACUTE RESPIRATORY INFECTION
disease and can be managed in the community with oral
1. Introduction cotrimoxazole. Severe ARI cases require urgent referral
Acute Respiratory Infection (ARI) is an important cause to a facility where injectable antibiotic therapy and
of infant and child mortality and also the commonest supportive care are available.
cause of morbidity among children below five years.
ARI is the infection of any part of respiratory tract,
2. Diagnosis & management of
which includes cough, common cold, pharyngitis, ARI
pneumonia, laryngitis and ear infection.
Classification and management of ARI is based upon
Acute respiratory infections in children can involve
three important factors. These are age of the child,
upper respiratory tract (nose, throat) or lower respiratory
respiratory rate and danger sign like chest in-drawing.
tract (bronchi, lung). Lower respiratory tract infections
(broadly termed as pneumonias) are a major cause of 2.1 Age of the child and respiratory
death of infants and children in India, accounting for rate
about 30% under-five deaths. Timely treatment, based
on well-researched algorithms can save most children Children are classified into three age groups for ARI
with ARI. Majority of the cases of ARI have non-severe management. These age groups and criteria for fast
breathing are given in table below:
Table 1: Cut off points for fast breathing

Sr. Age group Criteria for fast breathing
1 0 - 2 months Respiratory rate more than 60 / minute
2 2 months to 1 year Respiratory rate more than 50 / minute
3 1 year to 5 years Respiratory rate more than 40 / minute
2.2 Chest in-drawing Classification

- No pneumonia
In normal child, during respiration, chest expands when
- Severe pneumonia/Very severe illness
the child breathes in and compresses when the child
breathes out. In children with severe pneumonia, chest 2.3.1 No pneumonia
moves in when the child breathes in. This is called chest If respiratory rate of child is less than 60/minute, then
in-drawing. the child is classified as 'No Pneumonia'.
• Give Paracetamol ¼ tablet (500mg) if there is
2.3 Pneumonia in age group 0-2 fever and demonstrate to the mother how to clean
months nose with normal saline drops.
• Advise mother to continue breast-feeding.
Important aspects about pneumonia in age group 0-2
• Inform mother about danger signs of pneumonia,
months are as below:
e.g. breathlessness (rapid movement of abdomen),
• In these children, there are no usual features of
inability to drink, excessive drowsiness,
pneumonia like fever, cough, etc.
hypothermia, high fever etc.
• Child may have only fast breathing and/or chest in-
• Ask mother to immediately bring the child back to
drawing.
health facility, if she observes any of the signs
• Pneumonia in child less than 2 months of age is
mentioned above.
always severe & mortality is high
2.3.2 Severe pneumonia/Very severe illness
Such cases should be treated in the facility where
If child below 2 months presents with fast breathing (RR
specialist & ICU are available.
> 60/minute) and/or chest in-drawing
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Plus
One or more of the following signs • Hypothermia
• Inability to drink • Convulsions
• Excessive drowsiness Such child should be referred to specialist.
• Stridor, wheeze In case referral cannot be executed, treat the child as
• Cyanosis below
Table 2: Treatment of Pneumonia
Antibiotic Dosage Frequency Route
Age < 7 days Age > 7 days- 2 months
Inj. Benzyl penicillin OR 50,000 IU/kg/dose 12 hourly 6 hourly IV/IM
Inj. Ampicillin AND 50 mg/kg/dose 12 hourly 8 hourly IV/IM
Inj. Gentamycin 2.5 mg/kg/dose 12 hourly 8 hourly IV/IM
2.4. Pneumonia in age group 2 2.4.2 Pneumonia

If child has fast breathing (RR: 2-12 months > 50/ min.
months to 5 years & 1-5 years > 40/ min.) and no chest in-drawing,
Children with ARI of 2 months to 5 years of age are diagnose child as Pneumonia Treatment of pneumonia
classified into four groups as follows - • Give child Cotrimoxazole for 48 hrs.
• No pneumonia Treatment schedule for pediatric cotrimoxazole is -
• Pneumonia 2-12 months: 2 tablets twice daily or syrup 5 ml.
• Severe pneumonia twice daily
• Very severe illness 1-5 years: 3 tablets twice daily or syrup 7.5 ml.
twice daily.
2.4.1 No pneumonia Pediatric tablet contains Sulfamethoxazole 100 mg
When respiratory rate is normal and no sign of chest in- & Trimethoprim 20 mg.
drawing is seen child is diagnosed as ‘no pneumonia’. Syrup 5 ml. contains Sulfamethoxazole 200 mg
These children should be treated at home & observed for and Trimethoprim 40 mg.
appearance of danger signs (increase in RR and chest in- • If fever is present, give Tab. Paracetamol. (5 to 10
drawing) by mother. Following points should be advised mg./kg)
to mother - • Teach mother how to clean nose with normal
• Continue breast-feeding if child is breast-fed. saline. This will clear airway of child and improve
• Give plenty of oral fluids including water or ORS breast-feeding.
to child. • Keep baby warm by covering with warm clothes
• If fever is present, give Tab. Paracetamol(5 to 10 and keeping in lap.
mg/kg). • Assess child after 48 hrs:
• Teach mother how to clean nose with saline water. o If improvement - Continue CTZ for 3 Days
This will clear airway of child and improve breast- o Child has Chest in-drawing and RR may be fast
feeding. - complete 5-day course
• In community, many home remedies are used for o If no improvement or child gets deteriorated
ARI. One of the best among them is honey & refer child to specialist.
ginger. Advise mother to give honey and ginger to 2.4.3 Severe Pneumonia
child. Child with chest in-drawing & having RR normal or fast
• Inform mother about danger signs of pneumonia, is diagnosed as severe pneumonia and should be treated
e.g. breathlessness, inability to drink, excessive by specialist. Give oxygen if child has cyanosis till the
drowsiness, hypothermia, high fever etc. child is referred.
• Advise her to bring child back to health facility if
Treatment
she observes any of the danger sign.
a. Treat for first 48 hours by
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Table 3: Treatment of Severe Pneumonia
Antibiotic Dosage Interval Route
Inj. Benzyl penicillin OR 50,000 IU/kg/dose 6 hourly IM
Inj. Ampicillin OR 50 mg/kg/dose 6 hourly IM
Inj. Chloramphenicol 25 mg/kg/dose 6 hourly IM
b. Assess after 48 hrs
i. If improvement, continue for next 3 days as below
Table 4: Further management of Severe pneumonia
Antibiotic Dosage Interval Route
Inj. Procaine penicillin OR 50,000 IU/kg (Max 4 lac units) Once IM
Tab Ampicillin OR 50 mg/kg/dose 6 hourly Oral
Tab Chloramphenicol 25 mg/kg/dose 6 hourly Oral
ii. If no improvement, change antibiotic as below 2.4.4 Very severe illness

• If Ampicillin was given earlier then change to Inj. a) Child has:
Chloramphenicol Chest in-drawing and RR may be fast or normal
• If Chloramphenicol was given earlier change to Inj. Plus, One or more of following signs -
Cloxacillin 25 mg/kg/dose 6 hourly IM + • Inability to drink
Gentamycin 2.5 mg/kg/dose 8 hourly IM. • Excessive drowsiness
iii. Important aspects of antibiotic treatment • Stridor, wheeze
• Treatment with antibiotics should be continued for • Cyanosis
at least five days. • Hypothermia
• Continue treatment for at least 3 days after child • Convulsions
recovers. Diagnose the child as suffering from very severe illness
• If Cloxacillin & Gentamycin are started continue & refer the child to specialist having facility of intensive
for three weeks. care unit.
iv. In addition to this give following
• Administer Oxygen if required
3. Treatment of childhood
• Continue breast feeding during illness community-acquired pneumonia
• If fever, give tablet or syrup Paracetamol The management of pneumonia is guided by the severity
• If wheeze, treat by using bronchodilator of the disease as listed in Table below:
• Give plenty of oral fluids.
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3.1 Classification:
Table 5: Signs & symptoms
Sign or symptom Classification Treatment
• Central cyanosis • Admit to hospital
• Severe respiratory distress • Manage the airway
• Not able to drink due to respiratory Very severe pneumonia • Give oxygen
distress • Give recommended antibiotic
• Treat high fever if present
• Chest in drawing • Admit to hospital
Severe pneumonia • Give recommended antibiotic
• Treat high fever if present
• Fast breathing • Give appropriate antibiotic for 5
2 months to 12 months: ≥ 50 days
breaths/min • Soothe the throat and relieve cough
12 months to 5 years: ≥ 40 with a safe remedy
breaths/min Pneumonia • Treat high fever if present
• Definite crackles on auscultation
at home with oral Amoxicillin (15 mg/kg per dose

three times a day) plus IM Gentamicin (7.5 mg/kg
IM/IV once a day) daily for a further 5 days.
b) Alternatively, give Injectable Chloramphenicol (25
mg/kg IM or IV every 8 hours) until the child has
improved. Then continue the same drug orally in
the same dose for 3 times a day for a total course
of 10 days.
c) If the child does not improve by 48 hours to any
one of these treatments, reassess for complications
and switch to Injection Ceftriaxone (80 mg/kg IM
Figure 22.1 Signs of Respiratory distress or I/V once daily) for 10 days.
3.2 Treatment of very severe illness Staphylococcal pneumonia is suspected if:
3.2.1 Admit the child in hospital • There is a rapid progression of the disease, or
3.2.2 Obtain a radiograph of the chest if facilities are • There is pneumatocele, or pneumothorax, or
available for the same. Radiography in very severe pneumonia effusion on chest X-ray, or
is required at admission to assess the extent of disease and to • Child has large skin boils or abscess or infected
rule out presence of pneumothorax or effusion. In case of scabies, or
severe distress, stabilize and oxygenate the child before • Post-measles pneumonia which is not responding
sending for radiograph. within 48 hours to the initial therapy.
3.2.3 Give antibiotics If staphylococcal pneumonia is suspected, add Inj
a) Give Injectable Ampicillin (50 mg/kg IM/IV every 6 hours) Cloxacillin (50mg/kg/dose, every 6 hourly) to any of
and Gentamicin (7.5 mg/kg IM/IV once a day). If the child the above choice of antibiotics.
responds well, discharge after 5 days to continue treatment
Page 239
When the child improves, continue Cloxacillin orally 4 3.2.6 Monitor the child
times a day for a total course of 3 weeks at least. The child should be checked by nurses at least every 3
Children with complicated pneumonia (Empyema) hours and by a doctor at least twice a day. Monitor for
need longer therapy for 4-6 weeks. signs of improvement. A patient who is improving on
3.2.4 Give Oxygen treatment should have:
• Where pulse oximeter is available, use oxygen - An improvement in the respiratory rate.
saturation of the blood (SaO2) to guide oxygen - Less in-drawing of the lower chest wall.
therapy. Maintain SaO2 ≥ 92%. Continue with - Less fever, and /or
oxygen until the signs of hypoxia (such as severe - Improved ability to eat and drink.
lower chest wall in-drawing or breathing rate of ≥ 3.2.7 Watch for complications
70/min) are no longer present. If the child has not improved after two days, or if the
3.2.5 Give supportive care child’s condition has worsened, look for complications
• Ensure that the child receives daily maintenance or other diagnoses. If possible, obtain a repeat chest X-
fluids appropriate to child’s age. Encourage ray. Consider transfer to a higher facility in case of
breastfeeding and oral fluids once the distress poor response or deterioration despite second-line
settles and the child is able to feed. therapy.
• If the child has fever (≥38.5ºC) which appears to be 3.2.8 Monitoring
causing distress, give oral Paracetamol The child should be checked by nurses at least every 6
(15mg/kg/dose). hours and by a doctor at least once a day. Monitor for
• If wheeze is present, give a rapid-acting signs of improvement as discussed above.
bronchodilator (as described in the next section).
• Remove any thick secretions in the nose/throat,
which the child cannot clear, by gentle suction.
Table 6: Summary of management of ARI cases.

No. Type Who can manage Where can be managed
Age group 2 months to five years
1 No pneumonia ASHA Anganwadi Worker, MPW Home management
2 Pneumonia MPW/HA, MO Management at home or PHC
3 Severe pneumonia PHC MO / specialist PHC/ referral center
4 Very severe illness Specialist Specialist with ICU facility
Age group below 2 months
• Child should be referred immediately after giving one dose of CTZ
Bibliography:

Page 240
23. BRONCHIAL ASTHAMA
Less Preferred treatment: Montelukast, Theophylline,
1. Introduction: Cromoglycate and treatment of mild intermittent
Bronchial asthma is a disease characterized by an
asthma
increased responsiveness of the trachea and bronchi to
various stimuli. It manifests by widespread narrowing of 3.3. Moderate persistent
the airways causing paroxysmal dyspnea, wheezing or • Symptoms > 2 times/ week
cough. The diffuse obstruction to the airflow is • Nocturnal symptoms >1/week
reversible in a large majority of cases, either • PEFR 60-80%
spontaneously or in response to treatment. Bronchial 3.3.1Treatment
reactivity is a necessary component of asthma. Asthma • Inhaled steroid Medium dose
is a result of multifactorial inheritance. • If response not satisfactory
• Add inhaled LABA (Salmeterol/ Formoterol)/
2. Signs & Symptoms:
Montelukast/ long acting theophylline
• Recurrent cough
• Breathlessness
3.4. Severe Persistent
• Daily symptoms often severe
• Wheezing
• Activity limited
3. Clinical classification • Growth affected
• Mild Intermittent • Frequent Nocturnal symptoms
• Persistent • Frequent hospitalization
• Mild • PEFR<60%
• Moderate 3.4.1 Treatment
• Severe • Inhaled steroids high dose
3.1. Mild Intermittent • Inhaled LABA /Montelukast / Long acting
• Symptoms < 2times a week and asymptomatic in Theophylline
between • If response not satisfactory
• Nocturnal symptoms < 2 times /month • Oral Prednisolone 2mg/kg/day in three divided
3.1.1Treatment doses & inhaled Salbutamol as required
Salbutamol inhaled (100 MCG/puff) 1-2 puffs as per 3.4 Treatment Guidelines for acute
requirement for children less than 2 years use face mask exacerbation of Asthma
with spacer • O2 by mask (4-6 liters /min)
OR
• Salbutamol MDI (100MCG/puff) with spacer and
Salbutamol syrup/tablet
mask for < 2 years 4-8 puffs every 20 min x 3 OR
0.1-0.2 mg/kg/dose three times a day till symptoms
Salbutamol nebulization 0.15mg/kg (min 2-5mg)
subside
diluted in 3 ml saline can be repeated 3 times every
3.2. Mild Persistent 20 min
• Symptoms > 2times/week but ,1time/day • Inj. Adrenaline (1:1000) or Terbutaline
• Nocturnal symptoms > 2 times / month (0.01mg/kg) SC may be repeated thrice every20
• Asymptomatic in between exacerbations peak flow min if both above are not available
rate (PEFR) > 80% AND
3.2.1 Preference for Treatment • Inj. Hydrocortisone hemisuccinate 10mg/kg/dose 4
Preferred treatment: Inhaled steroids (low dose) 2 puffs times a day OR Inj. Dexamethasone0.2 mg
twice / day /kg/dose
• This must be converted to oral prednisolone once
patient is stable
Page 241
• If response not satisfactory refer to higher center
4. Investigation:
stat i. Pulmonary function test
IMP: Evaluate after 1 hour ii. Absolute Eosinophil count
• Good response iii. Chest X-ray
Send home: Salbutamol MDI+ Tab iv. Skin test & Allergy test
Prednisolone 2mg/kg/day x 5-7 days
Figure 23.1 Metered dose

inhaler
Table 1. Drugs used in the long-term control of asthma in children
Medication Dosage form Dosage
Formoterol DPI: 12 µg per single-use capsule 1. Capsule every 12 years
Salmeterol MDI: 25 µg per puff 1-2 puff every 12 hours
Fluticasone/salmeterol DPI:100, 250, or 500 µg of fluticasone 1 inhalation twice daily; dosage

depends on severity of asthma
with 50 µg of salmeterol
Cromolyn MDI: 1 mg per puff 1-2 puffs 3 to 4 times daily

Nebulizer solution: 20 mg per ampule 1 ampule 3 to 4 times daily
Nedocromil MDI: 1.75 mg per puff 1-2 puffs 2 to 4 times daily
Montelukast 4 or 5 mg chewable tablets, Age 12-23 months: 4 mg oral

4 mg packet of oral granules, granules at bedtime
10 mg tablets Age 2-5 years: 4 mg at bedtime
Zafirlukast 10 & 20 mg tablets Age 7-11 years: 20 mg twice

daily, 1 hour before or 2 hours
after meals
Page 242
Medication Dosage form Dosage
Theophylline Liquids, sustained- release Loading dosage is 5 mg /kg per

day
Tablets and capsules.
Maintenance dose
< 1 years: [(0.2 × age in weeks) +
5 mg] per kg day
> 1 years: 16 mg per kg per day
Bibliography:
April 2015
2. Hay Jr. WW, Levin MJ, Deterding RR, Abzug MJ. Current Diagnosis and Treatment: Pediatrics. 22nd
Edition. McGraw-Hill Education; 2014
Further reading:

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Page 243
24. Breath holding spell
• Less common, Apnea followed by pallor,
1. Introduction:
hypotonia and tonic seizure.
• A baby with crying followed by loss of
consciousness, tonic posturing (features of 3. Complication:
cerebral anoxia).
• Local trauma
• Cyanotic Breath holding spell more common
form • Aspiration pneumonia.
• Usual age of onset is 6 months, peak by 2 years,
abate by 5 years.
• After a shrill cry, forced expiration followed by
4. Management:
apnea and cyanosis leading to loss of • Examination to rule out other seizure mimicking
consciousness associated with clinical jerks or conditions.
posturing. • Reassurance of parent that these are not
seizures, EEG not required, inter-ictal EEG is
2. Signs & Symptoms: normal.
• Should not reinforce this behavior, put the child
• Baby may be cyanosed (blue)\ Baby may be
in safe place, avoid cuddling.
pale
• Iron supplements if anemia, delayed weaning
• History of a predictable stubborn behavior,
etc. (3 mg/kg for 3 months.)
precipitating event like upsetting the infant
• Syrup Piracetam (40-100 mg /kg twice a day)
• History of painful stimulus or hit on head
may be used for few months if the breath
cyanosis leading to loss of consciousness
holding spells are very frequent,
associated with clinical jerks or posturing.
• Parental counseling to prevent reinforcement of
this behavior.
Bibliography:
April 2015
Further reading:
1. Singh P, Seth A. Breath Holding Spells – A Tale of 50 Years. Indian pediatrics. 2015 Aug; 52(8):
695-6.
2. Sawires H, Botrous O. Placebo-controlled trial on the effect of piracetam on breath-holding spells. Eur
J Pediatr. 2012 Jul;171(7):1063-7.
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Page 244
25. Bronchiolitis
• Child should be treated in a humid atmosphere
1. Introduction:
preferably in sitting position with head and neck
• Viral in etiology (Respiratory syncytial virus)
elevated.
• Most frequently in children < 12 months of age
• Supportive measures such as oxygen by hood
(10 litre/ minute) or by mask (5 litre / minute).
2. Signs & Symptoms: • IV fluids if child is not able to feed orally.
Initial URI symptoms followed by Increasing • Antibiotics have no role.
cough, Respiratory distress, Wheeze and feeding • Monitor - Respiratory Rate, Respiratory
difficulty distress, pulse oximetry
• A trial dose of Nebulized salbutamol /
3. Investigations: epinephrine if wheezing is marked.
CXR: Hyper inflated lungs with patchy infiltrates • As child improves wean off oxygen and
increase oral feeds.
• If child develops severe respiratory distress,
4. Management: increasing hypoxemia, cyanosis or fatigue –
4.1 Treatment ventilatory support may be required.
• Treatment of bronchiolitis is essentially
symptomatic.
Figure 25.1: Clinical features of severe bronchiolitis in an infant. From Lissauer and Graham, 2002.
Bibliography:
April 2015
Page 245
Further reading:
2. Sharma S. Management of Bronchiolitis. Indian Pediatrics. 2014 Mar;51(3):235-6

Page 246
26. Empyema
• Diagnostic thoracocentesis: usually in fifth
1. Introduction:
intercostal space over mid-axillary line using a
• Characterized by presence of pus or large bore needle.
microorganisms in the pleural fluid • Pleural fluid for Gram stain, culture and
• Occurs as a complication of Pneumonia sensitivity
• Influenza, Streptococcus Pyogenes, Staph • Pleural fluid pH, sugar is reduced and protein is
aureus, Streptococcus Pneumoniae, elevated.
Haemophilus are the common organisms.
5. Management:
2. Signs & Symptoms:
5.1 Treatment comprises of chest
Common symptoms are
• Fever
drain and antibiotics.
• Chills • Chest drainage using an intercostal drainage
• Toxaemia tube inserted in the region of maximal dullness
• Respiratory distress (usually V or VI intercostal space in axillary
• Grunt and region) and connecting to a sterile under water
• Chest pain (pleuritic pain) drainage bottle.
• Chest drainage is kept till the drainage decreases
3. On examination to < 25 ml/day and there is good lung
expansion.
• Decreased chest expansion
• If there is no chest expansion by clinical or
• Diminished breath sounds
radiological methods, surgical opinion is sought
• Dullness on percussion on affected side and
• Mediastinal shift to opposite side 5.2. Antibiotics
4. Investigations: • Cloxacillin with Cefotaxime or Ceftriaxone is
the first line antibiotic; switch over to oral
• Chest X-Ray: Obliteration of costo-phrenic antibiotics after child becomes afebrile and
angle; diffuse homogenous opacity. chest tube is removed.
• USG chest: size, site of effusion, adhesions or • Total duration of 4 - 6 weeks of antibiotic
loculations can be made out. therapy
- Cloxacillin: 100 - 200 mg/kg/day in 4 div.
doses
- Cefotaxime: 150 - 200 mg/kg/day in 3 or 4
div. doses
5.3. Supportive care: Oxygen, good
nutrition
Figure 26.1: Chest X-Ray in empyema
Page 247
Bibliography:
April 2015
Further reading:
1. Ranjini EK, Agarwal I, Kirubakaran C. Pneumococcal subdural empyema in young infants. Indian
Pediatrics. 2004 May;41(5):505-8

Page 248
27. Approach to Fever
• Total count, differential count, peripheral smear,
1. History:
Platelet count
• Type of fever
• Urine analysis, urine culture and sensitivity
• Associated symptoms – chills / rigor, cough,
sore throat, ear pain, urinary symptoms, bleeds • Blood culture and sensitivity
etc. • Chest x-ray
• Previous illness and treatment. • C-reactive protein
• If any Feeding difficulty, respiratory distress. • Mantoux test
• CSF analysis if required
• Other investigations
2. Clinical Examination - Liver function test
• Check Temperature, Blood pressure, Pulse, - Renal function test
Perfusion
- USG abdomen
• Skin: Rashes, Bleed, Cyanosis - Blood for leptospirosis
• Eyes: Pallor, Icterus - Serology for dengue
• Mouth: Ulcer, Thrush - Widal test
• Ear: Discharge, Redness, Tenderness - Bone marrow
• Throat: Congestion, Tonsillitis
• CNS: Meningeal irritation, altered sensorium
4. Refer if:
• Abdominal examination: Hepatomegaly, • Fever with unconsciousness
Splenomegaly
• Fever with shock
• Respiratory System: Tachypnea, Retraction,
• Severe respiratory diseases
Crepitation, Wheeze
• Bleeding diathesis
• Refractory seizures
3. Basic investigations in high
risk group and fever beyond
5 days in low risk:
Bibliography:
April 2015
3. Engorn B, Flerlage J. The Harriet Lane Handbook. 20th Edition. Saunders; May 2014.
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Page 249
28. ACUTE FLACCID PARALYSIS (AFP)
1. Definition: 2. Salient Features
• Acute flaccid paralysis is defined as sudden • The paralysis is of acute onset (<4 weeks) and
onset of weakness and floppiness in any part of the affected limb(s) are flaccid (floppy or limp).
the body in a child < 15 years of age or • If the AFP is due to polio, then sensation is
paralysis in a person of any age in whom polio never affected. Other important differentials to
is suspected [without any obvious cause (e.g. be considered in cases with AFP are detailed in
severe trauma or electrolyte imbalance like Table-1.
(hypokalemia)]. • This includes possible illness due to Guillain-
• AFP is a notifiable disease and all cases must be Barre syndrome, Transverse Myelitis,
reported immediately to Nodal Officer and Traumatic Neuritis, viral infections caused by
District Surveillance Officer, NPSP Unit, other Enteroviruses, toxins and Tumours.
Directorate of Family Welfare. • Isolated facial paralysis is also included.
• India has shifted to the Virological system of • Pseudo paralysis due to pain in Congenital
case classification, i.e. within 90 days of Syphilis, Osteomyelitis, Abscess, Scurvy,
paralysis onset; all cases should undergo final unrecognized trauma leading to contusions,
classification as confirmed polio, non-polio slipped epiphysis or fractures, etc. can also
AFP or compatible with poliomyelitis. mimic AFP.
3. Differential Diagnosis:
Table 1- Important differential diagnosis of AFP (adapted from Field Guide, MOHFW, GOI)
Signs and Polio GBS Transverse Traumatic
symptoms myelitis or injection
neuritis
Age Most cases occur Usually above 2 Mostly above 4 No age limit
under 3 years of age years of age years of age
Progression of 24-48 h onset to Hours to days Hours to 4 days Hours to 4 days
paralysis full paralysis
Fever onset High always Not common Rare Commonly
present at onset of present before,
flaccid paralysis during and after
disappears the paralysis
following day
Flaccidity Acute, Acute, Acute Acute,
asymmetrical, symmetrical, lower limbs asymmetrical
Proximal Distal symmetrical Limb
Muscle tone Diminished Diminished Diminished in Diminished in
lower limbs affected limb
Deep tendon Decreased or Absent Absent in lower Decreased or
reflexes absent extremities, later absent
hyper-reflexia
Sensation Severe myalgia but Cramps, tingling Anaesthesia of Pain in gluteal
no sensory deficit hypoanaesthesia of the lower limbs region
palms and soles with sensory loss
Page 250
Signs and Polio GBS Transverse Traumatic
symptoms myelitis or injection
neuritis
Cranial nerve Only in bulbar or Often present Absent Absent
bulbospinal cases. affecting VII, IX,
Loss of gag reflex X, XI, XII
most common Only
in bulbar or
bulbospinal cases.
Loss of gag reflex
most common
Respiratory Only when bulbar In severe cases Sometimes Absent
insufficiency and bulbospinal
involving
respiratory muscles
CSF WBCs High WBCs. <10 Normal Normal
proteins Normal or slightly High Normal or Normal
Increased slightly elevated
Bladder Absent Transient Present Never
dysfunction
Nerve Abnormal, anterior Abnormal, Normal of Abnormal in
conduction horn cell disease demyelination abnormal has no sciatic nerve
velocity in 3rd diagnostic value
EMG 3rd week Abnormal Normal Normal Normal
Sequelae at 3 Severe Symmetrical Flaccid Moderate
months and up asymmetrical atrophy of distal atrophy only in
to a year atrophy, skeletal muscles, diplegia, affected lower
deformities may atrophy after years limb
develop later
4. Confirmation • The final classification of the case as “compatible

“or discarded as “non-polio AFP” is determined by
• An AFP case is “confirmed” as Polio only by the the National Expert Review Committee (ERC)
isolation of wild poliovirus from any stool which meets every month in New Delhi to review
specimen. all such cases.
• An AFP case is classified as “non-polio AFP” if • Adequate stool: Two specimens collected within
wild poliovirus is not isolated from adequate stool 14 days of paralysis onset and at least 24 hours
specimens. apart; each specimen must be of adequate volume
• If stool specimens are inadequate, final (8-10 grams) and arrive at a WHO-accredited
classification of the AFP case as either non-polio laboratory in good condition (i.e., no desiccation,
AFP or compatible with Polio will depend on the no leakage, with adequate documentation and
results of 60-days follow-up examination. evidence that the cold chain was maintained.)
• If the 60-days follow-up examination shows no
residual weakness, the case is classified as non-
polio AFP.
Page 251
progression of paralysis, respiratory distress,
5. Treatment for Acute Polio bulbar involvement, paralysis of upper limbs
like illness which is <3 days old (there is higher risk of
All cases should be treated as below except patients diaphragmatic involvement in such cases),
with isolated single lower limb involvement and marked drowsiness or any other complication.
reporting after 4 days of onset of paralysis and
currently not progressing for more than 48 hours.
5.3. Patient/parent education
• No dietary restrictions, however, continue
5.1. Nonpharmacological breastfeeding or other regular feeding.
• Complete bed rest and correct positioning of the • Paralysis progresses usually for about 4-7 days
affected limbs in the optimal position as after onset. Recovery may start thereafter over
follows: days to weeks with little recovery of strength
- Hip—slight flexion, knee—5° flexion, foot— after 6 months of illness. A regular
90° with support against the soles. physiotherapy facilitates recovery of muscles.
- Both legs should be supported from the lateral Note: Post-polio residual paralysis should be
sides with pillows or rolled towels or salt/sand referred for rehabilitative services to an
packs to prevent rotation. appropriate centre.
• When pain subsides, passive movements of the
joints for about 10 minutes, 2-3 times a day.
• Warm water fomentation using hot packs with
6. Action expected on
soaked towels wrapped around the affected admission of suspected AFP
parts for about 10 minutes, 2-3 times a day help case:
in relieving pain.
• If transient urinary retention occurs, alternate • Report to higher authority immediately
hot and cold compresses over the suprapubic • Take adequate stool sample
region. • Send the stool sample maintaining cold chain to
Caution: No massage or intramuscular district headquarter
injections as it may further precipitate
paralysis. Watch for progression, particularly
for the involvement of the respiratory muscles.
• There is no specific drug therapy for polio. For
fever and pain, use Paracetamol or Ibuprofen
• Referral to a tertiary care center with a
ventilatory support facility, if there is
Figure 28.1: A child

with a deformity of
her right leg due to
polio
Page 252
Figure 28.2 Virological Classification
Bibliography:
April 2015
Further reading:
1. Government of India, Ministry of Health and Family Welfare. Field Guide - Surveillance of Acute
Flaccid Paralysis. 3rd edition. 2005: New Delhi, MOHFW-NPSP; pg-42.
2. Francis PT. Surveillance of acute flaccid paralysis in India. The Lancet. 2007 Apr 21; 369(9570):
1322-3
3. Francis PT. Non-Polio AFP rate and Polio Eradication. Indian Pediatrics. 2008 May;45(5):422-3.
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Page 253
29. FEBRILE SEIZURES
1. Introduction
• Febrile seizures are brief (2-5 min), generalized
tonic-clonic and self-limited seizures followed
by a brief post-ictal period of drowsiness, in an
otherwise healthy, febrile child of 6 months to 5
years of age, without any evidence of
underlying neurological disease.
• They are the most common seizure disorder
during childhood, with a uniformly excellent
prognosis. Figure 29.1 Tonic-Clonic Seizure
• They occur rarely before 6 months and after 5
years of age. The peak age of onset is 3. Investigations
approximately 14-18 months of age, found in 3-
• Lumbar puncture: A lumbar puncture with
4% of young children.
examination of CSF is essential to rule out
• There is a strong family history of febrile possibility of meningitis in cases with first
convulsions in siblings and parents, suggesting episode of febrile seizures.
a genetic predisposition.
• EEG has no role in case of simple febrile
• Except for the cases at high risk, simple febrile seizures. However, in cases with atypical febrile
seizures rarely develop into epilepsy. seizure or in a child with high risk for
developing epilepsy, it may be helpful.
2. SALIENT FEATURES
• Febrile seizures usually occur when the 4. High risk for developing
temperature is rising rapidly, to generally 39°C
(102°F) or more of core temperature. They are Epilepsy
of two types: It includes a positive family history of Epilepsy,
(i) Typical (simple) febrile seizure occurs on Initial febrile convulsion prior to 9 months of age, a
day 1 of fever, does not last for more than 10 prolonged or atypical febrile seizure, delayed
minutes; generalized tonic-clonic; generally, not developmental milestones and an abnormal
more than one episode within 24 hours. neurological examination.
(ii) Atypical or complex febrile seizure may
persist for more than 15 minutes; it could be 5. Treatment
focal in nature; more than one episode of
Most febrile seizures are brief and would be over
seizure in 24 hours; associated with abnormal
by the time a child is brought to the doctor or health
neurological findings or deficits. An organic
facility. Management includes definitive diagnosis,
cause such as an infectious or toxic process
restraint in investigations, treatment of an acute
should be considered and investigated.
episode, prophylaxis for future episodes and family
• Late onset febrile seizures, persistent febrile counselling. Role of defervescence in preventing
seizures, generalized epilepsy and Febrile febrile seizures is questionable.
seizure plus (GEFS+) and febrile status
epilepticus (FSE) are part of the Spectrum of
febrile seizures
5.1. Nonpharmacological
Clear the airway, semi-prone lateral position and
Oxygen therapy.
Page 254
5.2. Pharmacological Phenobarbitone and Valproate may be used in
• In cases presenting with seizures, the mainstay infants and older children, respectively, for 1-
of management is prompt administration of 2 years. Carbamazepine and Phenytoin are not
anticonvulsants. useful.
• The best drug is Diazepam / Midazolam/
Lorazepam in a dose of 0.3 mg/kg by slow 6. Patient/parent education
intravenous or rectal route. It can be repeated, if • The parents and caretaker should be assured of
seizures do not subside (per rectal dose may be the benign nature of the disease and should be
given up to 0.5 mg/kg/dose). told that no neurological deficit or mental
• Intermittent prophylaxis (during febrile illness) retardation occurs as a result of simple febrile
- It is a safe and effective method of seizure.
prophylaxis but does not reduce the risk of • They should be taught about control of fever at
future Epilepsy. home.
- Tab Clobazam 0.75 mg/kg for 2-3 days in 2 • They can be taught to give Diazepam per
divided doses during fever or Tab/Syr. rectally at home.
Diazepam 0.3 mg/kg/dose every 8 hours (1 • Routine immunization as per schedule should be
mg/kg/day) for 2-3 days of febrile illness, followed.
started on the day of onset of fever. Dose can
• After DPT vaccination, oral Paracetamol 15
be adjusted, if over sedation or ataxia noted.
mg/kg/dose every 6 h for 2 or 3 days and
• Continuous prophylaxis similarly, after measles vaccination, oral
- Febrile status, complex and recurrent febrile Paracetamol in the same dose started from the
seizures (>6/year in spite of intermittent day of vaccination and given for 3 to 4 days to
prophylaxis) may need EEG, neuroimaging avoid precipitation of febrile seizures.
and continuous prophylaxis with AED.
Bibliography:
April 2015
Further reading:
1. Pratibha D. Singhi, M. Srinivas. Febrile Seizures. Indian Pediatrics. 2001; 38: 733-740.
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Page 255
30. Acute Nephritis
- Oral Penicillin 25000-50000u/kg/Day
1. Introduction: OR
• It follows streptococcal infection of throat or
- Inj. Penicillin 25000-50000 U/kg/Day IM/IV
skin by 1-2 weeks. Glomerular injury will
in 4 divided doses x 10 days
clinically present as acute nephritis.
OR
• In majority of pediatric patients, it is Post
- Erythromycin 40mg/kg/day in 4 divided doses
Streptococcal glomerulonephritis.
X 10 days
• Age group 3-12 years.
Although a 10-day course of systemic antibiotic
• Disease is self-limiting and generally resolves in
therapy with penicillin is recommended to limit
one month; however, microscopic urinary
the spread of the nephritogenic organisms to
changes may persist up to one year.
other children’s, antibiotic therapy does not
affect the natural history of acute nephritis.
2. Signs & Symptoms: • Diuretics: Frusemide1-2mg/kg/day in 1-2
Hematuria, Oedema, Hypertension, Varying degree divided doses
of oliguria or anuria. May present with CCF. Many • Antihypertensive:
primary or secondary Glomerular diseases will (a) Nifidepine: Usual Pediatric Dose of nifidepine
present as acute Nephritis. for Hypertensive Emergency
- Immediate release capsules: 0.25 to 0.5
3. Lab Investigations: mg/kg/dose (maximum 10 mg/dose) repeated
• Urine exam: RBCs, RBC casts, significant every 4 to 6 hours if necessary. Maximum
dose: 1 to 2 mg/kg/day.
proteinuria2+/3+
- Initial doses less than or equal to 0.25
• ASO titre increases mg/kg/dose may result in a less dramatic
• Chest X-ray: Cardiomegaly, Pulmonary decrease in blood pressure and be safer than
vascular congestion, Effusion larger initial doses. Some centers use initial
• Haemogram: Normocytic normochromic doses of 0.1 mg/kg/dose.
anaemia (b) Enalapril: Usual Pediatric Dose for
• BUL, Serum Creatinine raised Hypertension
- Oral tablets or solution: Children 1 month to
17 years: Initial dose: 0.08 mg/kg/day (up to 5
4. Complication: mg) in 1 to 2 divided doses. Adjust dosage
Congestive heart failure, encephalopathy may occur based on patient response.
in a few patients. - Maximum dose: Doses greater than 0.58
mg/kg (40 mg) have not been evaluated in
pediatric patients.
5. Treatment
5.4 Rest
5.1 Diet-Proteins, sodium, potassium should be
restricted. Urine output should be measured 6. Refer patient to higher
accurately. center in case of following
5.2 Daily monitoring of weight. condition
Protein restriction up to 0.6mg/kg/day • CCF
5.3 Drugs: • Uncontrolled HTN or its complications
• Antibiotics
Page 256
Bibliography:
April 2015
3. Hay Jr. WW, Levin MJ, Deterding RR, Abzug MJ. Current Diagnosis and Treatment: Pediatrics.
22nd Edition. McGraw-Hill Education; 2014


Page 257
31. Nephrotic Syndrome
1. Introduction: 4. Complication
• Nephrotic syndrome is characterized by massive Spontaneous bacterial peritonitis is the most common
proteinuria, hypoalbuminemia and edema. complication which should be treated adequately before
Hyperlipidemia is usually associated; hematuria, starting steroids
hypertension and impaired renal function are 5. Management
occasionally seen.
• More than 90% of childhood nephritic syndrome is
5.1. 1st Episode
primary (idiopathic). Other causes are • The child should receive a high protein diet no
Amyloidosis, Vasculitis, SLE, Post-infectious GN extra salt is given.
and Hepatitis B Nephropathy. • Prednisolone (2mg/kg/day) in 2-3 divided doses
• Nephrotic syndrome in children can be divided into along with antacid given till patient goes into
two groups based on renal histological remission (Urine Albumin 1+/absent for 5 days)
characteristics: OR up to 8 weeks and then tapered to
i) Minimal change nephritic syndrome (MCNS): 2mg/kg/alternate day x3-6 months and then
This is usually sensitive to steroids with a stopped
satisfactory long-term outcome. • Ideal calculation 60mg/m2 BSA
ii) Nephrotic syndrome with significant lesions: 5.2. Relapse:
It is usually associated with less satisfactory • Urine Albumin 2+ >5 days / oedema. Sometimes
course, tends to be steroid resistant and a resolves in a week if precipitated by infection, then
significant proportion progress to chronic renal infection is treated.
failure. • If not resolved continue Prednisolone 2mg/kg/day
in 2-3 doses till urine is protein free for 5 days,
2. Clinical Features: then taper alternate day x 4 week and then stop.
• The onset is insidious with edema first noticed • General care
around the eyes and subsequently around the legs. • Ca++ & K+ supplement if on Frusemide
• Gradually edema may become generalized, with • Frusemide: 1-2mg/kg/day for edema with expert
ascites, hydrothorax and hydrocele. Severe muscles advice.
wasting are seen. 5.3. Treatment of frequent relapses:
• It is a triad of hypoproteinemia, hyper • Long term alternate day Prednisolone: Following
cholesterolemia and proteinuria. completion of treatment for relapse, alternate day
Prednisolone is slowly tapered to minimum
maintenance dose (0.3 – 0.7mg/kg). The dose is
maintained for 9-12 months.
• Levamisole: After inducing a remission,
Levamisole is administered at a dose of 2-2.5
mg/kg on alternate days. Co-treatment with
Alternate day Prednisolone is given in decreasing
doses, until a dose of 0.3-0.5mg/kg is reached, for
2-3 months.
• Cyclophosphamide and Cyclosporine A are used
in some cases.
6. Refer to higher center
Fig 31.1 Edema Around Eyes & Generalized Edema • For confirmation of diagnosis
• Systemic features: Arthritis/ Rash/
3. Investigations: Hepatosplenomegaly
• Urine >3+ proteinuria, No RBCs/ Casts • Persistence of Hypertension / Azotemia/
• Azotemia not significant Hematuria
• Serum proteins< 3.2gm/dL • Steroid dependent or resistant or frequent relapse
• Serum cholesterol raised
Page 258
Bibliography:
April 2015
Further reading:
1. Bagga A. Revised guidelines for management of steroid-sensitive nephrotic syndrome. Indian Journal
of Nephrology. 2008;18(1):31-39.
2. Indian Pediatric Nephrology Group, Indian Academy of Pediatrics. Consensus Statement on
Management of Steroid Sensitive Nephrotic Syndrome. Indian Pediatrics. 2001 Sep; 38(9):975-86.
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32. Congestive Heart Failure (CHF)
Slow weight gain, easy fatigability, persistent
1.Introduction: horse crying, wheezing, excessive perspiration,
Every Cardiac patient has potential to develop CHF.
puffiness of face, edema, not able to suck at
It is not a diagnosis. It is a clinical syndrome due to
mother’s breast due to breathlessness.
an underlying anatomical or pathological cause
which is the primary diagnosis.
2.Definition: Congestive cardiac failure is
defined as “inability of the heart to maintain an
output, at rest or during stress, necessary for the
metabolic needs of the body (systolic failure) and
inability to receive blood into the ventricular cavities
at low pressure during diastolic (diastolic failure)”.
3.Etiology
The causes of diastolic failure are given below:
i) Mitral or tricuspid stenosis.
ii) Constrictive pericarditis
iii) Restrictive cardiomyopathy
iv) Acute volume overload (acute aortic or mitral
regurgitation)
v) Myocardial ischemia
vi) Marked ventricular hypertrophy
vii) Dilated cardiomyopathy
The causes of systolic failure or mixed systolic Figure 32.1: Symptoms of CHF
diastolic failure can be divided into two groups
according to age.
5. Signs:
• The commonest cause of CCF in infants is
• Left sided failure is indicated by tachypnea and
Congenital heart disease, whereas in the older
tachycardia.
children it is Rheumatic fever and Rheumatic
heart disease. • Persistent cough, wheezing, crepts in the chest.
• Causes of Congestive Cardiac Failure • Right sided failure signs are hepatomegaly,
Infants: facial edema, edema on feet.
- Congenital heart disease
- Myocarditis and primary myocardial disease
- Paroxysmal tachycardia
- Anemia
Children:
- Rheumatic fever and RHD
- CHD complicated by anemia infection
- Hypertension
- Myocarditis
- Upper respiratory obstruction.
4. Symptoms: Figure 32.2: Edema on feet
Page 260
6. Treatment: 6.2 Oral Diuretics
It is based on following principles: • Frusemide: 1 - 2 mg/kg/day or
i. Reducing cardiac work. • Hydrochlorothiazide: 1 - 1.5 mg/kg/dose every
ii. Augmenting myocardial contractility. 12 - 24 hours or
iii. Improving cardiac performance by reducing the • Spironolactone: 1 - 2 mg/kg/day
heart size.
iv. Correcting the underlying cause. 6.3 ACE inhibitors
• Indicated for all patients with congestive heart
• Control of excessive salt and water retention failure.
with diuretics.
• Captopril: 0.1 to 0.5 mg/kg/dose oral every 8 to
• Improve cardiac contractility with digoxin. 12 hourly upto 4 mg/kg/day or
• Prevent and reverse neuro-hormonal changes • Enalapril: 0.1 mg/kg/dose oral every 12 - 24
that lead to progressive worsening of cardiac hourly upto 0.5 mg/kg/day
status with beta blockers, ACE inhibitors.
6.4 β-blockers
6.1 Digoxin • β-blockers is an integral part of congestive heart
• Drug of choice in chronic CHF with atrial failure therapy nowadays.
fibrillation.
• Metaprolol or carvedilol is also used
• In CHF with sinus rhythm it gives symptomatic
benefit
• Dose
6.5 Diet
Calories - Recommended daily dietary allowance
- Total digitalizing dose in children: 30 - 40
plus 20 - 30% in shunt lesions Avoid salty foods and
mcg/kg. ½ the total dose stat: ¼ after 8 hrs; ¼
additional salt in cooking Iron supplementation
after 16 hrs.
- Daily maintenance dose: ¼ of total
digitalizing dose. Once daily or 2 divided 7. When to refer
doses. • Severe respiratory distress
• Hypokalemia may aggravate digitalis toxicity • Acute pulmonary oedema
especially with concomitant diuretic • Refractory CCF
administration. Use oral KCl supplement or use
• Cardiogenic shock
potassium sparing diuretics such as
spironolactone.
Bibliography:
April 2015
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33. PICA
1. Introduction: 2. Signs & Symptoms:
• Pica involves repeated and chronic ingestion of Pallor and chronic abdominal pain are main
non-nutrient substances including mud, plaster, complaints.
paint, earth, clay, etc.
• Children with PICA usually have history of 3. Treatment
neonatal insults. • Pica below two years does not need any
• Most of the time, it is self-limiting and intervention.
represents manifestations of family • Children with pica are at increased risk of lead
disorganization, poor supervision, and poisoning, iron deficiency, and parasitic
affectional neglect. infections. They should be investigated for these
• Testing or mouthing of strange objects is normal problems and if present, treated suitably.
in infant and children up to age of 2 years. • Education, guidance and counselling of the
• Common in children from lower socioeconomic family.
strata and at times in the malnourished and • The child has to be kept occupied in other tasks
mentally subnormal children. and provided with the environmental
stimulation.
Bibliography:
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34. NOCTURNAL ENURESIS
1. Introduction: 6. Treatment
Enuresis is defined as normal nearly complete 6.1. Nonpharmacological (effective in
evacuation of the bladder at a wrong place and time
30% cases)
at least twice a month after the fifth year of life.
• Rule out organic causes.
Bedwetting at night is known as nocturnal enuresis.
• Restrict fluid intake in the evening.
Enuresis may be primary or secondary:
• Bladder exercises:
- Hold urine as long as possible during the day.
2. Primary enuresis: - Practice repeated starting and stopping the
Repeated passage of urine into clothes/bed during stream at the toilet bowl.
night in a child more than 5 years of age. Most • Emotional support to child.
common cause in primary enuresis is inappropriate • Behaviour modification- Child should not be
toilet training. Other causes could be genetic, sleep given liquids after meal in the evening. Practice
disorder, reduced Anti Diuretic Hormone (ADH) at getting up from bed and going to the bathroom
night. In some cases, there may be organic etiology at bed time before sleep.
such as obstructive uropathy or UTI. There may be • Alarm device- alarm device is used to elicit a
associated with mental retardation or spinal cord conditioned response of awakening to the
abnormalities. sensation of a full bladder.
3. Secondary enuresis: Indicated only in children > 6 years where
The child has been dry for several months and again sufficient trial of non-pharmacological management
starts bed wetting. Too enthusiastic and immature has failed with following:
toilet training, emotional stress, parent child • Tab. Imipramine: (0.9-1.5 mg/kg/day/PO) 6-8
maladjustment, urinary tract infections, diabetes year (25 mg), 9-12 year (50 mg), >12 year (75
mellitus or diabetes insipidus. can cause secondary mg) once a day at bedtime. Success rate 30-
enuresis. 60%, relapse rate 90%. or
• Tab. Desmopressin: 0.1-0.5 mg at bedtime.
4. Signs & Symptoms: Or
Involuntary discharge of urine after the age at which • Desmopressin acetate (nasal spray, 10 mcg per
bladder control should have been established (5 spray): Start with 10 mcg given at bedtime daily
years). and increase gradually by 10 mcg/per week to a
In primary nocturnal enuresis, child has never been maximum of 40 mcg per day. If effective, it
dry at night while in secondary, child has been should be used for 3-6 months. Success rate is
continent for at least 6 months before the child begins 40-60%; relapse rate is 90%.
to wet again. (Caution: Not effectively absorbed in rhinorrhea. If
not used properly may cause hyponatremia)
5. Investigations:
• Full medical history
7. Referral
• Genital and neurological examination Refer the patient to a higher centre, if organic cause
• Urine for albumin, sugar, microscopy, specific is suspected or when diagnosis is in doubt.
gravity and culture.
• USG voiding cystourethrogram and urodynamic
studies.
Page 263
• Ask the parents to maintain a diary record of dry
8. Parent education
nights; reward the child for such nights. Avoid
• Reassure the parents that condition is self-
punitive measures.
limiting.
Bibliography:
April 2015
Further reading:
1. Mathew JL. Evidence-Based Management of Nocturnal Enuresis: An Overview of Systematic
Reviews. Indian Pediatrics. 2010 Sep;47(9):777-80.
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Page 264
35. Thrush / Candidiasis
1. Introduction: 2. Salient Diagnostic Features:
• Candida fungal infection in the oral cavity is • Thick white patches on an angry red base in the
common and may be seen as early as 7 to 10 mouth may spread to involve the lips, buccal
days of age (peak 4th week of life). mucosa, tongue and palate.
• After infancy it is usually secondary to • Asymptornatic or may cause pain in the mouth,
treatment with broad-spectrum antibiotic. discomfort, anorexia and feeding difficulty.
• Chronic or recurrent oral candidiasis is seen in • Diagnosis is confirmed by the fact that on
children having immuno-deficiency. removing the plaques, spots of bleeding are seen
HIV_AIDS, undergoing cancer therapy and in on the mucosal surface.
severe malnutrition. • Faulty sterilization of bottle and nipple causes
• Hypoparathyroidism, Addison's disease, persistent or recurrent infections / thrush.
Autoimmune disorders are other rare causes.
Figure 35.1: Candidiasis / oral thrush
• In resistant/ chronic cases (patients with major

3. Treatment: Drugs
underlying disease)
• In case of breast fed baby, the medicine has to
Tab. Fluconazole 3-6 mg/kg once daily for 5-7
be applied to mother’s nipples also to prevent
days.
cross / re-infection.
• Clotrimazole 1% cream, gel or lotion, oral 4. Prevention:
application 3-4 times/day after feeding for 5-7 • Emphasize on avoiding bottle feeding /bottle
days (or 1-2 days beyond recovery). hygiene, care/ hygiene of the nipple and
Or treatment of vaginal candidiasis in expectant
• Gentian violet 1% aqueous solution, 1-2 times a mother.
day, for 5-7 days (can stain tissues and clothes).
Bibliography:
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36. Congenital Hypothyroidism
1. Introduction:
• It may be familial or sporadic, goitrous or non-
goitrous. 4. Treatment of Congenital
• In about 85% cases the etiology is dysgenesis.
Hypothyroidism
• All new born babies should be screened.
As soon as possible diagnosis.
2. Signs & Symptoms: 4.1 Counseling of Parents

At birth – 4.2 Eltroxin
• Lethargy • 10-15 microgram/kg---start higher dose
• Prolonged Unconjugated Hyperbilirubinemia • Do NOT use liquid preparation
• Constipation • On above dose, T4 Normalises in 1 week and
• Hypothermia TSH in one month
• Bradycardia • Aim: to normalize serum T4, avoid
• Large Anterior fontanelle hyperthyroidism, promote normal growth and
• Posterior fontanelle more than 0.5 cm which is development
normal in only 3% neonate
• Somnolence and Choking spells during nursing
are present during first month of life
• Affected infants cry little, sleep much
Develop with passage of time
• Large tongue
• Hoarse cry
• Facial Puffiness
• Umbilical Hernia
• Hypotonia
• Mottling
• Cold hands and feet
3. Investigation: Fig 36.1: Congenital Hypothyroidism: Before &
• TSH level should be estimated after 72 hours of after treatment
life if TSH is more than 20 mU/L then
Hypothyroidism is considered and Eltroxin 4.3 Repeat T4 and TSH at 2 and 4
should be started. weeks after initiation of therapy.
• Second screening at 2 to 6 weeks (routinely in
• After one year tests to be done 1-2 monthly
VLBW and NICU graduates)
• Between 1 and 3 years do tests 2 to 3 monthly
• Over 3 years do tests yearly till growth is
complete.
Page 266
Bibliography:
1. Kliegman R, Stanton B, Geme JS, Schor N. Nelson’s Textbook of Pediatrics. 20 th Edition. Elsevier;
April 2015
Further reading:
1. Rose SR et. al. Update on newborn screening and therapy for congenital hypothyroidism. Pediatrics.
2006 Jun;117(6):2290-303.
2. Nair PS, Sobhakumar S, Kailas L. Diagnostic re-evaluation of children with congenital
hypothyroidism. Indian Pediatrics. 2010 Sep;47(9):757-60.
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37. Urinary Tract Infection (UTI)
1. Introduction: 3.3 USG Abdomen and Pelvis,
Approximately 8% of girls and 1 - 2% of boys are Voiding Cystourethrogram
likely to get UTI during childhood. A significant These will identify upper and lower urinary tract
proportion of children less than 2 years developing abnormalities, including vesicoureteral reflux in
UTI have underlying urinary tract anomalies, most complicated UTI
often vesico-ureteric reflux (VUR). UTI in a
setting of VUR may lead to renal scarring, an
important cause of chronic renal disease. Early 4. Common organisms
recognition and treatment of UTI and urinary
anomalies is essential to prevent such
responsible for UTI:
• E. coli, Occasionally Klebsiella, Staph
complications.
epidermidis or Strep fecalis may be responsible.
• A colony count of > 105 colony forming units
2. Signs & Symptoms (CFU) / ml of single species in a clean catch
2.1 Neonates specimen indicate significant bacteriuria.
Sepsis like features with fever or hypothermia, • Presence of any bacteriuria in suprapubic
lethargy, poor feeding, poor weight gain, jaundice specimen is significant.
and shock; urinary symptoms may be absent.
2.2 Infants and children below 2 5. Treatment
For the purpose of management UTI is divided into
years complicated and uncomplicated UTI.
Unexplained fever; urinary symptoms minimal or
absent. 5.1 Complicated UTI
• Temperature > 39°C, persistent vomiting, renal
2.3 Adolescents angle tenderness and systemic toxicity are
Mostly related to lower urinary tract such as
features of complicated UTI
dysuria, frequency, urgency and suprapubic pain.
• Infants below 3 months of age and those with
Renal parenchymal involvement is indicated by
complicated UTI should receive parenteral
high fever, chills, rigors and flank pain.
antibiotics initially.
• In young infants (< 3 months) entire treatment is
3. Investigations: parenteral
3.1 Urine analysis - Cefotaxime 100 - 150 mg/kg/day in 3 div
May suggest UTI in the form of increased doses, or
leukocytes in urine. Gram stain of centrifuged urine - Ceftriaxone 75 mg/kg/day in 1-2 doses, or
specimen may show bacteria. Dipstick for nitrite - Gentamycin 5 - 7.5 mg/kg/day single dose,
reduction and leukocyte esterase may help in rapid or
diagnosis. - Amikacin 15 - 20 mg/kg/day single dose, or
• For older children, after first 2 - 3 days, oral
3.2 Urine culture antibiotics may be started based on
• This is the only confirmatory test for UTI. antimicrobial sensitivity. Total duration of
Every effort must be made to properly collect treatment is 10 - 14 days.
and send a urine sample before antibiotic is • Oral antibiotics
started. In infants and young children UTI - Amoxicillin 20 - 40 mg/kg/day in 2 - 3
should be suspected if there is unexplained doses, or
fever. - Cefadroxil 30 mg/kg/day in 2 doses, or
• A midstream clean catch specimen is ideal. - Cephalexin 50 mg/kg/day in 3 doses, or
Soap or antiseptic solution should not be used - Cefixime 8 mg/kg/day in 2 doses, or
before collection. In infants, urine can be - Ciprofloxacin 10 - 20 mg/kg/day in 2 doses
obtained by suprapubic aspiration.
Page 268
5.2 Uncomplicated UTI kg) or Cefadroxil (5 to 10 mg per kg) for 7 to 10
days (based on sensitivity).
• Children > 3 months of age and those who do
not have features of complicated UTI can be • Though fluoroquinolones are effective and safe
treated with oral Amoxicillin (10 to 15 mg per for UTI, they are not the first-line antibiotics.
Bibliography:
April 2015
Further reading:
1. Lin CW, Chiou YH, Chen YY, et. al. Urinary tract Infection in neonates. Clinical Neonatology. 1999;
6 (2). [cited 18 July 2016]
Available from: http://www.son.org.tw/upload/Jour/2/199912/1.pdf
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Page 269
Obstetrics &
Gynaecology
3. Obstetrics and Gynaecology
1 Normal Pregnancy 270
2 Normal Labour 276
3 Clinical Care for high risk pregnancy 282
4 Obstetric complications 290
5 Medical disorders complicating pregnancy 309
6 Comprehensive Abortion Care 319
7 Common Gynaecological problems 322

1. NORMAL PREGNANCY
Antenatal period is the most crucial period as the complications after delivery (PPH, Retained
services provided during this period can have positive Placenta, Infection)
impact on health of both the mother and her child. • Past history: Hypertension, Diabetes Mellitus,
Tuberculosis, Asthma, Heart disease, any other
Essential obstetric care to surgical procedures undergone, medications
taken during peri conceptional period, history of
every pregnant woman bleeding.
• H/O current symptoms, perception of fetal
1. Registration before 12 weeks movements if pregnancy > 16 weeks.
2. Detailed history at first visit 3. Schedule of Examination

• Menstrual history: Regularity of cycles, date of Ideally all the ANCs should be examined monthly
LMP, calculate EDD and record on Mother after registration. If it is not possible to attend ANC
Child Protection (MCP) card clinic monthly, then checkup should be carried out at
• Obstetric history: Number of prior pregnancies least five times during the pregnancy. First 8-12
and outcome of each pregnancy (full term birth, weeks, second between 14-20 weeks, third at 22-26
preterm birth, abortion), place and mode of weeks, fourth at 28-32 weeks and fifth at 36-40
delivery, weight of baby, Live birth/stillbirth, weeks.
Table 1: Examination at Antenatal Clinic

*Height *Breast examination
Weight: Compare with previous visit (calculate *Systemic examination: Auscultate chest
BMI in first trimester)
Pallor, icterus P/A: Fundal height & its correlation with period of
amenorrhea (POA)
Edema over feet, hands, face Fetal presentation and position after 32 weeks
Blood pressure Fetal heart rate
* During first check up

• The last two visits are important as many of the • Medical officer should perform at least one
pregnancy complications are detected during checkup during the third trimester and
last trimester. For 'high risk' mothers more auscultate her chest to rule out any systemic
frequent examinations will be required. abnormality.
Page 270
4. Investigations
Table 2
Hemoglobin estimation VDRL
Urine Analysis: Protein and sugar Blood sugar testing
Test for sickling in selected tribal area Malarial parasite testing in endemic area.
Blood grouping, Rh typing Hepatitis B surface antigen (HBsAg)
Voluntary HIV testing Ultrasonography (around 18 weeks)
5. Examination and action to be taken during ANC check up

Table 3
Examination Action
Edema • Examine whether edema is on one leg or both legs and is it pitting. Look for
edema over face, hands, and abdomen. Check for proteinuria and
hypertension.
• High blood pressure and albuminuria present, refer to specialist as she has pre-
eclampsia.
• History of kidney disease, if yes refer to specialist.
• If edema is on one leg, refer to specialist.
• If bilateral pedal edema without albuminuria and normal BP: Reassure mother,
check for anemia and give IFA tablets as required
Weight gain • Record monthly weight on MCP card of mother, calculate weight gain since
the previous visit
• Weight gain more than 3 kg. in a month: Suspect preeclampsia
• Weight gain less than 1 kg. in a month: Suspect fetal growth retardation.
Blood Pressure • If 140 / 90 mm Hg or more, advise mother to rest for half hour and then repeat
the BP recording. Check for proteinuria
• If systolic between 140-160 and /or diastolic 90 or above: advise extra rest
and refer to MO PHC
• If systolic 160 or more or diastolic > 100: refer to specialist
Fundal Height Examine fundal height in weeks and compare with calculated duration of
pregnancy as per LMP. If it is greater or lesser refer to specialist. Causes of fundal
height less or more than expected are given in table below.
Fetal Presentation Non-cephalic at 34-36 weeks. Refer to Obs/Gyn specialist (correction can be
attempted at 36 weeks in suitable cases).
Fetal Heart Rate FHR < 120 or > 160 /minute: Refer to specialist.
Hemoglobin % Hb 11 gm% or more: IFA 1 tablet daily for 180 days

Hb between 7-11 gram%: Start IFA double dose* and re-examine after one month -
If improvement of Hb by more than 1gm%, continue IFA. Give tab Albendazole
Page 271
Examination Action
(during second trimester)
Hb< 7 gm % - Refer anemia treatment guidelines
Proteinuria If proteinuria present suspect pre-eclampsia and refer to specialist.
Risk factors All high-risk pregnancies should be checked by MO and then referred to specialist
if necessary for further checkup or during delivery depending upon the risk factor.
* For better absorption, IFA tablets should be taken 1.30 hours before meals
Table 4
Fundal height < Period of Amenorrhea Fundal height > Period of Amenorrhea
Wrong dates Wrong dates
Infrequent periods prior to conception Polyhydramnios
Intrauterine Growth retardation(IUGR) Twins
Oligohydramnios Big baby
Intrauterine fetal death. Hydatidiform mole
Uterine fibroids
• Practicing safe sex.

6. Education and counseling • Self-reporting of danger signals, e.g. Abdominal
regarding care during pain, severe headache, giddiness, palpitations,
pregnancy easy fatigability, breathlessness, fever,
generalized edema, vaginal bleeding, watery
6.1. First and second trimester: discharge per vaginum, blurred vision,
excessive vomiting, reduced fetal movements.
• Diet: Two meals, breakfast and evening snacks.
Rich in proteins, iron, calcium, vitamins, 6.2. Third trimester:
inclusion of sprouted legumes, pulses, green
leafy and other vegetables, seasonal fruits, milk- • Avoid heavy work and jerky travel on bad
milk products. Consumption of Iodized salt roads.
• Consumption of Folic acid tablets in first 12 • Importance of institutional delivery, safe
weeks, iron folic acid tablets after 12 weeks for delivery, inform Toll Free No.102 and 108 for
180 days for anemia prophylaxis. free ambulance service, JSY, JSSK and other
• Tetanus Toxoid 2 doses/booster dose. benefits, Plan for place of delivery, preparation
• Consumption of Calcium carbonate (500mg) + for delivery.
Vitamin D tablets 1 tab twice a day. • Importance of early initiation of colostrum
• Rest: 2 hours in afternoon and 8 hours at night feeding within half an hour of birth & exclusive
in lateral position. breast-feeding for 6 months, child immunization
and contraception especially PPIUCD.
• Exercise: Walking for 30 minutes daily.
• Identify birth companion.
• Habits: Avoid tobacco in any form, avoid
alcohol.
Page 272
7. Identify high-risk mothers:
Table 5:
Risk factors detectable during Abnormalities developing during

first check up Current pregnancy
• Age: Teenage/ elderly primi • Anemia

• Para 4 and above • Hypertension, proteinuria
• Short stature, limping gait, vertebral spine • Vaginal bleeding during pregnancy
abnormalities
• Premature rupture of membranes (PROM)
• Bad obstetric history: H/O stillbirth, neonatal
death, LBW baby, recurrent abortions • Gestational Diabetes Mellitus (GDM)
• Previous Caesarean delivery • Fundal height < POA or > POA
• H/O Preeclampsia/eclampsia, PPH, retained • Uterine over distension: Twins,

placenta during previous pregnancies Polyhydramnios
• Preexisting medical conditions: Heart • Fetal malpresentation persisting near term

disease, Diabetes Mellitus, renal disease • Pregnancy > 41 weeks
• HIV /VDRL positive gravida • Reduced fetal movements
• Rh negative gravida
7.1. Actions suggested for some high-risk indicators
Table 6:
RISKS ACTION
1. Elderly Primi
• Hypertension during pregnancy • Refer to specialist soon after registration for evaluations to
exclude fetal anomalies (biochemical markers and
• Gestational Diabetes ultrasonography)
• Difficult labour - Chances of • Regular ANC: B.P, urine analysis every month
caesarean section are higher
• Pelvic assessment at or after 36 weeks.
• Fetal abnormalities.
• Institutional delivery under care of specialist.
2. Teenage primi
• Hypertension during pregnancy • Regular antenatal care

• Anemia • Hb%, BP, urine analysis more frequently
• Pre-term labour • Adequate rest
• Fetal growth retardation. • IFA tablets, nutrition guidance
• Difficult labour • Pelvic assessment at 36 weeks
• Hospital delivery.
Page 273
RISKS ACTION
3. Primi: Height less than 145 cms Regular ANC checkup.
Difficult labour Assessment of place of delivery by specialist. Observe progress
of labour partographically.
4.Primi having vertebral /limb deformity Regular checkup at PHC,
Difficult labour Assessment by specialist for place of delivery.
5. Grand multipara (para 4 and more)
• Anemia • Supplement IFA, nutrition guidance
• Malpresentation • At 34 and 36 weeks look for fetal malpresentation & refer
• Atonic PPH • Hospital delivery - Active management of 3rd stage of
labour - Keep IV line ready
• Uterine rupture
• Avoid injudicious use of oxytocics for augmenting labour
Bibliography
1. Government of India, Ministry of Health and Family Welfare National guidelines for calcium
supplementation during pregnancy and lactation. 2014. New Delhi: MoHFW.
2. Government of India, Ministry of Health and Family Welfare. National guidelines for deworming
during pregnancy. Dec 2014. New Delhi: MoHFW.
3. Government of India, Ministry of Health and Family Welfare. National Iron + Initiative; Guidelines for
control of Iron deficiency Anaemia; 2013. New Delhi: MoHFW.
4. Government of India, Ministry of Health and Family Welfare. Guidelines for ANC & Skilled
attendance at Birth by ANMs, LHVs, SN, 2010
5. Government of India, Ministry of Health and Family Welfare. Skilled birth attendance: A handbook
for ANMs, LHVs & Staff Nurses, 2010
6. Government of India, Ministry of Health and Family Welfare. Trainer’s guide for conducting Training
of ANMs, LHVs & staff Nurses, 2010
7. Government of India. MH Protocol posters: Maternal health division, Ministry of Health & Family
Welfare
Further reading
1. Dutta DC. Ed: Konar H. Textbook of Obstetrics. 7th Edition. Kolkata: New Central Book Agency Pvt
Ltd; 2010
2. Maternal Health Guidelines. Maternal health division, Ministry of Health and Family Welfare,
Government of India. [Internet] [Cited 2016 July 8]
Available from: http://nrhm.gov.in/nrhm-components/rmnch-a/maternal-health/guidelines.html
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Page 274
Figure 1.1: Fundal Height Measurement and Obstetric Examination
Page 275
2. NORMAL LABOUR
Every delivery should be conducted by a skilled birth Fetal heart rate: Normal FHR 120-160/min, regular.
attendant. At a PHC, cases admitted for delivery need
to be assessed for detection of any abnormality and 3.Vaginal Examination:
complications. It is necessary to give initial care to
the complicated cases and execute appropriate Take adequate aseptic precautions and note:
referrals.
Cervical dilatation in cm and effacement as
When a woman is admitted for delivery, review ANC
percentage
card (Lab test results, weight gain, risk factors,
complication if any) and perform complete Membranes intact or ruptured. If ruptured, since how
examination. many hours?
Color of liquor: Clear, meconium stained or blood
1.General examination: Pulse,
stained.
temperature, blood pressure, pallor, icterus, edema
Presenting part: Vertex or other than vertex.
2. Obstetric examination per
Position: Occiput anterior or posterior
abdomen:
Head is well flexed (posterior fontanel felt easily) or
Uterine contractions: Frequency(No/10minutes), deflexed (anterior fontanel also felt easily)
duration in seconds and intensity
Station of presenting part in relation to ischial spines
Fundal height: Proportionate to POA or greater or
Presence of caput or molding
lesser than POA
Assessment of pelvis and test for CPD
Presentation: Cephalic or non-cephalic
Engagement of head: 2/5th or less fetal head 3.1. Pelvic Assessment
palpable per abdomen
Table 1
Parameter Adequate Suggestive of abnormality

Sacral promontory
Not felt Felt easily
figure 1
Diagonal Conjugate* >11.5 cms < 11.5 cms
Sacral curvature Well curved Flat
Lateral Pelvic walls Parallel Converging
Ischial spines Both cannot be palpated simultaneously Both can be palpated simultaneously
Subpubic Angle Accommodates two fingers (850) Acute
Inter tuberous diameter Accommodates closed fist (4 Knuckles) Cannot accommodate 4 knuckles
* If sacral promontory is felt, distance between sacral promontory and lower border of pubic symphysis is
measured.
Page 276
Fig 2.1. Palpating Sacral Promontory & Measuring Diagonal Conjugate
Figure 2.2. Assessing transverse diameter of Outlet Figure 2.3. Assessing Subpubic Angle
3.2. Clinical Examination for CPD
• Place the woman in dorsal position.
• Hold the fetal head by left hand.
• Place two fingers of gloved right hand into the vagina at the level of ischial spines.
• Place the thumb of right hand on the pubic symphysis.
• Push the head into the pelvic inlet and note whether it descends into the pelvis (felt by fingers in vagina) or
overhangs on the pubic symphysis. If head descends with no overlap at pubic symphysis: No inlet CPD.
• If the head is engaged, it indicates that the pelvic inlet is adequate.
4. Monitoring during active phase

Table 2
Examination / Observation Periodicity
Maternal pulse and FHR Every 30 minutes
Uterine contractions Every 30 minutes
Maternal temperature, BP, urine volume Every four hours
Vaginal Examination Every four hours
Note the time of rupture of membranes and • To assess cervical dilatation, station and
perform vaginal examination immediately position of presenting part.
• To rule out cord prolapse and see the color of Assess and monitor the progress of labour
liquor. by using ‘Simplified Partograph’ adopted by
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GOI to record FHR, liquor, cervical dilatation,
uterine contractions, medications administered
5. Management of Labour
during labour, maternal pulse, blood pressure
and temperature. 5.1 First stage of labour showing
Points to Remember satisfactory progress
• This graph is used only during active phase of Continue observation till second stage starts.
labour.
• The complications requiring immediate
5.2 Second stage of Labour
intervention need to be excluded first. • Cervix is fully dilated.
• Signs of imminent delivery: Mother starts
4.1. Partograph pushing (bearing down). Fetal scalp seen at
vulva, perineum bulges, anus gapes. Mother
On this graph, one square represents one hour on gets sensation of defecation.
horizontal axis. On vertical axis, one square • Encourage the mother to push only during
represents cervical dilation of one centimeter. contraction.
4.1.1 Phases of first stage and alert and • Monitor progress and fetal wellbeing during
action line: second stage.
• Latent phase: Cervix dilates very slowly up to 4 • Note FHR every 15 minutes.
centimeters. It may take up to eight hours for • Assess descent of presenting part (fetal station)
this. every 15 min.
• Active phase: 4 cm onwards; cervix dilates • Look for caput, moulding, meconium staining
rapidly at the rate of about 1 centimeter per of liquor.
hour. • Support the perineum and deliver the head
• Alert Line: An oblique line on the graph from 4 gently
to 10 centimeters progressing at the rate of 1 • Deliver the shoulders
centimeter per hour. • Keep the baby on mother’s abdomen on a pre-
• Action Line: Parallel line four hours to the right warmed towel and give immediate care.
of alert line • Follow universal bio safety precautions.
• Delivery of baby takes place usually within 30
4.1.2 Recording on partograph: minutes in a multi and 60 minutes in a primi.
• Initiate recording when cervix is 4 cm dilated • Give mediolateral episiotomy under local
and immediately if the cervix is > 4 cm dilated infiltration anesthesia by injecting 1%
on admission to the labour ward. lignocaine, if mother is unable to push or if
• Record the dilatation in cm (symbol x) on the there is undue delay.
alert line and record the time at which
observation has been made on the horizontal 5.3 Third stage of Labour
axis below this point. Deliver the placenta by active management of third
• Perform vaginal examination every 4 hours and stage of labour (AMTSL).
note the cervical dilatation and mark it on the
graph. Active management of 3rd stage of labour reduces
the amount of blood loss due to uterine atony,
• Join the points and interpret the observations.
reduces the chances of having atonic PPH and
requirement of blood transfusion significantly
4.1.3 Interpretation and Action: thereby helping to reduce maternal mortality due to
• Satisfactory progress: Cervical dilatation lies severe PPH.
on left side of alert line, active phase
progression > 1 cm/ hour, Fetal and maternal It is an integral part of skilled attendance at birth and
health parameters are normal. is mandatory for all deliveries. The steps are as
• Slow progress: Alert line crossed, careful follows:
monitoring to note the progress. At sub centre • After the childbirth, exclude presence of another
and PHC the arrangements for referral to FRU. baby by abdominal palpation
• Action line reached or crossed: Careful review • Give Inj. Oxytocin 10 IU IM. immediately after
to find the cause for delay followed by birth (Oxytocin should be kept in refrigerator).
appropriate interventions. When Oxytocin is unavailable, tablet
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Misoprostol 600 mcg (3 tablets) may be given uterus upwards towards umbilicus. Repeat this
orally. during contraction as required. Only trained
• Check for uterine contraction. SBA should give CCT figure 4.
• Clamp and cut the cord (1-3 min after birth) • After delivery of placenta, give uterine massage
• Deliver the placenta by controlled cord traction to keep the uterus contracted.
(CCT). When the uterus is well contracted give
gentle downward traction on cord while giving
counter traction by other hand pushing the
Figure 2.4: Controlled Cord Traction
6. Care after delivery 7. Augmentation of Labour

• Examine the perineum, vulva, lower vagina for 7.1. Slow progress of Labour
tears.
• Alert line crossed or the action line reached
• Examine the placenta and membranes carefully
• Causes: Hypotonic uterine action, occipito-
for completeness and any abnormality.
posterior position, deflexed head, CPD etc.
• Observe the mother every 15 minutes for two
Refer the case to higher level of care.
hours for general condition, pulse, vaginal
bleeding, pallor, uterine contraction. Labour augmentation is done only when there is
• Repeat uterine massage every 15 minutes for 2 unsatisfactory progress of labour. Amniotomy
hours. (artificial rupture of membranes) and Oxytocin
• Encourage mother to take the baby to breast infusion are offered as per the clinical situation.
within ½ hour of delivery. Labour augmentation should be done in places
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where clinical expertise and facilities for operative • Hyperstimulation: > 5 uterine contractions / 10
delivery are available.
minutes, each lasting for > 60 sec
• If vertex is engaged and cervix is well applied • Uterus failing to relax between the contractions
to the vertex, then controlled ARM can be • Fetal bradycardia (distress)
performed to hasten the progress. • Uterine rupture – if drip is not supervised
• After ARM review progress after two hours. If vigilantly.
progress is still slow, assess uterine • Water intoxication if too much of electrolyte
contractions. If uterine contractions are free infusion is administered.
infrequent and weak then consider Oxytocin • Neonatal hyperbilirubinemia
augmentation after excluding
contraindications.
• If there is no progress after augmentation or if 7.2.4 Treatment of Hyperstimulation:
signs of fetal distress develop, an emergency
Caesarean Section might be required. Hence • Discontinue the drip
such a woman should be referred to a well- • Maternal repositioning (left lateral position),
equipped maternity unit. Oxygen therapy
• Terbutaline 250 mcg can be given IV slowly
over 5 minutes for tocolysis if required
7.2. Oxytocin Augmentation: (only
where specialist is available) Caution:
• For augmentation of labour Oxytocin should
Exclude contraindications before starting never be given intramuscularly.
Oxytocin • Cautious use in multiparous women as the
• CPD, Fetal distress uterus tends to rupture.
• Grand Multiparity, Malpresentation • Misoprostol should not be used for labour
• Scar on the uterus augmentation.
7.2.1 Dose and Administration
• Add 2.5 IU Oxytocin to 500 ml of normal
7.2.5 When to discontinue the drip:
saline or ringer’s lactate. Start infusion at the
rate of 10 drops/min. Observe uterine • If six hours of strong stimulated uterine activity
contractions. is unable to bring progress of labour,
• If contractions are mild increase the drip rate discontinue the drip and review the case.
by 10 drops /min every 30 min until she gets 3 • If there are signs suggestive of fetal distress.
contractions in 10 minutes, each contraction • If after initial satisfactory progress, cervical
lasts for 40-45 seconds and there is good dilatation does not progress for two hours or
relaxation of uterus in between the more in established active phase of labour then
contractions (optimum response). review her. This could be due to cephalo-pelvic
disproportion or large head with deflexion. Such
Drip rate can be increased maximum up to 60 patient may need operative intervention.
drops/minutes. If the contractions are inadequate at
this rate, prepare another drip with 5 IU /500 ml
and start it at the rate of 30 drops/min, increase by 8 Prolonged second stage
8-10 drops every 30 minutes and observe the
response.
If second stage is prolonged for more than 2 hours in
primi and for > 1 hour in multi, then
7.2.2 Monitoring: • Assess size of baby and pelvis again.
Monitor following parameters every 15 minutes, • See whether fetal head is still palpable in
• Drip rate, Uterine contractions – frequency suprapubic region.
and intensity
• FHR and Maternal pulse Refer the case to FRU/DH if:
• Progress of labour
• Failure of fetal head to descend (station fails to
advance)
7.2.3 Complications:
• Increasing caput or molding
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• Suspected CPD including mid-pelvic and outlet • Maternal exhaustion
contraction • Fetal distress
• Occipito-posterior/Occipito-transverse position
Cases of prolonged second stage may require assisted
with arrest at mid-pelvis
instrumental delivery or Caesarean Section.
Bibliography
1. Government of India, Ministry of Health and Family Welfare. Guidelines for ANC & Skilled
attendance at Birth by ANMs, LHVs, SN, 2010
2. World Health Organization. Managing complications in pregnancy and childbirth: A guide for
midwives and doctors. Section 3 – Procedures, 2000/2007
3. World Health Organization. WHO Recommendations for Augmentation of labor. Geneva: WHO, 2014
4. Government of India, Ministry of Health and Family Welfare. Guidelines for pregnancy care and
Management of common obstetric complications by Medical Officers: June 2005. Reviewed by State,
Feb 2006, SFWB, Pune.
5. Government of India, Ministry of Health and Family Welfare. Trainees’ handbook, Trainers’ guide and
Workbook for training of medical officers in pregnancy care and management of common obstetric
complications. Maternal health division, August 2009
6. Government of India, Ministry of Health and Family Welfare. Dakshata: Empowering providers for
improved MNH care during institutional deliveries, April 2015.
7. Government of India, Ministry of Health and Family Welfare. Guidance Note on Use of Uterotonics
during Labour. Maternal health division, Sep 2015.
8. Government of India, Ministry of Health and Family Welfare. Guidance note on Prevention and
Management of Postpartum Hemorrhage, Maternal health division, Dec 2015
Further reading
Ltd; 2010

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3. CLINICAL CARE OF HIGH RISK
PREGNANCY
Common Risk Indicators: 1.1.3 Risk Factors:
• Risk is highest among couples where the age of
• Bad obstetric history (BOH): Recurrent woman is ≥35 years.
pregnancy loss (RPL) • The risk increases after each successive
• Cervical incompetence pregnancy loss, reaching approximately 40%
• Hypothyroidism after three consecutive pregnancy losses.
• Infections: Syphilis
• Rh negative pregnant woman, husband Rh +ve 1.1.4 History:
• Post caesarean pregnancy. • Detailed obstetric history about each pregnancy.
• Diagnosed twins, polyhydramnios. Duration of pregnancy at mishap. Whether USG
• Pregnancy beyond 41 weeks. documented cardiac activity was seen, fetus was
• Hypertension, Preeclampsia live born/stillborn (fresh/macerated stillbirth),
• Vaginal bleeding during pregnancy, APH. baby normal/abnormal.
• Fetal malpresentation persisting at 36 weeks. • H/O Consanguinity, history of infertility,
• Medical diseases: Anemia, Diabetes Mellitus, menstrual abnormality, infections, STD.
Cardiac disease, Chronic Hypertension, Kidney • Personal history: Tobacco, alcohol, caffeine,
disease, Tuberculosis. (Subsequent chapters) medications.
• Other high risk indicators (refer chapter 1). • Personal/familial H/O thrombosis, autoimmune
disorder.
1. Bad Obstetric History
1.1.5 Physical examination:
Bad obstetric history is a term used in day to day a) Look for obesity, hirsutism, acanthosis, thyroid
practice for describing unsuccessful pregnancy enlargement, galactorrhea
outcome in previous pregnancies. A variety of b) P/S & P/V examination: Look for uterine
unsuccessful outcomes are included in this such as fibroids, double uterus, bicornuate uterus,
previous H/O stillbirth, early neonatal death, preterm genital infection, torn or short cervix
delivery, recurrent mid-trimester/early abortions. c) Investigations: Carry out the relevant
investigations as indicated and available
1.1. Recurrent Pregnancy Loss depending on whether the woman has presented
during pregnancy or after the mishap.
1.1.1 Definition: Three or more consecutive
d) During pregnancy:
pregnancy losses
• Hematology, blood group and Rh typing,
1.1.2 Causes: VDRL
• Urine analysis
• Genetic • Rule out Diabetes
• Environmental and occupational exposure to • Antiphospholipid antibody testing
organic solvents, ionizing radiation, toxins, • USG: For uterine abnormalities, Monitoring
tobacco, alcohol early pregnancy
• Uterine anomalies, Cervical incompetence, • Thyroid function, Prolactin
Intrauterine adhesions, Uterine fibroids e) Non pregnant state:
• Infections • Pelvic USG for polycystic ovaries (PCOS),
• Endocrine dysfunction: Polycystic ovary • Hysterosalpingography (HSG), Hysteroscopy
syndrome (PCOS), Luteal phase inadequacy for uterine abnormalities
(LPI), Diabetes Mellitus, Thyroid dysfunction, • Parental karyotype
Prolactin disorders. • Mid luteal serum progesterone and
• Antiphospholipid antibody syndrome (APLAS) thrombophilia profile if available
• Unexplained: In some cases, no cause can be f) Soon after miscarriage:
detected. Chromosomal studies of conceptus
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1.1.6 General Measures: 3. Infections
• Quitting cigarette smoking, tobacco, alcohol and Generally, cause sporadic pregnancy loss.
caffeine consumption Toxoplasmosis, Rubella, Cytomegalovirus, Herpes
• Weight reduction in PCOS cases and Listeria infections do not cause recurrent
• Therapies depending upon cause. pregnancy loss and routine TORCH screening is not
• Psychological counseling & support is indicated. Active syphilis during pregnancy can lead
extremely helpful. to recurrent pregnancy loss.
• 50% Success even if no treatment is given.
3.1. Syphilis during pregnancy
2. Cervical incompetence 3.1.1 Effects: Late abortions, stillbirths, neonatal
deaths, infant having active congenital
• Premature softening and dilatation of internal
syphilis.
cervical os during pregnancy can lead to
protrusion of membranes, rupture of membranes 3.1.2 Diagnosis is serological: VDRL at
and fetal expulsion during second trimester or booking. Treponemal test (TPHA) is
early third trimester confirmatory, however not mandatory.
• Typical obstetric history is diagnostic: Repeated 3.1.3 Treatment:
mid-trimester or early third trimester pregnancy Treatment of maternal disease can prevent fetal
terminations, relatively painless, rapid, often infection and also treat established fetal disease
preceded by rupture of membranes followed by
expulsion of fresh still birth or live fetus • Benzathine penicillin single injection 2.4 Mega
• Symptoms: Low backache, mucoid vaginal units deep IM after sensitivity test as Penicillin
discharge may precede is the only antibiotic that can cross the placenta
• P/S: Bag of membranes may be seen through in adequate amounts to treat the fetus. Check
the cervical os emergency drug tray.
• Vaginal examination: Internal cervical os • For latent disease > 1-year duration, 3 Injections
dilated in absence of uterine contractions, cervix at weekly interval.
may be short. • Penicillin sensitive individuals require
desensitization.
2.1 Investigation: • Erythromycin 2 gms daily in divided doses for
USG may show short cervix, funneling of 14 days can be considered however Penicillin is
cervix, membranes dipping into the cervical recommended during pregnancy.
canal.
• Infant of a VDRL positive mother needs blood
USG assessment of cervical length (25mm or testing, penicillin treatment and care by
less) by transvaginal scan before 24 weeks in specialist.
women having previous history of preterm • Partner testing, Safe sex counseling, voluntary
labour is considered significant for prediction of HIV testing
preterm labour.
2.2 Treatment:
At PHC: Refer the case to specialist soon after
registration.
At RH/DH: Prophylactic cervical os tightening
at 16 weeks by McDonald method under short
general anesthesia.
• Follow up: Extra rest, avoid exertion. Fig 3.1. Congenital Syphilis: Blistering Skin rash
• Stitch removal at 37 weeks or at the onset of
labour whichever is earlier. Anticipate rapid 4. Hypothyroidism
delivery.
• Hypothyroidism can be due to iodine deficiency
or thyroid autoantibodies.
• Infertility, menstrual problems due to ovulation
disturbances.
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• Increased risk of miscarriage due to luteal phase • Note history of receiving anti D
insufficiency. immunoglobulin, time, dose during/following
• Anemia, gestational hypertension, placental every pregnancy.
abruption and postpartum hemorrhage are • Perform Indirect Coombs test (ICT) on blood
common. sample to detect maternal sensitization.
• Fetal/neonatal problems: Preterm birth, low
birth weight, congenital malformations, 5.2.1 Nonsensitized woman:
neonatal respiratory distress, perinatal death.
Cretinism. • Negative ICT indicates that the woman does not
• Diagnosis by testing serum TSH. If elevated, have detectable antibodies against Rh antigens.
thyroid function tests and antibody testing. Refer her to gynecologist at FRU. ICT is
• Treatment by Thyroxine can correct ovulatory repeated at 28 weeks2.
dysfunction and help achieving pregnancy and • Do not perform external cephalic version for
successful outcome. malpresentation. Any episode of bleeding or
• Counsel pregnant women for consumption of manipulation, procedure such as amniocentesis
iodized salt. should be followed by administration of anti D
• Targeted case finding approach is followed. immunoglobulin.
Universal TSH screening is currently not • It is recommended to give 300 mcg anti D
recommended. immunoglobulin during pregnancy at 28 weeks
for reducing the risk of antepartum sensitization.
• At delivery, cord blood sample to be tested for:
5. Rh Negative Pregnant Infant’s Rh, ABO grouping, hemoglobin,
Woman hematocrit. Direct Coombs test and direct and
indirect bilirubin estimation.
A major cause of hemolytic disease of newborn • Administration of 300 mcg of anti D Ig IM to
(HDN) is Rh blood group incompatibility between mother within 72 hours of delivery. 300 mcg
the mother and her fetus. When Rh negative mother neutralizes 15 ml of feto-placental hemorrhage
bears Rh positive fetus, the Rh antigen from fetal red (FMH). If it has not been given within 72 hours,
cells enters the maternal circulation and results in can be given up to 28 days with some benefit.
antibody formation in mother. These antibodies cross • The baby is referred to neonatology specialist
the placenta and cause destruction of fetal red cells and is observed for icterus, anemia.
resulting in fetal anemia. Prevention of such
sensitization is possible by antenatal screening and 5.2.2 Sensitized woman:
appropriate care. • If ICT is positive, it indicates that the woman is
sensitized and has got antibodies against Rh
5.1. Pregnancy outcome antigen in her blood. Note the titers reported.
There is no use of giving Anti D Ig to sensitized
First child usually escapes. Subsequent babies suffer mother.
from mild hemolytic anemia, rapidly increasing • Sensitized woman must be referred to a tertiary
hyperbilirubinemia within 24 hours of birth or care centre having equipment and expertise for
hydrops fetalis resulting in intrauterine fetal death.
Doppler middle cerebral artery peak systolic
The adverse perinatal outcome occurs earlier during
pregnancy with each subsequent pregnancy.
flow velocity studies, Cordocentesis and
intravascular fetal transfusion as required.
5.2. Management
• Every pregnant woman should be tested for Rh
6. Post Caesarean Pregnancy
typing at registration.
Pregnancy with h/o previous Caesarean Section (CS)
• Those testing negative should have their is a high risk condition as there is increased risk of
husband’s Rh typing done. complications during childbirth after each Caesarean
• Take detailed history about every pregnancy Section (Scar rupture, placenta praevia, adherent
and its outcome. H/O neonatal jaundice, placenta, PPH)
hydrops, stillbirths etc.
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6.1 Risks
Table 1: Risks to Pregnant Woman and Baby
Maternal Fetal/neonatal
Scar dehiscence during labour Fetal distress
Scar rupture leading to severe Fetal death due to scar rupture

haemorrhage & shock
Chances of repeat CS are high Neonatal asphyxia
All cases having Cesarean Section in previous • Exclude pregnancy complication: Twins,
delivery should be referred to specialist at polyhydramnios, APH.
FRU/district hospital during third trimester. At 36 • Look for scar tenderness.
weeks she should have a review by specialist • Perform clinical pelvic assessment at or after 36
regarding plan for delivery either by repeat elective weeks.
Cesarean Section or trial for vaginal birth after
Cesarean Section which depends on indication of
6.4 Investigations
prior Cesarean Section and assessment of scar USG assessment of fetal weight, localization of
integrity. placenta. Look for morbidly adherent placenta if
placenta praevia.
6.2 History 6.5 Selection for Trial of Labour
• Indication for Cesarean Section, elective or after Caesarean Section
emergency, when in labour it was done.
• Place and person operating, performed at term • Indication for previous Cesarean Section non
or preterm. recurrent (eg fetal distress, breech, placenta
• Type of Cesarean Section: Lower segment praevia.)
transverse incision or classical. (Vertical scar is • Only one prior low transverse Cesarean Section
very weak having high chances of scar rupture delivery. No other uterine scars or previous
which is likely to happen during late pregnancy rupture.
and during labour with increased risk to the • Vertex presentation, clinically adequate pelvis.
mother and fetus hence elective caesarean • No other obstetric complication (eg APH,
section should be performed at term in such breech presentation)
cases) • Surgeon, Anesthetist immediately available for
• Review operation notes regarding emergency Cesarean Section.
complications, inverted T extension of incision,
or lateral extension of tears, post-operative
infection, blood transfusion, prolonged hospital All post caesarean pregnancies should only be
stays. managed in equipped hospitals with personnel
readily available for emergency caesarean section
• Inter pregnancy interval < 24 months increases
when needed. Carefully selected women can be
the risk of scar rupture.
allowed to have trial of vaginal birth under expert
6.3 Examination supervision.
Repeat Cesarean Section: Women not eligible for

• Anemia: Correction before term is important as vaginal trial will need an elective repeat Cesarean
the chances of requiring repeat Cesarean Section which should be performed at 39 weeks for
Section are high. the best neonatal outcome, if there is no maternal or
• Note the size of baby, presentation, presence of fetal indication to perform it earlier.
any other risk factor or complication in current
pregnancy.
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6.5.1 Management of labour following • Postpartum IUCD insertion at operation before
Caesarean Section: closure of uterine incision is safe.
• Refer post Caesarean delivery to higher centers. 7. Twin Pregnancy

• Counseling and informed consent for trial of
labour. 7.1 Antenatal Diagnosis and
• Keep operation theatre ready for CS, arrange
blood.
Management
• Monitor progress of labour. The incidence of twin gestation is increasing as a
• Watch for early signs of fetal distress, scar result of infertility treatment. With modern assisted
dehiscence and perform immediate caesarean reproduction techniques higher order of multifetal
section if these signs appear. gestation is common.
• If satisfactory progress, cut short the second
stage of labour and deliver. 7.1.1 History:
• After vaginal delivery, watch for PPH/intra
peritoneal hemorrhage. • Ovulation induction by Clomiphene or
Gonadotropin Injections for infertility.
6.5.2 Symptoms & Signs of impending • Maternal family history of twins, advanced age,
rupture during labour: high parity.
• Suprapubic pain persisting in between uterine
contractions. 7.1.2 Signs:
• Slight fresh vaginal bleeding.
• Suspect twins when the fundal height is greater
• Unexplained tachycardia, tenderness over
than the period of amenorrhea and multiple
uterine scar.
fetal parts are felt.
• Alteration in fetal heart rate, sudden signs of
• Palpation of 2 heads, 3 major poles
fetal distress.
• May have associated polyhydramnios
• Hematuria.
• Two persons simultaneously hearing FHS at
• Falling BP with increasing pallor is a late sign
two different locations with a difference of > 10
of uterine rupture.
beats/min.
6.5.3 Contraception: 7.1.3 Investigation:
• Counseling for contraception for increasing
inter pregnancy interval. Ultrasonography. Early sonography in second
trimester helps in assessing chorionicity
7.2Risks
Table 2: Risk to Pregnant Woman and Baby
Pregnant Woman Baby
Hyperemesis gravidarum Prematurity

Anemia IUGR
Pre-eclampsia Fetal Malpresentation
Antepartum haemorrhage due to Placenta praevia and Fetal asphyxia
also abruptio placentae is likely
Preterm labour Twin-to-twin transfusion
Hypotonic uterine action, prolonged labour Fetal malformations
Postpartum haemorrhage Fetal death
Difficult delivery Perinatal mortality is high
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7.3 Management during pregnancy 8.2. Causes
• Detection and correction of anemia.
• Nutrition counseling, extra nutrients to meet the • Fetal anomalies: Anencephaly, esophageal
need of two fetuses. atresia.
• Avoiding exertion, extra rest in left lateral • Maternal Diabetes, Multiple pregnancy.
position.
• Early diagnosis of preeclampsia. • Idiopathic, Placental chorioangioma.
• Refer to specialist for antenatal care and Can be mild, moderate or severe.
delivery at FRU.
• Explaining warning signals for preterm Labour. Development can be acute or chronic
8. Polyhydramnios 8.3 Risks

8.1. Definition
Excessive volume of amniotic fluid
Table 3: Risks to Pregnant Woman and Baby
Pregnant Woman Baby
Hypertension Prematurity
Risks due to associated Diabetes Mellitus Malpresentation
Risks due to associated twins Fetal asphyxia due to cord prolapse or placental
abruption
APH: Placental abruption Fetal malformations
Preterm labour, PROM, cord prolapse Problems due to associated complications:
twins/preeclampsia/APH
Hypotonic uterine action, prolonged labour
Postpartum haemorrhage
Difficult delivery
8.4. Diagnosis
Mild cases: No intervention required. Extra rest in
• Fundal height is > POA. Abdomen is over comfortable position.
distended.
Symptomatic women need to be hospitalized.
• Fluid thrill can be demonstrated.
• Fetal parts are not well felt if the abdomen is Specialist can offer following interventions
tense. FHS may not be clearly heard. depending upon the case.
• USG confirms the diagnosis by demonstrating
• Tablet Indomethacin: 50-100 mg stat followed
large amount of amniotic fluid. Amniotic fluid
by maximum 200 mg in 24 hrs. for 1-2 days at <
index (AFI) 24-25 cm
30-32 weeks of pregnancy (As there is risk of
• Association with twins and fetal malformations
premature closure of fetal ductus arteriosus)
need to be looked for.
• Amniocentesis to relieve the maternal distress.
• Severe hydramnios can lead to edema, severe
The success is transient and repeated fluid
breathlessness, inability to sleep and may
removal is required. Complications such as
require immediate attention by specialist.
preterm labour, rupture of membranes,
• Maternal Diabetes Mellitus needs to be chorioamnionitis, and placental abruption are
excluded. likely.
• Hydramnios should be differentiated from • Delivery in a well-equipped institution under
ascites and large ovarian cyst. care of a specialist.
• Oxytocin augmentation if contractions are
8.5 Management weak.
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• Risk of placental abruption is high when the • Instruct ASHA, ANM to refer a woman who has
membranes rupture and a large volume of crossed her EDD to the medical officer.
amniotic fluid is drained suddenly. Preserving • At 40 weeks: Check for any complications. In
membranes is important. When required, pregnancies complicated by hypertension,
controlled ARM is done. preeclampsia, IUGR the fetus is at greater risk
• Active management of third stage as there is a of asphyxia. Hence these women should not be
risk of atonic PPH. allowed to cross their EDD. They should be
• Examine the baby for congenital malformations referred to specialist as they need to be
(Esophageal atresia or trachea- esophageal delivered early.
fistula) • Uncomplicated pregnancy: Wait until 41 weeks.
Instruct the woman to report if fetal movements
are reduced.
9. Prolonged Pregnancy • Vaginal examination: Assess whether the cervix
is ripe or unripe (Bishop Score).
9.1. Definitions • Sweeping of membranes should be done during
this examination as it decreases the chances of
Post term pregnancy: Pregnancy that has crossed 42 post term pregnancy.
weeks. • At 41 weeks: At PHC, once pregnancy has
reached 41 weeks, refer her to FRU for further
9.2. Risks evaluation and interventions.
• Post maturity syndrome: In about 20 % cases
of prolonged pregnancy there is placental 9.5 Management of post term
insufficiency which results in a pathologic pregnancy at FRU
syndrome in which there is fetal growth
retardation associated with meconium stained There are two options of managing 41 weeks
amniotic fluid, oligohydramnios and fetal pregnancy: Immediate induction of labour or
distress. The newborn is at risk of meconium expectant management until 42 weeks, while
aspiration syndrome. The baby shows loss of monitoring the fetal wellbeing.
subcutaneous fat, wrinkled, dry, cracked skin 9.5.1 In low-risk pregnancies routine induction of
(old man look). It has long thin body and long labour at 41 weeks is associated with reduction in the
nails. Associated oligohydramnios increases the risk of fetal distress and in perinatal mortality. Hence
likelihood of post-maturity. induction of labour is recommended.
• In other cases, not complicated by placental 9.5.2 Follow up: If expectant management option
insufficiency, there is continued growth of the is chosen, the mothers should be advised to come for
fetus leading to macrosomia, with increased risk fetal surveillance test at 41 weeks and twice between
of abnormal labour, shoulder dystocia, and 41 and 42 weeks.
Injuries to baby.
• Increased perinatal mortality in pregnancies a) History: Accurate assessment of gestational age
continuing > 42 weeks. to avoid delivery of a preterm baby. Errors
• Mother: Difficulties in labour due to fetal likely if prior irregular menstrual cycles or if
macrosomia, Shoulder dystocia. she has conceived soon after cessation of oral
• Increased chance of caesarean delivery. contraceptive pills. Review the early USG
reports and the date of detection of positive
UPT. Ask H/O of diminished fetal movements.
9.3 . Risk Factors
Primiparity, pervious history of post term b) On examination: Less amount of liquor on
pregnancy, sedentary life style, anencephalic abdominal palpation, baby may be of large size.
fetus. Genetic predisposition c) USG: Look for oligohydramnios: Amniotic fluid
index (AFI) 5 cm or less or there is no vertical
9.4 Prevention pocket > 2 cm. This is a marker for fetal
compromise. Note estimated fetal weight and
• Accurate calculation of EDD. Ask whether check for macrosomia.
menstrual cycles before conception had been
d) Non-stress test: Reactive or nonreactive.
regular.
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[Reactive: FHR increased by > 15 beats lasting in bishop score. Induction can then be carried
for 15 seconds in response to fetal movement] out with Oxytocin infusion.
• Favorable cervix: Induction can be done with
Fetal compromise is indicated by reduced AFI,
Oxytocin infusion and ARM.
nonreactive NST, reduced fetal movements
when immediate delivery is indicated. 9.7 During labour (Induced or
e) At 42 weeks: Labour is induced. If the baby is spontaneous)
too large or severely compromised, caesarean
section is performed. • Partographic monitoring of labour. Monitor
FHS and color of liquor, (electronic monitoring
9.6 Induction of labour if available). Watch for signs of fetal distress.
• Cervix unfavorable (Bishop’s score < 6): • CS is indicated for intra partum fetal distress
Vaginal Misoprostol 25 mcg 6 hourly for and for large baby.
induction of labour. Oral Misoprostol 25 mcg 2 • Second stage: Anticipate risk of shoulder
hourly can be used. dystocia.
• Pre induction cervical ripening can also be • Episiotomy, assisted delivery may be performed
achieved by intra cervical PGE2 gel or by Foley as required.
catheter. Cervix is reassessed for improvement
Table 4: Bishop Score
Parameters 0 1 2 3
Cervical dilatation in cm Closed 1-2 3-4 5+
Cervical effacement in % 0-30 40-50 60-70 80+
Fetal station -3 -2 0, +1 +2, +3
Cervical consistency Firm Medium Soft
Cervical position Posterior Middle Anterior
Bibliography
1. Government of India, Ministry of Health and Family Welfare. Guidelines for Screening of
Hypothyroidism during pregnancy, Dec 2014
2. Government of India, Ministry of Health and Family Welfare. Screening for syphilis during pregnancy,
technical & operational guidelines. Maternal health division, Dec 2014
3. RCOG Green top guideline No 65: The management of women with red cell antibodies during
pregnancy, May 2014
4. SOGC Clinical practice guidelines No 133: Prevention of Rh Alloimmunization, Sep 2003
5. RCOG Green top guideline No 45: Birth after previous caesarean birth, Feb 2007
6. WHO, Induction of labour: 2011
7. ACOG, Induction of labour: 2009
8. NICE, Induction of labour: 2008
Further reading
1. Dutta DC. Ed: Konar H. Textbook of Obstetrics. 7th Edition. Kolkata: New Central Book Agency Pvt Ltd;
2010

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4. OBSTETRIC COMPLICATIONS
• Proteinuria: One plus or more.
1. Preeclampsia and Eclampsia
Oedema of hands, face, abdominal wall (generalized
Pre-eclampsia is a condition specific to pregnancy,
edema) may be present but it is not a diagnostic
arising after the 20th week of gestation, characterized
feature. Excessive weight gain. 1 kg or more in a
by hypertension and proteinuria.
week or 3 kg in a month could be a warning signal.
Eclampsia is preeclampsia with convulsions.
1.2 Classification of pre-eclampsia
1.1. Signs of preeclampsia Mild and severe.
• Hypertension: BP 140/90 mmHg or more on at
least 2 occasions 4 hours apart after 20 weeks of
gestation.
Table-1: Classification of Preeclampsia
Finding Mild Pre-eclampsia Severe Pre-eclampsia

Blood Pressure (BP) BP ≥ 140/90 but <160/110 BP 160/110 mm Hg or
mmHg more
Proteinuria Present, 2+ or less *3+ or greater
Generalised Oedema (including in the face & hand) May or may not be Present
present
Headache Absent Present
Visual Disturbances Absent Present
Upper abdominal pain Absent Present
Oliguria Absent Present
Fetal growth restriction (IUGR) Absent Present
Pulmonary Oedema Absent Present
Decreased foetal Movement Absent Present
Platelet count Normal Less than 100,000
It is not necessary that all these signs are present in all cases
1.3. Diagnosis At each prenatal visit, check the woman's BP, urine
for presence of protein; look for oedema and record
her weight. If there is a rise in BP, monitor the
There are no symptoms in mild preeclampsia. Look woman's BP weekly.
for signs
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Table-2: Dangers
Maternal Fetal/Neonatal
Eclampsia IUGR
Cerebral oedema, haemorrhage, thrombosis, Stillbirth
Acute renal failure Neonatal asphyxia
Aspiration bronchopneumonia, Pulmonary oedema,
HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count)
Disseminated intravascular coagulopathy (DIC) leading to hemorrhage
1.4 Management of mild • Tab Nifedipine sustained release preparation 10

mg orally twice a day (maximum up to 80 mg in
pre-eclampsia 24 hrs.) OR
• Tab Labetalol 100 mg orally twice a day
1.4.1 Gestation more than 37 weeks: • Terminate pregnancy if there are signs of fetal
compromise, BP is persistently rising or if there
• Admit the woman to a hospital. Check BP. Test is worsening proteinuria.
for proteinuria. Monitor FHR. • Mode of delivery: Vaginal or caesarean section
• Assess cervix. Induce labour if cervix is ripe. depending on gestational age, cervical status,
Do not allow her to cross her EDD. maternal and fetal condition.
• In mild cases, when maternal and fetal condition Anytime during observation if systolic BP is ≥ 160
are well, can wait for spontaneous onset of mm Hg &/or diastolic BP ≥110 mm Hg: Manage as
labour until 37-38 weeks. severe preeclampsia. She should be referred to a
1.4.2 Gestation less than 37 weeks district hospital/ medical college for further care.
Advise her to avoid exertion. Encourage her to rest in 1.5. Management of Severe pre-
left lateral position. Counsel her about diet. She is eclampsia
allowed to take normal salt in food but no extra salt
should be added to the food. • Hospitalize patient.
• Control hypertension: Give anti-hypertensive
• Hospitalization.
drugs. Maintain diastolic blood pressure
• Check BP, urine protein, urine output, weight between 90-100 mmHg.
daily.
• Check for generalized body oedema. Nifedipine 10 mg orally. After 30 minutes, if BP
• Exclude symptoms of severe pre-eclampsia is not brought under control, another 10 mg of
• Monitor foetal growth, ask the woman about the drug can be repeated. Caution needed while
foetal movements, check daily fetal movement using Nifedipine as there may be sudden and
count (DFMC), FHR. massive fall in B P.
• Biweekly LFT, KFT, Platelet count, NST Labetalol can be given.
• Antihypertensive drugs are not beneficial in
mild hypertension. • Monitor vital signs, reflexes & fetal heart rate.
• Diuretics are not recommended. • Auscultate lung bases frequently and look for
• During observation if BP starts rising, signs of pulmonary edema. If rales are heard
(diastolic BP 100 mm Hg or more) start give Inj. Frusemide 40 mg IV.
antihypertensive medicines. • Perform bedside clotting test.
• Tab Alpha Methyl Dopa 250-500 mg 6-8 hourly • Watch for warning symptoms and signs which
orally (maximum up to 2 gm in 24 hours) OR may appear before getting fits. Sharp rise of
BP, increased proteinuria, exaggerated knee
jerk. Severe headache, drowsiness, mental
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confusion, visual disturbances (e.g. blurred 2.1. Differential diagnosis of
vision, flashes of light, double vision) epigastric
pain, nausea, vomiting, decreased urinary convulsions during pregnancy
output.
• Eclampsia: Hypertension, proteinuria.
• Prevent fits: Give prophylactic Magnesium
Sulphate (full loading & maintenance dose as in
• Epilepsy: Past H/O fits, normal BP.
Eclampsia) • Cerebral malaria: Fever, Anemia, jaundice,
Malaria tests positive.
• Encourage the woman for delivery at the FRU
• Meningitis/encephalitis, Tetanus.
1.6. Investigations
2.2. Management of Eclampsia
Urine- Albumin, sugar, culture, 24 hrs. urine protein,
Hb%, PCV, Platelets, bleeding time, clotting time, Principles:
serum fibrinogen, Blood urea, serum creatinine,
serum uric acid, serum bilirubin, serum proteins, i. General care
SGOT, SGPT. Fundoscopy.
ii. Control fits
1.7. Obstetric management iii. Control blood pressure
iv. Expedite delivery
• Gestation < 24 weeks: Fetal salvage is difficult
v. Maintain fluid balance
so proceed with termination of pregnancy.
• If gestation > 24 weeks - < 34 weeks: vi. Postpartum care
Treatment should be individualized.
2.2.1 General care
• Give Inj. Dexamethasone 6 mg 12 hourly 4
doses. • Keep the patient in a quiet room in a bed with
padded rails on sides. Place the woman on her
• If BP controlled keep woman under regular
left side.
maternal & fetal surveillance.
• Evaluate vital signs.
• Deliver the woman at 37 wks. Induce labour • Clean the mouth & nostrils by applying gentle
before 37 weeks if BP uncontrolled or suction.
worsening of clinical/ biochemical parameters • Give oxygen.
or appearance of signs of fetal compromise.
• Prevent Injury to tongue by putting airway or by
• Assess cervical status. If cervix is unripe placing padded tongue blades.
induction by oral or vaginal Misoprostol. 25 • Start IV line with Ringer lactate/ normal saline:
mcg tablets. Intra cervical Dinoprostone gel can 60 ml/hour.
be used for pre-induction ripening of the cervix. • Catheterize patient. Monitor hourly urine
• If cervix is ripe induction can be done with output.
Oxytocin infusion and Amniotomy. • Send investigations as for severe pre-eclampsia
• If not breathing check airway and give bag and
• LSCS may be done for deteriorating maternal mask ventilation.
condition, adverse fetal condition, failed
induction or other obstetric indications. 2.2.2 Controlling fits
Magnesium sulfate is the drug of choice.
2. Eclampsia
• Loading Dose: Give Inj. Magnesium sulphate 4
Eclampsia is characterized by hypertension and gm (20 ml of 20% solution) slow IV in 5 min.
proteinuria. (Preeclampsia) and convulsions/fits (not to be given as a bolus rapidly). Then
followed by coma. administer Inj. Magnesium sulphate 10 gm deep
IM, 5 g in each gluteus muscle (10 ml of 50%
Convulsions may occur in the antepartum, intra solution, in each buttock) with 1 ml of 2%
partum or the postpartum period. Lignocaine in the same syringe.
Status eclampticus: Convulsions continue one after • If convulsions recur after 15 minutes, give
the other. additional 2 g of Magnesium sulphate (10 ml of
20 % solution) IV over 5 minutes.
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• Maintenance Dose: Give 5 gm of 50% o The Urine output is at least 100 ml in
Magnesium sulphate solution IM with 1 ml of 2 previous 4 hours.
% Lignocaine every 4 hours alternately in each o Knee jerk reflexes are present
buttock. o The respiratory rate (RR) is at least 16
• Magnesium sulphate to be continued till 24 breaths/min.
hours after delivery or the last convulsion • Postpone the next dose if the above criteria are
whichever occurs later. not met.
• Before giving the next dose of Magnesium
sulphate, ensure:
Table-3: Magnesium sulphate solution for loading dose
Preparation of 20 % Magnesium sulphate solution for loading dose
➢ Inj. Magnesium sulphate is supplied as a 50 % solution in 2 ml vial. 1 amp of 2 ml = 1 gm MgSO4

➢ 4 amp of 2 ml 50% solution = 4 gm Magnesium sulphate in 8 ml solution
➢ Add 12 ml distilled water or saline to make 20 ml 20 % Magnesium sulphate solution
➢ Give slowly IV in 5 min
For initial intramuscular dose:

➢ 5 amp of 2 ml 50% solution =5 gm MgSO4. Give 10 ml deep IM in each buttock
Table-4: Magnesium sulphate for maintenance dose
Preparation of 50 % Magnesium sulphate for maintenance dose
1 amp 2 ml 50% solution = 1gm. 5 amp = 5 gm Magnesium sulphate

Give 10 ml deep IM in alternate buttock every 4 hourly
Table-5: Precautions
Precautions:
• DO NOT give 50 % Magnesium sulphate solution IV without diluting it to 20 %
• DO NOT give rapid IV infusion of MgSO4 as it can cause respiratory failure or death.
• If respiratory depression occurs (RR < 16 breaths/minute) do not give the next dose.
• Give antidote Calcium gluconate 1 g IV (10 ml of 10 %) over a period of 10 minutes.
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2.2.3 Controlling blood pressure 2.2.6 Post-Partum Care
Fits can also occur for the first time in the immediate
Nifedipine the drug of choice for controlling BP.
postpartum period. Monitor BP and the urine output
Tab. Nifedipine 10 mg orally, followed by 6 hourly,
after delivery. Continue antihypertensive to maintain
after taking BP.
diastolic BP between 90 – 100 mm Hg. Advise the
Labetalol: Intravenous Labetalol (α1β blocker) is woman to have her BP checked regularly until BP
another commonly used drug for severe hypertension. returns to normal. If BP remains high at 12 weeks
It is given in a dose of 20 mg IV initially. If BP has diagnose her as chronic hypertension and refer her to
not decreased to the desirable level in 10 min then 40 physician for evaluation.
mg is given. If the BP has still not decreased in the
next 10 minutes, an incremental dose of 80 mg may 3. Vaginal Bleeding During
be given. This may be followed by another 80 mg
every 10 min if needed till a maximum of 220 mg has Early Pregnancy
been administered. Cardiac monitoring is required.
A woman may present with history of a short period
Avoid in bronchial asthma and in cardiac disease.
of amenorrhea followed by vaginal bleeding.
2.2.4 Delivering the baby Abortion, vesicular mole and ectopic pregnancy are
the common underlying conditions, while an
The mode of delivery should be decided depending occasional woman may simply have a delayed
on whether or not the woman has gone into labour menstruation.
and the stage and progress of labour. In eclampsia,
delivery should occur within 12 hours of the onset of 3.1 Ask patient following
convulsions.
• If woman is in active labour: Monitor the • Period of amenorrhea, LMP, symptoms
progress of labour and deliver. Watch for signs suggestive of pregnancy. Prior H/O abortion,
of fetal distress. Augment labour by Amniotomy ectopic pregnancy.
and Oxytocin infusion as required. • Amount and duration of bleeding, it may be
• Cut short the second stage of labour. scanty in threatened and missed abortion and
profuse in incomplete / inevitable abortion.
• Do not give Inj. Methyl ergometrine.
• If woman is not in labour: Assess condition of
• Nature and severity of pain (severe in ruptured
ectopic pregnancy)
cervix and induce labour with vaginal or oral
Misoprostol 25 mcg tablets or ARM & • Clinical presentation may be as Threatened
Oxytocin infusion. abortion, Inevitable abortion, Incomplete
abortion, Complete abortion, Missed abortion or
• Mode of delivery depending on fetal condition
Septic abortion.
and condition of cervix.
• Perform LSCS if: Cervix unfavorable, Fetal
• Arrange for ultrasonography and pregnancy test.
distress, Fits are not controlled, labour is not • Arrive at the diagnosis with the help of
progressing well despite induction/ following chart. (Table-6)
augmentation or for any other obstetric • Refer to specialist for further management.
indication.
2.2.5 Maintaining the fluid balance
• Monitor urine output. It should be at least 30

ml/hour.
• Record the fluid intake. Give all the necessary
fluids slow IV @ 60 ml per hour.
• Maintenance of proper fluid balance is essential
to prevent water intoxication, dehydration,
hyponatremia, or pulmonary oedema.
• Diuretics should not be used unless there are
signs of pulmonary edema.
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3.2 Differential diagnosis
Table 6: Differentiating Features according to Condition
Particulars Threatened Incomplete Missed abortion Hydatidiform Ectopic

abortion abortion Mole pregnancy
Uterine Size Equal Smaller Smaller Bigger Smaller

to POA Internal os open
Internal os closed
Vaginal Slight Profuse Absent or Recurrent Slight

bleeding brownish small
discharge
Pain Mild or Absent Cramping pain Absent Absent Severe,

significant continuous
G.C. pallor Fair Proportional to Fair Fair Out of

/tachycardia blood loss proportion to
visible blood
loss.
Tenderness Absent Absent (Unless Absent Absent Marked

Abdominal infected)
/vaginal
USG Intrauterine viable Some products in Nonviable Snowstorm Empty uterus

pregnancy uterine cavity pregnancy appearance pelvic / adnexal
mass
Risks Preterm Hemorrhage Blood Hemorrhage Shock

coagulation
/IUGR Sepsis
failure
Management Expectant Surgical evacuation Termination of Suction Laparoscopy or

pregnancy evacuation
Antibiotics Laparotomy,
Blood
Blood
transfusion if
transfusion
required
3.3. Management of Threatened recommended. The role of progesterone therapy or

human chorionic gonadotropin is unproven.
abortion
Follow up: Regular ANC check up every 15 days.
Avoiding exertion, sexual abstinence and regular The pregnancy has higher risk of having recurrent
follow up to monitor the growth of the fetus are episodes of bleeding, bleeding in late pregnancy due
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to APH, fetal growth retardation and preterm UPT positive; ultrasonography reveals an empty
delivery. uterus.
3.4. Management of Missed Refer to specialist for laparoscopic surgery.

Abortion Medical management for selected cases: Inj
Methotrexate under careful monitoring.
Investigation: Ultrasonography. Bleeding time,
3.6.2 Tubal abortion:
clotting time, prothrombin time, platelet count (risk
of coagulation failure with prolonged retention of Symptoms:
dead fetus).
Treatment: The pregnancy needs to be terminated Significant pain in lower abdomen, vaginal bleeding
for maternal anxiety and for risk of blood coagulation could be slight or even absent.
failure leading to excessive bleeding. Signs: Tenderness in lower abdomen.
Uterus < 12 weeks: Manual/electrical vacuum P/V: Cervical movements extremely painful and
aspiration. tenderness in fornices.
Uterus > 12 weeks: Pregnancy termination by Pallor and tachycardia depending on the amount of
Misoprostol. internal bleeding.
3.5. Septic abortion Clinical condition usually Stable.
Investigations: Ultrasonography reveals free fluid in
Causes: Unsafe abortion. Anemia, delay in emptying
abdomen.
the uterus in cases of incomplete abortion, failure to
follow adequate aseptic precautions. Treatment: Referral to gynecologist for surgical
management.
Symptoms and signs: Fever, tachycardia, lower
abdominal pain, offensive vaginal discharge and 3.6.3 Ruptured ectopic pregnancy:
pelvic tenderness.
Severe and acute pain in abdomen with severe
Investigations - Bleeding time, clotting time, intraperitoneal bleeding which is continuing.
prothrombin time, platelet count are done as there is
risk of coagulation failure. Signs: The patient presents with tachycardia, severe
pallor and hypotension. The abdomen is tender and
Treatment: Antibiotics. Inj. Ampicillin 1gm stat IV
distended. Signs of free fluid in abdomen (shifting
followed by Inj. ampicillin 500 mg.6 hourly, Inj.
dullness). Vaginal examination is extremely painful
Gentamicin 80 mg 12 hourly, Inj. Metronidazole 100 and an ill-defined mass may be felt in posterior and
ml IV 8 hourly slowly. lateral fornix.
Surgical evacuation of uterus if there are retained
USG: Free fluid in abdomen and vague ill-defined
products.
pelvic mass may be seen.
Cases having severe sepsis with complications need
Culdocentesis: Blood is aspirated which fails to clot
to be referred to district hospital.
on observation.
3.6. Ectopic pregnancy Treatment: Management of shock. Urgent surgical
exploration to stop the bleeding. Blood transfusion as
The commonest site of ectopic pregnancy is the
required.
fallopian tube.
Clinical presentation: Unruptured tubal pregnancy; 3.7 Hydatidiform Mole
tubal abortion or tubal rupture with severe
intraperitoneal bleeding leading to shock. An abnormal pregnancy where there is no fetus, no
amniotic sac and the uterus is full of proliferated
3.6.1 Unruptured ectopic pregnancy: trophoblastic tissue.
Diagnosis requires a high index of suspicion. The Symptoms: The pregnancy vomiting is often
woman can reveal some of the risk factors for ectopic exaggerated and there is recurrent vaginal bleeding
pregnancy, will present with signs and symptoms of rarely with passage of grape like vesicles.
pregnancy, may have a unilateral adnexal mass.
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Signs: Uterus is larger than the POA and soft /
doughy in consistency. Tachycardia, pallor.
Investigation: Ultrasonography reveals snow storm
appearance, absence of fetus, amniotic fluid. The
ovaries may be enlarged with multiple cysts.
Pregnancy hormone beta HCG is markedly elevated.
Treatment: The pregnancy is terminated by suction
evacuation under general anesthesia. Blood is
arranged.
Figure 4.1: Placenta praevia
Complications:
• Severe hemorrhage and uterine perforation 4.2. Dangers:

during evacuation. Maternal mortality is high due to hemorrhagic shock
• Infection. and its complications like acute renal failure (ARF),
• Development of gestational trophoblastic coagulation failure due to DIC. There is increased
neoplasia. risk of atonic PPH after delivery. Lacerations of
friable cervix also cause bleeding. Operative delivery
Follow up: Baseline X ray chest and  HCG levels rates are high.
tested before discharge. Regular  HCG monitoring Fetal and neonatal mortality is high due to
till it falls to normal level and for 6 months thereafter prematurity (Spontaneous & iatrogenic), LBW and
as there is risk of development of gestational asphyxia.
trophoblastic neoplasia.
It is important to avoid pregnancy by using reliable 4.3. Case Management of APH
contraception during this follow up period. Oral pills
can be given. Intrauterine contraception is not 4.3.1 History:
recommended. • Ask the period of amenorrhea, fetal movements,
During follow up: Look for abnormal vaginal time of onset of bleeding, amount, prior H/O
bleeding, enlarged soft uterus, evidence of any warning hemorrhages.
metastasis (lungs, brain, anterior vaginal wall) • Abdominal pain present or absent and its
severity.
Pregnancy is allowed when  HCG remains normal
• Passage of urine.
for 6 months. Referral to tertiary care center is
indicated for chemotherapy if  HCG levels show • Prior USG reports if available.
initial decline followed by a rise or it remains static • H/O trauma, internal examination/ coitus
(plateau). aggravating the bleeding.
4.3.2 Examination:
4.Antepartum Haemorrhage
• Note pallor, tachycardia, general condition,
(APH) record blood pressure.
4.1. Definition: • In concealed accidental hemorrhage, although
the woman is in shock, her BP may be normal
Bleeding from vagina after 20 weeks of pregnancy as she could be having prior hypertension.
and before the birth of child. Two major causes: Therefore, degree of pallor and tachycardia are
more important for assessment of amount of
• Abruptio placentae: Bleeding from premature bleeding and general condition.
separation of normally located placenta in the
upper uterine segment.
• P/A:
o Uterus is relaxed, contracting and relaxing
• Placenta Previa: Bleeding from premature or hard.
separation of low lying placenta located in lower o Uterine tenderness present/absent (localized
uterine segment. or generalized)
o Fetal presentation, FHS
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No vaginal examination to be done until placenta • Blood tests: Hb, PCV, Coagulation profile
praevia is ruled out (Bleeding & clotting time, clot observation test,
platelet count, prothrombin time).
4.3.3 Investigations:
• Liver function and renal function tests.
• Urgent USG to locate placenta and assess the
fetal condition and its gestational age.
4.4 Placenta Previa
4.4.1 Differentiate between Placenta Previa and Abruptio placentae

Table-7: Differentiation between Placenta Previa and Mixed Abruptio Placentae
Particular Placenta praevia Concealed or mixed abruptio placentae
Pain Painless recurrent vaginal bleeding Painful bleeding
General Pallor, tachycardia, restlessness proportional Pallor, tachycardia disproportionately more

condition to visible amount of blood lost than the visible amount of vaginal bleeding
Uterus Relaxed, non-tender, fetal parts felt well Tense, tender, woody hard, fetal parts
cannot be felt
Presentation May be abnormal or head may be high floating Presentation cannot be made out
Fetus Fetal condition usually well if mother not in Fetus often distressed or dead. FHS may not
shock be heard
Maternal Hypovolemic shock Shock, acute renal failure, DIC
Dangers
Action No P/V examination. IV fluids, referral IV fluids, referral, monitor
• If pregnancy duration is > 36 weeks or if there
4.4.2 Complications: is life threatening bleeding, then pregnancy is
terminated.
Maternal: Hypovolemic shock, malpresentation, • Expectant management until 36 weeks for
operative delivery, PPH clinically stable patient with moderate blood
loss having fetus alive and preterm
Baby: Prematurity, low birth weight, fetal/neonatal • P/S: Exclude local genital causes (cervical
asphyxia growth, polyps, vascular ectropion)
4.4.3. Management: • Pregnancy is terminated in maternal interest at
any time during the observation period if there
• Even if bleeding is only a very small amount, is furious uncontrolled bleeding or when
hospitalization is required. pregnancy > 36 weeks.
• Assess the blood loss.
• Full blood count and clotting studies. 4.4.4 Mode of delivery:
• Arrange cross matched blood • Caesarean section for major degree placenta
Perform gentle palpation of abdomen to assess the praevia and for cases having type II posterior
placenta praevia with a salvageable fetus.
gestational age of fetus, presentation and position.
• Previous CS & anterior placenta praevia: There
• Assess fetal condition. Arrange urgent is risk of morbidly adherent placenta leading to
ultrasound. furious hemorrhage. Refer such case to tertiary
• Rh negative woman: With every episode of care centre. Such case needs to have 4 units of
bleeding, give prophylactic anti-D blood to be kept ready and preparations for CS
immunoglobulin. hysterectomy if required.
• Cases having low lying placenta, (type II
anterior) can be delivered vaginally by
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Amniotomy followed by Oxytocin infusion. 4.5.2 Management:
Arranging blood and the delivery at well-
equipped institution is necessary.
• If fetus is alive and salvageable an urgent CS is
performed, hence referral to nearest facility is
4.5 Abruptio Placentae indicated.
• If fetus is dead, it indicates massive
retroplacental hemorrhage. Hemodynamic
stability is assessed (pulse, BP, pallor). Foley’s
catheter is introduced and hourly urine output is
monitored. Coagulation profile is checked.
• Correction of hypovolemia: Ringer lactate
infusion and by blood transfusion.
• Refer the woman to tertiary level of care having
facility of providing blood and blood products
for treatment of DIC.
• Induce labour by ARM and Oxytocin infusion.
Figure 4.2: Abruptio placentae 4.5.3 During Labour:
4.5.1 Diagnosis: • First stage of labour is augmented by ARM and

Oxytocin infusion.
• May present with vaginal bleeding and • If fetus is alive, watch for signs of fetal distress.
abdominal pain.
• Second stage of labour is cut short.
• Ask H/O trauma, prior hypertension.
• Active management of third stage of labour.
• Assess blood loss: Look for pallor, tachycardia,
general condition, urine output, record BP. • Placenta is examined and the retro placental clot
Hypertension and proteinuria may be present. is weighed.
• P/A uterus hard, tender, not relaxing • Hemoglobin and hematocrit estimation
(Hypertonus) following delivery.
• In cases of severe abruption, fetal parts may not
be felt well, fetus may be distressed/dead. When
the fetus is dead at least 1,500 ml of blood is
5. Preterm labour
lost, hence shock is usual, uterus is firm-to-hard Prematurity and low birth weight is the important
and very tender. Blood pressure may be normal causes of neonatal deaths in India.
in spite of being in shock as the initial BP may
be high. Coagulation failure leading to severe Preterm labour is onset of labour from 24 weeks to
bleeding is common. before 37 completed weeks of gestation.
• USG shows placenta in upper uterine segment
and may show retroplacental hematoma. From survival point of view, the gestational age of 34
weeks is important as after this period the fetal lungs
Avoid Errors in Diagnosis are mature enough for independent survival outside
the uterus.
• The case could be misdiagnosed as preterm
labour. A single course of antenatal corticosteroids
• A patient of concealed accidental hemorrhage administered between 24 to 34 weeks of pregnancy
can be misdiagnosed as patient in labour with has been shown to reduce the neonatal mortality
severe anemia with fetal death. significantly in preterm born babies.
• In labour, uterine rupture can be misdiagnosed
as concealed accidental hemorrhage. 5.1. Risk Factors
• Maternal weight < 40 Kg in first trimester.
(BMI < 19.8 kg/m2), Obesity (BMI > 30
kg/m2).
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• Teenage pregnant women Confirm onset of labour: Intermittent painful uterine
• Short inter pregnancy interval. contractions (4 in 20 min or 8 in 60 mins) along with
progressive change in the cervical dilatation and
• Short stature, maternal undernutrition, anemia.
effacement assessed over 2 hours
• Inadequate weight gains during pregnancy
• Strenuous working, long hours of work, 5.5. Management principles
inability to take adequate rest.
• Tobacco, smoking, heavy alcohol use, illicit 5.5.1 If pregnancy is < 34 weeks
drug use.
• Previous H/O preterm birth, mid trimester
• Antenatal Dexamethasone therapy
abortion. Risk increases with each additional • Inhibition of preterm labour by administering
preterm birth. tocolytic medicine.
• Incompetent cervix, uterine malformations. • ‘In Utero transfer’.
• Vaginal infections: Bacterial vaginosis. • Safe conduct of preterm labour.
• Over distended uterus (Twins, polyhydramnios), • Special care of preterm neonate.
Vaginal bleeding during pregnancy,
Chorioamnionitis. a) Antenatal corticosteroid therapy
• Diabetes, hypothyroidism, heart disease, chronic • Injection Dexamethasone administered between
hypertension, HIV illness, urinary tract 24- 34 weeks of pregnancy in cases of
infection(UTI), periodontal infections. threatened preterm labour is effective in
• Fall, psychological stress, abdominal surgery lowering the risk of respiratory distress
during pregnancy. syndrome (RDS) & neonatal mortality if birth
was delayed by at least 24 hours after initiation
5.2. Prevention of therapy. The effect persists for 7 days after
completion of course of steroid therapy.
• Treatment for UTI, correction of anemia, • Injection Dexamethasone 6 mg IM 12 hourly for
improving oral hygiene. 48 hours, total 4 doses. Repeated courses should
• Nutritious diet and consumption of IFA tablets. not be given.
• Counseling: Avoid strenuous work, take extra
rest, quitting tobacco, alcohol. Who can receive the therapy?
• Women with previous history of preterm birth:
• All women having spontaneous onset of preterm
Refer to specialist.
labour and those having complicated
• Vaginal sonography to see the length of cervix. pregnancies (Severe preeclampsia, antepartum
• Weekly Injections of 17 hydroxyprogesterone. hemorrhage etc).
• Cervical os tightening in selected cases are • Preterm rupture of membranes before the onset
some of the preventive interventions. of labour pains (PROM)
5.3. Prediction by warning
Which women should not receive corticosteroid
symptoms therapy?
• Cramping discomfort/pain in lower abdomen, If there is chorioamnionitis, (infection of fetal
low backache. membranes) delivery is not to be postponed. Early
• Increased mucoid vaginal discharge. delivery is safer for both mother and her baby.
• Intermittent uterine contractions felt during Signs are.
discomfort.
• Fever, lower abdominal pain, Tenderness over
• Heaviness in pelvis (something descending the uterus
down).
• Fetal tachycardia (FHR > 160/minute), Foul
smelling liquor
5.4. Diagnosis
b) Inhibition of uterine contractions by tocolytic
Assess pregnancy duration accurately drugs:
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Tocolytic drugs stop contractions temporarily but dose few hours before delivery has some
rarely prevent preterm birth. However, the beneficial effects.
delivery is delayed long enough for getting the • Check fetal presentation as possibility of
benefits of administration of Dexamethasone. abnormal presentations is higher in preterm
Indication for Tocolysis labour needing skilled attendance.
• Monitor the progress of labour.
• If labour starts between 24 weeks to 34 weeks. • Prevent birth trauma and birth asphyxia while
• The cervix is < 3 cm dilated. conducting breech delivery.
• There is no foetal distress. • Avoid delay in second stage by giving
• Tocolysis is not indicated in Amnionitis, pre- episiotomy to prevent trauma to the baby’s
eclampsia, active bleeding & foetal distress. head. Do not use vacuum extractor as the risk of
• Nifedipine 20 mg oral stat followed by 10 mg 4 intracranial bleeding is high.
hourly till contractions stop or maternal pulse • If labour continues and the gestation period is <
exceeds 120 beats/min. Continue drug till 37 weeks; although evidence is not in favour of
steroid cover is complete or for 8 hours after last prophylactic antibiotics but as woman is coming
contraction. Then taper the dose slowly. from hygienically poor area, antibiotics can be
• Alternatively, beta adrenergic receptor agonists given to reduce the chances of infection in the
(Ritodrine, Terbutaline, Isoxsuprine) can be neonate. (Cap. Ampicillin, Tab Metronidazole
given. However, their value is not proven. and Inj. Gentamicin)
Terbutaline is a selective beta agonist having
lesser cardiovascular side effects and can be e) Special care of preterm neonate
administered subcutaneously.
• Cardiac disease needs to be excluded before If needed, refer neonate to the nearest NICU/
giving these drugs. While administering SNCU after appropriately stabilizing new born
tocolytic drugs careful monitoring is required
for side effects. Monitor pulse, BP, signs of
respiratory distress, uterine contractions, loss of 6. Intrapartum & Postpartum
amniotic fluid or blood, FHR, fluid balance,
blood glucose. Watch for maternal acute Complications
pulmonary oedema when combination of
steroids and tocolysis is used. 6.1 Abnormal Presentation:
• Do NOT give tocolytic drugs for more than 48
During labour fetal malpresentation is diagnosed by
hours.
palpating the presenting part on vaginal examination.
c) ‘In Utero transfer’: If the period of gestation is <
34 weeks, and labour continues despite tocolysis, or 6.1.1 Breech Presentation
if the woman is already having cervical dilatation >3
In complete breech presentation the presenting part is
cm, refer to district hospital/medical college with
buttocks with feet, in frank breech buttocks only and
NICU/ SNCU facility for delivery. Before referral
in footling presentation only feet are felt.
always give at least the initial shot of steroid
mentioning the time on the referral note. Record BP, The chance of cord prolapse is highest in footling
urine test result on referral note. breech while it is lowest in frank breech. It is
necessary to avoid rupturing membranes during
d) Safe conduct of preterm labour
vaginal examination.
• Do not inhibit preterm labour and allow it to 6.1.2 Transverse lie
progress if
o The cervix is > 3 cm dilated. Fetal shoulder felt. After rupture of membranes hand
o There is active bleeding, severe pre- prolapse occurs, cord prolapse may occur. These
eclampsia, Amnionitis cases need to be referred to FRU urgently for
o Fetus is distressed, dead or has an anomaly caesarean delivery.
incompatible with survival.
6.1.3 Face presentation:
• If a woman presents with preterm labour which
is progressing rapidly, there may not be Chin and face felt. If the chin is anterior (left or right
adequate time available for referral. Still give mento-anterior position) vaginal face delivery is
the first dose of Inj. Dexamethasone as even 1 possible specially in a multipara having average sized
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baby. However, in mentoposterior position, caesarean • Check whether arms are on the chest. Allow the
delivery is often required. Refer these women to arms to get rotated and disengage
FRU, however a midwife should accompany with a spontaneously.
delivery tray during referral. • If the arms are stretched above the head or
6.1.4 Brow presentation: folded around the neck (Winging of the
scapulae indicates extension of arms) use
Baby’s forehead and part of the face is felt and chin Lovset’s manoeuvre to deliver arms.
is not easily felt. A good sized baby’s head is unable • Deliver the head by Burns Marshal manoeuvre
to get engaged in the pelvis and the labour is likely to or Mauriceau-Smellie-Veit manoeuvre (jaw
get obstructed. Such woman should be referred to flexion and shoulder traction).
FRU for caesarean section. • Observe baby’s breathing and initiate
resuscitation as required (Breech born baby
7. Breech delivery takes longer time to start normal breathing)
If the full term breech presentation is diagnosed in • Perform active management of the third stage of
early labour the case should be referred to higher labour.
centre. Decision to deliver by Caesarean Section or • Check the birth canal for tears and repair
allowing vaginal delivery needs to be taken after episiotomy.
careful evaluation by specialist. Maternal age, parity,
pelvic capacity, status of membranes, type of breech, 8. Twins delivery
estimated weight of baby, other complicating medical
/obstetrical conditions, scar on uterus are some of the A case of diagnosed twin pregnancy arriving in early
important considerations for this decision. labour should be referred immediately as the babies
are often LBW and require special care. However, if
However sometimes woman arrives in advanced the mother is admitted in advanced labour the
labour when you are required to conduct her delivery following steps should be taken to deliver her.
by performing the following steps:
• Check presentation of first baby, check FHS
• Check the delivery tray, episiotomy tray, baby • Start IV Ringer lactate
tray and newborn resuscitation equipments
• If first baby is presenting by vertex allow labour
• Start IV infusion to progress and deliver the first baby. Leave a
• Tell the woman to bear down with contractions clamp on the maternal end of the cord of the
only when the cervix is fully dilated and the first twin and do not give Oxytocin.
buttocks are in the vagina • Palpate abdomen to determine the lie of second
• Wash hands with soap and water and put on fetus. If it is breech or transverse attempt to
sterile gloves. perform external cephalic version.
• Take the woman to the edge of the table • Check the presentation of second baby by
• Clean the vulva with antiseptic solution and vaginal examination. If vertex, allow labour to
drape the mother. progress and deliver the baby.
• Catheterize the bladder, if necessary. • If the uterine contractions become weak and
• Give pudendal block or local perineal delivery of second baby is getting delayed start
infiltration for episiotomy. Oxytocin drip slowly.
• Give episiotomy when the buttocks distend the • If the presenting part is breech, conduct breech
perineum. delivery. If delivery is getting delayed or if fetus
• Do not pull the baby or interfere in any way shows signs of distress, perform breech
• When the baby is born up to umbilicus, pull a extraction carefully.
loop of cord and keep it aside. Cover the baby • If second baby is transverse refer to FRU for
with a clean sheet and gently hold the buttocks CS. (If the baby is small and very preterm
of the baby, but do not pull. sometimes it may deliver spontaneously, hence
• If the legs do not deliver spontaneously, deliver it is necessary to accompany her with
one leg at a time. preparations to conduct delivery during transfer)
• Ask the mother to continue pushing with • Give Oxytocin soon after delivery of second
contractions. baby and conduct active management of third
stage of labour.
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• Anticipate risk of PPH and check for hardness • Apply Mc Roberts maneuver i.e. bring knees as
of uterus and massage the uterus. Start IV far as possible up to the chest and abduct and
Oxytocin infusion (20 IU in 500 ml of Ringer rotate legs outwards
lactate) • Apply firm suprapubic pressure using the heel
• Weigh both babies and take steps for special of the hands
care needs if the babies are LBW. • Make adequate episiotomy
• Rotate the baby’s body so that the posterior
9. Cord Prolapse shoulder moves anteriorly.
• If these measures fail to deliver shoulders,
Cord prolapse is more common if the presentation is
attempt internal rotation maneuvers to deliver
breech or transverse. In vertex presentation cord gets
anterior or posterior shoulder. (Application of
severely compressed as head descends and baby gets
pressure to the anterior/posterior shoulder in the
severely asphyxiated and needs urgent delivery and
direction of the baby’s chest)
prompt resuscitation
• Check baby’s breathing and initiate
• Determine the lie and the presenting part resuscitation
• Note the fetal heart rate • Complications: PPH, vaginal/perineal tears and
• P/V examination to determine the stage of Injuries to baby.
labour and the presenting part
• Gently feel for the cord pulsations. Push the 11. Obstructed Labour
cord in the vagina
• If first stage; push the head upwards to relieve
11.1 Causes
pressure by presenting part on cord and give • Cephalopelvic disproportion due to contracted
head low position to mother. Alternatively, pelvis or large head.
insert a Foley catheter in urinary bladder and • Transverse lie, Brow presentation, Mento
rapidly fill the bladder with 300-500 ml Normal posterior face presentation, Deep transverse
Saline to elevate the fetal presenting part. arrest of fetal head.
Clamp the catheter. The clamp must be released
and the bladder drained before any delivery 11.2 Diagnosis
attempt.
• Refer immediately to FRU for Caesarean • Non progressive labour, prolonged labour.
Section. • Maternal exhaustion: Tachycardia, restlessness,
• If in second stage; expedite delivery with sweating, mild fever, signs of dehydration.
episiotomy and vacuum/forceps delivery. • Signs of fetal distress or death.
• Perform breech extraction, if the baby is
presenting by breech. 11.3 Signs of obstruction
• Check for breathing and resuscitate the • Lower uterine segment over stretched
newborn. • Bandl’s ring seen which is rising progressively
• If the baby is very premature or dead towards umbilicus.
spontaneous delivery can be awaited. • Suprapubic bulge – Edematous bladder.
• Presenting part – High, abnormal or showing
excessive molding.
10. Shoulder Dystocia • On catheterization, scanty high colored/ blood
If the baby is big the chances of shoulders getting stained urine.
stuck after delivery of head are high. Many babies die • Early signs include edematous cervical lip,
within few minutes of the head being delivered. It is increasing molding of fetal head.
important, therefore, to manage the problem
efficiently and carefully so as to avoid injuries to the 11.4 Action
baby or mother.
Urgent referral. IV infusion during referral will help
• Call for help in correcting dehydration. Delay in referral can result
• Discourage maternal bearing down effort in uterine rupture, infection due to prolonged labour
and foetal death.
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Vesicovaginal fistula may develop if presenting part 12.4 Action
is deep in the pelvis for prolonged period as in deep
transverse arrest. • Urgent referral to tertiary care centre where
blood transfusion facility is available.
At the institution the patient will be delivered mostly
by Caesarean Section. • IV infusion of 1 liter of fluids, start antibiotics,
monitor vitals.
12. Uterine Rupture • Exploratory laparotomy, blood transfusion.
• At laparotomy: Hysterectomy or repair of tear.
12.1 Causes • If only repair of the rent is done, there is risk of
uterine rupture in subsequent pregnancy and an
• Scarred uterus (previous Caesarean Section, elective Caesarean Section is required.
uterine perforation etc.)
• Obstructed labour 13. Third Stage Complications
• Incorrect use of oxytocic agents like Oxytocin,
Prostaglandins 13.1 Postpartum Hemorrhage
• Internal Podalic version, manual removal of
placenta. 13.1.1Definition:
Excessive vaginal bleeding > 500 ml after delivery.
12.2 Diagnosis
Even moderate amount of bleeding could lead to
• Cessation of uterine contractions after shock in women who are anemic or have
prolonged obstructed labour. preeclampsia.
• Continuous pain in abdomen.
13.1.2 Types:
• Maternal tachycardia, restlessness, increasing
pallor, hypotension, fresh vaginal bleeding, Immediate (Primary) PPH: Within first 24 hours
haematuria. after childbirth.
• Fetus dead. Delayed (Secondary) PPH: After 24 hours up to 42
• Abdomen distended, tender all over, fetal parts days after childbirth.
may be felt easily.
Although PPH is more common in cases of twin
• Signs of free fluid in abdomen.
pregnancy, APH, over distended uterus, grand
• In labour, presenting part may recede upwards. multiparas, it is an unpredictable complication and
can occur in any low risk woman.
12.3 Dangers:
Maternal shock and death due to severe internal
13.1.3 Probable cause of Excessive Bleeding
hemorrhage. and Shock after childbirth.
Table 8: Causes of Excessive Bleeding and Shock after Childbirth.
Clinical Presentation Probable diagnosis

Uterus is flabby, not contracted, fundus is rising. Atonic PPH
Uterus is well contracted. Speculum examination of cervix and vagina Traumatic PPH
reveals cervical/vaginal lacerations/tears.
Placenta not delivered within 30 minutes after delivery. Retained placenta
Placenta incomplete, torn vessels in the membranes. Retained lobe of placenta
Bleeding continues even after treatment. Blood does not clot for > 15 Coagulation failure
minutes.
Uterine fundus not felt per abdominally. Inverted uterus seen in vagina or Acute Uterine Inversion
outside vulva.
Delayed PPH. Uterus is larger for the postnatal day, soft, may be tender, Uterine infection, retained
bleeding may have foul smell. lobe/fragments of placenta
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13.1.4 Initial Management of Atonic PPH: • Monitor woman’s GC, pulse, blood pressure,
respiratory rate, temperature every 15 minutes.
The management includes, uterine massage, Note pallor. Assess whether the woman has
bimanual compression of uterus, administering heavy bleeding and she is in shock.
uterotonic drugs along with blood volume • Uterine tamponade with condom catheter may
replacement and evaluation to look for other causes. be tried.
• Check for flabby uterus, retained placenta, tears • If bleeding is controlled by drugs, repeat uterine
and lacerations in vagina and cervix. massage every 15 minutes for 2 hours.
• If the uterus is flabby/soft, give continuous • Monitor vitals closely every 10 minutes for 30
uterine massage and bimanual compression of minutes, every 15 min for next 30 mins, and
uterus immediately (Fig 4.3). every 30 min for next 3-6 hours or until stable.
• Secure intravenous access and collect blood Continue Oxytocin infusion. (max 100 IU in 24
samples – Two 16 or 18 gauge cannulae are hours)
inserted in two veins for correcting • If the bleeding does not stop, explore uterine
hypovolemia by rapid infusion of IV Ringer cavity for retained placental bits/lobe.
lactate/Normal Saline. • If the uterus is hard, explore the lower genital
• Start Oxytocin infusion 20 IU in 500 ml of tract in good light to look for genital trauma and
Ringer lactate@ 40-60 drops/minute. If uterus repair any tears followed by firm packing of
remains flabby, other oxytocic agents (Inj vagina to stop the oozing from lacerations.
Methyl ergometrine, tablets Misoprostol, Inj 15 • If the blood sample fails to clot, reversal of
methyl PGF2 à,) can be given in dosage given in coagulation defects needs to be achieved by
table 9. administering blood and blood products.
• Send blood sample for cross matching of 3-4 Execute urgent referral to higher facility.
units of blood • Arrange urgent referral to FRU, with
• Send blood sample to laboratory for full blood accompanying HCW and relatives. Continue
count, coagulation profile, baseline urea and Oxytocin infusion & oxygen during transit.
electrolytes testing. • If the woman is in shock manage shock. The
• Inspect placenta if she is recently delivered. first drip should be fast and timed for
• Auscultate lung bases frequently to rule out approximately 1 litre in 20 min. Estimated
pulmonary edema. replacement is usually 3 times the blood loss.
Attempt compressing the abdominal aorta by
• Oxygen is given by face mask: 8 L/min
firm pressure with a closed fist just above the
• Keep the woman warm. Elevate the legs. umbilicus during transit (Fig 4.4).
• Wash hands and wear surgical gloves. • If it is delayed PPH, look for signs of infection
• Insert Foley catheter and monitor hourly urine and administer the first dose of antibiotic.
output. Urine output less than 20 ml /hour
indicates poor perfusion of tissues.
Table-9: Management of Atonic PPH
Oxytocin Methyl Ergometrine Misoprostol 15 Methyl

PGF2alfa
Dose & Route IV infusion 20 IU 0.2 mg IM or IV slowly. 800 micrograms (4 0.25 mg IM Can
in 500 ml of Can be repeated after 15 tablets of 200 mcg be repeated
RL/NS @ 40-60 mins, thereafter 4 hourly each) per rectally every 15 minutes
drops/min if required
Maximum dose 100 IU in 24 hours 5 Injections (Total 1.0 800 micrograms 8 doses (Total 2
mg) mg)
Precautions & Do not give as IV Preeclampsia, Safe drug Rule out Asthma
contraindications bolus Inj hypertension
Side effects Hypotension if Vomiting Nausea, vomiting, Nausea,
given IV bolus chills vomiting,
diarrhea
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Oxytocin Methyl Ergometrine Misoprostol 15 Methyl
PGF2alfa
Remarks Safe and effective Causes sustained Stable at room Refrigeration is
retraction of uterus temperature, cheap required
Refrigeration is
required Refrigeration is required
a) Oxytocics for Management of Atonic PPH • Hold the cord with left hand and introduce the
whole right hand in the vagina, pass it through
First start Oxytocin, if not responded give Methyl the cervical canal into the uterine cavity.
Ergometrine, if uterus still flabby Misoprostol, if no Support the fundus with left hand. Locate the
response 15 Methyl PGF2 alfa. edge of the placenta, separate it completely by
b) Uterine Tamponade with a sterile condom is a slicing movement, remove the separated
simple procedure which can be carried out by any placenta and explore the uterine cavity to check
SBA as a life saving measure before referral. After that it is empty Continue Oxytocin drip,
putting the patient in the lithotomy position, under massage the uterus.
aseptic precautions, a sterile rubber catheter is • Inspect the birth canal for any injury.
inserted within the condom and tied near the mouth • Give antibiotics. Monitor the vital signs.
of the condom by a silk thread and introduced in the
uterine cavity. The condom is inflated with 250-500 If the placenta cannot be removed completely, if the
ml normal saline. The uterine condom kept in woman is in shock and needs blood transfusion refer
position by ribbon gauze pack placed in the vagina. her to tertiary care centre immediately.
The condom catheter is kept for 24-48 hours, If placenta cannot be separated suspect morbid
depending upon the initial intensity of blood loss. It adhesion and refer her as morbidly adherent placenta
is gradually deflated when bleeding is controlled. causes furious bleeding requiring urgent lifesaving
Uterine contraction is maintained by Oxytocin drip hysterectomy.
for at least 6 hours after the procedure. Antibiotic
cover is given.
For uncontrolled PPH surgical procedures may be 13.3 Acute Inversion of Uterus
required.
13.3.1 Definition:
13.2 Retained Placenta Uterus turns inside out and may protrude outside
vulva.
13.2.1 Definition:
The woman gets very severe hemorrhage and goes in
When the placenta fails to deliver for 30 minutes
profound shock.
after the birth of baby in spite of routine measures
including administration of Oxytocin Injection and Usually occurs due to mismanaged third stage, giving
controlled cord traction, it is necessary to perform traction on cord when placenta is yet not separated
manual removal of placenta (MRP) and the uterus is relaxed.
13.2.2 Management (Manual removal of 13.3.2 Management:
placenta) O/E: Pulse feeble and fast. Hypotension.
• Check woman’s pulse, blood pressure, P/A: Cupping of fundus, fundus may not be felt at
respiration. Assess the amount of blood loss. all.
Check whether she is in shock.
• Wash hands, Wear plastic apron, gown, mask Inverted uterine fundus may be seen at vulva or in
and long surgical gloves. vagina.
• Start IV Ringer lactate, start Oxytocin infusion. Check whether placenta is separated and delivered or
• Catheterize the bladder and monitor urine is still attached.
output.
No oxytocics to be given until the fundus is
• Give premedication. Clean the perineum and the manually reposed.
vagina with antiseptic solution.
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Start IV infusion preferably in two veins, give Ringer • Local examination: Episiotomy wound
lactate infusion, arrange Blood transfusion and treat oedematous, pus discharge, foul smelling
Shock. lochia.
The freshly inverted uterus can be often replaced in • Vaginal examination: Uterus subinvoluted,
position by pushing up on the fundus with the hand tender, fornices tender, Bogginess in posterior
immediately after inversion. In case of delayed fornix if pelvic abscess.
diagnosis short uterine relaxant inhalation anesthesia
helps successful reposition. 14.4 Risk Factors:
After reposition, inhalation anesthesia is discontinued
and Oxytocin 20 IU in 500 ml of Ringer lactate is
• Prolonged labour, PROM, Unclean delivery.
given along with bimanual compression of the uterus • Anaemia, Undernutrition, Diabetes Mellitus,
to maintain the uterine retraction and the reposition. HIV infection.
Correct management of third stage of labour is

important for preventing this dangerous 14..5 Investigations:
complication. Do not give any traction on cord until
• Complete blood count with WBC total and
the uterus is firmly contracted and retracted which
differential count.
indicates the onset of placental separation.
• Smear for malarial parasite.
14 Puerperal Sepsis • Urine routine, microscopy, culture & sensitivity
in suspected cases of UTI.
About 8% of maternal deaths are attributed to post- • USG for retained products, collection in pelvis.
abortal or postpartum sepsis. It is a preventable • Chest X-ray.
complication. Early detection and prompt treatment
can save a lot of morbidity associated with it. • High vaginal and cervical swab – smear, culture
sensitivity.
14.1 Causes of Fever in Puerperium: • Blood culture in seriously ill cases.
• Wound infection: Episiotomy, Caesarean 14.6. Management:

Section.
a) Genital sepsis
• Puerperal sepsis due to postpartum On examination patient has pallor, tachycardia,
endomyometritis, pelvic cellulitis, septicemia uterus is soft, tender, subinvoluted (i.e. large for the
• Urinary tract infection day of puerperium), abdomen soft, non-tender.
• Mastitis, Breast abscess.
Mild sepsis can be treated at PHC level by giving
• Thrombophlebitis, deep vein thrombosis
oral antibiotics for 7 days.
• Malaria, Pneumonia, Typhoid, HIV related
infections. Cap Ampicillin/Amoxicillin orally 500 mg 6 hourly
for 7 days, Tab Metronidazole 400 mg orally 3 times
14.2 Symptoms: a day.
• Fever with chills and rigors, Foul smelling Give Haematinics. Review after 48 hours.
lochia. If response is seen, continue treatment for 7 days. In
• Malaise, headache, nausea, anorexia, vomiting. case of deterioration, refer the patient. Antibiotics
including Inj. Gentamicin 80 mg IM should be
initiated by ANM/MO at the first suspicion of sepsis
14.3 Signs:
before referral.
Depending upon severity of infection b) Pelvic peritonitis
• Tachycardia, fever, hypotension in septic shock, If P/A examination reveals tenderness in lower
swelling in one leg, calf tenderness. (DVT) abdomen (iliac fosse) with or without distention and
• P/A: Subinvoluted tender uterus, tenderness in guarding, suspect pelvic peritonitis and refer to FRU
iliac fossae, distension, guarding, absent after giving loading dose of antibiotics. Inj.
peristalsis in peritonitis. Ampicillin 1 gm IV, Inj. Gentamicin 80 mg, IV
Metronidazole 500 mg.
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This patient needs hospitalization and parenteral Any degree of puerperal sepsis when associated
antibiotics for 7-10 days. Inj. Ampicillin 1 gm IV with severe anemia, there is risk of rapid
followed by 500 mg 6 hourly. Inj. Gentamicin 80 mg deterioration. Hence refer such patient to a
twice a day I.M. IV Metronidazole 500 mg 8 hourly. specialist at district hospital.
IV fluids are given. After 48 hours if patient
d) Surgical treatment:
improves and resumes oral intake, Cap Ampicillin
and Tab Metronidazole can be given orally. • Retained products in uterine cavity: Evacuation
Change in antibiotics as per results of antibiotic of uterine cavity.
sensitivity testing is required if there is no response to • Pelvic abscess is drained by colpotomy.
treatment within 48 hours. • General peritonitis may require laparotomy.
c) Generalized peritonitis or septicemia: • Breast abscess: Incision and drainage.
If a patient of puerperal sepsis is looking very ill, 14.7 Prevention of sepsis:

febrile, restless, has marked tachycardia and has
distention of abdomen, guarding, tenderness over • During pregnancy: Nutrition, IFA prophylaxis,
abdomen, peristalsis is sluggish or absent then such Anaemia correction, Diabetes control.
patient is having generalized peritonitis. She may • Intranatal and postnatal: Strict aseptic measures,
have septicemia. Refer her to tertiary care center, as minimum number of vaginal examinations, early
she requires special care in critical care unit, higher delivery in PROM cases & antibiotic
antibiotics and may need surgical interventions. prophylaxis.
There is risk of death due to Endotoxic shock, acute
renal failure, DIC.
Fig 4.3: Bimanual Compression of uterus Fig 4.4: External Aortic compression
Bibliography
1. Government of India, Ministry of Health and Family Welfare. EmOC training Manual, 2013
2. Government of India, Ministry of Health and Family Welfare. MH Protocol posters: Maternal health
division
3. Government of India, Ministry of Health and Family Welfare. Use of Antenatal Corticosteroids in
Preterm Labour: Operational Guidelines, Child Health Division, June 2014
4. Government of India, Ministry of Health and Family Welfare. Prevention of PPH through community
distribution of Misoprostol: Operational guidelines, Nov 2013
5. WHO, Prevention and management of preeclampsia, 2011, 2013
6. WHO, Calcium supplementation in pregnant women, 2013
Further reading
Ltd; 2010

Page 308
5. MEDICAL DISORDERS COMPLICATING
PREGNANCY
1. Anemia in Pregnancy 1.1. Definition:
Anemia during pregnancy is a major contributory Anemia in pregnant women is Haemoglobin level of
cause for maternal deaths. Nutritional deficiency is less than 11 g/dL.
the commonest cause.
Table-1: Anemia Classification
Degree Hb(gm/dl)
No Anemia 11
Mild 9 -10.9
Moderate 7- 8.9
Severe Less than 7
1.2. Causes of Anemia During • Precordial soft systolic murmur.

• Signs of cardiac failure, crepitation at the base
Pregnancy of lungs.
i. Nutritional (Iron, folic acid, proteins)-
deficiency anemia commonest cause. 1.5. Investigations
ii. Worm infestations.
iii. Twin/ multifetal pregnancy. • Hb estimation, Haematocrit, Blood counts.
iv. Malaria. • Peripheral blood smear (PBS) to know whether
v. Urinary tract infection, Tuberculosis. Iron deficiency or B 12/ Folate deficiency.
vi. Blood loss. • Haematological indices- MCV, MCH, MCHC.
vii. Acquired hemolytic anemia.
To find out the cause of anemia.
viii. Haemoglobinopathies: Sickle cell disease,
Thalassemia. • Examination of stool for worms and occult
ix. Rare causes: Aplastic Anemia, Leukemia. blood.
• Urine examination routine, microscopic, culture
1.3. Symptoms if required.
• PBS (thick and thin smear) for malarial parasite.
Weakness, Lassitude and fatigue, Anorexia and • Sickling test: Solubility test.
indigestion, palpitation, dyspnoea, giddiness and
• Hemoglobin electrophoresis, HPLC in
swelling of legs.
suspected haemoglobinopathy.
1.4. Signs • Serum bilirubin: Hemolysis, Megaloblastic
anemia.
• Pallor, glossitis and stomatitis, edema, signs of
nutritional deficiencies, Koilonychias, 1.6. Complications
Platonychia.
Anemia contributes to 20 % of maternal death
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Table 2: Complications
Maternal Baby
Increased risk of cardiac failure. Fetal growth restriction. (IUGR)
Inability to withstand third stage hemorrhage, can go in Prematurity
shock with moderate blood loss.
During Puerperium: Risk of puerperal sepsis, Poor Poor stores of iron at birth, risk of
establishment of lactation. anemia during infancy.
Puerperal venous thrombosis, Pulmonary embolism.
Iron sucrose is safe. It helps in replenishing iron

1.7 Treatment stores faster than oral iron.
Treatment depends upon: Calculated dose: (2.4 × W × D +500mg for storage
Severity of anemia, cause of anemia and gestational iron)
period at which anemia is detected. Where,
1.7.1 Nutritional deficiency anemia W= weight in kg (Pre-pregnancy),
a) Prophylaxis (Hb =/> 11 G/dl): D = (target Hb in gm% - actual Hb in gm %),

Rounded up to the nearest 100 mg.
Oral IFA tablets (Elemental iron 100mg with Folic
acid 0.5mg/day) one tablet daily for 6 months during Total iron is given in divided doses.
pregnancy and 6 months during lactation.
Oral iron is to be stopped before 24 hours.
b) Mild/Moderate anemia: (Hb< 11 G/dl): 200 mg iron sucrose in at least 200 ml of normal
Therapeutic double dose: Oral IFA one tablet twice a saline is given over a period of 30 minutes on
day. For better absorption it should be taken before alternate days. Keeping emergency drugs is a must at
meals. Check response after 4 weeks. The treatment every clinic.
should be continued till the Hb becomes normal, then
e) Severe anemia:
one tablet daily is to be continued to replenish the
iron stores. Patients with Hb level <7gm% or moderately anemic
Nutritional guidance is given. Protein is patients with associated obstetrical or medical
supplemented. complications should be referred to specialist for
evaluation and management. Hospitalization helps in
Tab Albendazole (400mg) single dose after first complete evaluation for cause of anemia.
trimester for deworming.
Blood transfusion is indicated if
c) Response of therapy is evidenced by
• Sense of well-being, increased appetite within • Hb< 5 gm/dl any time during pregnancy
3-4 days. • Severe anemia seen after 36wks of pregnancy
• After a lapse of 2 weeks, haemoglobin starts • Refractory anemia
rising at the rate of 1gm % per week. • Patients needing operative delivery
• If no significant improvement is evident • Continued bleeding
clinically and haematologically, after 4 weeks
refer the woman to FRU as diagnostic re- Packed red cells are transfused slowly and under
evaluation is needed. supervision, diuretics are given to avoid circulatory
d) Parenteral iron therapy is indicated if: overload.
• Intolerance to oral iron. 1.7.2 Treatment of other causes for anemia
• Patient not co-operative to take oral iron.
• Poor responders to oral iron. Should be given as indicated. Antimalarial treatment,
appropriate care for bleeding piles etc.
• Severely anemic mothers.
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1.7.3 Management during Labour Special care if low birth weight. Iron supplements as
stores are poor.
a) 1st Stage:
1.7.4 Patient education and counseling
• The patient should be in bed, propped up
position, Oxygen inhalation. • Proteins, Iron and vitamin rich diet
• Strict asepsis. Monitor vitals, auscultate lung • Correct cooking habits
bases. • Precaution against malaria
b) 2nd Stage: • Spacing between pregnancies
• Avoid exertion and delay: Episiotomy, 2. Diabetes Mellitus (DM) in

prophylactic low forceps or vacuum delivery.
Pregnancy
c) 3rd Stage:
Due to lifestyle factors and dietary habits, incidence
• Active management of 3rd stage of labour with of type 2 DM is increasing. Gestational Diabetes
prophylactic Oxytocin. Mellitus (GDM) results in higher maternal and
• Blood transfusion if required perinatal morbidity and requires meticulous control
• Precaution against post-partum overloading of and special care. Of all GDM patients, > 50%
heart. develop type 2 DM in later life.
d) Puerperium 2.1. Two types of cases
• Prophylactic antibiotics • Pre-Gestational DM: DM diagnosed before
• Anti anemic therapy continued till 3 months pregnancy.
after normalization of Hb. • Gestational DM: Glucose intolerance detected
Baby: for the first time during pregnancy.
Prone to sepsis in neonatal period.
2.2. Effects of GDM on the Mother & Baby

Table-3: Effects of GDM
Mother Baby
Pre-eclampsia Unexplained sudden fetal death during third trimester.
Polyhydramnios Congenital abnormalities.
Caesarian section more common due to fetal Macrosomia (big baby > 4 Kg), Birth trauma. (due to
macrosomia and CPD. shoulder dystocia)
Shoulder dystocia, maternal Injuries due to Neonatal hypoglycemia
macrosomia.
Chorioamnionitis and postpartum endometritis. Hyaline membrane disease. (RDS)
Miscarriages in uncontrolled Diabetes. Hypocalcemia, hypomagnesemia.
Recurrent UTI, Fungal vaginitis, skin infections. Prematurity, Jaundice, Apnea and bradycardia.
Long term risk of type-2 Diabetes Mellitus. Polycythemia/Hyperviscosity syndrome.
The risk of fetal anomalies is high in pre-gestational 2.3. Screening and diagnosis of
DM. It is not increased in GDM patients. However,
the risks of unexplained still births (during the last 4- Diabetes in pregnancy
8 weeks of gestation) is similar to pre-gestational
Diabetes. All Indian women should be screened for gestational
Diabetes Mellitus as they belong to a high risk
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ethnicity. Screening should be done at first visit (12- 2.4.4 Obstetrical Management:
16 weeks) and again between the 24th and 28th weeks
of pregnancy. One step screening and diagnostic test Antepartum foetal monitoring: Non-Stress test and
is very convenient for pregnant women in Indian Amniotic fluid index are performed periodically
scenario. As recommended by GOI guidelines 75 gm during third trimester to prevent IUD and plan
Glucose load is given orally to women attending delivery. Umbilical artery Doppler studies help in
ANC irrespective of meal status and blood sugar is timing the delivery. More frequent monitoring is
estimated after 2 hours. done if there is history of stillbirth, hypertension, and
uncontrolled blood sugar. Women with GDM with
A plasma glucose value of 140 mg and above is poor glucose control, those with hypertension,
considered diagnostic of GDM. A value of < 120 previous still birth & other complications often
mg/dl is normal. Value between 120 – 139 mg/dl is require to be delivered earlier. The timing of delivery
considered as gestational glucose intolerance. should be discussed with the obstetrician.
For well controlled uncomplicated cases can wait
2.4. Management of Diabetes in upto 40 weeks. It is safe not to allow to cross EDD in
Pregnancy any case.
Caesarean Section is done for large baby and other
The woman should be referred to gynecologist at obstetric indications.
district hospital. A team of specialists including
Management during labour:
Diabetologist, Sonologist and neonatologist should
manage the case in consultation.
• Regular glucose monitoring and urine testing
for sugar and ketones.
2.4.1 Medical Nutrition Therapy(MNT): • Regular insulin: Low-dose infusion depending
Calories calculation for 24 hours according to weight upon blood sugar levels.
and occupation.
• Prophylactic antibiotics.
30-35 kcal/ kg body weight and for obese women 25-
• Baby: Monitoring for hypoglycemia and for
30 kcal/kg/day.
other complications like respiratory distress, and
Composition of diet– It should include carbohydrates needs special care.
(50-55%), proteins (20-30%) and fats 20-30%) with
saturated fat <10%. 2.4.5 Postpartum management:
Three major meals and 3 snacks are advised. After delivery insulin requirement decreases hence
dose needs to be adjusted. Fasting and postprandial
2.4.2 Exercise: blood sugar should be checked before discharge.
Walking 3- 4 times weekly for 20-30 min/session. Patients who are diagnosed to have GDM during
pregnancy are subjected to oral glucose tolerance test
Blood sugar monitoring should be done after 2 weeks with 75g glucose at 6 weeks.
of starting diabetic diet.
2.4.6 Contraception:
Recommended glycemic goals: Fasting blood
glucose < 95 mg/dl Condoms. Intrauterine device safe
Two-hour postprandial blood glucose < 120 mg/dl 2.5. Care of Pre-Gestational
BSL monitoring twice weekly up to 28 weeks, Diabetes Mellitus
weekly from 28 weeks onwards. More frequently as
required. 2.5.1 Before pregnancy:
2.4.3 Insulin Therapy: If MNT fails to achieve To reduce the risk of fetal malformations and fetal
glycemic goals within two weeks of therapy. macrosomia, counsel for planning pregnancy when
glycated hemoglobin levels are normal. Advise pre
Insulin requirements increase as pregnancy advances. conceptional Folic acid 5 mg daily 3 months prior to
Consult a physician or endocrinologist for insulin conception. Optimize BMI.
administration. Oral antidiabetic medicines are not to
be given during pregnancy as they are not yet proven 2.5.2 During pregnancy: Special investigations
to be safe for the baby. Refer Annexure and national for detecting fetal malformations, as practicable.
guidelines for details of MNT and insulin therapy.
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First trimester biochemical screening (PAPP – A, safe practice unless indicated earlier. Elective LSCS
hCG), USG for nuchal translucency (11-12 weeks). if foetal weight 4 kg.
Second trimester biochemical screen (16-18 weeks),
USG (18-20 weeks)
3. Pregnancy with Cardiac
2.5.3 Third trimester:
Disease
Assess fetal growth and liquor volume by USG. NST Cardiac disease complicates around 1% of
and umbilical artery Doppler studies to decide time pregnancies. The disease worsens during pregnancy,
and mode of delivery. delivery and postpartum period. It is one of the
important indirect cause of maternal mortality.
2.5.4 Delivery: Rheumatic valvular disease (Mitral stenosis,
For uncomplicated pregnancy with well controlled regurgitation) is common form in India. Currently
Diabetes one can wait until 40 weeks. However, in congenital heart disease cases are being diagnosed
view of adverse perinatal outcomes associated with early and surgically corrected. Such women are also
poor control, induction of labour at 38 -39 weeks is a presenting during pregnancy.
3.1. Risks
Table-4: Maternal, Fetal/Neonatal Risks in Cardiac Disease
Maternal Fetal/Neonatal
Cardiac failure, Acute pulmonary edema Prematurity
Subacute bacterial endocarditis IUGR leading to LBW
Thromboembolic complications
Atrial fibrillation & other arrhythmias
• Twins, polyhydramnios
3.2. Risk of failure • Tachycardia due to any cause: Physical
exertion, emotional upset
The cardiac patient faces greater risk of cardiac
failure at each stage when there is significant rise in 3.3. Diagnosis
cardiac output. (E.g. at around 12-16 weeks, 28-32
weeks, during labour with each successive stage of Normal pregnancy is associated with fatigue,
labour, soon after delivery and first 24 hours after dyspnea, decreased exercise capacity, peripheral
delivery). edema, and jugular venous distention. Most
pregnant women have audible physiologic
The following obstetric and medical complications systolic murmurs and a physiologic third heart
increase the risk of cardiac failure. sound (S3). This makes diagnosis of heart disease
difficult during pregnancy.
• Infection: Urinary, Respiratory, Dental.
• Anemia, Hypertension, Preeclampsia,
Hyperthyroidism.
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Table-5: New York Heart Association (NYHA) Functional Classification
NYHA Class Symptoms
I No symptoms on ordinary physical activity such as walking or climbing stairs.
II Mild symptoms and slight limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-ordinary

activity such as walking short distances (20-100 m). Comfortable only at rest.
IV Severe limitations. Experiences symptoms even while at rest.
examination. Suspected cases must be referred

3.4. Symptoms to physician.
• Complete evaluation by physician/ cardiologist.
• In grade 1 and 2 the woman may not have any Risk determination, counseling
symptoms. • Watch for signs of cardiac failure.
• Grade 3: Breathlessness on accustomed • Care of teeth, treatment of urinary tract
exertion, fatigue, syncope, chest pain. infection.
• Grade 4: Breathlessness even at rest, nocturnal • Prevention or early correction of anemia.
cough, hemoptysis. • Monitoring blood pressure.
3.5. Signs • Early detection and prompt treatment of
pregnancy complications.
• Cardiac murmurs: Systolic grade 3 or more, any 3.7.3 Hospitalization:
diastolic murmur.
• Abnormal heart sounds, Arrhythmias. • Grade 3 & 4 dyspnoea kept in hospital
throughout pregnancy.
• Signs of cardiac failure: Progressive dyspnoea,
Neck veins engorged, Palpable tender liver, • Women with obstetric or medical
HJR positive. complications.
• Pitting oedema over feet. • Around 28-32 weeks depending on social
circumstances.
• Crepitation at the lung bases.
3.7.4 Care during labour:
3.6. Investigations
Await spontaneous labour. Induction only for
• ECG, 2D Echo Cardiography obstetric indications.
3.7. Management: a) First stage:
3.7.1 Before conception • Rest in propped up position; Avoid fluid

overload.
Women with preexisting cardiac lesions should • Prophylactic antibiotics depending upon risk of
receive preconception counseling regarding maternal complications: Ampicillin, Gentamicin.
and fetal risks during pregnancy and long-term
• Pain relief.
maternal morbidity and mortality. Women with
NYHA class III and IV face a high mortality and • Monitor pulse, respiratory rate, BP, temperature,
morbidity. These women should be strongly lung bases.
cautioned against pregnancy. • Monitor oxygen saturation; Oxygen as required.
• Keep cardiac drug tray ready.
3.7.2 Care during pregnancy: • Monitor labour progress, fetal condition.
• Every pregnant woman should be completely b) Second stage:
examined between 4-6th month by the medical
officer. Chest auscultation is a must during this
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• Do not allow the woman to have strenuous 3.8.2 Management
bearing down effort.
Medical management includes fluid and salt
• Cut short the 2nd stage by prophylactic restriction, Digoxin, Diuretics, Vasodilators, and
vacuum/forceps delivery. Anticoagulants. These women need to be in a tertiary
c) Third stage: care centre having cardiac ICU facility under care of
cardiologist.
• Do not give Inj. Methyl ergometrine. Provide
physiologic management.
• Give Inj. Oxytocin IM 10 IU if there is
3.9 Pregnant Women receiving
excessive bleeding. anticoagulation for surgically
d) During Postpartum period: corrected heart disease
• Monitor vitals. Watch for signs of failure. Women with surgically corrected heart disease with
prosthetic valves are receiving Warfarin, a vitamin K
• Encourage ambulation to prevent
antagonist orally for anticoagulation. Warfarin freely
thromboembolism.
crosses the placenta and causes adverse fetal effects.
• Watch for signs of puerperal sepsis and give The risk of Warfarin Embryopathy is highest when
antibiotics. Warfarin is administered during 6 to 12 weeks of
• Breast feeding is advisable. gestation. Heparin does not cross the placenta and is
safe for the fetus.
3.7.5 Contraception:
• Anticoagulation: Warfarin must be
• Combined Oral Contraceptive pills are discontinued and Heparin should be
contraindicated. administered during this period. After 12 weeks,
• Condom is safe. Heparin is stopped and Warfarin is restarted and
• After completing family tubal ligation can be continued until 36 weeks. After 36 weeks again
performed at district hospital or in tertiary care LMWH or unfractionated Heparin is started
centre. Male partner may be encouraged to which is stopped 4-6 hours before delivery and
undergo vasectomy. restarted 6 hours after delivery if there are no
• MTP (if requested) can be performed at district bleeding complications (24 hours after
hospital after stabilizing cardiac condition. Caesarean Section).
• There is risk of profuse bleeding hence delivery
should always take place in tertiary care
3.8. Peripartum Cardiomyopathy institution. Protamine sulfate is antidote.
This is an idiopathic dilated cardiomyopathy that
• These cases need regular laboratory monitoring
to adjust the dose of medications. Also they
develops in the last month of pregnancy or within 5
might need fresh frozen plasma for bleeding
months of delivery and is characterized by left
hence they should be under care of specialists at
ventricular systolic dysfunction with ejection fraction
the tertiary care centre during pregnancy and
(LVEF) < 45%.
delivery.
3.8.1 Risk factors: • Breast feeding is allowed.
Advanced maternal age, Multiparity, multiple • Combined Oral Contraceptives are
gestation, obesity, malnutrition, gestational contraindicated.
hypertension, preeclampsia, cesarean section, family
history, abuse of tobacco, alcohol, or cocaine. 4. Malaria during Pregnancy
The mortality rate is 25% to 50%, half of those die
within the first month of presentation and the Malaria during pregnancy is more common, more
majority die within three months postpartum. Death atypical, can be more serious and fatal.
results from progressive cardiac failure,
thromboembolic events, and arrhythmias. Of the 4.1. Effects on Pregnancy Outcome
patients who survive, approximately 50% recover
normal left heart function. Prognosis is related to left • The chances of spontaneous abortion, preterm
ventricular dysfunction at presentation. birth, fetal growth retardation, fetal distress and
still birth are increased.
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• Rarely transplacental spread to the foetus • Fetal growth retardation.
resulting in congenital malaria.
4.4. Diagnosis
4.2. Complications
• Microscopy of stained thick & thin smear is the
Profound Anaemia may develop rapidly as there is a gold standard.
reduction in Haemoglobin. Anaemia can have serious • Rapid diagnostic tests. All fevers particularly in
consequences during labour. In the last two decades Malaria endemic areas should be tested for
in India, an increasing proportion of P. falciparum Malaria.
infections is proving to be resistant to Chloroquine.
• In endemic areas the pregnant woman should be
4.3. Clinical presentation routinely tested for Malaria at all antenatal visits
by RDT even if she does not manifest any
symptoms of Malaria.
• Fever, Splenomegaly
• Anemia may be the presenting feature of
Malaria; therefore, all cases of anemia should be
tested for M.P.
Table-6: Treatment of Uncomplicated Malaria during Pregnancy
Day 1 Day 2 Day3
P. Vivax CQ 250 mg, (150 mg base) 4 tablets CQ 250 mg, 4 tablets CQ 250 mg, 2 tablets
P. Falciparum
First trimester Quinine Quinine Quinine 10mg/kg 3

times daily Continue
10mg/kg 3 times daily. 10mg/kg 3 times daily.
upto 7 days.
2nd, 3rd AS 200 mg 1 tablet SP 2 tablets (750 + AS 200 mg 1 tablet AS 200 mg 1 tablet
trimester 37.5mg each)
P. Vivax + P. AS 4 tablets of 50 mg 3 SP tablets AS 4 tablets of 50 mg AS 4 tablets of 50 mg

Falciparum
(500mg + 25 mg
(Mixed)
each)
CQ: Chloroquine 250 mg tablet (150 mg base); 25 mg/kg body weight divided over three days i.e.10 mg/kg on day 1,
10 mg/kg on day 2 and 5 mg/kg on day 3. AS: Artesunate SP: Sulfadoxine + Pyrimethamine
• Treatment during first trimester: Quinine. It may
4.5. Treatment • Induce hypoglycemia; do not give Quinine on

AS: Artesunate SP:Sulfadoxine+ Pyrimethamine empty stomach and tell the woman to eat
4.5.1 Vivax Malaria: Chloroquine for 3 days.
regularly, while on Quinine treatment.
Primaquine is contraindicated in pregnant women. To
prevent the relapse, suppressive chemoprophylaxis • ACT is not to be given in first trimester of
with Chloroquine 300mg base, once a week until pregnancy
delivery.
• During 2nd & 3rd trimester: ACT+ SP
4.5.2 P. Falciparum Malaria: As pregnant
women having falciparum Malaria are more prone to 4.5.3 Mixed infections (P. vivax + P. falciparum)
develop complications, they should be referred to treated as falciparum Malaria
nearest FRU immediately.
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4.6 Prevention: advanced labour, conduct delivery by following
principles:
Use of personal protection measures including
insecticide treated bed nets (ITN) / Long lasting • Follow universal safety precautions
insecticidal nets (LLIN) should be encouraged. • Minimum number of vaginal examinations
• Do not rupture membranes unless indicated.
5. HIV Infected Pregnant • Avoid: Routine Episiotomy, perineal injuries,
Woman vacuum delivery.
• Avoid suctioning of baby unless there is
Every pregnant woman during her first visit should meconium staining
be counseled for voluntary HIV testing at an ICTC to • Give ARV medicines as per protocol.
know her HIV status. • Clean the baby of the maternal blood and body
fluids before handing over to the relatives.
5.1. Care of HIV positive pregnant
woman during pregnancy 5.3 Care of mother after delivery
• Refer to PPTCT centre for care of mother and
5.1.1 Points to be noted in history: baby.
• Watch for signs of sepsis.
• High risk behavior of herself and her spouse
• Nutritious diet, nutrient supplements.
• Pregnancy duration, number of previous
pregnancies, live children, receipt of any • Encourage to use reliable contraception; safe
antiretroviral medicines earlier. sex practices.
• If pregnancy is unwanted and is < 20 weeks
refer her to MTP Centre.
5.4 Treatment at PPTCT/ART
• If she wishes to continue current pregnancy, Centre
refer her to PPTCT Centre soon after • The new protocol consists of giving triple ART
confirmation of pregnancy to start the to pregnant woman and extended Nevirapine
antiretroviral medicines for reducing the risk of therapy for the exposed infant.
vertical transmission. ART Centre will be • Triple antiretroviral therapy (ART) initiated
initiating anti-retroviral medicines from 14 from 14 weeks irrespective of CD4 count and
weeks and will be doing CD4 testing and other continued lifelong. Refer table below.
evaluations. • If there is no prior exposure to EFV/NVP, triple
• Screen for TB and STI at every visit. ARV regime consisting of Tenofovir,
5.1.2 Specific education & counseling Lamivudine and Efavirenz is started from 14
regarding: weeks onwards to be continued throughout
pregnancy, labour, postpartum period and
• Nutritious diet, consumption of micronutrient thereafter.
supplements. • If there is H/O prior exposure to NVP/EFV then
• Safe sex practices for preventing new STIs and EFV is not given and a protease inhibitor is
other strains of HIV which could harm the baby. given (Lopinavir/Ritonavir).
• Adherence to HIV medicines. • Baseline investigations: Hb, urine, VDRL,
screening for hepatitis B and C, ALT, CD4,
• Follow up at ART & PPTCT centers as
urea/creatinine, blood sugar, lipid profile.
instructed.
• If CD4 is < 250 Cotrimoxazole (CPT) 1 ds tab
• Institutional delivery.
daily.
• Safe infant feeding practices, infant care.
Laboratory tests:
5.2 Care during delivery • After 2 weeks of initiating ARV  Hb, ALT.
• At 4 ,8,12 weeks Hb testing.
Insist on institutional delivery at a PPTCT Centre as • Every 6 months BUN, Sr. Creatinine, ALT,
she requires ARV medicines during labour which CD4, Urine analysis (imp in TDF based
need to be continued postpartum. C. section is regimes).
performed only for obstetric indications. If she is in • If on PI based treatment: BSL & Lipid profile
every 6 months.
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Table-7: Dosage Schedule and Associated Side Effects of ARV Medicines
Name of ARV Dose Major Side Effects

Tenofovir (TDF) 300 mg Once a day Nephrotoxicity, hypophosphatemia
Lamivudine (3 TC) 300mg Once a day Very few. Hypersensitivity, rarely pancreatitis
Efavirenz (EFV) 600 mg Once a day Neuropsychiatric symptoms (hallucinations, suicidal
ideation, nightmare)
*Lopinavir/Ritonavir 400/100 mg BD GI disturbance, glucose intolerance, lipo-dystrophy
(LPV/r) & hyperlipidemia
* For prior exposure to EFV or NVP; LPV/r FDC tablet of LPV 200 mg/r 50 mg: 2 tablets BD
5.5 Care of HIV Exposed Infant: 5.5.4 After 6 months, if breast feeding option has
been chosen, breast feeding is continued as
5.5.1 Infant is given Nevirapine (NVP) syrup for per EID status:
6 or 12 weeks as advised by PPTCT Centre • EID –ve babies: Continue BF upto 1 year
depending on duration of ART received by + Complementary feeding; No abrupt
mother. stopping of breast feeding
5.5.2 Appropriate infant feeding is initiated as per • EID +ve baby on ART: Breast feeding
informed choice following AFASS continued upto 2 years
counseling: Upto 6 months: Exclusive 5.5.5 Growth & nutrition monitoring,
breast feeding (preferred option) or immunization as per schedule.
exclusive replacement feeding. No 5.5.6 Confirm HIV status:
mixed feeding. Repeat HIV testing at 6, 12 months and 6 weeks
5.5.3 At 6 weeks: after stoppage of breast feeding; (If rapid test +
• Start Cotrimoxazole (CPT) prophylaxis, ve DBS followed by WBS).
• Early infant diagnosis (EID) by dry blood At 18 months: Confirmation of HIV status by 3
spot test (DBS); if DBS +ve Whole blood spot rapid antibody tests.
(WBS) confirmatory testing. 5.5.7 Counseling: Counsel for adherence to ARV
• EID +ve babies are started on ART at and AKT if co-infected with tuberculosis.
pediatric ART Centre irrespective of CD4 Encourage safe infant feeding practices.
Bibliography
1. Government of India, Ministry of Health and Family Welfare. Guidelines for control of Iron deficiency
Anaemia; National Iron + Initiative, 2013
2. Government of India, Ministry of Health and Family Welfare. National guidelines for deworming during
pregnancy Dec 2014
3. Government of India, Ministry of Health and Family Welfare. National guidelines for Diagnosis &
Management of Gestational Diabetes Mellitus, Maternal Health Division, Dec 2014
4. WHO, Prevention of neural tube defects (IMPAC): Folic acid supplementation. Integrated management of
pregnancy and childbirth (IMPAC). Standards of Maternal and Neonatal care, 2006
5. NACO, Updated guidelines for Prevention of parent to child transmission of HIV using Multi drug Anti-
Retroviral Regimen in India, Dec 2013
6. WHO, Neonatal IMCI – Evidence based Interventions (PAHO guidelines), 2011
7. Government of India, Ministry of Health and Family Welfare. Diagnosis and treatment of Malaria;
Directorate of National Vector borne disease control programme, 2013
Further reading
1. WHO, Guidelines for treatment of malaria. 2nd edition, 2010

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6. COMPREHENSIVE ABORTION CARE:
MEDICAL TERMINATION OF PREGNANCY
Unsafe abortion still accounts for nearly 9 %

maternal deaths. Provision of easily accessible, free
7. Methods for first trimester
safe abortion service can reduce the burden of MTP
maternal morbidity and mortality.
7.1 Surgical methods
1. Legal limit
Upto 20 weeks of pregnancy. A trained medical • Manual vacuum aspiration (MVA) is the safe
officer at Primary Health Center is authorized to recommended technique for pregnancy up to 12
perform MTPs up to 12 weeks. weeks.
• Electrical vacuum aspiration is also safe and
2. Indications effective.
• Pregnancy likely to endanger woman’s life or • D&C should not be used as a method for MTP.
likely to cause grave Injury to her physical or • Give antibiotics prophylaxis: Cap. Doxycycline
mental health. 100 mg orally twice a day for seven days may
• Child is likely to suffer from serious physical or be given.
mental disability. • Follow adequate infection control practices.
• Pregnancy caused by rape.
• Pregnancy following contraceptive failure. a) Before MVA:
3. Consent for MTP • Check the eligibility and consent

An adult woman who is not mentally ill can undergo • Give pain relief
MTP with only her own consent. Consent of legal • Start prophylactic antibiotics
guardian is required for minors and mentally ill • If uterus is > 9 weeks of size, cervical softening
women. can be achieved by administering 400 mcg (2
tablets) of Misoprostol orally/vaginally 3-4
4. Record and register hours before MVA.
• Consent in form C of the MTP Act. • Keep the charged syringe ready, perform the
• Certify MTP within 3 hours on form I MVA procedure.
specifying the indication. b) Complications:
• Admission register (Form III). This register is a
secret document. • Incomplete abortion, hemorrhage, infection,
• Uterine perforation
5. Clinical evaluation • Anesthesia related complications.
Medical history, date of LMP, complete physical • Failed termination with continuation of
examination. Determine size of uterus on vaginal pregnancy. Woman should be counseled to
examination. report if she continues to be amenorrhoeic after
MTP. Repeat termination of pregnancy can be
6. Investigations undertaken.
• Hemoglobin, blood group, Rh typing, urine 7.2. Mifepristone-Misoprostol
testing for sugar and protein.
• Ultrasonography is not mandatory. It may be abortion (MMA)
helpful for knowing the pregnancy duration in MMA is permitted up to 49 days by MTP Act.
women having irregular cycles, Lactational
amenorrhea, when on examination the uterine a) Information to Women:
size is uncertain or discrepant with the period of
amenorrhea and to exclude an ectopic gestation. MMA is safe and effective. Success rate 95-98 %
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• Three visits are necessary, day 1 Mifepristone, • Vaginal bleeding and uterine cramping may
day 3 Misoprostol tablets and day 14 for post occur for 7-14 days.
treatment evaluation b) Protocol
• If treatment fails, surgical termination is
necessary; pregnancy cannot be continued, as
there is risk of fetal malformation.
Table-1: Protocols for Mifepristone-Misoprostol Abortion
Mifepristone Misoprostol
Day 1 Day 3
Gest Age Dose Route Dose Route
Upto 49 days 200 mg (1 tab) oral 400 mcg (200 mcg, 2 tablets) Oral/vaginal
The clinic where medical abortion drugs are prescribed by an RMP as under the MTP Act, does not need
site approval as long as it has referral linkage to an MTP approved site. The clinic should display a
certificate to this effect from the owner of the approved place.
The Central Drugs Standard Control Organization, Director general of health services, Govt. of India has
approved a Combi pack of one 200 mg tablet of mifepristone and four 200 mcg tablets of Misoprostol
for MTP for gestation between 49-63 days. However, MTP Act allows MMA up to 7 weeks
In the event that vomiting ensues within 30 minutes of • OC pills or Inj. DMPA can be started on day 3
oral Misoprostol the medication should be repeated. or day 15 when abortion process appears to be
There is no need to keep a woman in the facility till complete.
she aborts. • IUCD insertion after one normal menstrual
Misoprostol given by vaginal route has lesser side period.
effects, is absorbed slowly and is effective for a • Tubal ligation after next cycle.
longer time whereas by oral route it is absorbed
quickly, is effective for a shorter time and leads to e) Counseling:
more gastrointestinal side effects. Early abortion is safer. MTPs should not be
c) Contraindications: performed repeatedly. Using contraception is
important. Concomitant female sterilization or IUCD
• Ectopic pregnancy, either confirmed or insertion at the time of surgical abortion is safe.
suspected, or undiagnosed adnexal mass Inform the woman to report early for symptoms
• Hemorrhagic disorder. suggestive of complications.
• Allergy to mifepristone, Misoprostol or another
prostaglandin. 8. Methods for Second
• Current anticoagulant therapy, Current use of Trimester MTPs
long-term systemic corticosteroids.
• Intrauterine device in place (remove before
giving Mifepristone). a) Mifepristone –Misoprostol:
• Chronic adrenal failure. Inherited porphyria.
• Caution: Haemoglobin<8 gm %. These drugs are recommended by WHO for second
• Uncontrolled hypertension, BP > 160/100 trimester MTPs. Combination improves the efficacy.
• Uncontrolled seizure disorder. The suggested protocol is 200 mg mifepristone
d) Contraception after MMA: followed after 36 – 48 hours by 400 micrograms of
vaginal, sublingual or oral, Misoprostol every 3 – 6
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hours up to 5 doses. Before 18 weeks 3-4 hourly Safe method, however the drug is not currently
interval is preferred. At or after 18 weeks consider 6 available.
hourly dosing interval.
d) Abdominal Hysterotomy:
Vaginal Misoprostol is more effective than oral Major surgery, done only in selected cases. Eg.
Cancer cervix.
Cautious use in cases having scarred uterus. Check
and record vital signs 4 hourly until onset of strong Second trimesters MTP procedures require
contractions, thereafter 2 hourly. hospitalization for few days. They are likely to be
associated with more bleeding, more chances of
b) Use of Misoprostol alone
incomplete abortion and other complications.
Is less effective as compared to combination
Provider needs to make sure that the woman is not
400 mcg 3-6 hourly upto 5 doses. seeking a sex selective abortion.
If fetal expulsion does not occur after 24 hours from Additional legal requirements: MTP Centre approved
initial dose perform abdominal examination and USG for 2nd trimester MTP, experienced RMP as stated in
to rule out uterine rupture. MTP Act, and the requirement of opinions of two
registered medical practitioners are necessary.
c) Extra amniotic Instillation of Ethacridine
Lactate, 0.1 %, 150 ml

Bibliography
1. MTP Act 1971.MTP Rules 2003
2. Government of India, Ministry of Health and Family Welfare. Comprehensive abortion care; training
& service delivery guidelines, 2010 (2nd edition 2014)
3. IPAS, Refresher course for medical abortion services Reference manual, 2009
4. Government of India, Ministry of Health and Family Welfare. Guidance on Ensuring Access to Safe
Abortion and Addressing Gender Biased Sex Selection; Feb 2015
5. Government of India, Ministry of Health and Family Welfare. Handbook on Medical Methods of
Abortion to Expand Access to New Technologies for Safe Abortion, Jan 2016
6. Government of India, Ministry of Health and Family Welfare. Comprehensive Abortion Care Training
Package, 2014.
7. World Health Organization (WHO): Clinical practice handbook for Safe Abortions. Geneva, 2014
Further reading
Ltd; 2010


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7. COMMON GYNAECOLOGICAL PROBLEMS
1. Dysmenorrhoea d) Investigations:
1.1 Definition:
• Ultrasonography to detect pelvic pathology
Dysmenorrhoea is painful menstruation.
(adnexal mass, ovarian cyst).
• Diagnostic laparoscopy helps in diagnosis of
1.2 Types: genital TB, endometriosis, adhesions.
Spasmodic (Primary) and Congestive (Secondary).
e) Treatment:
1.2.1 Spasmodic Dysmenorrhoea
• Assurance and treatment of cause.
a) Symptoms: Colicky pain in lower abdomen starts • NSAIDs for pain relief: Mefenamic acid,
on first day of menstruation and usually lasts for a Ibuprofen.
day. Nausea, vomiting may occur. • Antibiotics for treatment of PID.
• Progestins for Endometriosis.
b) Treatment: • Specialist referral for treatment of
Endometriosis, genital TB.
• Usually reassurance is adequate.
• Laparoscopy for diagnosis of cause for chronic
• Majority get relief with antispasmodics pelvic pain and treatment of adhesions,
(Dicyclomine) or antiprostaglandins like endometriosis.
Mefenamic acid 500 mg t.d.s as needed.
• If no response: Combined oral contraceptive
pills for 3 cycles.
• Rarely pain may be very severe not responding 2. Abnormal Uterine Bleeding
to medicines and may need further evaluation
and management by specialist. Abnormal uterine bleeding (AUB) accounts for 20%
of all gynecologic visits.
c) Investigations: If pain is persistent, USG to rule
out Endometriosis, Uterine anomalies, or Submucous 2.1 . Definitions
myoma. • Menorrhagia: Excessive uterine bleeding
occurring at regular intervals or prolonged
1.2.2 Congestive Dysmenorrhoea: uterine bleeding lasting > 7 days.
• Dysfunctional uterine bleeding (DUB):
a) Common causes: Chronic Pelvic inflammatory
Abnormal uterine bleeding occurring in the
disease (PID), endometriosis, Genital Tuberculosis,
absence of identifiable pathology. It can be
Pelvic adhesions.
ovulatory or anovulatory DUB.
b) Symptoms: Chronic pelvic pain. Pain is • Metrorrhagia: Acyclical intermenstrual
experienced few days before period and is usually bleeding occurring at irregular intervals.
relieved with the onset of menstrual bleeding. It is • Breakthrough bleeding: Unpredictable
continuous dull aching pain in lower abdomen and bleeding that occurs while on exogenous
low backache. Often associated with dyspareunia, hormones (eg hormonal contraception).
vaginal discharge, menorrhagia and infertility. • Oligomenorrhea: A menstrual cycle interval of
more than 35 days.
c) Signs of chronic PID: • Polymenorrhea: A menstrual cycle interval of
P/A: Tenderness in lower abdomen less than 21 days.
P/S: Discharge from cervical canal in STIs • Postmenopausal bleeding: Vaginal bleeding
P/V: Retroverted fixed uterus, cervical movements occurring more than 12 months after the last
painful. Tenderness in fornices and tender menstrual period.
adnexal mass. Nodularity in posterior fornix in • Amenorrhea: Absence of menstrual bleeding.
endometriosis.
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2.2. Differential diagnosis of AUB 2.2.3. Investigations
Abnormal uterine bleeding can occur in all age • Complete blood count
groups. The diagnostic testing and treatment
approach should take into consideration the age
• Ultrasonography abdomen and pelvis and
transvaginal ultrasonography (TVUS) for
group and fertility choices of the woman.
diagnosing fibroids, polyps, adnexal mass.
• Adolescent girls: Anovular DUB is common. Thickness of endometrium can be measured.
Pregnancy related conditions should be kept in Intrauterine pregnancy and ectopic pregnancy
mind. Bleeding disorders can be present in some can be excluded.
cases.
• Endometrial biopsy in women over age 35 and
• Women between 20-40 years: Pregnancy related women having risk factors for endometrial
conditions, ovular DUB, pelvic infection and cancer. It helps in diagnosing ovular or anovular
benign neoplasia like fibroids are common. bleeding, endometrial hyperplasia, endometrial
• Perimenopausal AUB is commonly due to precancerous lesions and endometrial
anovulation and fibroids. However, it is carcinoma.
necessary to exclude polyps, endometrial
hyperplasia and malignancies. • Endometrial sampling is a rapid, safe, and cost-
• Postmenopausal bleeding: Malignancy needs to effective procedure that can be performed in the
be excluded. office to evaluate AUB. A potential drawback is
that the biopsy does not sample the entire
2.2.1. History endometrium and a localized lesion may be
missed.
• Detailed menstrual history, sexual history, past • Dilation and Curettage (D&C) can be both
medical history, gynecologic and obstetric diagnostic and therapeutic.
history. Note any change in the patient's
weight, and exercise pattern. • Hysteroscopy is the gold standard for evaluating
• History of bleeding disorders, possible the endometrial cavity. It provides direct
pregnancy. visualization of the endometrial cavity and can
• H/O Drugs, IUCD. be performed in the office setting or operating
room. It can be both diagnostic and therapeutic,
• Antipsychotic medications (Dopamine
allowing for directed biopsies and excision of
antagonists), Phenothiazine and antidepressants
polyps and small sub mucus myomas.
can cause hyperprolactinemia and AUB.
• Combination OC pills can cause breakthrough • Saline infusion Sonohysterography for detecting
bleeding. endometrial polyps or uterine leiomyoma.
• Prolonged use of high doses of progestational
• Thyroid stimulating hormone (TSH) and
agents.
Prolactin estimation: Hypothyroidism and
• Anticoagulant medications. hyperprolactinemia can lead to anovulation and
• Digitalis, Phenytoin, and Corticosteroids. DUB.
• Copper- intrauterine devices.
• Bleeding disorders should be evaluated if
historical or clinical features suggest specific
2.2.2. Physical Exam
conditions.
• Note pallor, thyroid examination. 2.3. Dysfunctional Uterine Bleeding
• Breast examination: Galactorrhea.
• P/A examination: Pelvic mass (fibroids), • Dysfunctional uterine bleeding (DUB) is a
tenderness in lower abdomen. (PID) diagnosis by exclusion of other causes of AUB
• Speculum examination: Cervical pathology. without a demonstrable pathologic cause. The
(growth, ulcer, polyp) predominant causes of DUB are anovulation or
• P/V: Cervical motion tenderness, size and oligo ovulation.
contour of uterus, and presence of any palpable
• Long-term anovulation, polycystic ovary
adnexal masses or tenderness.
syndrome: Resulting unopposed estrogen state
increases the risk of endometrial hyperplasia.
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Morbid obesity with associated elevated • Endometrial ablation: Endometrial ablation is
estrogen levels can also cause DUB. not recommended in women who desire future
fertility.
• In some cases, DUB may be associated with
ovulatory cycles. • Hysterectomy provides definitive treatment for
menorrhagia and may be a reasonable option in
2.3.1 Medical therapy: women with severe menorrhagia, who have
completed their childbearing and are refractory
Treatment of Anemia should be initiated. Women
to medical and less invasive surgical therapy.
who are severely anemic or not responding to
medical treatment should be referred to specialist. The women not responding to medical line of
treatment should be referred to specialist at FRU/DH
a) Nonsteroidal anti-inflammatory drugs
for surgical treatment.
(NSAIDs) may reduce menstrual blood loss by about
30% in women with menorrhagia and can be given as
the first line therapy. They need to be taken during
menses only. The options are:
2.4 AUB: Other Conditions
i. General medical causes associated with
• Mefenamic acid 500 mg three times a day for 5 menorrhagia: Hypertension, cardiac failure,
days during menstruation. hepatic dysfunction can be associated with AUB.
• Ibuprofen 600-1200 mg /day.
• Naproxen sodium 500 mg × 1, then 250 mg ii. Genital Infection: Chronic PID and genital
every 6-8 hourly. tuberculosis.
iii. Endometrial Pathology & Genital Neoplasia:
b) Hormones:
a. Endometrial Polyps can present as Menorrhagia
or Metrorrhagia. Diagnosis is by saline infusion
• Oral Progestins: Useful in anovulatory bleeding.
sonogram and hysteroscopy. Endometrial polyps
For acute heavy bleeding: Medroxyprogesterone can be removed by operative hysteroscopy.
acetate 10 mg tablet 2-3 times a day till bleeding
Cervical polyps can be removed by grasping with
stops. It is tapered and continued 1 tab daily for
forceps, twisting them off, and cauterizing the base.
a total duration of 21 days. Withdrawal bleeding
starts in few days. Further cyclical therapy (10 b. Endometrial Hyperplasia: A precursor to
mg daily) is given from day 5 to 25 th day for 2 endometrial carcinoma. It is classified into simple
more cycles. Response is awaited. or complex, based on architectural features, and
Norethisterone tablet 5 mg can be used similarly typical or atypical, based on cytological features.
for a period of 21 days, initially 1 tab 3 times a Endometrial hyperplasia tends to occur during
day until bleeding stops, then 1 tab twice a day periods of long-term unopposed estrogen exposure,
for few days and then tapered to 1 tab daily either secondary to anovulatory cycles or
thereafter. Side effects of Progestins include exogenous use. AUB is the most common
breast tenderness, weight gain, and headaches. presenting symptom.
• Combined oral contraceptive pills can be given • Diagnosis by endometrial biopsy
from day 5 to 25 for 3-6 cycles in women • Treatment depends upon age, desire for future
between 20-40 years of age not having fertility and presence of atypia in the pathology
contraindications for estrogens and who also specimen.
wish to have contraception. • Simple hyperplasia can be treated with
c) Antifibrinolytic medications (e.g. Tranexamic progestogens.
acid) decrease menstrual blood flow by 50%, and • Cyclic Medroxyprogesterone Acetate (MPA 10
need to be taken during menses only. However, there mg/day for 12 to 14 days/cycle for 3 to 6
are concerns about their pro-thrombotic potential. months) in young anovulatory women to induce
monthly withdrawal bleeding.
2.3.2 Surgical Treatment for DUB:
• Local Progesterone administration:
• Diagnostic D&C may have some therapeutic Levonorgestrel-releasing intrauterine system.
effect. However, it does not have a sustained (LNG IUS)
therapeutic effect. • Atypical endometrial hyperplasia is more likely
to progress to carcinoma or may coexist with
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endometrial carcinoma. Hence hysterectomy is f) Ovarian Cancer: Estrogen-producing ovarian
advised. tumors, can produce endometrial hyperplasia and
AUB. USG will reveal the tumor. The woman
should be referred to district hospital or a cancer
c) Uterine Fibroids: Menorrhagia is the most
treatment centre for surgical treatment.
common presenting symptom. Diagnosis is by
USG. Symptomatic fibroids need surgical
treatment by a specialist. 3. Postmenopausal Bleeding
d) Endometrial Cancer: It is mostly seen in 3.1 Definition:
postmenopausal women and is rare in patients
younger than 40. Postmenopausal bleeding is the Vaginal bleeding occurring one year after cessation
presenting symptom which should be assumed to of menses.
represent endometrial cancer until proven Uterine bleeding is often due to endometrial cancer,
otherwise. The women should be referred to polyps or endometrial hyperplasia. Genital tract
specialist for further evaluation and treatment. malignancy and precancerous conditions need to be
excluded in these cases. Hence immediate referral to
e) Cervical Cancer: Bleeding patterns associated
gynecologist is necessary for further evaluation and
with cervical carcinoma are intermenstrual and
treatment.
post-coital bleeding. Cervical biopsy is
diagnostic. The woman should be referred early 3.2 Differential diagnosis:
to district hospital or a cancer treatment centre.
Table-1: Differential Diagnosis of Postmenopausal Vaginal Bleeding.
Endometrial causes Ovarian causes

➢ Endometrial Hyperplasia ➢ Benign tumors of ovary
➢ Endometrial carcinoma ➢ Malignant tumors of ovary
➢ DUB ➢ Hormone secreting tumors of Ovary
➢ Endometrial polyp (Granulosa- theca cell tumor)
➢ Senile endometritis
➢ TB endometritis
Cervical causes: Exogenous Estrogens –

➢ Cancer cervix, Polyp, ➢ HRT for menopausal symptoms can cause
➢ Decubitus ulcer on prolapse irregular bleeding
➢ Cervicitis
Vulvovaginal causes: Non genital causes:

➢ Senile atrophic vaginitis ➢ Hypertension
➢ Foreign body in vagina like pessary ➢ Bleeding diathesis
➢ Malignant lesions on vulva ➢ Urethral and rectal bleeding can sometimes
be misreported as vaginal bleeding
3.2.1 Endometrial Cancer in the body (endogenous) or given in medicinal

form (exogenous)
a) Risk Factors for Endometrial Cancer: • Age at menopause > 52 years
• Nulliparity, infertility.
• Conditions associated with excessive estrogens • Obesity, Hypertension, Diabetes Mellitus
unopposed by cyclical Progesterone are
• Family history of uterine, breast, colorectal
commonly responsible for postmenopausal
cancer
bleeding. Estrogens could have been produced
• Drugs: Estrogen therapy, Tamoxifen
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b) Management: • Fractional curettage under GA if hysteroscope
unavailable
At PHC: • Treatment is planned according to pathology
found.
History:
➢ Endometrial hyperplasia: Abdominal total
• Ask symptoms: Irregular bleeding, spotting, hysterectomy with bilateral salpingo
brown discharge, post-coital bleeding, number oophorectomy
of bleeding episodes ➢ Cervical / Endometrial malignancy:
Treatment as per stage
• Age of woman, late menopause (> 52 years),
Nulliparity,
➢ Ovarian tumors: Staging laparotomy (Total
hysterectomy + bilateral salpingo-
• H/O receiving hormones (estrogen oophorectomy for benign tumors. Treatment
/progestogen), drugs (tamoxifen) as per stage for malignant tumors)
• Family history of endometrial cancer ➢ Senile vaginitis: Vaginal estrogen therapy
• Diabetes Mellitus, Hypertension
d. Screening for endometrial cancer:
Examination:
TVS for endometrial thickness is a simple, non-
• Look for Obesity, Hypertension invasive, reliable screening technique for the
• Examination of vulva for any lesion, ulcers, diagnosis of Ca Endometrium. All postmenopausal
growth, atrophy, polyp. women should have annual trans vaginal sonographic
• P/S examination of vagina and cervix to look assessment for endometrial thickness. Women having
for any growth, polyp, ulcer, estrogenization, endometrial thickness > 4 mm need further
infection. If cervical pathology is seen refer to evaluation to rule out endometrial cancer.
gynecologist for cervical biopsy, polypectomy 3.2.2 Cervical Cancer
as necessary
• Vaginal examination: Look for uterine Cervical cancer is the second most common cancer
enlargement, Suspect Pyometra if soft among women in India, the first being breast cancer.
uniformly enlarged tender uterus with In 2012, about 1,23,000 new cases of cancer cervix
intermittent offensive vaginal discharge. were detected in India and 67,000 women died due to
Suspect uterine myoma or malignancy if firm cervical cancer, but this cancer can be prevented.
irregularly enlarged uterus Human papillomavirus (HPV) is the causal agent for
• Refer the woman to the gynecologist for further cervical cancer and about 15 high-risk types of HPV
evaluation. are known. HPV infection is a very common
• Refer for USG including TVS for assessment of infection. Those women who cannot clear this
endometrial thickness and other uterine and infection by their natural immunity are at risk of
ovarian pathology. cervical cancer.
c. Management a. Screening for Cervical Cancer:
At RH/DH:
Cervical cancer is preceded by a long phase of
premalignant lesion called as Cervical
• If gross cervical pathology seen cervical biopsy, Intraepithelial Neoplasia (CIN). This stage may last
Polypectomy
for about 10-20 years before developing into a frank
• Pap smear if no gross lesion seen malignancy. When the abnormal cells are limited to
• Colposcopy for unhealthy cervix, abnormal Pap the lower third of the epithelium it is labeled as CIN
smear, vulval lesions 1, when lower two thirds of the epithelium are
• Ultrasonography: TVS or Saline infusion involved, it is termed as CIN II and when the entire
sonography thickness of the epithelium is involved, it is termed as
• Hysteroscopy and directed biopsy is the gold CIN III. CIN can be diagnosed by a pathologist on
standard for evaluation: It permits direct visual histopathological examination of cervical biopsy
inspection of uterine cavity with greater specimen. CIN lesions can be treated by simple
accuracy of diagnosis as focal lesions are not treatment modalities and cervical cancer can be
missed. It is superior to blind dilatation and prevented.
curettage in which neoplasia may be missed.
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The World Health Organization (WHO) has solution, 95% ethanol or ether-alcohol mixture, glass
recommended that at a minimum, as a priority, slides.
screening is recommended for every woman 30–49 Procedure:
years of age at least once in a life time. Screening • Schedule the procedure following abstinence for
should be initiated at 30 years of age. For HIV- 24 hours and when there is no vaginal bleeding.
infected women screening should be initiated as soon Confirm that no vaginal examination has been
as the infection is diagnosed. done in previous 24 hours. No vaginal
antiseptics should be used
Cervical cancer screening can be done by following • Use speculum to inspect the cervix
different tests:
• Do not take smear if there is vaginal bleeding or
• Pap smear (cytology screening) active infection
• Visual inspection of cervix with acetic acid • Place the Ayre’s spatula against the cervix and
(VIA) rotate it firmly against the cervix through 360
• HPV testing for high risk types (it is expensive degrees to scrape the transformation zone.
and available only in some centers. Useful in Spread the sample on the spatula evenly on a
increasing the screening interval in women glass slide. Endocervical cells are obtained by
above 30 years of age) endo-brush or cotton tipped applicator rolled in
cervical canal. Place the sample on another
i) Pap smear (cytology screening): glass slide (Fig 1 & 2)
Pap smear requires laboratory infrastructure, quality • Fix the smears by putting in fixative jar or by a
control, a system for informing the results to the fixative spray. Send the smears to an expert
women and further referral for colposcopy. cytopathologist
Material: Cusco’s bivalve speculum, Ayre’s spatula,
• Currently Bethesda system (2001) is used for
endo-brush, fixative spray or jar containing fixative
reporting of smears.
Figure 7.1: Scraping from Ectocervix Figure 7.2: Endocervical sampling
ii) Visual inspection of cervix with acetic acid: Procedure:
VIA involves application of 5% acetic acid on the • Insert a bivalve speculum, view the cervix
cervix for one minute and visual inspection of • Remove any discharge, blood or mucus from
colour changes in the cervix. VIA is simple, cheap, the cervix by a saline moistened cotton swab
it can be performed by trained health care workers • Identify the squamocolumnar junction (SCJ)
and provides an opportunity to treat screen positive and the area around it
women during the same sitting thus reducing the • Apply acetic acid to the cervix for one minute
challenges of lost to follow up. and simultaneously observe if any color change
Materials and equipment needed for screening: develops
• Observe any changes in the color/ appearance of
• Sterile gloves and Cusco’s speculum the cervix after one minute. Give special
• Autoclaved cotton balls and sponge holding attention to abnormalities close to the SCJ
forceps/ autoclaved cotton-tipped swabs • Look for any raised and thickened white plaques
• Freshly prepared acetic acid solution (5%) or acetowhite epithelium.
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• Use a fresh swab to remove any remaining Primary prevention of cervical cancer is now
acetic acid solution from the cervix and vagina. possible by HPV vaccination of girls between 9 to 13
Gently remove the speculum. years of age before initiation of sexual activity. But
HPV vaccines are currently expensive and not yet
The test results are reported as follows: available in the government programs.
• VIA positive (Fig 3) - when there is a dense
white, opaque lesion touching the A comprehensive approach to cervical cancer
squamocolumnar junction (SCJ) prevention and control involves health education
• VIA negative when such lesion is not seen and screening of all women and treatment before
• VIA positive-invasive cancer when there is a progression to invasive disease. Awareness among
clinically visible growth which turns dense women and doctors that cervical cancer can be
acetowhite and bleeds on touch. prevented by early detection and treatment of CIN
is critical for the success of cervical screening.
4. Infertility
4.1 Definition:
Infertility is defined as failure to conceive after one
year of regular, unprotected sexual intercourse. It can
be primary or secondary:
Primary: The woman has never conceived in past.
Secondary: The woman has previously conceived but
Figure 7.3: VIA positive cervix is subsequently unable to conceive for 12 months.
Infertility affects 10 – 15% of the general population.
After screening
It is the problem of the couple. Male factor is
responsible in 30%, female factor in 50%, and the
• If the test is negative, repeat test in 3-5 years.
combined factors are responsible in 10%.
• For HIV infected woman repeat testing within 3 Unexplained infertility is observed in 10%.
years.
4.1.1 Infertility – Male Factor
b) Treatment strategy for screen positive cases: a) History in Male Partner: Age, occupation,
previous marriage if any, substance abuse, coital
GOI-WHO (2006): Screening women between age history (Frequency of intercourse / Knowledge of
30 -59, by VIA by trained HCW at PHC. Referral of fertile period / Coital difficulties related to erection /
VIA positive to district hospital (DH). penetration / ejaculation).
At DH repeat VIA followed by pap smear, Past history:
colposcopy, directed biopsy from abnormal areas Mumps/Genital trauma/STIs/Surgery/Tuberculosis,
followed by cryotherapy /LEEP as required at the Current history: Any illness, drug treatment.
same sitting.
b) Physical Examination - Rule out Hernia,
WHO guidelines (2013): Hydrocele, Undescended testis, Absence of Testis.
Note the size of testis. Look for Varicocele in upright
“Screen and Treat” approach, using a screening test position.
giving immediate results (like VIA) followed by “on
the spot” treatment (cryotherapy) of detected lesions c) Investigations:
to eligible women, without any further tests, when Semen Analysis: Sample collected after 2-3 days of
there is no suspicion of cancer. This has been shown abstinence and examined within 2 hours of
to be an effective strategy. This is a single visit collection. Male partner should be evaluated first by
approach which is convenient for rural women. performing semen analysis. In humans it takes about
75 days for spermatogonia to develop into mature
spermatozoa.
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Blood and urine routine testing Tubal infertility:
Table 2: Minimum normal criteria for semen Genital Tuberculosis, PID, Tubectomy
analysis: WHO revised criteria.4
Uterine factors:
Submucous fibroids, Tubercular endometritis,
Parameter Lower Ref Limit Endometrial polyps, Intrauterine adhesions.
Volume 1.5 ml
Peritoneal factors: Endometriosis, Chronic PID
Sperm concentration 15 million/ml
Progressive motility 32 % Cervical factors:
Normal forms 4%
Immunologic, infections, surgical trauma
(amputation, conization, deep cauterization of
If semen report is abnormal, the test should be cervix).
repeated twice at least at 2-4 weeks of interval before
considering it as abnormal. Ideally, a period of 3 b) History in female Partner:
months should be considered for evaluation of any
Age, years since marriage, occupation, substance
improvement as a result of therapy.
abuse. History suggestive of reproductive tract
Persistently abnormal semen parameters require infections (Vaginal discharge/Pruritus
further evaluation at specialty infertility clinic vulvae/Chronic pelvic pain), Tuberculosis,
Endocrinopathy (Weight & hair changes/discharge
d) Counselling for male:
from nipples/cold intolerance/dryness of skin),
Regular intercourse 2-3 times/week, stop smoking, Premature ovarian failure (H/O Mumps, hot
alcohol & any addictive drugs, wear loose fitting flushes/Oligomenorrhea/amenorrhea), Abdominal
underwear and trousers, and avoid occupational or Surgery. coital frequency & knowledge of fertile
social situations that might cause testicular heating. period, dyspareunia
Treat any psycho-sexual problem if present.
H/O previous pregnancies, post-partum infection.
e) Male Partner- Treatment
Family history: e.g. Tuberculosis
i. Medical therapy: Antioxidants, clomiphene
Menstrual history: Menarche, regularity of cycles,
citrate, gonadotropins.
Dysmenorrhoea, flow, LMP: Regular cycles,
ii. Intra-uterine Insemination (IUI): Mild male
Dysmenorrhoea, Mittelschmerz (mid cycle pain),
factor infertility.
premenstrual breast heaviness and mastalgia are
iii. Donor insemination: For azoospermia
suggestive of ovulatory cycles.
(Primary testicular failure)
iv. Adoption: For cases with recurrent unexplained
c) Examination of female partner:
failed IVF cycles.
v. Surgical restoration of duct patency: For Look for obesity or gross underweight (BMI),
obstructive azoospermia (previous vasectomy). Lymphadenopathy, Thyroid enlargement, Hirsutism,
vi. Intra-cytoplasmic Sperm Injection (ICSI): Galactorrhea, Acanthosis Nigricans.
For severe male factor or for recurrent
unexplained failed IVF cycles. Systemic exam
Speculum & per vaginal exam: Look for anatomic
4.1.2 Infertility – Female Factors abnormalities.
a) Causes d) Investigation in Female Partner
Anovulatory infertility- • Pelvic USG: Diagnosis of PCOS, uterine

fibroids, adnexal mass, uterine malformations,
i. Polycystic ovarian disease. endometrioma.
ii. Thyroid disorders, Hyperprolactinemia • Serial trans-vaginal sonography for
iii. Decreased ovarian reserve, Premature ovarian confirmation of ovulation and timing of
failure. ovulation.
iv. Anorexia nervosa / Stress related / Exercise
• Hormonal assay: Mid luteal serum
induced.
progesterone.
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• TSH, Prolactin, FSH & LH in selected patients f) Treatment of Female Partner:
with anovulation
• Induction of Ovulation:
For women with ovulatory dysfunction.
• Endometrial sample collected by premenstrual
curettage is sent for histopathological and
microbiological evaluation to exclude • Clomiphene citrate is the first line drug for
endometrial tuberculosis in suspected cases. ovulation induction.
50 mg orally daily for 5 days from day 2 to day
Laparoscopy helps in diagnosis.
6 of menstrual cycle. Ovulation is monitored by
USG follicle monitoring. If ovulation does not
• Hysterosalpingography (HSG)- Tubal patency occur, the dose can be increased by 50 mg daily
test. It also helps in detecting intra uterine in successive cycles up to 150 mg daily. Risk of
pathology. Performed between Day 6 – Day 11 multiple pregnancies should be explained.
of the menstrual cycle, at the Radio- diagnosis Failure of ovulation or conception after
department. treatment for 3 cycles requires careful review
Contraindications: Current PID, suspected and evaluation.
Genital TB, cervicitis. • Women with polycystic ovary syndrome who
have not responded to clomiphene citrate should
• Laparoscopy with chromotubation – be offered laparoscopic ovarian drilling
This is an invasive surgical procedure indicated • Gonadotropins for ovulation induction requires
when HSG is abnormal, there is failure to special expertise and careful monitoring. There
conceive within 6 months in spite of a normal is risk of multiple pregnancy
HSG, and for suspicion of endometriosis. • Hyperprolactinemia: Treatment with
Usually done in the pre ovulatory period. bromocriptine.
Diagnostic laparoscopy helps in diagnosing • Hypothyroidism: Thyroxine therapy restores
tubal, uterine pathology and also helps in ovulatory cycles
detecting Endometriosis, Pelvic adhesions,
Pelvic Tuberculosis. Surgical treatment for Intra-uterine Insemination (IUI): Unexplained
adhesions, Endometriosis can be done infertility and cases with minimal endometriosis.
laparoscopically.
Surgical Treatment
• Hysteroscopy:
Endoscopic direct visualization of the uterine i. Laparoscopic adhesiolysis
cavity. Submucous fibroids, Endometrial ii. Hysteroscopic tubal cannulation, resection of
polyps, adhesions, Malformations and Foreign intrauterine adhesions, polyp or submucous
bodies can be visualized. myoma.
Hysteroscopic resection of uterine septum, iii. Laparotomy for tubal reconstructive surgery.
submucous myoma and adhesiolysis for
intrauterine adhesions can be offered.
Laparoscopy can be combined with
hysteroscopy.
5. Pelvic Organ Prolapse
Pelvic organ prolapse (POP) is a common
e) Counselling for Female Partner:
gynaecological problem in women above the age of
Regular intercourse 2-3 times/week. stop smoking, 40 years.
alcohol and addictive drugs, and follow a supervised
weight loss programme if obese. Treat psycho-sexual
problem if present. POP includes anterior vaginal prolapse (cystocele),
uterine prolapse, and posterior vaginal prolapse
(rectocele, enterocele).
Page 330
5.1 Symptoms
Table-3: Symptoms
Lower urinary tract symptoms Bowel symptoms Sexual symptoms Other symptoms
Incomplete emptying, Constipation Interference with Pelvic pressure,

sexual activity heaviness, pain
recurrent UTI, frequency,
urgency, nocturia
Stress urinary incontinence Straining Dyspareunia Presence of vaginal

bulge/mass
Voiding difficulty: may require to Incomplete Decreased sexual Low back pain
reduce prolapse before passing evacuation desire
urine
5.2. Signs 5.4. Management

• P/A: Look for any lump, ascites, obesity
5.4.1 At PHC:
• Local exam: Inspection of the vulva with
coughing and straining – demonstrate severe
Preoperative care given at PHC can help in
prolapse and may demonstrate stress
shortening the hospital stay and reduce the number of
incontinence (provided the bladder is full)
visits to the district hospital.
• Examination using Sims speculum: Note type of
• Treat urinary tract infection. Correct Anemia,
prolapse, degree of uterine descent, anterior and
control Diabetes
posterior vaginal wall prolapse. Look for
decubitus ulcer on cervix, elongation of cervix • Treat the decubitus ulcer before surgery:
Reposition of prolapse and maintaining it in
• Vaginal examination: Note uterine size,
reposed position helps in healing of ulcer.
position, adnexal mass
Glycerine-acriflavine vaginal packing daily
• Rectal examination, to differentiate rectocele helps in healing. In older women having severe
from enterocele vaginal atrophy, vaginal application of estrogen
• Assess anal sphincter tone, assess levator tone, cream helps in rapid healing. The ulcer will
perineal body usually heal within 7 days.
5.4.2 At FRU/DH:
5.3. Predisposing factors
The women should be evaluated completely for
• Injuries to supports of pelvic organs during planning the treatment modality. Most women will be
childbirth candidates for surgical treatment. In a young woman
following childbirth conservative measures should be
• Obesity, chronic cough, chronic constipation, advised for 3 to 4 months.
• Atrophy and loss of tone due to aging, estrogen
deficiency a) The nonsurgical treatment is useful in following
• Congenital weakness of tissues can lead to women
nulliparous prolapse • Women having mild degree of prolapse
• Pregnancy and Postpartum
• Unfit or unwilling to undergo surgery.
Page 331
Kegel exercises to strengthen the pelvic supports. women, vaginal hysterectomy with repair of the
pelvic floor is performed.
Ring pessary: Can provide temporary relief for 5.5. Prevention
woman unfit for surgery,
• Antenatal physiotherapy, relaxation exercises
and due attention to weight gain and Anemia
b) Surgical treatment:
correction are important.
Surgery can be of two types. • Proper management of second stage of labour.
• Vaginal hysterectomy with vaginal wall Avoiding undue prolongation of second stage
prolapse repair and by timely assisted delivery.
• Uterus conserving surgical repair. • Immediate and accurate suturing of perineal tear
Choice of surgical procedure depends on age, after delivery.
parity and wish for further pregnancy and • Postnatal exercises and physiotherapy are
medical fitness. beneficial.
• Early postnatal ambulation.
In younger women desirous of retaining fertility, • Provision of adequate rest for the first 6 months
conservative surgical repair operations are indicated, after delivery
whereas in the peri-menopausal and menopausal • Contraception: Too many births at too short
intervals are avoided.

Bibliography
1. Government of India, Ministry of Health and Family Welfare - World Health Organization
Collaborative Programme Guidelines for Cervical Cancer Screening Programme (2004-2005), June
2006.
2. World Health Organization (WHO): Screening and treatment of precancerous lesions for cervical
cancer prevention (2013) [Cited 2016 July 10]
Available from: http://www.who.int/reproductivehealth/publications/cancers
3. World Health Organization (WHO): Comprehensive cervical cancer prevention and control - a
healthier future for girls and women. (2013) [Cited 2016 July 10]
Available from: http://www.who.int/immunization/documents/diseases
4. Laboratory manual for examination and processing of human semen 2010
Further reading
Ltd; 2010

Page 332
Annexure 1
Simplified Partograph
Page 333
Annexure 2
Page 334
Annexure 3
Page 335
Dermatology
4. Dermatology
1 Infections of Skin 336

Bacterial
Viral
Fungal
Parasitic
2 Noninfectious Skin Conditions 342
Urticaria
Psoriasis
Lichen Planus
Pityriasis Rosea
Pityriasis Alba
Acne
Miliaria
Eczema / Dermatitis
Atopic Dermatitis
3 Sexually Transmitted infections (STI) 347
Syphilis
Chancroid
LymphoGranuloma Venereum (LGV)
Gonorrhoea
Chlamydial infection
Bacterial Vaginosis
Trichomoniasis
Candidiasis
Wart
Herpes Genitalis
4 Syndromic management of STDS 352
5 HIV AIDS 354

1. INFECTIONS OF SKIN
Rule out Diabetes Mellitus in case of recurrent

1. Bacterial Infections of Skin furunculosis and carbuncle
It is infection of skin caused by bacteria. Persons
with poor personal hygiene, old age, Diabetes and
Immunocompromised patients are prone to bacterial
infection of skin.
1.1. Pyoderma
1.1.1 Types
a. Impetigo
 Starts as an erythematous macule
 Develops into a vesicle with erythematous halo
 Vesicle breaks down with oozing Figure 1.2 Carbuncle
 Dries to form golden yellow crust, spreads by 1.1.2 Investigations: - CBC, BSL (R)
auto inoculation
1.1.3 Treatment guidelines:
b. Ecthyma  Good personal hygiene
 Deeper infection  Wash with soap and water
 An ulcer covered with adherent crust  Topical antibacterial cream – Neomycin 0.5% /
Framycetin 1% / Mupirocin / Fusidic acid -
 Heals with scarring local application two times in a day for 7 days
 Rule out Diabetes Mellitus in case of recurrent  Systemic antibiotics – Erythromycin 250 or
furunculosis and carbuncle. 500 mg QID / Cefadroxil 250 or 500mg BD
for 7 days
c. Folliculitis
 Follicular oriented pustules without peri-  Azithromycin 250 mg BD for 7 days
follicular oedema. For recurrent pyoderma:
d. Furuncle  Topical application of Mupirocin 2% to carrier
 Erythematous, painful, tender sites especially anterior nares and natal clefts
for 2 weeks
 Forms discrete follicular nodules with
1.1.4 Erysipelas
perifollicular edema.
 Erysipelas is a superficial form of bacterial
cellulitis
 Usually seen over the face
 H/o minor injury may be present
 Present as sharply defined erythematous tender
swelling
Figure 1.1 Furuncle

e. Carbuncle
 Infection of multiple adjoining hair follicles
 Presents with painful, tender plaque with
ulceration.
Figure 1.3 Erysipelas
Page 336
 With partial alopecia showing broken off hair. appearance of black dot.
Treatment:  Diffuse and poorly circumscribed lesions with
 Systemic antibiotics- Azithromycin 250 BD low grade folliculitis.
for 5-7 days / Cloxacillin / Amoxicillin-
c. Kerion
Clavulanic Acid - 625 mg BD for 7 days.
 Boggy purulent inflammatory nodules and
 IV antibiotics for severe cases -Inj. Cefotaxime
plaques with sinus formation and pus discharge
1 gm IV BD for 7 days.
which leads to thick crusting and matting of
 Non-steroidal anti-inflammatory drugs - Tab. adjacent hair.
Ibuprofen for pain & fever
d. Favus
1.1.5 Cellulitis  Perifollicular erythema and matting of hair
with fetid odour
 Cellulitis is a deep subcutaneous infection with
lymphangitis and adenopathy  Heals with scarring alopecia.
 Borders of the lesion are poorly demarcated e. Investigation: - CBC, BSL (R)
 Vesicles and bullae may be seen over the
surface in both conditions.
Figure 1.5 Tinea Capitis

f. Treatment
Figure 1.4 Cellulitis Topical anti-fungals (lotions / creams)
 Clotrimazole - 1% local application BD for 15
Treatment: days – 1 month.
 Non-steroidal anti-inflammatory drugs - Tab.  Miconazole - 2% local application BD for 15

Ibuprofen 1 BD for 7 days. days – 1 month.
 Amoxycillin-Clavulinic Acid 625mg BD / Systemic anti-fungals

Cloxacillin for 7-10 days  Tab. Griseofulvin 10mg/kg/day for 4 to 6
 IV antibiotics for severe cases - Inj. weeks
Cefotaxime 1 gm IV BD for 7 days.
2. Fungal infections of skin

2.1 Dermatophyte infections
Superficial fungal infections of keratinized tissue
caused by dermatophyte fungi. Persons with
Diabetes, Obesity and Immunocompromised
patients are prone to infections.
Dermatophytosis is classified according to the body
Figure 1.6 Kerion
part involved.
2.1.1 Tinea Capitis Systemic antibiotics in case of secondary
Presents with different clinical types and is more infection - Azithromycin 250 BD for 5-7 days /
common in children. Cloxacillin / Amoxicillin - Clavulanic Acid -
a. Gray patch 625 mg BD for 7 days.
 Well defined scaly circular patches
 Tab. Fluconazole 150 mg / week for 4 to 6
b. Black dot weeks.
 Broken off hair near the surface give
Page 337
2.1.2 Tinea Corporis
Dermatophytosis of the skin with the exclusion of
palms, soles and groin is called Tinea Corporis
 Well defined scaly annular patches

 With or without vesicles, pustules at margin
 Single or multiple scattered lesions
 Itching present
Figure 1.9 Tinea Capitis
2.1.5 Tinea Manuum

Dermatophyte infection of palms and inter-digital
areas of hand.
Treatment:
Topical
 Clotrimazole- 1% local application BD for 4-6
weeks.
Figure 1.7 Tinea Corporis  Miconazole - 2% local application BD for 4-6
weeks.
2.1.3 Tinea Cruris Systemic
Infection of groin area and includes infection of  Tab. Griseofulvin 250 to 500 mg BD for 3-6
genitalia, pubic area, perianal and perineal skin. weeks
 Tab. Fluconazole 150mg one per week for 4-6
weeks
2.1.6 Tinea Unguium

Dermatophyte infection of nail plate causing
whitish or brownish yellow discoloration of nail,
separation of nail bed and nail plate
 Nails becomes friable and discolored
Treatment:
 Griseofulvin 1 gm per day for 4-6 months for
finger nails and 12-18 months for toe nails
Figure 1.8 Tinea Cruris  Tab. Fluconazole 150mg one per week for 6
Treatment: months for finger nails & 12 months for toe
nails.
Topical
2.1.7 Candidiasis:
 Clotrimazole - 1% local application BD for 4-6
Caused by yeast like fungi Candida albicans
weeks.
a. Chronic Paronychia
 Miconazole - 1% local application BD for 4-6
weeks.  Infection of nail fold
 Erythema and swelling of finger tips
Systemic
 Tab. Griseofulvin 250 to 500 mg BD for 3 b. Intertrigo
weeks
 Seen over intertriginous areas, groin, in
 Tab. Fluconazole 150mg one per week for 4 -6 between toes, below the neck in children
weeks  Sharply demarcated polycyclic erythematous
eroded patches with satellite pustules
2.1.4 Tinea Pedis  Rule out underlying Diabetes Mellitus
Dermatophyte infection of the feet.
Page 338
c. Diagnosis
 KOH mount Direct examination of scrapings
under microscope from lesions with KOH
mount will reveal budding yeasts with hyphae
or pseudo-hyphae.
d. Treatment
 Keep intertriginous areas dry
 Clotrimazole– 1% local application BD for 4-6
weeks.
Figure 1.11 Herpes Zoster
 Miconazole– 2% local application BD for 4-6
3.1.1 Prodromal Symptoms
weeks.
 Tab. Fluconazole 150 mg per week for 4 weeks.  Pain at the site
 Treat underlying Diabetes mellitus  Closely grouped reddish papules, vesicles and
pustules in continuous or interrupted band in
2.1.8 Tinea Versicolor one or adjacent dermatomes
 Usually unilateral and does not cross the
Chronic superficial fungal infection caused by
midline
Malassezia furfur. Lesion vary color from white,
 Thoracic segments most commonly involved.
pink to brown usually consisting of coalescing
macules, patches with fine scales on trunk and neck. 3.1.2 Treatment
 Tab. Acyclovir 800mg 1-1-1-2 for 5-7 days.
3.1.3 Herpes Eye: In Herpes Zoster
Ophthalmicus, refer to ophthalmologist for further
management.
Disseminated herpes zoster occurs in
immunocompromised individuals
3.2 Herpes simplex

3.2.1 Infection occurs in two types
Figure 1.10 Tinea Versicolor a. HSV1 usually responsible for cutaneous,
a. Treatment oropharyngeal and ocular infections.
b. HSV2 involved in genital infections and
 Oral Fluconazole given as single dose of 400 infections of new born.
mg
 Oral Infections shows vesicles, erosions on
b. Topical buccal mucosa or peri-oral skin with severe
pain and high fever.
 Ketoconazole 2% shampoo – Local application  Vulvo-vaginitis in female and painful penile
half an hour before bath for 4 weeks. lesions in men with appearance of vesicles and
 Selenium sulphide suspension - Local erosions seen.
application half an hour before bath for 4
weeks.
 Clotrimazole 2% solution local application for
4 to 6 weeks
3. Viral infections
3.1 Herpes Zoster
Figure 1.12 Herpes Zoster

3.2.2 Treatment:
Tab. Acyclovir 200mg 1-1-1-2 for 5-7 days
Page 339
3.3 Molluscum Contagiosum
3.3.1 Clinical manifestations:
Molluscum Contagiosum – A viral infection of the
skin caused by a poxvirus. It is a contagious disease
particularly common in young children. After
approximately two to three months of the virus
incubating, small, round growths begin to emerge.
These are light pink or tan coloured and can look Figure 1.15 Planter Warts
similar to warts. They can sometimes become red e. Treatment:
and irritated or have a tiny white depressed spot in
the centre.  Spontaneous resolution possible
 Topical keratolytics
3.3.2 Treatment:
 Needling o 16.7% Salicylic acid and 16.7% Lactic acid
 Curette – most common, cryotherapy with in collodion base local application daily till
liquid Nitrogen resolution
 Electrocautery OR
 Topical 50% Trichloroacetic Acid – Twice a o 50% Trichloroacetic acid applied weekly till
week till resolution resolution
OR
3.4 Warts o Topical 5% Fluorouracil ointment local
 Filliform or digitate warts application daily till resolution.
 Plantar warts  Electrocautery or liquid Nitrogen therapy
 Podophyllin 25% for genital wart twice weekly
a. Common warts: till resolution
 Firm keratotic papules with rough horny  Cryotherapy with liquid nitrogen for genital
surface wart
4. Cutaneous Tuberculosis
It is infection of skin caused by mycobacterium
tuberculosis. Persons with malnutrition and
immuno-compromised patients are prone to
tuberculosis.
4.1 Clinical types

Figure 1.13 Common warts  Lupus vulgaris
b. Plane warts  Tuberculosis verrucosa cutis
 Multiple smooth, flat or slightly elevated  Scrofuloderma
round or polygonal papules (1 to 5 mm)
4.1.1 Lupus vulgaris:
Reddish brown plaque which spreads with foci
of scarring
 It has an active advancing edge and areas of

scarring.
Figure 1.14 Filiform or Digitate

c. Filiform or Digitate
 Composed of one or more finger like
projections 2 to 10 mm in length.
d. Planter Warts
Figure 1.16 Lupus Vulgaris
 Sharply defined rough keratotic lesion.
 Surrounded by a smooth collar of thickened 4.1.2 Tuberculosis Verrucosa Cutis:
horn.  Indurated warty papule or nodule or a plaque,
with surrounding erythema.
Page 340
 There may be fissuring and discharge from the Tuberculosis.
surface.  Skin biopsy to confirm diagnosis.
 Irregular extension leads to serpiginous  Treatment after confirmation.
margin.
4.1.3 Scrofuloderma: 4.3 Treatment
 It occurs over the underlying focus of Anti-tubercular treatment – 6 months
tuberculosis like caseating lymph gland, bone,  4 Drugs – 2 months
joint etc.
 2 Drugs – 4 months
 Present as painless bluish red swelling which Refer RNTCP guidelines.
breaks down to from sinus or undermined
ulcer.
4.2 Investigations
 TT (Tuberculin Test)
 X-ray chest PA view – Screen for Pulmonary
Bibliography
1. Khopkar U. An Illustrated Handbook of Skin Diseases and Sexually Transmitted Infections with an
Update on HIV. 6th Edition. India: Bhalani Publications.
2. IADVL Textbook of Dermatology. 4th Edition. India: Bhalani Publications. 2015
Further reading
1. British Journal of Dermatology. United Kingdom: Blackwell Publishing. [Cited 2016 July 10]
Available from: http://onlinelibrary.wiley.com/journal/10.1111/(issn)1365-2133/issues
2. Indian Journal of Dermatology, Venereology and Leprology. India: Wolters Kluwer- Medknow
Publications. [Cited 2016 July 10]
Available from: www.ijdvl.com
3. Indian Journal of Dermatology. [Cited 2016 July 10]
Available from: www.e-ijd.org
4. Journal of The American Academy of Dermatology. [Cited 2016 July 10]
Available from:www.jaad.org
5. Rook’s Textbook of Dermatology. 9th Edition. United States: Wiley & Sons. 2016.
6. Chiller K, Selkin B, Murakawa G. Skin Microflora and Bacterial Infections of the Skin. Journal of
Investigative Dermatology Symposium Proceedings. 2001; 6(3): 170-174.
7. Bernad P. Management of common bacterial infections of skin. Current Opinions in Infectious Diseases,
2008; 21(2): 122-128.
8. Rossi R, Bruscino N, Ricceri F, Grazzini M, Dindelli M, Lotti T. Photodynamic Treatment for Viral
Infections of the Skin. Europe PMC. 2009; 144(1): 79-83.

Page 341
2. NON INFECTIOUS SKIN CONDITIONS
1. Urticaria 2. Psoriasis
 Elevated erythematous itchy swelling 2.1 Clinical features
 Transient in nature i. Erythematous well defined scaly plaques
 Worsened by scratching ii. Predominantly extensor aspect of the body
 Acute < 6 weeks iii. Scales are silvery and loosely attached to the
 Chronic >6 weeks lesion
iv. Koebner phenomenon (it is isomorphic reaction to
 Angioedema involves the deeper structures
trauma or injury) in which positive new lesion
1.1. Provoking factors occurs at the site of trauma
i. Drugs
ii. Food
iii. Infection
iv. Stress
v. Systemic Diseases
Figure 2.2: Psoriasis

Scalp:
 Scaling that extends beyond the hair line
Nails:
Collection of keratotic material under the nail lifting
the distal part of the nail from the nail bed and Nail
Figure 2.1: Urticaria pitting.
Joints may be involved.
1.2. Treatment
2.2 Treatment
 Eradication of the etiological factor
i. Potent topical steroids for localized lesion–
 In Acute Urticaria with laryngopharyngeal edema Clobetasol Propionate 0.05% local application
0.5 to 1 ml of subcutaneous epinephrine. twice daily for 2 weeks.
Antihistamines ii. Topical keratolytics– Salicylic acid 3% or 6%
 Tab. Cetirizine 10 mg /day for 2 to 4 weeks twice daily for 2 weeks.
OR iii. Liquid paraffin for external use or use of any other

emollients local application twice daily for 2
 Tab. Levocetirizine 5 mg per day for 2 to 4 weeks.
weeks
iv. Tab. Cetirizine 10 mg per day if itching persists
OR
v. 5% Coal tar ointment local application twice daily
 Tab. Loratadine 10 mg /day for 2 to 4 weeks for 2 weeks.
Severe extensive cases or unresponsive cases vi. Calcipotriol cream local application twice daily
for 2 weeks.
 Tab. Prednisolone 0.5 to 1 mg /kg per day and
gradually tapered Patients with extensive involvement, arthropathy,
pustular psoriasis, erythrodermic psoriasis refer to
 Tab. Albendazole 400 mg single dose higher centre.
Refer to higher centre if no response
Page 342
3. Lichen Planus
3.1 Clinical features
 Well defined, violaceous, polygonal flat topped
papules
 Itching present
 Common Sites: leg’s and forearm
 Koebner Phenomenon +ve
 Involvement of hair leads to alopecia
 Oral mucosa: lacy network of whitish patches
Figure 2.4 Pityriasis Rosea
5. Acne
Common in adolescents
Present as comedones, papules, pustules, nodules,
abscess, cysts, scars
Sites –Face, chest, back, shoulder
Figure 2.3 Lichen Planus

5.2 Treatment
5.2.1 Grade I
3.2 Treatment Comedones / Occasional papules.
 Topical steroids - Clobetasol Propionate 0.05%  Washing of face with soap and water when it
twice daily for 2 weeks. becomes oily.
 Tab. Cetrizine 10 mg daily for 2 weeks.  Removal of comedones by comedone extractor.
 Generalized forms - Systemic steroids like  Topical Retinoic acid (0.025%) local application
Tab. Prednisolone 0.5 mg/kg per day. Gradually HS for half hour for 2 to 4 weeks.
tapered over the next 4-6 weeks  Benzoyl Peroxide (2.5%) local application HS for
 Refer to higher centre for extensive lesions. half hour for 2 to 4 weeks
5.2.2 Grade II
4. Pityriasis Rosea Papules, comedones, pustules:
 Washing of face with soap and water when it
4.1 Clinical features becomes oily.
 Initial lesion 2 to 6 cm circular asymptomatic  Topical antibiotics Clindamycin local application
erythematous scaly plaque called herald patch BD for 2 weeks.
 Within days, crops of papules and oval patches  Erythromycin 2 to 4% local application BD for 2
with wrinkling surface and a border of fine scales weeks.
 Trunk and proximal extremities are commonly  Benzoyl peroxide local application HS for half
involved (covered part) hour for 2 to 4 weeks.
 Lesion heal with hyper or hypo pigmentation  Retinoic acid local application HS for half hour for
2 to 4 weeks.
4.2 Differential diagnosis: 5.2.3 Grade III
Predominant, pustules, nodules, abscesses:
 Psoriasis Washing of face with soap and water when it becomes
 Secondary syphilis oily.
 Tinea Corporis  Topical benzoyl peroxide local application HS for
Note - Systemic Steroids should be avoided half hour for 2 to 4 weeks.
 Retinoic acid local application HS for half hour for
4.3 Treatment 2 to 4 weeks.
 Azithromycin 500 mg OD 3 days per week, may be
 Mostly do not require treatment
repeated; maximum duration 3 months, or
 Symptomatic treatment like topical moisturizers
 Doxycycline 100 mg OD for 2 to 6 weeks, or
local application BD for 7 days.
 Isotretinoin 0.5mg/kg/day for 16 to 24 weeks (only
 Tab. Cetirizine 10 mg per day if itching is present
after expert opinion)
Daily sun exposure of covered part if possible.
Sequelae: Hyper pigmentation and scarring.
Page 343
5.2.4 Grade IV 8. Eczema
Mainly cysts, abscess, widespread scarring
 Washing of Face with soap and water when it 8.1 Stages
becomes oily.  These are synonymous terms signifying
 Systemic antibiotics and Isotretinoin as in grade inflammatory response of skin to different factors
III  Caused by exogenous or endogenous factors
 Aspiration of cysts  Generally, 3 stages – acute, subacute and chronic
 Intralesional steroids for cysts Inj. Triamcinolone
Acetonide 10 mg / ml weekly.
6. Pityriasis Alba
 Asymptomatic round or oval hypo-pigmented
scaly patches usually on the face.
 Single or multiple
 Spontaneous resolution may recur.
 Age group 3 years to puberty Figure 2.5 Eczema / Dermatitis
6.2 Differential diagnosis 8.1.1 Acute Stage- Characterised by erythema,

 Early vitiligo oedema, vesicles and oozing
 Pityriasis versicolor
 Leprosy 8.1.2 Subacute stage- Erythema, oedema, vesicles
decrease and are replaced by moderate oozing,
 Post inflammatory hypo pigmentation
crusting & Scaling
6.3 Treatment 8.1.3 Chronic Stage- Mainly consists of hyper
 Reassurance pigmentation and lichenification. Highly
 Bland emollients for external application like pruritic in all stages.
liquid paraffin local application BD.
 Multivitamins like Calcium carbonate+ Vitamin 8.2 Treatment
D3 Syrup 1 tsp HS for 1 month.  Treatment is according to stage of dermatitis.
 Treatment of worm infestation if any– Tab.
Albendazole 400 mg HS single dose. 8.2.1 Acute Eczema
 Cap. Vitamin A 50,000 IU OD for 4-6 wks.  Wet soaks / compresses of Potassium
permanganate (4-5crystals in 500ml water) local
application 3 times in a day.
7. Miliaria  Antihistaminic Tab. Cetirizine 10 mg BD for 5
7.1 Clinical features days.
 Small discrete itchy non follicular erythematous  Topical corticosteroids- Clobetasone 0.05% local
confluent macules or papules forming sheets application 3 times in a day.
 Pricking sensation
 Occurs more in summer and heat condition.  Systemic Antibiotics if secondary infections.
8.2.2 Subacute Eczema
7.2 Treatment  Wet compresses for crust removal like acute
 Avoidance of excessive exposure to heat Eczema local application 3 times in a day.
 Calamine lotion local application BD for 5 days.
 Antihistamines – Tab. Cetirizine 10 mg HS for 5  Betamethasone or Mometasone topical application
days. in cream form local application 3 times in a day.
 Tab. Vitamin C – 500 mg OD for 5 days.
 Loose cotton dresses
 Plenty of oral fluids etc.
Page 344
 Systemic Antibiotics if secondary infections.
8.2.3 Chronic eczema
 Corticosteroid ointments - Clobetasone 0.05%
local application 3 times in a day.
 Tab. Cetirizine 10mg BD for 5 to 10 days.
8.2.4 Acute infected Eczema
i. Wet dressing with light weak pink potassium Figure 2.6 Atopic Dermatitis
permanganate soaks for 5 days where indicated
ii. Whenever infection is present, it has to be treated 9.3 General Guidelines
with appropriate antibiotics like Azithromycin  Use soft non irritating cotton clothing
250 BD for 5-7 days / Cloxacillin 500mg three  Use emollients such as oils applied over wet skin.
times a day 5 to 7 days / Amoxicillin-Clavulanic Avoid foods which tend to aggravate lesions e.g.
acid - 625 mg BD for 7 days. nuts, eggs, wheat, cow's milk, fish.
iii. Emollients like liquid paraffin applied daily.  Accentuation under Wood’s lamp
 Skin as well as mucous membranes can get
iv. Mild cases– Hydrocortisone 1% ointment daily
involved.
v. Moderate cases- Betamethasone 0.1% cream or
ointment twice daily 9.4 Treatment
8.2.5 Symptomatic relief by Antihistamines  Moderately potent corticosteroids - Fluticasone /
Mometasone cream topically for 6 weeks
Tab. Chlorpheniramine (4 mg) TID as needed or Tab.  Tacrolimus 0.03% for face; 0.1% for trunk and
Promethazine (10-25 mg) 6-8 hourly as needed in extremities for 3 months
severe cases.
 Extensive / resistant cases – refer to higher centre
Refer to higher centre to confirm diagnosis and for
management of complicated cases.
10. Alopecia Areata
8.2.6 Management as per severity 10.1 Diagnostic features
Mild or Moderate Infected Eczema Loss of hair in patches
 Soaks or compresses of plain tepid water or  Patches of non-scarring alopecia especially over
normal saline the scalp and the beard area. Usually round or oval
in shape with a normal appearing superficial skin.
Severe Eczema Asymptomatic, Exclamation mark appearance of
 Tab. Prednisolone (5 or 10 mg) 0.5 to 1mg/kg the hair
with gradual tapering,  Avoid irritating strong soap chemicals
 If infected, Tab. Erythromycin (250 to 500  Exclusive breast feeding in infants
mg) QID for 5 to 10 days  Review patient after 2 weeks.
 Tab. Chlorpheniramine Maleate (4 mg) TDS
for 5 to 10 days. 10.2 Treatment
Moderately potent corticosteroids (Mometasone
9. Dermatitis Furoate, Fluocinolone Acetonide, Fluticasone) for 6 to
9.1 Atopic Dermatitis Diagnostic 12 weeks
Feature 11. Vitiligo
 Chronic pruritic dermatitis over face, neck and
flexures. Seen mainly in infants and children 11.1 Diagnostic feature
 Depigmented macules and patches which can
occur anywhere on the body (Fig. 7)
9.2 Treatment Guidelines
 Tab. Chlorpheniramine (4 mg) TDS for 3 Days 12. Androgenic Alopecia
 Topical steroid (Clobetasone-Butyrate cream
(0.05%)) BD for 3 weeks. Underlying susceptibility of hair follicles to androgenic
 Tacrolimus 0.03% BD for 3 months topically miniaturization.
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Affects up to 70% of men and 40% of women
Treatment:
Topical Minoxidil solution (2 to 5%) BD application
for 4 to 6 months.
Figure 2.7: Vitiligo


Bibliography
Further reading

Page 346
3. SEXUALLY TRANSMITTED INFECTION
(STI)
 Tab. Erythromycin 500 mg orally QID for 2
1. Syphilis weeks
1.1 Early Syphilis c. Follow Up:
1.1.1 Primary Syphilis After treatment the patient should be examined
 Causative agent– Treponema pallidum clinically and serologically once a month for first 3
 Incubation period -9 to 90 days months and quarterly till the end of second year
 Genital ulcer (primary chancre)– classical
lesion 1.2 Late Syphilis
 Regional lymphadenopathy in 50% of cases In untreated early syphilitic patients will have the
 Primary chancre resolves in 3 to 6 weeks late syphilitic manifestations after 5-15 years from
 After 3 weeks of appearance of chancre, the onset of infection
VDRL becomes reactive 1.2.1 Late latent syphilis
 Treponema pallidum can be demonstrated from After 2 years from the onset of infection No signs
the chancre and symptoms
In the case of untreated primary syphilis, patient Non-infectious
may develop secondary syphilitic lesions in 3-6 1.2.2 Late benign syphilis (Gumma)
months interval. After 5-7 years from the onset of infection, visceral
gumma
1.1.2 Secondary Syphilis 1.2.3 Cardiovascular syphilis
Skin Rash After 10-15 years from the onset of infection;
Maculopapular, Uncomplicated aortitis, aortic regurgitation,
Psoriasiform or Papulosquamous coronary ostial stenosis, aortic aneurysm
Annular 1.2.4 Neuro-syphilis
Pustular Follicular After 10-15 years from the onset of infection;
 Rash is generalized, bilaterally symmetrical meningitis, meningo-vascular, General Paresis of
non itchy Insane (GPI), Tabes dorsalis, CNS gumma
 Mucosal lesion
 Snail track ulcers 1.2.5 Treatment:
 Condylomata lata a. Late Latent Syphilis and Late Benign Syphilis
 Painless discrete, rubbery lymph nodes, (Gumma)
systemic manifestations  Inj. Benzathine Penicillin 2.4 mega units IM
 Highly reactive VDRL weekly for 4 consecutive weeks
OR
Treponema pallidum can be demonstrated from the  Inj. Procaine Penicillin 1.2 mega units IM daily
skin lesions, Cutaneous gumma for 21 days
b. Cardiovascular syphilis and Neuro-syphilis
1.1.3 Early latent Syphilis  Inj. Procaine Penicillin 1.2 mega units IM /day
 No Signs and symptoms for 21 days under the cover of steroids.
 2years period is demarcation between early and c. Inj. Penicilin allergic patients
late latent syphilis  Cap. Doxycycline 100 mg orally BD for 4
weeks
1.1.4 Treatment:  Cap. Tetracycline 500 mg orally QID for 4
For all the above 3 conditions weeks
a. Penicillin treatments OR
Inj. Benzathine penicillin 2.4 mega units deep IM  Tab. Erythromycin 500 mg orally QID for 4
after test dose Weeks
b. In Penicillin allergic patients: d. Follow-up
 Cap. Doxycycline 100mg orally BD for 2 The patient should be monitored at 6 months
weeks interval, clinically and serologically along with
OR repeat Cerebrospinal examination.
 Cap. Tetracycline 500 mg orally QID for 2
weeks
OR
Page 347
1.3 Congenital syphilis
Untreated early syphilitic mother may deliver a
congenital syphilitic child.
1.3.1 Early:
 Skin lesions, rash, bullae, Condylomata lata
 Lymphadenitis, hepatosplenomegaly,
osteochondritis
 CNS, kidneys, lungs, testes involvement.
1.3.2 Late:
 Interstitial keratitis Figure 3.1 Chancroid
 Neurosyphilis 2.2 Treatment
 Bone and joint involvement  Cap. Doxycycline 100mg oral BD for 14 days
 Sensorineural deafness OR
 Gummatous lesions  Tab. Erythromycin 500mg orally QID for 14
 Cardiovascular syphilis involvement. days
1.3.3 Stigmata: OR
 Bulldog facies  Tab. Azithromycin 1 gm oral stat
 Hutchinson’s teeth OR
 Rhagades  Tab. Ciprofloxacin 500 mg oral BD for 3 days
 Salt and pepper fundus
 Gummatous scars 3. Lymphogranuloma
1.3.4 Treatment:
Venereum (LGV)
a. Early: Inj. Benzathine Penicillin 5000
units/kg/day divided in 6 hourly doses for 7 days. 3.1 Clinical features
 Caused by Chlamydia trachomatis serovars L1,
b. Patient Education: L2, L3
 To seek early and appropriate treatment  Incubation period – 3 to 12 days
 To avoid sexual contact until the treatment is
completed  Primary – Transient genital ulcer Lymph nodes
 Insisting epidemiological treatment of sex (bubo)
partners with regular follow-up
c. Prevention:
 Sexual abstinence
 Avoid high risk behavior
 Consistent and correct usage of condoms
 Safer sex practices
2. Chancroid
 Causative agent – Haemophilus ducreyi Figure 3.2 Lymphogranuloma Venereum
 Incubation period – Usually 3 to 5 days but it
can extend up to 14 days. Tertiary complications include:
 Multiple, painful, non-indurated ulcers with Elephantiasis of genitalia Fistulae Strictures
ragged and undermined edges. Floor is covered
by a yellowish grey necrotic exudates 3.2 Treatment
overlying granulation tissue that bleeds on  Cap. Doxycycline 100mg oral BD for 3 weeks
manipulation. OR
 In 50% of the patients, a tender inguinal  Tab. Erythromycin 500mg oral QID for 3
adenitis (usually unilateral) occurs weeks
(Inflammatory Bubo)
 “School of fish appearance” in smears
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4. Venereal Granuloma 5.2.3 Other forms:
 Disseminated gonococcal infection
(Donovanosis)  Gonococcal arthritis
4.1 Clinical features  Meningitis
 Causative agent- Klebsiella granulomatis  Anorectal
(Calymmatobacterium granulomatis)  Pharyngeal gonorrhea
 Incubation period – 1 to 3 months
 Granulomatous ulcer
5.3 Treatment
 Tab. Azithromycin 2 g oral stat (or)
 Calymmatobacterium granulomatis (Donovan
bodies) seen inside large mononuclear cells in  Inj. Ceftriaxone 250 mg IM stat
tissue smears.
6. Non–gonococcal urethritis
4.2Treatment
6.1 Clinical manifestation
 Cap. Doxycycline (100mg) BD  Causative agent: Chlamydia trachomatis
OR Ureaplasma urealyticum, Mycoplasma
 Tab. Cotrimoxazole (800mg + 160 mg) BD genitalium
OR  Urethritis
 Tab. Erythromycin (500mg) 4 times a day in  Increased Polymorphonuclear leucocytes in
pregnant women for14 Days urethral smear or sediment of first voided
OR urine.
 Inj. Ceftriaxone (1gm) daily IM injection for 7
days 7. Chlamydial infections
5. Gonorrhoea  Agent- Chlamydia trachomatis
5.1 Clinical features  Incubation period -1 to 3 weeks
 Causative agent – Neisseria gonorrhoeae
 Incubation period – 1 to 14 days
7.2 Complications
 Presents as urethritis in male and cervicitis in 7.2.1 Male:
female Urethritis, Littritis, Epididymitis, Prostatitis,
Proctitis, Reiter’s syndrome
7.2.2 Female:
Cervicitis, Urethritis, Bartholinitis, Endometritis,
Salpingitis
Fitz Hugh Curtis Syndrome (It is fever with lower
abdominal pain after cervical movement. There are
adhesions in pelvic cavity, may lead to infertility.)
Figure 3.3 Gonorrhoea 7.3 Treatment
5.2 Complications  Tab. Azithromycin 1 gm oral stat
5.2.1 Male: OR
 Posterior urethritis  Cap. Doxycycline 100 mg oral BD for 14 days
 Infection of Cowper’s and Tyson’s gland OR
 Epididymitis  Tab. Erythromycin 500 mg QID for 14 days
 Prostatitis
 Seminal Vesiculitis 8. Bacterial Vaginosis
 Peri-urethral abscesses
5.2.2 Female:
8.1 Clinical aspects
 Salpingitis,  Polymicrobial Syndrome
 Peritonitis,  Gardnerella Vaginalis
 PID  Mycoplasma hominis, bacteroides
 Bartholinitis,  Excessive, homogenous, uniformly adherent
 Proctitis vaginal discharge, elevated vaginal pH > 4.5
 Chronic urethritis  Positive Amine test (Whiff test)
 Presence of ‘Clue–Cells’ (Epithelial cells
Page 349
studded with organisms) 10.2 Treatment
8.2 Treatment  Commonly used antifungals include oral
Fluconazole and topical Clotrimazole.
 Tab. Metronidazole 400 mg BD for 14 days
 Vaginal candidiasis – a single dose of oral
OR
Fluconazole (150mg)
 Tab. Secnidazole 2g stat dose
 Clotrimazole pessary for 7 days Daily
9. Trichomoniasis  Clotrimazole cream (1%) or Miconazole cream
(2%) daily BD
9.1 Epidemiology  Application for 7 to 14 days
 Caused by Trichomonas vaginalis 11. Warts (Condylomata

 Incubation period – 4 to 28 days
Acuminata)
9.2 Clinical features 11.1 Clinical features
 Copious, homogenous, malodorous, yellowish
Caused by Human Papilloma Virus
green vaginal discharge
 Punctuate hemorrhages over cervix –
 Incubation period – 1 to 8 month
Strawberry cervix
 Skin coloured multiple verrucous lesions
 Demonstration of motile trichomonads in wet
film smears under direct microscopy 11.2 Treatment
 Culture – gold standard for diagnosis
 Topical Podophyllin 25% local application
9.3 Treatment twice weekly.
 Tab. Metronidazole 400 mg BD for 14 days  Cryotherapy
OR  Cautery
 Tab. Secnidazole 2g stat dose  Surgery
10. Candidiasis 11.3 Treatment

10.1 Clinical features 11.3.1 For Primary
 Tab. Acyclovir 200 mg 5 times a day for 7
 Predominantly caused by Candida albicans days
 Predisposed by pregnancy, diabetes, HIV and
immunosuppression 11.3.2 For Recurrence
 Causes Balanoposthitis in males  Tab. Acyclovir 400 mg 3 times a day for 5
days
 Clinically erythema and swelling with a
macular /papular rash over glans penis.
 A white sub-preputial discharge, increased skin
12. Herpes Genitalis
marking, fissuring of the glans and foreskin
occasionally regional lymphadenopathy may
be present  Predominantly by HSV -2 & also by HSV – 1
 Causes Vulvo-vaginal candidiasis in females,
oedema, fissures, erosions, curdy white  Incubation period – 5 to 14 days
discharge.  Ballooning degeneration and giant cells seen in
 Demonstration of candidiasis by 10% KOH – HPE
yeast cells, mycelia seen.
 Primary – Severe associated with systemic
symptoms starts as grouped vesicles – ulcerate
- polycyclic margin
 Recurrence – less severe
12.2 Complications
 CNS involvement dissemination Secondary
infection
 Recurrence
 Transmissible during pregnancy and delivery
Figure 3.4 Warts (Condylomata Acuminata)
Page 350
Figure 3.5: Herpes Genitalis
Bibliography
Further reading
1. Global Prevalence and Incidence of Selected Curable Sexually Transmitted Infections: Overview and
Estimates. WHO: 2001. [cited 2016 July 8].
Available from: http://www.who.int/iris/handle/10665/66818
7. Sexually Transmitted Infections. United Kingdom: BMJ Publishing. [Cited 2016 July 10]
Available from: http://sti.bmj.com/
8. World Health Organisation. Guidelines for the Management of Sexually Transmitted Infections. Geneva:
WHO 2003.
9. Workowski K, Berman S. Sexually Transmitted Diseases Treatment Guidelines. Centers for Disease
Control and Prevention: 2010. [cited 2016 July 8]
Available from: http://hdl.handle.net/123456789/682

Page 351
4. SYNDROMIC MANAGEMENT OF STD
1. Syndromic Approach 2. Why Syndromic Management
 Provision of STI/RTI care services is a very  STI signs and symptoms are rarely specific to a
important strategy to prevent HIV transmission particular causative agent.
and promote sexual and reproductive health under  Laboratory services may not be available.
the National AIDS Control Programme (NACP III)  Dual infections are quite common and both
and Reproductive and Child Health (RCH II) clinician and laboratory may miss one of them.
 Syndromic case management (SCM) with  Waiting time for lab. Results may discourage
appropriate laboratory tests is the cornerstone of some patients.
STI/RTI management under NACP III.  Failure of cure at first contact.
 SCM is a comprehensive approach for STI/RTI
control endorsed by the WHO.
 Diagnosis is based on the identification of 3. The common STD Syndromes
syndromes, which are combinations of the  Genital ulcer diseases
symptoms the client reports and the signs the  Urethral discharge
health care provider observes.  Vaginal discharge
 The provision of the most effective therapy at  Bubo (inguinal swelling)
patient's first contact with a health or medical  Lower abdominal pain in female
facility.  Scrotal swelling
 The recommended treatment is effective for all the  Ophthalmia neonatorum
diseases that could cause the identified syndrome.
Syndromic approach for STI s is useful and practical
 Provides single does treatment as far as possible.
strategy for offering, high quality, effective and
 Comprehensive to include patient education on
acceptable care for prevention and treatment of sexually
risk reduction, counseling, condom promotion and
transmitted infections (Guidelines from National Aids
provision, partner notification, follow up.
Control Organization (NACO) has been used)
Table 1: NACO Guidelines
Kit Color Composition of kit Syndrome / disease
1 Grey Tab. Azithromycin 1 g stat + Tab. Urethral discharge (UD), cervical discharge (CD),
Cefixime 400 mg. anorectal discharge (ARD), Presumptive treatment
(PT), Painful scrotal swelling.
2 Green Tab. Secnidazole 2 g stat + cap. VD (Vaginal discharge)
Fluconazole 150 stat
3 White Inj. Benzathine Penicillin 2.4 MU Genital ulcerative disease (GUD); non herpetic
IM stat + Tab. Azithromycin 1 g stat
4 Blue Cap. Doxycycline 100 mg BD for15 (GUD; non herpetic)
days + Tab. Azithromycin 1 g stat
5 Red Tab. Acyclovir 400 mg TDS for 7 (GUD; herpetic)
days
6 Yellow Tab. Cefixime 400 mg stat + Tab. Lower abdominal pain (LAP)
Metronidazole 400 mg BD for 14
days + Cap. Doxycycline 100 mg
BD for 14 days
7 Black Cap. Doxycycline 100 mg BD for IB (Inguinal Bubo)
21 days + Tab. Azithromycin 1 g
stat
Page 352
Bibliography
Further reading
7. Thulkar J, Kriplani A, Agarwal N. Utility of pH Test and Whiff Test in Syndromic Approach to Abnormal
Vaginal Discharge. Index Medicus for South East Asia Region. 2010. [cited 2016 July 8].
Available from: http://imsear.hellis.org/handle/123456789/135459

Page 353
5. HIV – AIDS
1. HIV  Mild symptoms
 Infected person can infect other people
Invades the helper T-cells (CD4 cells) in the body of the
host (defense mechanism of a person)
4.2 Stage 2 – Asymptomatic
‘Human Immunodeficiency Virus’ a unique type of  Lasts for an average of ten years
virus (a retrovirus)
 This stage is free from symptoms
Preventable, manageable but not curable.  There may be swollen glands
 The level of HIV in the blood drops to low levels
2. AIDS  HIV antibodies are detectable in the blood
‘Acquired Immunodeficiency Syndrome’ HIV is the
virus that causes AIDS
4.3 Stage 3 – Symptomatic
Disease limits the body’s ability to fight infection due to  The immune system deteriorates
markedly reduced helper T-cells.  Opportunistic infections and cancers start to
Patients predisposed to multiple opportunistic infections appear.
leading to death.
4.4 Stage 4 - HIV AIDS
 The immune system weakens too much as CD4
cells decrease in number.
5. Opportunistic Infections
associated with AIDS
CD4 < 200
Bacterial infections, Tuberculosis (TB), Herpes
Simplex, Herpes Zoster, Vaginal candidiasis, Hairy
leukoplakia, Kaposi’s sarcoma
Figure 5.1 The Viral Genome

5.1 TB & HIV Co-Infection
 TB is the most common opportunistic infection in
3. Modes of HIV/AIDS HIV and the first cause of mortality in HIV
infected patients (10-30%)
Transmission  10 million patients co-infected in the world.
 Through Bodily Fluids  Immunosuppression induced by HIV modifies the
 Blood products semen and vaginal fluids clinical presentation of TB: Subnormal clinical
 Sharing needles without sterilization Increases the and roentgen presentation
chances of contracting HIV  High rate of MDR / XDR
 Unsterilized blades  High rate of treatment failure and relapse (5% Vs.
 Through unprotected intercourse oral, sexual, anal < 1% in HIV)
 Mother-to-Baby: before birth, during birth, after
birth
6. Testing Options for HIV
4. Stages 6.1Anonymous Testing
 No name is used
4.1 Stage 1 – Primary  Unique identifying number
 Short, flu-like illness - occurs one to six weeks  Results issued only to test recipient
after infection
6.2 Blood Test
Page 354
Blood Detection Tests: Table No. 1
HIV enzyme-linked immune-sorbent assay (ELISA) Screening test for HIV; Sensitivity > 99.9%
Western Blot Confirmatory test
Specificity > 99.9% (when combined with ELISA)
HIV rapid antibody test Screening test for HIV
Simple to perform
Absolute CD4 lymphocyte count Predictor of HIV progression
Risk of opportunistic infections and AIDS when <200
HIV viral load tests Best test for diagnosis of acute HIV
infection correlates with disease
progression and response to HAART
7. Treatment Options
7.1 Treatment of Opportunistic Infections (OIs)
Table 2: Managing OIs before starting ART
Drug reaction Do not start ART during an acute reaction
Acute diarrhea which may reduce absorption of ART Diagnose and treat first, start ART when diarrhea is
stabilized or controlled
Non-severe anemia (Hb <8g/ liters) Start ART if no other causes for anemia are found
(HIV is often the case of anemia), avoid AZT
Skin conditions such as PPE and seborrheic dermatitis, Start ART (ART may resolve these problems)
psoriasis, HIV-related exfoliative dermatitis.
Suspected MAC, Cryptosporidiosis and Start ART (ART may resolve these problems)
Microsporidiosis
Cytomegalovirus infection Treat if drugs available; if not, start ART
Toxoplasmosis Treat; start ART after 6 weeks of treatment and when

patient is stabilized.
Page 355
Figure 5.2 HAART (Highly active anti-retroviral treatment)
7.2 Antiretroviral Therapy advantages (procurement and stock management),

improve adherence to treatment and thus reduce
Regimens the chances of development of drug resistance. The
Currently, the national programme provides the current national experience shows that BD
following drugs / combinations for first-line regimen. regimens of FDCs are well tolerated and complied
with.
Fixed- dose combinations (FDCs) are preferred
because they are easy to use, have distribution
Page 356
Table 3: Revised NACO ART Regimen 2012
Regimen I Zidovudine + First line Regimen for patients with Hb ≥ 9 gm/dl and not on
Lamivudine + concomitant ATT
Nevirapine
Regimen I (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
Nevirapine
Regimen II Zidovudine + First line Regimen for patients with Hb ≥ 9 gm/dl and not on
Efavirenz
Regimen II (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
Lamivudine + concomitant ATT. First line for all patients with Hepatitis B and /
or Hepatitis C co-infection First line Regimen for pregnant
Efavirenz women,with no exposure to sd-NVP in the past.
Regimen III Zidovudine + Regimen for patients on AZT containing first line regimen, who
Lamivudine + develop toxicity to both NVP and EFV Also second line regimen
for those who are on TDF containing first line regimen if Hb ≥ 9
+ Atazanavir/ gm/dl
Ritonavir
Regimen III (a) Tenofovir + For patients of regimen III who develop severe Atazanavir
Lamivudine + toxicity First line regimen for patients with HIV-2 infection with
Hb ≥ 9 gm/dl
+ Lopinavir /
Ritonavir
Regimen IV Tenofovir + Second line regimen for those who are on AZT / d4T containing
Lamivudine + regimen in the first line. Also for patients on TDF containing first
line regimen who develop toxicity to both NVP and EFV.
Atazanavir / Ritonavir
Regimen IV (a) Tenofovir + For patients on regimen IV who develop severe Atazanavir
Lamivudine + toxicity First-line Regimen for patient with HIV 2 infection with
Lopinavir / Hb ≤ 9 gm/dl First-line Regimen for all women exposed to sd-
Ritonavir NVP in the past.
Regimen V Stavudine + Second line for those who are on TDF containing regmen in the
Lamivudine + first line if Hb ≤ 9 gm/dl
Atazanavir / Ritonavir
Regimen V (a) Stavudine + For patients on Regimen V who develop severe Atazanavir
Lamivudine + toxicity.
Lopinavir / Ritonavir
Page 357
Antiretroviral Drugs – Highly active anti- 9.1. Actions to be taken
retroviral treatments Immediately following on exposure:
i. Needle pricks and cuts should be washed with
 Nucleoside Reverse Transcriptase inhibitors soap and water
(NRTI)
o AZT (Zidovudine), Lamivudine, ii. Splashes to the nose, mouth or skin should be
Ditanosine, Abacavir, Empricitadine, flushed with water
Tenofovir iii. Eyes should be irrigated with clear water, saline
 Non-Nucleoside Transcriptase inhibitors or sterile irrigant
(NNRTI)
o Nevirapine (Viramune), Efavirenz iv. Do not panic
 Protease inhibitors (PI) v. Pricked finger should not be put in to mouth by
o Ritonavir, Lopinavir reflex
vi. Do not squeeze the pricked finger to expel the
8. Primary Prevention contaminated blood
Five ways to protect yourself: vii. PEP should be started within 72 hours of
 Abstinence exposure, within 2 hours is ideal.
 Monogamous Relationship
 Protected Sex 9.2. Post Exposure Prophylaxis
 Sterile needles (PEP)
 New shaving / cutting blades
The decision to start PEP is made on the basis of
9. Post Exposure Prophylaxis degree of exposure to HIV and the HIV status of the
(PEP) source from where the exposure infection has
occurred.
Steps to be taken on exposure to HIV infected blood,
body fluids and contaminated sharps etc.
9.2.1 Exposure Code Determination
Page 358
Figure 5.3. Exposure Code Determination
Is the source of material – blood, body fluid, other potentially

infectious material (OPIM) or an instrument contaminated with one
of these substances
YES No No PEP Needed
OPIM Blood or Body Fluid
What Type of Exposure has occurred?
Mucous membrane or Skin Intact Skin only Percutaneous

integrity contaminated Exposure
Volume No PEP needed Severity
Small i.e. Few drops, Large e.g. several Less severe e.g. solid More severe e.g.
short duration drops major blood needle superficial large base hollow
splash and / or scratch needle, deep
longer duration punctures, visible
(i.e. several blood or device,
minutes or more) or needle used in
source patients
EC1 EC2 EC2 EC3
Page 359
9.2.2 Determination of HIV status of source:
Figure. 5.4 Exposure Source
The HIV Status of the Exposure Source
HIV Negative HIV Status Source

Positive Unknown Unknown
No PEP
Needed
Lower titre Higher titre exposure

exposure (e.g. (E.g. Advanced aids,
Asymptomatic and Primary HIV infection &
High CD4 count) Higher increasing viral
Load or low CD4 count)
HIV SC1
HIV SC2
HIV SC
UNKNOWN
Page 360
9.2.3. PEP recommendation based on exposure code & source code
Figure 5.5. PEP
EC HIVSC PEP Recommendation

1 1 PEP may not be warranted
1 2 Considered basic regimen
2 1 Recommend basic regime

(most exposures are in this category)
2 2 Recommend expanded regimen
3 1 or 2 Recommend expanded regimen
2/3 Unknown If the source (in the case of an unknown source) the settings were the exposure
occurred suggested a possible risk for HIV
exposure and EC 2 or 3 consider PEP basic regimen
9.2.4. PEP regimen formulations should be used. Dual drug regimen should
not be used any longer in any situation for PEP. The
In case of intolerance to Efavirenz, regimen first dose of PEP regular should be administered as
containing Tenofovir + Lamivudine + Pl soon as possible, preferably within 2 hours of exposure
and subsequent dose should be given at bed time with
a. (ATV/r or LPV/r) can be used after expert clear instruction to take it 2-3 hours after dinner & to
consultation by an experienced physician. avoid fatty food in dinner.
b. Wherever PEP is indicated and source is ART
9.2.5 In case of Sexual Assault:
naïve or unknown: recommended regimen is
Tenofovir 300 mg + Lamivudine 300 mg + PEP should be provided to exposed person in case of
Efavirenz 600 mg once daily for 28 days. sexual assault as a part of overall package of post
Wherever available, single pill containing these sexual assault care.
Bibliography
1. Khopkar U. An Illustrated Handbook of Skin Diseases and Sexually Transmitted Infections with an Update
on HIV. 6th Edition. India: Bhalani Publications.
Further reading
1. AIDS Research and Treatment. United States: Hindawi Publishing.
3. Indian Journal of Dermatology, Venereology and Leprology. India: Wolters Kluwer- Medknow Publications.
[Cited 2016 July 10]
Page 361
8. Chopra S, Arora U. Skin and Mucocutaneous Manifestations: Useful Clinical Predictors of HIV/
AIDS. J Clin Diagn Res. 2012 Dec; 6(10): 1695–1698 [cited 2016 July 8]

Page 362
Psychiatry
5. Psychiatry
Sr. No. Contents Pae No.
1 Mental Illness 363

2 Evaluation: History and Mental Status Examination (MSE) 364
3 Schizophrenia 366
4 Bipolar Mood Disorder 369
5 Major Depressive Disorder (MDD) 373
6 Anxiety Disorder 375
7 Somatization Disorder 378
8 Organic Brain Syndrome 379
9 Drug Abuse and Substance Use Disorder 381
10 Intellectual Sub normality 384
11 Child and Adolescent Psychiatry 386
12 Psychiatric Emergencies 389
13 Procedure for Admission to a Mental Hospital 391
1. MENTAL ILLNESS
in thinking, motions and behavior leading to severe
1. Introduction impairment in Social and Occupational functioning)
 Schizophrenia
 15 to 20% of general population suffers from  Bipolar Mood Disorder
major or minor type of psychiatric illness
 Major Depressive Disorder
causing significant degree of morbidity and
mortality in society.
 It is therefore necessary to know about 2.1.2 Other disorders
commonly occurring mental illnesses and their a) Anxiety disorders
primary management.  General Anxiety disorders
 Phobias
 Obsessive and Compulsive Disorders
2. Classification of Psychiatric  Somatoform Disorder and Conversion Disorder
Disorders
b) Special Group Disorders
2.1 Psychiatric illnesses can be  Dementia / Alzheimer’s Disorder
 Substance use disorder
broadly divided into two  Children and Adolescent Disorder
categories:  Intelligence Disability Disorder
2.1.1 Major psychiatric illnesses (Abnormality  Psychiatric Emergencies ex. suicide, violence
Bibliography
1. Ahuja N. A Short Textbook of Psychiatry. 7th Edition. New Delhi: Jaypee Publications. 2011.
2. Sadock B, Sadock V. Synopsis of Psychiatry: Behavioral Sciences / Clinical Psychiatry. 10 th Edition. USA:
Wolters Kluwer and Lippincot Wiliams and Wilkins. 2007.
3. World Health Organisation. The ICD-10 Classification of Mental and Behavioral Disorders: Clinical
Descriptions and Diagnostic Guidelines. W.H.O. 2002.
4. Diagnostic and Statistical Manual of Mental Disorders. 5th Edition. USA: American Psychiatrist’s
Association. 2013
Further Reading
1. American Journal of Psychiatry. United States: American Psychiatric Publishing. [cited 2016 July 8].
Available from: www.ajp.org
2. British Journal of Psychiatry. United Kingdom: Royal College of Psychiatrists. [cited 2016 July 8].
Available from: www.bjp.rcpsych.org
3. Depression and Anxiety. United States: John Wiley & Sons Inc. [cited 2016 July 8].
Available from: www.adaa.org
4. Indian Journal of Psychiatry. India: Wolters Kluwer –Medknow Publications. [cited 2016 July 8].
Available from: www.indianjpsychiatry.org
5. Indian Journal of Social Psychiatry. India: Wolters Kluwer –Medknow Publications. [cited 2016 July 8].
Available from: www.indjsp.org/
6. Indian Journal of Psychological Medicine. India: Wolters Kluwer –Medknow Publications. [cited 2016 July
8].
Available from: www.ijpm.info
7. Schizophrenia Bulletin. United Kingdom: Oxford University Press. [cited 2016 July 8].
Available from: www.schizophreniabulletin.oxfordjournals.org

Page 363
2. EVALUATION: HISTORY AND MENTAL
STATUS EXAMINATION (MSE)
 History: Data from patient (subjective) / from procedures, head injury, Epilepsy and Medico-
reliable informant (objective) Legal issues
 Demographic details:  Family h/o of psychiatric illness, addictions,
o Name suicide
o Sex/Age  Developmental history
o Address  Level of education
 Presenting complaints  Occupational history
 Onset / duration / progress  Marital history
 Past h/o of psychiatric illness / treatment  Personal history – any addiction
 Past h/o of medical illnesses (Hypertension,  Premorbid personality
Diabetes, TB, Enteric Fever etc) / surgical
Table No. 1: Mental Status Examination Format
1. Appearance Tidy Untidy Appropriately Over dressed

dressed
2. Attitude Cooperative Uncooperative
3. Behavior (psychomotor Dull Normal Increased
activity)
4. Eye to eye contact Present Absent
5. Rapport Established Difficult to Not Established
Establish
6. Speech Normal Mute Speaking very Over talkative
few words
Coherent Incoherent
Relevant Irrelevant
Flight of ideas Thought block
7. Mood Euthymic Anxious Irritable
Elevated Sad Depressed
8. Affect Normal Cheerful Happy
Tearful Depressed Blunt
9. Hallucinations Auditory Visual Olfactory
(Abnormal perception Tactile Gustatory
without external stimulus)
10. Delusions Persecution Grandiosity Reference Infidelity
(Firm and false belief)
11. Obsessive thoughts / Cleaning Washing Arranging
compulsive behaviors Rituals Verbal
12. Suicidal / Homicidal Present Absent
ideation
13. Level of consciousness Alert Drowsy Stuporous
14. Orientation Time Place Person
15. Attention and Sustained Not sustained
concentration
16. Memory Intact Impaired
17. Intelligence Average Below average
18. Judgment Intact Impaired
19. Insight Present Absent
Page 364
**Delusions and Hallucinations are the cardinal features of Schizophrenia / Psychosis
Bibliography
6. Sadock B, Sadock V. Synopsis of Psychiatry: Behavioral Sciences / Clinical Psychiatry. 10 th Edition. USA:
Wolters Kluwer and Lippincot Wiliams and Wilkins. 2007.
7. World Health Organisation. The ICD-10 Classification of Mental and Behavioral Disorders: Clinical
Descriptions and Diagnostic Guidelines. W.H.O. 2002.
Association. 2013
Further Reading
8].

Page 365
3. SCHIZOPHRENIA
 Anxious and fearful affect
1. Introduction  Poverty of speech
 Delusion of Persecution and/or Reference
Schizophrenia is a mental disorder of chronic nature
in which there is primary impairment of thoughts,  Auditory Hallucinations
emotions and behavior which leads to severe socio-  Lack of Insight
occupational impairment and personality  Impaired Judgment
deterioration.
4. Investigations
2. Symptoms  No diagnostic investigations available.
 Suspiciousness  Complete Haemogram, Blood Sugar, Renal
 Fearfulness Function Test, Liver Function Test, Serum
 Social withdrawal Electrolytes, Urine Routine, Chest X-Ray (If
 Muttering / smiling to self necessary)
 Poor self-care
 Disturbed sleep
5. Complications
 Work impairment  Severe agitative behavior
 Homicidal tendencies
3. Signs  Self-harm / Suicidal behavior
 Unkempt appearance  Catatonic Stupor / Excitement
 Increased or decreased psychomotor activity
6. Treatment and Management

6.1 Antipsychotics: Primary care physician can start single drug and titrate it up to optimum level
Table No. 1 Antipsychotics
Name Strength Recommended doses** Duration/ Remark

Trifluoperazine 5 mg 10-40 mg/day Drugs to be started in low
Trihexyphenidyl 2 mg 2-6 mg/day doses and gradually
Haloperidol 5 mg 10-30 mg/day increase till 80 %
Risperidone 2 mg 4-8 mg/day improvement.
Olanzapine 5 mg 5-20 mg/day
Quetiapine 50/100 mg 50-300 mg/day Maintenance doses to be
Clozapine 50 mg 50-200 mg/day continued long term
Chlorpromazine 50 mg 50-200 mg/day
**To be given in divided doses: It is to be monitored by psychiatrist.
6.2 Sedatives:
Table No.2 Sedatives
Name Strength Recommended doses Duration/ Remark

Lorazepam 2 mg 1-4 mg HS Drugs to be started in low
Diazepam 5 mg 5-10 mg HS doses preferably at night
Clonazepam 0.5 mg 0.5-1 mg HS and to be tapered off
Nitrazepam 5 mg 5-10 mg HS within 2 weeks
Page 366
6.3 Modified Electro-Convulsive 6.5 Maintenance Therapy:
Therapy: All patients with Schizophrenia have to be
Minimum of 8-15 sessions of modified ECT are maintained on long term antipsychotics oral or
required. injectable treatment.
Depot Injections:
6.4 Treatment and Management of Inj. Haloperidol Decanoate, 50mg, once a month,
Complications: deep IM
 Inj. Haloperidol, 10mg, BD/ SOS for 2/3 days OR
 Inj. Promethazine*, 50 mg, BD / SOS for 2/3
days Inj. Fluphenazine 25mg, once a month, deep IM
(*Not to exceed 100mg/day) OR
 Electro-convulsive Therapy Inj. Flupenthixol, 40mg, once a month, deep IM

 Inj. Diazepam, 10mg or Lorazepam, 4mg if
required
6.6 Side effects and management:

Table No. 3 Common Side Effects and Management
Side Effect Management Duration/ Remark

Tremors at extremities / Salivation Trihexyphenidyl 2-6mg along with antipsychotic
drugs.
Dystonic Reaction / Rigidity Inj. Promethazine 50mg Stat / SOS SOS
Dry Mouth / Constipation Reduce dose of Trihexyphenidyl 1 week
Neuroleptic Malignant Syndrome Stop Antipsychotics Till patient recovers and CPK level
(Rigidity, Fever, Disorientation, comes to normal.
Inj. Lorazepam,
Reduced urine output)
Tab. Bromocriptine,
Supportive Management
6.7 Counseling and Psychotherapy

Refer to higher center if needed.
Bibliography
2. Sadock B., Sadock V. Synopsis of Psychiatry: Behavioral Sciences / Clinical Psychiatry. 10th Edition.
USA: Wolter’s Kluwer and Lippincot Wiliams and Wilkins. 2007.
3. The ICD-10 Classification of Mental and Behavioral Disorders: Clinical Descriptions and Diagnostic
Guidelines. W.H.O. 2002.
Association. 2013
Further Reading
Page 367
3. Guitart X. σ Receptors and Schizophrenia. Sigma Receptors: Chemistry, Cell Biology and Clinical
Implications. USA:2007. Springer. 273-292 [cited 2016 July 8].
Available from: http://link.springer.com/chapter/10.1007/978-0-387-36514-5_13
8]. Available from: www.ijpm.info
7. Iritani S, Neuropathology of Schizophrenia—From a New Perspective. Brain and Nerve = Shinkei Kyunko
no Shinpo [cited 2016 July 8].
Available from: http://europepmc.org/abstract/med/17585592
8. Kay S, Flszbein A, Opfer L., The Positive and Negative Syndrome Scale (PANSS) for Schizophrenia.
Schizophrenia Bulletin.1987, 13(2): 261-276 [cited 2016 July 8].
Available from: http://psycnet.apa.org/journals/szb/13/2/261/
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Page 368
4. BIPOLAR MOOD DISORDER
1. Introduction 5. Signs of Depression
 Distinctive episodes of abnormally and  Dull, withdrawn
persistently elevated, expansive, irritable or  Poor eye contact
depressive mood  Decreased productivity of speech
 Patient may be in Mania or Depression or  Crying spells
present with mixed features  Feeling of guilt
 Suicidal thoughts, ideas and plans
2. Symptoms of Mania  Decreased appetite
 Over talkative  Sleep disturbances
 Hyperactive
 Over familiar / over religious / over spending /
over grooming 6. Investigations
 Big talks  No diagnostic investigations available.
 Decreased need for sleep  Complete haemogram, Blood Sugar, Renal
 Work impairment Function Test, Liver Function Test, Serum
Electrolytes, Urine Routine, chest X-Ray (If
3. Signs of Mania necessary).
 Increased psychomotor activity
 Pressured speech / flight of ideas
7. Complications
 Grandiosity 7.1 Mania:
 Easily distractible / irritable  Severe agitative behavior
 Hypersexual behavior  Homicidal tendencies
 Auditory hallucinations of God / actors talking
to him 7.2 Depression:
 Self-harm / Suicidal behavior
4. Symptoms of Depression
 Persistent and pervasive low / sad mood
 Lack of energy / interest / initiative
8. Treatment and Management
 Hopelessness / worthlessness / helplessness of Mania
 Feeling of guilt, agitation 8.1 Antipsychotics:
 Suicidal ideas / attempts Primary care physician can start single drug and
 Decreased sleep, appetite and libido titrate it up to optimum level.
 Sometimes hearing of voices
 Work impairment
Table No. 1 Antipsychotics
Name Strength Recommended doses* Duration/ Remark

Trifluoperazine 5mg 10-40mg/day Drugs to be started in low
Trihexyphenidyl 2mg 2-6 mg/day doses and gradually
Risperidone 2mg 4-8mg/day increased till 80 %
Olanzapine 5mg 5-20mg/day improvement.
Quetiapine 50/100mg 50-300mg/day
Chlorpromazine 50mg 50-200mg/day Maintenance doses to be
continued long term
*To be given in divided doses
Page 369
8.2 Sedatives:
Table No. 2 Sedatives

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg HS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks.
**To be given in divided doses
8.3 Mood Stabilizers

Table No. 3 Mood Stabilizers
Name Strength Recommended Duration/ Remark

doses***
Carbamazepine 100/200mg 100-600mg/ day Drugs to be started in low
Lithium 300mg 300-900mg/day doses and gradually
Divalproex 250/500mg 500-1500mg/day increase till 80 %
improvement.
Maintenance doses to be
continued long term
***To be given in divided doses
8.3.1 Side effects of mood stabilizer: Minimum of 8-15 sessions of modified ECT are
 Carbamazepine- Giddiness, blurred required.
vision, rash, hypotension
 Lithium- Tremors, muscle twitching, 9. Treatment and Management
disorientation
 Divalproex Sodium- Gastric irritation, of Depression
weight gain, lethargy, confusion, 9.1 Antidepressants:
tremors Primary care physician can start single drug and
titrate it up to optimum level.
8.4 Modified Electro-Convulsive
Therapy:
Table No. 4 Treatment and Management of Depression

Imipramine 25mg 50 to 150mg/day To be started in low doses
Amitriptyline 25mg 50 to 150mg/day and gradually increase till
Sertraline 25/50mg 25 to 100mg/day 80% improvement. To
Escitalopram 5/10mg 5 to 20mg/day continue at least 6 months
Mirtazapine 7.5/15mg 15 to 30mg/day and more if necessary
Desvenlafaxine 50mg 50 to 100mg/day
**To be given in divided doses
Page 370
9.2 Sedatives
Table No. 5 Sedatives

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg HS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks
9.3 Modified Electro-Convulsive 9.5 Precautions for Suicidal patients

Therapy: 8-15 sessions if needed.  24 hrs. continuous supervision.
 Do not isolate the patient.
9.4 Treatment and Management of  Do not keep any sharp objects, ropes, blades
near patient.
Complications during Mania:  Do not allow patient to lock room / bathroom
 Inj. Haloperidol 10mg BD/ SOS for 2/3 days. from inside.
 Inj. Promethazine* 50mg BD/ SOS for 2/3 days
(*Not to exceed 100mg/day) Note - Reduce doses of mood stabilizers if above
 Electro-convulsive Therapy. side effects are seen.
 Inj. Diazepam(5mg) or Lorazepam(2mg) stat if
needed. 9.6 Counseling and Psychotherapy
 In case of Depression, Electro-convulsive Refer to higher centre if needed.
Therapy 8-12 sessions if patient shows suicidal
tendencies.
Bibliography
Association. 2013.
Further Reading
2. Atre-Vaidya N, Taylor MA, Seidenberg M, Reed R, Perrine A, Glick-Oberwise F et.al. Cognitive deficits,
Psychopathology and Psycho-social functioning in Bipolar Mood Disorder. July 1998. Cognitive and
Behavioral Neurology 11(3). [cited 2016 July 8].
Available from:
http://journals.lww.com/cogbehavneurol/Abstract/1998/07000/Cognitive_Deficits,_Psychopathology,_and.
2.aspx
5. Goodwin F, Jamison R. Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression. Oxford
University Press, USA.
Page 371
8].
9. Oquendo MA, Waternaux C, Brodsky B, Parsons B, Haas GL, Malone KM, et al. Suicidal Behavior in
Bipolar Mood Disorder: Clinical Characteristics of Attempters and Non-Attempters. Journal of Affective
Disorders. August 2000. 59(2):107-117. [cited 2016 July 8].
Available from: http://www.sciencedirect.com/science/article/pii/S0165032799001299



Page 372
5. MAJOR DEPRESSIVE DISORDER (MDD)
 Sometimes psychotic symptoms like
1. Introduction hallucination and reference ideas
 Depression is major public health problem
 Hopelessness, helplessness, worthlessness
 By 2020, it will be the major cause of
 Suicidal thoughts, ideas or attempts
worldwide morbidity and mortality
 Atypical symptoms
 MDD is a disabling condition that severely
o Overeating
affects a person’s family work, sleeping, eating
o Oversleeping
habits and general health
o Agitation
 It is the leading cause of suicide o Decreased libido
2. Types: Mild, Moderate and Severe
4. Investigations
3. Signs and Symptoms of  No diagnostic investigations available.
 Complete Haemogram, Blood Sugar, Renal
MDD Function Test, Liver Function Test, Serum
 Pervasive and persistent low mood Electrolytes, Urine Routine, Chest X-Ray (If
 Low self esteem necessary)
 Loss of interest or pleasure in normally enjoyed
activities
 Lack of energy and enthusiasm, easy fatigue 5. Complications
 Loss of appetite, weight loss Self-harm / Suicidal behavior
 Disturbed sleep
6. Treatment and Management of Depression

6.1 Antidepressants:
Table No. 1 Treatment and Management of Depression
Name Strength Recommended doses Duration/ Remark

Imipramine 25mg 50 to 150mg/day To be started in low doses and
gradually increased till 80%
Amitriptyline 25mg 50 to 150mg/day
improvement. To continue at least
Sertraline 25/50mg 25 to 100mg/day 6 months and more if necessary.
Escitalopram 5/10mg 5 to 20mg/day
Mirtazapine 7.5/15mg 15 to 30mg/day
Desvenlafaxine 50mg 50 to 100mg/day
6.2 Sedatives: Table No. 2 Sedatives

Lorazepam 2mg 1-4mg HS Drugs to be started in low doses
preferably at night and to be
Diazepam 5mg 5-10mg HS tapered off within 2 weeks
Clonazepam 0.5mg 0.5-1mg HS
Nitrazepam 5mg 5-10mg HS
**To be given in divided doses; if psychotic features are present, add low dose antipsychotics.
Page 373
6.3 Modified Electro-Convulsive Precautions for Suicidal patients
 24 hrs continuous supervision.
Therapy: 8-15 sessions are required.  Do not isolate the patient.
6.4 Treatment and Management of  Do not allow patient to lock room/ bathroom
Complications from inside.
Electro-Convulsive Therapy Counseling and Psychotherapy play a major role.
Daily ECTs (if needed), minimum for three Refer to higher centre if needed.
days.
Bibliography
Association. 2013
Further Reading
8].



Page 374
6. ANXIETY DISORDER
E.g. Fear of public places, closed spaces, heights,
1. Introduction animals, water etc.
 Anxiety is a normal emotion experienced by
everyone at times of stress
 Symptoms of anxiety are psychological, 2.4 Post-Traumatic Stress Disorder
physical or mixture of both (PTSD)
 Anxiety becomes a disorder when symptoms Disabling fear, intrusive flashbacks or vivid
become severe, disabling and reduce quality of dreams and emotional disturbances after
life traumatic life event causing avoidance of similar
 Anxiety spectrum disorders tend to be chronic situations
2. Presentation 2.5 Obsessive Compulsive Disorder

Frequent intrusive thoughts producing
apprehension and fear or worry and leading to
2.1 Generalized Anxiety Disorder compulsive, repetitive behavior aimed to reduce
(GAD) the anxiety
This involves excessive, unrealistic worry and
E.g. Frequent thoughts of contamination leading
tension without any definite reason.
to compulsive washing; frequent checking of
Signs and Symptoms
locks, gas knobs, counting money etc.
Palpitations, dry mouth, tremors, sweating,
difficulty in breathing, frequency of urination,
abnormal feeling in the gut, muscle tension,
3. Investigations
dizziness.  No diagnostic investigations available
2.2 Panic Attacks  Complete Haemogram, Blood Sugar, Renal
 Can occur in patients with GAD Function Test, Liver Function Test, Serum
 Signs and symptoms include all of the above Electrolytes, Urine Routine, Chest X-Ray (If
with severe choking sensation and shortness of necessary).
breath with impending feeling of death or going
crazy. The attack lasts for few minutes and 4. Complications
subsides on its own Any of the anxiety spectrum disorder can lead to
 If panic attacks occur frequently, then it is ‘Major Depressive Disorder’, making person
called as Panic Disorder vulnerable to suicide.
2.3 Phobia
Intense and irrational fear of a specific object or 5. Treatment and Management
situation leading to phobic avoidance
Includes Drug and Non-drug treatment
Page 375
5.1 Drug Treatment
Table No. 1 Drug Treatment
Drug Treatment Duration/ Remarks

SSRIs (Any One) As anxiety disorders tend to be chronic, treatments
1. Escitalopram 10-20mg/day should be given for long duration.
2. Paroxetine 12.5-25mg/day
3. Mirtazapine 7.5-15mg/day
4. Fluvoxamine 50-150mg/day (Preferred in OCD)
5. Sertraline 25-50mg/day
TCA
Clomipramine 25-75mg/day
Anxiolytic Drugs (Any One)

1. Clonazepam 0.5-1mg/day
2. Lorazepam 1-2mg/day
3. Diazepam 5-10mg/day
β-Blocker
Propranolol 10-40mg only in panic disorder
5.2 Non Drug Treatments

Table No. 2 Non Drug Treatment
 Reassurance
 Supportive Therapy
 Relaxation Therapy
 Exposure and Response Prevention Therapy
 Cognitive Behavior Therapy
 Yoga and Exercises
 Self-help techniques
Comprehensive treatment including drugs and psychotherapies are most effective.
Bibliography
Association. 2013.
Further Reading
Page 376
8].
7. Schizophrenia bulletin. United Kingdom: Oxford University Press. [cited 2016 July 8].

Page 377
7. SOMATIZATION DISORDER
Reaction.
1. Introduction
 Excessive thoughts, feelings or behavior related 4. Investigations
to the somatic symptoms or associated health  Psychiatric assessment
concern  Laboratory Investigation
 Persistently high level of anxiety about health o No diagnostic investigations available.
symptoms o Complete Haemogram, Blood Sugar, Renal
 Excessive time and energy spent over these Function Test, Liver Function Test, Serum
symptoms and their investigations and Electrolytes, Urine Routine, Chest X-Ray (If
treatments Necessary)
2. Signs and Symptoms 5. Management

 Pain in different areas- Head / Back / Stomach / 5.1 Antidepressants (Any One)
Joint etc a) Tab. Sertraline 25-200mg/day in divided doses
 GI symptoms like nausea, vomiting b) Tab. Amitriptyline 25-100mg/day in divided
 One pseudo-neurological condition doses
(Paresis, loss of voice, loss of vision) c) Tab. Escitalopram 5-20mg/day in divided doses
 Symptoms cannot be explained by a medical 5.2 Anxiolytics (Any One)
condition
a) Tab. Lorazepam 2mg HS/SOS
b) Tab. Clonazepam 0.5-1mg HS/SOS
3. Conversion Reaction c) Tab. Diazepam 5-10mg HS/SOS
 Altered voluntary motor or sensory function 5.3 Counseling and Psychotherapy-
with incompatibility between the symptom and Supportive, Cognitive Behavioral, REBT
recognized medical/neurological condition
 Causes significant distress in social,
5.4 Stress Management and Life
occupational and other important areas of style changes.
functioning
 Possession Attack is an example of Conversion
Bibliography
Association. 2013
Further Reading
8]. Available from: www.ijpm.info

Page 378
8. ORGANIC BRAIN SYNDROME
1. Introduction 2.1.6. Management
 Identify and treat the precipitating cause
 Primary biochemical or structural disturbances
 Provide environmental and supportive care
(damage) to the brain resulting in impairment of
mental functions affecting memory, orientation  Avoid sedation, but for severely agitated
and cognition patients it may be necessary to induce sedation
in order to facilitate investigations and treatment
 Regular clinical review, close vigilance
2. Types of organic brain
2.1.7. Medication
syndrome Important:
 Acute organic brain syndrome- Delirium Watch for level of consciousness before giving
 Chronic organic brain syndrome- Dementia injectable
 Other / Sub-acute organic brain syndrome-
Use single medication - Start low, go slow
Amnestic syndrome.
 Haloperidol - 1-4mg /day Initially for 3
2.1 Delirium  Lorazepam - 0.5-1mg daily days,
2.1.1. Definition Review and
 It is a clinical syndrome of fluctuating global  Risperidone - 1mg daily
titrate
cognitive impairment of consciousness,  Quetiapine - 25mg – 100mg daily
attention and orientation the dose
 Additional disturbances in memory, language (To be given in divided doses)
and perception may occur All anti-psychotics and sedatives to be tapered
 Commonly occurs in hospitalized patient with gradually, once symptoms are relieved
history of major preexisting medical,
neurological or surgical illnesses 2.1.8. Refer to higher center
2.1.2. Causative Factors For counseling and psychotherapy
 Substance intoxication (alcohol, cannabis,
opioid etc) 2.2. Dementia
 Substance withdrawal 2.2.1. Definition
 Medicine induced It is a syndrome characterized by progressive, usually
 Delirium due to preexisting medical conditions irreversible, global cognitive deficits primarily
e.g. Hepatic Encephalopathy characterized by memory impairment and
2.1.3. Risk factors dysfunction in Activity of Daily Living (ADL)
Old age, preexisting dementia, very young, 2.2.2. Common Causes of Dementia
postoperative, burns victim, alcoholic and
Benzodiazepine dependence  Vascular dementia (20%)
 Substance Use Disorders (10%)
 Subdural hematoma
2.1.4. Signs and Symptoms  Vitamin B12 deficiency
 Confusion
 Metabolic causes, Hypothyroidism
 Clouding of consciousness All Anti psychotics and Sedatives to be tapered
 Visual illusion and hallucination gradually once symptoms are relieved
 Labile affect Refer to higher centre for Counseling and
 Disorientation to time, place, person Psychotherapy
 Hyperactivity or hypoactivity
2.1.5. Investigations 2.2.3. Signs and Symptoms:
Complete Haemogram, Blood Sugar, Renal Function  Memory impairment.
Test, Liver Function Test, Serum Electrolytes, Urine  Dysphasia–Deficiency of words, name
Routine, Chest X-Ray (If necessary). generation
 Agnosia –Inability to recognize parts of body
Page 379
 Apraxia – Inability to perform purposeful c. Associated Depression / Insomnia
action and draw objects  Tab. Sertraline 25mg/day, for 2 months and then
 Impaired executive function– Inability to plan titrate the dose
and take action accordingly  Tab. Escitalopram 10mg/day, Lorazepam 0.5
 Personality disintegration– Resulting in mg/day
maladaptive behavior
Anti-psychotics and Anti-depressants to be
2.2.4. Investigations: discontinued once symptoms relieved.
 Complete Haemogram, Blood Sugar, Renal
Function Test, Liver Function Test, Serum 2.2.6. Treatment of co-morbid medical
Electrolytes, Urine Routine, Chest X-Ray, illnesses:
Thyroid Function Test, HIV, Vit. B12, Folate
levels, ECG, CT brain, MRI a. Supportive:
 EEG – abnormal depending upon the cause High doses of Multivitamins
b. Assistance:
2.2.5 Treatment and Management For routine activities like bath, food etc.
a. Cognitive Enhancers – Keep surroundings of patient safe and calm and
(ACE inhibiter) well lit
Oral Donepezil 2.5-10mg / day lifetime c. Psychological support:
To both patient and caregiver
b. NMDA antagonist–
Oral Memantine 5mg d. Functional management:
Associated Psychosis/agitation– Maximize mobility and independence, assist
Tab. Quetiapine 25mg, ½ - ½ - 1 communication
OR e. Social management:
Tab. Risperidone 1mg/day, titrate the dose, regular Shelter homes, recreational activities, assistance
follow up and then stabilize the dose for two years. in financial and legal matters
Taper the dose after two years.
Bibliography
Association. 2013.
Further Reading
8].
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Page 380
9. DRUG ABUSE AND SUBSTANCE USE
DISORDER
consequences in physical, social, legal aspects
1. Introduction of life.
 When substances like alcohol, caffeine,
cannabis, inhalants, opioids, sedatives and  Patients of addictions, especially of alcohol, are
hypnotics etc. are taken in excess quantities, the most commonly treated cases in rural set up.
they produce intense activation of the brain and
disinhibition.
2. Common Substance
 Addiction- Repeated, compulsive use of a
substance that continues in spite of negative
Disorder
Table No. 1 Common Substance Disorders
Condition Sign and Symptoms Management Duration

Alcohol intoxication Aggressive behavior, mood No active treatment Till symptoms
Caused by excessive lability, slurred speech, needs to be given. recover
consumption of Alcohol incoordination, unsteady gait, Manage
nystagmus, impaired symptomatically.
judgment.
If excited- Inj.
Haloperidol 5mg + Inj.
Phenergan 50mg IM.
IV fluids SOS.
Alcohol withdrawal Autonomic hyperactivity, Inj. Thiamine 100mg 5-7 doses on alternate
tremulousness, insomnia, and Multivitamin days
Caused by Cessation or
psychomotor agitation, infusion.
reduction of alcohol use that
nausea / vomiting, transient
has been heavy and Inj. Lorazepam 1 2-3 days
visual, tactile, auditory
prolonged earlier. ampule BD/ HS.
illusion or hallucinations.
4-5 days and taper
Shift to Tab.
gradually
Lorazepam 1mg TDS
/SOS.
IV Fluids As necessary
Delirium Tremens Tremors, disorientation, 1. IV Inj. Thiamine 10 days

It is a severe form of confusion, hyperactivity, 100mg /day in 100
Withdrawal insomnia, illusions, ml NS.
severe anxiety, seizures 2. IV 5% Dextrose As needed
Close monitoring of vital hallucinations and DNS.
functions like pulse, BP, 3. Inj. Diazepam 5mg 5 days
temperature, input and IM TDS or Inj.
output is very essential. Lorazepam 2 mg
IM/IV TDS.
4. Tab. Diazepam As needed
5mg TDS or Tab.
Lorazepam 6-12
mg/day in divided
doses.
Page 381
Condition Sign and Symptoms Management Duration
5. Inj. MVI (Multi 6 days
Vitamin Injection)
+ 5% Dextrose drip.
6. If severe agitation
or perceptual Till psychotic symptoms
abnormality present recover
Tab. Olanzapine
2.5-10mg or
Tab. Risperidone
2-4mg per day in
divided doses.
Cannabis intoxication Dryness of mouth, 1. Supportive As needed
tachycardia, reduced motor treatment and IV
skills, euphoria, sleepiness, Fluids.
apathy, laughter, paranoia, 2. Benzodiazepines
hallucinations. eg. Clonazepam
0.5mg / Lorazepam
1mg TDS.
3. Tab. Olanzapine 5 days
5mg HS.
Cannabis withdrawal Anxiety, irritability, 1. Supportive 3-5 days
depressed mood, restlessness, treatment and IV
insomnia, loose motions, Fluids
2. Benzodiazepines
eg. Clonazepam
0.5mg / Lorazepam
1mg TDS.
Opioid withdrawal Dysphoric mood, 1. Lorazepam 1-2 mg 2-3 times a day for 1st
Heroin, Gard, Afeem, MD, insomnia, muscle aches, oral/I.M./I.V. for week
Brown Sugar, Inj. Fortwin nausea or vomiting, anxiety and
diarrhea, lacrimation or decreased sleep.
rhinorrhea, yawning.
2. Tab. Ibuprofen As needed
400mg or Tab.
Naproxen 250 –
500mg or Tab.
Paracetamol TDS.
3. Tab. Clonidine As needed
0.1mg can be given
2-3 times a day
during
detoxification.
4. IV fluids and As needed
Supportive Care.
Remark:
All patients with substance addiction should be motivated to enroll in de-addiction centres and to attend support
groups like Alcohol Anonymous (AA) and Narcotic Anonymous (NA).
All other Substance Use Disorder patients should be treated symptomatically and referred to higher centre.
Page 382
Bibliography
Guidelines. WHO 2002.
4. Diagnostic and Statistical Manual of Mental disorders. 5th Edition. USA: American Psychiatrist’s
Association. 2013
Further Reading
1. Abuse S. Results from the 2010 National Survey on Drug Use and Health: Mental Health Findings. 2012.
3. Babor TF, McRee BG, Kassebaum PA, Grimaldi PL, Ahmed K, Bray J. Screening, Brief Intervention and
Referral to Treatment (SBIRT) toward a Public Health Approach to the Management of Substance Abuse.
Substance abuse. 2007 Nov 21:28(3):7-30. [cited 2016 July 8].
Available from: http://www.tandfonline.com/doi/abs/10.1300/J465v28n03_03
Available from:www.adaa.org
6. Guidelines for the Psychosocially Assisted Pharmacological Treatment of Opiod Dependence. WHO 2009.
Available from:www.indjsp.org/
8].
Available from:www.ijpm.info
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Page 383
10. INTELLECTUAL SUBNORMALITY
A state of mind with intellectual and functional iii. Postnatal – CNS infections, trauma,
deficits is commonly known as Mental Retardation. uncontrolled epilepsy.
1. Incidence 3. Types of Mental Retardation

3 to 4 cases per 1000 population.
1. Borderline
2. Etiology: 2. Mild
3. Moderate
i. Prenatal (1 in 1000 live birth) due to genetic,
4. Severe
intrauterine viral infections, injuries, maternal
5. Profound
metabolic disorders
Refer to the table for details and management.
ii. Perinatal - All causes leading to hypoxia during
birth.
Table No. 1 Mental Retardation Classifications
Types Borderline Mild Moderate Severe Profound

Dull Slow
Normal Learner
IQ range 80 to 90 70 to 80 50 to 70 35 to 50 35 to 15 up to 15
Salient - Scholastic - Can tell right - May not be - May not be - Cannot feed
backwardness in left laterality able to tell able to name self
Clinical
some subjects - Can recognize laterality organs - Cannot protect
features but may coins - May not - May not be self
complete - Can use recognize able to
- 10th Standard money all coins recognize
with extra years - Can do simple - May not o Colors
- And additional calculation tell all o Coins
coaching - Can tell colors o Count
relations - May not - May not
- Can pass 10th count recognize own
std. in selected beyond 10 family
subjects - May not be members but
able to recognize
recognize familiar faces
relations
like
cousins,
uncles
ADL - Independent - Independent - May need - Needs - Needs to be
- Can travel on - Can use help for assistance for fed, bathed,
(Activities of
own telephone grooming, bath, protected
Daily - Good social bath cleanliness but
skills - May be Can feed self
Living) able to
e.g. bath, move in
village but
food, not far
grooming etc. away.
Page 384
Types Borderline Mild Moderate Severe Profound
Trainability - Trainable - Trainable - Trainable - Non trainable - Non trainable
- Can earn - Can earn for - So remains - So remains
repetitive dependent for dependent for
work under life long life long
supervision
- May be
able to earn
as
shepherd,
helper
% Disability <50 but eligible for > 40 % > 50 % > 75 % 100%
subject selection.
4. Management
 Anti-Psychotics in low doses for behavioral 5. Special Guidance
disturbances.
Get IQ assessment certificate and Disability
 Anti-Epileptics – if the patient has co-morbid certificate from concerned Civil Hospital.
Epilepsy.
 ADL training. Enrollment in government employment facility for
 Vocational training. gainful employment
 Caregiver education.
Bibliography
USA: Wolter’s Kluwer and Lippincot Williams and Wilkins. 2007.
Association. 2013
Further Reading
1. American Journal of Psychiatry. United States: American Psychiatric Publishing.
2. British Journal of Psychiatry. United Kingdom: Royal College of Psychiatrists.
3. Indian Journal of Psychiatry. India: Wolters Kluwer –Medknow Publications.
4. Indian Journal of Social Psychiatry. India: Wolters Kluwer –Medknow Publications.
5. Indian Journal of Psychological Medicine. India: Wolters Kluwer –Medknow Publications.
6. Lukasson R, Schalock R., Spitalnik D., Mental Retardation: Definition, Classification and Systems of
Support. 10th Edition. USA: 2002, AAMR. [cited 2016 July 8].
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Page 385
11. CHILD AND ALDOLESCENT PSYCHIATRY
Certified patients can avail the provision of a writer
1. Introduction and extended time to write a paper in 10th std. and
 Child and adolescent form a major percentage 12th std. board examinations. Remedial teaching by
of population specially trained teachers either one to one or in
 Many psychiatric problems are present in this groups of a few children is very effective.
age group.
 Early detection and treatment of these
conditions will prevent complications and B. Pervasive Developmental Disorder of
significantly reduce the morbidity. Childhood or Autism –
 Commonly seen disorders are behavior Such children do not mix or communicate verbally or
disorders, anxiety disorders and depressive emotionally even with their parents. They are self-
disorders. engrossed in non-goal directed activities. Usually
non-complaining and self-sufficient, odd motor
2. Presentation movements, peculiar speech pattern, attracted by
music. Those with normal IQ may excel in some arts
The child usually presents as poor scholastic like music, drawing.
performance, disobedience, somatic pain.
Some such patients may need small dose
antipsychotic if self-destructive.
2.1 Assessment: Tab. Haloperidol 1.5 mg half tablet HS.
 History to be taken from parents, school teacher
and care taker as well as other colleague They need special training in one to one setup.
children.
 Child to be taken into confidence by talking to 2.2.2 Psycho emotional disorders
him alone.
A large number of these age group patients belong to A. Attention Deficit Hyper Activity Disorder
the intellectual sub normality disorder. ADHD/ADD is not uncommon
Clinical symptoms -
2.2 Important childhood  Inattention – i.e. not able to mentally focus at a
disorders: given task adequate enough to understand it or
2.2.1 Psycho-developmental disorders perform it. Easily distractible and so, forgetful
 Hyperactivity – Always driven by some
A. Learning Disorders or Dyslexia– movements; cannot sit still; runs around; climbs
IQ of the child is normal but still he lags in scholastic windows; cupboards
performance due to specific learning disability i. e.  Impulsivity – Acts before thinking; shifts from
one activity to another; disruptive
 Writing dyslexia - wrong spellings and
grammatical mistakes. Plenty of complaints from the school, neighbors.
 Reading dyslexia - unable to read sentences and Most of the children show good response to psycho
words with proper pronunciations. stimulant medicine.
 Arithmetical dyslexia - confusion in  Tab. Methylphenidate 5 to 10mg once a day
mathematical symbols e. g. +, -, x, 3, 6, OR
i.e. geometrically reverse symbols, resulting
 Cap. Atomoxetine 10 to 25mg once a day.
into poor performance in solving and
understanding mathematics. B. Childhood Depression – common.
 Global dyslexia - all of above.
C. Nocturnal Enuresis due to environmental
Detection of dyslexia is usually done by the school stress.
teacher and confirmation has to be done by
 Common
government approved agency such as special units in
 Shows good response to Tab. Imipramine 25mg
teaching hospitals / medical colleges.
H.S.
Page 386
2.2.3 Performance Anxiety, Phobia, Oppositional – disobedient, negativistic, temper
Childhood Depression, Tension tantrums, argumentative, stubborn, not yielding to
headache, Somatization disorder are also rules.
commonly seen among children facing stress Management:
at home or at Aashram-shala or in the school.  Small doses of antidepressant e.g. Tab.
They need to be managed with medication Imipramine 25mg, 0-0-1 or Tab. Sertraline 25
(discussed already) and along with counseling. mg ½ - 0 – 0 to 1-0-0 for a short period
Clinical symptoms:  Benzodiazepines should be avoided.
 Headache, pain in abdomen, migraine, loose  Behavioral modification using positive /
motions, vomiting, exacerbations of asthma, negative reinforcers
fever, skin rash  Childhood psychoemotional disorders are
 Irrational fear and phobia of animals, ghosts, usually secondary to environmental stress. So,
darkness, school which ultimately resulting into modification of the stressful environment and
avoidance to school improving child’s coping capacity must be
 Sleep disturbances, nightmares, enuresis taken care to relieve symptoms. Medication is
 Child remains withdrawn and introvert, not as mentioned, to be given only till symptoms
playing, crying spells, excessively shy, Temper active, and in dosages appropriate to weight.
Tantrums
 Small doses of antidepressant e.g. Tab.
Imipramine 25 mg HS or Tab. Sertraline 25 mg Note: All suspected cases need exhaustive evaluation
½ - 0 – 0 to 1-0-0 for a short period. by psychiatrist, so must be referred if not
Benzodiazepines should be avoided responding to above medication.
2.2.4 Conduct disorder

In adolescents – Antisocial behaviors like violating
rules, showing aggression, running away from home,
lying, stealing, lack of guilt feeling.
Bibliography
Association. 2013
Further Reading
2. Aneshensel CS, Sucoff CA. The Neighborhood Context Of Adolescent Mental Health. Journal of Health
and Social Behavior. 1996 Dec 1:293-310.
Available from: http://www.jstor.org/stable/2137258?seq=1#fndtn-page_scan_tab_contents
4. Depression and Anxiety. United States: John Wiley & Sons Inc.
5. Hoagwood K, Burns BJ, Kiser L, Ringeisen H, Schoenwald SK. Evidence-based practice in child and
adolescent mental health services. Psychiatric Services. 2001 Sep 1.
Available from: http://ps.psychiatryonline.org/doi/full/10.1176/appi.ps.52.9.1179
Page 387
9. World Health Organization, World Psychiatric Association, International Association for Child, Adolescent
Psychiatry, Allied Professions. Atlas: child and adolescent mental health resources: global concerns,
implications for the future. World Health Organization; 2005.
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Page 388
12. PSYCHIATRIC EMERGENCIES
1. Suicidal Attempt 4. Catatonic Stupor
Patient develops complete mental and physical
1.1 Causes: inactivity, becomes statue like and non-
 Severe depression - associated with financial communicative. Does not eat for many days and
burden, crop failure, love affair failure develops dehydration.
 Schizophrenia
 Drug induced psychoses like alcoholic 4.1 Causes:
hallucinations  Depression
 Impulsive act  Psychotic illness
 Organic brain disorder
1.2 Management:
 Immediate physical resuscitation 4.2 Management:
 Treatment for psychiatric illness – ECT and  I.V. fluids
medicines  Inj.Lorazepam1mg slowly BD till symptoms
 24 hrs continuous supervision reduce
 Do not isolate the patient  Ryle’s tube feeding
 Do not keep any sharp objects, ropes, blades  ECTs
near patient  Low doses of antipsychotic
 Do not allow patient to lock room/ bathroom
from inside
 Counseling and psychotherapy 5. Dystonic Reaction
Sustained muscles contractions causing twisting
and repetitive movements or abnormal postures
2. Psychotic excitement e.g. neck dystonia, tongue protrusion
2.1 Causes:
 Schizophrenia 5.1 Causes: -Use of antipsychotics like
 Mania Haloperidol, Trifluoperazine, Risperidone,
 Psychoactive drug abuse like charas, ganja, Olanzapine
alcohol
5.2 Management:
2.2 Management:  Taper off the anti-psychotic.
 Inj. Haloperidol 10mg IM twice a day  Inj. Phenergan 50mg IM twice a day to be
 Inj. Promethazine 50mgIM twice a day till tapered off over next 4-5 days depending
excitement controlled upon symptom relief.
 Restrain the patient to avoid injuries to self or  Tab. Benzhexol 2mg 1-1-1 till symptoms
others or destruction of property subside.
 I.V. fluids if patient not eating / R. T. feeding to  I.V. fluids till patient able to eat orally.
maintain hydration and nutrition  Change of antipsychotic by Psychiatrist.
 Oral antipsychotics
 ECTs Note: all patients of psychiatric emergencies need to
be referred to psychiatrist as early as possible, once
they are fit to travel.
3. Delirium
Management is given under topic of same name.
Bibliography
Page 389
Association. 2013.
Further Reading
3. Depression and Anxiety. United States: John Wiley & Sons Inc.
7. Schizophrenia Bulletin. United Kingdom: Oxford University Press.
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Page 390
13. PROCEDURE FOR ADMISSION TO A
MENTAL HOSPITAL
the ‘Reception Order’ from the concerned (i.e.
1. Introduction: the district of the patient’s residence) court.
All admissions to any government or private mental
hospital are governed by the Mental Health Act- 2.4 Reception Order-
1987.  By the concerned District Civil Court is issued
 The act provides guidance for - admission and only on confirmation of the mental illness and
discharge procedures of civil and criminal then, the patient can stay beyond 90 days till
patients. recovery.
 Management of property of the patients.  Such a patient even on discharge can extend his
 Safeguarding human rights of the patients. order with the ‘leave of absence facility’ for 60
days forever (i.e. he can be readmitted with the
original R.O. any time in future without further
2. Admissions legal procedures).
2.1 Voluntary Boarder- Patient himself
signs the application requesting the 3. Documents required
superintendent of a mental hospital to allow him Documents required for above legal procedures:
to stay in the hospital for treatment of his mental 1. Address proof of the patient or his caretaker.
illness. Maximum stay 90 days. 2. Photographs of the patient and his caretaker.
2.2 U/s. 19 (Mental health Act)-When 3. Undertaking to pay hospital charges by the
patient not capable of signing above application caretaker unless exempted by court order or by
due to his mental illness then, he is examined by provisions under the GR (1)
2 Psychiatrist independently and if found to need 4. Medical Certificates by 2 Psychiatrist for U/s.
admission, can be admitted for maximum 90 19 and for obtaining R. O. if patient admitted as
days. D.O.
2.3 Detention Order- A suspected mentally 5. Medical Certificates in prescribed format by one
Medical Officer in government service and by
ill person can be admitted to a mental hospital
any Registered Medical Practitioner for
for 10 days of observation period by the
application for R.O.
Detention Order of the Hon. District Civil Judge
or the CP of the area.
Note:
This section usually used for admission of
i. All court procedures to be done during court
wandering mentally ill people suffering of
timing i.e. between 10 am to 5:45 pm.
schizophrenia, mental sub normality, delirium,
ii. Patient and all documents to be presented to the
dementia etc. also for criminal people behaving
court.
abnormally.
iii. No legal procedures needed for admission at a
On certification after observation period, the stay
Civil Hospital or a General Hospital, as the
in the hospital for treatment can be extended by
patient is not isolated from society. Hence, such
admissions to be encouraged.
Bibliography
Further Reading
1. Mental Health ACT 1987. [Cited 2016 July 8]
Available from: https://sadm.maharashtra.gov.in/sadm/GRs/Mental%20health%20act.pdf
2. Narayan CL, Shikha D. Indian legal system and mental health. Indian Journal of Psychiatry. 2013;55
(Suppl 2): S177-S181. doi:10.4103/0019-5545.105521.
3. Math SB, Murthy P, Chandrashekar CR. Mental Health Act (1987): Need for a paradigm shift from
custodial to community care. The Indian Journal of Medical Research. 2011;133(3):246-249.
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Page 391
Ear, Nose & Throat
6. ENT
1 Acute Otitis Media 392

2 Chronic suppurative Otitis Media 393
3 Acute Parotis 397
4 Furuncle 399
5 Otomycosis 400
6 Neck Swellings 401
7 Atrophic Rhinities 402
8 NasalMyasis 403
9 Forign body in the Nose 404
10 Deviated nasal septum 405
11 Nasal obstruction 407
12 Tonsillitis 408
13 Adenoiditis 410
14 Peritonsillar abscess 412
15 Acute Pharyngitis 414
16 Hoarseness of voice 415
17 Stridor 416
18 Facial Palsy 417
19 Sensory Neural Hearing Loss 419
20 Vertigo 421
21 Fracture Involving Nasal Bone 423
22 Fracture Involving Maxilla 424
23 Penetrating neck injury 427
24 Blunt External Laryngeal Trauma 430
25 Epistaxis 432
26 Premalignant lesion of oral cavity 434
27 Acute upper airway obstruction 436
28 Deaf mutism 438
1. ACUTE OTITIS MEDIA (AOM)
1. Acute Otitis Media 1.3 Treatment –
Level 1 (PHC) & Level 2 (Rural Hospital):

1.1 Definition - An acute inflammatory Diagnosis & above-mentioned treatment with regular
condition of the middle ear space. Common in checkup. Non-improvement or deterioration, then
children – usually associated with fever. refer to higher center.
i. Counselling- Bed rest, advice mother about
correct feeding techniques and plenty of fluids.
No ear drops, ear mopping to be done only with
good illumination facility, not to blow nose
ii. Antibiotics (Ampicillin, Amoxicillin, 3rd
generation Cephalosoprins like Cefixime,
Cefpodoxime, Cotrimoxazole (Septran)
iii. Analgesic (For adults: Tab. Diclofenac -50 mg
TID x 5 days)
For children: Ibuprofen 200mg TID, Antipyretic
Fig 1.1 Congestion of eardrum
(Paracetamol-325 mg TID x5days) infant
&child over 3 months 5 to 10 mg/kg 3-4
times/day max. Daily dose 40 mg/kg/day)
iv. Decongestant nasal drops (1% for adults and
0.5% for children), like Oxymetazoline
(Nasivion) or Xylometazoline (Otrivin). This
will reduce congestion
v. Symptomatic – Application of dry local heat to
relieve pain
At Level 3-Distrtict Hospitals, Referral Hospital
Fig 1.2 Diagramatic representation of middle ear 1. Diagnosis, Investigations and Treatment of the
with otitis media case.
2. Referred case from Level 1 & Level 2,
1.2 Symptoms & Signs - Reassessment & further treatment.
i. Severe earache Fever, vomiting, may have Treatment:
convulsions
 If the tympanic membrane is bulging or if
ii. Mastoid tenderness & tinnitus, complication is suspected myringotomy should
iii. Congestion of the eardrum (Tympanic be done by ENT specialist under microscope
membrane), Bulging Tympanic Membrane & with a coverage of antibiotics
loss of normal light reflex (Ampicillin/Amoxycillin (25mg/kg/day for
pediatric patients for 5 days) / Adult dose
iv. Hearing Impairment (conductive deafness) 500mg TID/QID for 5 days/Amoxycillin +
Clavulanic Acid 625 mg BD for 5 days.
v. Usually associated with chronic rhinitis &
sinusitis, Nasal allergy, Cleft palate, tonsillitis,  Decongestants - Oxymetazoline nasal drops,
adenoids, measles 0.1% Nasal drops, 2-3 in each Nostril thrice
daily/ Xylometazoline Nasal Drop 0.05% in
vi. Young children may cry in agony, pull the children.
affected ear or bang their heads
Page 392
 Mastoid exploration may be required in cases of a. Systematic Antibiotics - Ampicillin
coalescent mastoiditis or other complication. /Amoxycillin (25mg/kg/day for pediatric
 Neurological / Pediatric Physician, patients for 5 days / Adult dose 500mg QID for
Ophthalmologist Consultation may be required 5 days).
in unresolved cases & management in b. Anti inflammatory /Anti pyretic Ibuprofen
accordance with them. (200mg) with Paracetamol (325 mg) in divided
doses for 5 days.
2. Acute Suppurative Otitis c. Decongestant - Oxymetazoline nasal drops,
0.1% nasal drops, 2-3 in each nostril thrice
Media (ASOM) daily/ Xylometazoline Nasal Drop 0.05% in
children.
2.1. Definition -
An Acute inflammatory condition of middle ear cleft 2.3.2 Level 3 (Referral Hospital / Dist.
which includes Eustachian tubes, middle ear, Antrum Hospital)
(opening of mastoid air cells in middle ear) with pus 1. Dry mopping/ Suction Clearance
discharge from external auditory canal due to
bacterial infection or following exanthematous 2. Antibiotic (Ampicillin/Amoxycillin 500 mg
fevers. It is also called safe ear if infection limited to thrice daily or, Amoxycillin + Clavulanic Acid
lower part of Eardrum. 625 mg BD x 5 days). If needed parenteral
antibiotics IV Cefotaxime 1 gm 12 hourly in
adult for 5 days.
3. Anti inflammatory drugs (Tab Ibuprofen 200
mg + Paracetamol 325 mg BD)
4. Decongestant - Oxymetazoline nasal drops,
0.1% nasal drops, 2-3 in each nostril thrice
daily/ Xylometazoline Nasal Drop 0.05% in
Fig 1.3 Perforated ear drum with pus discharge. children.
2.2. Symptoms- 2.3.3 Stages
i. Severe Pain, Fever a) Inactive stage -
ii. General malaise
Antibiotic not required and ear toileting may be
iii. Vomiting
done regularly Antibiotic ear drops (Ciprofloxacin
iv. Irritability
ear drop 2 drops BID) may be needed.
v. Discharge from ears:
vi. Mucopurulent discharge after dry mopping or b) Quiescent stage may not require any active
suction. Tympanic membrane may show treatment, as the ear is dry
congestion, perforation and pulsatile discharge
vii. Signs of upper respiratory tract infection like c) Active stage:
sinus, nasal & throat involvement.
In active case of the disease
2.3. Treatment- Symptoms and Signs:
2.3.1 Level 1 (at PHC level) & Level 2 (Rural 1. Ear Discharge - Non-foul, smelling /
intermittent / profuse and associated with upper
Hospital)
respiratory tract infection.
1. Dry mopping, suction, clearance of ear
discharge. A wick moistened with antibiotics 2. Hearing Loss - conductive in nature and
may be inserted. gradually progressive
2. Treatment of other septic focus - Eg. Acute 3. May be associated with tinnitus, Autophony
Adenotonsillitis, Rhinosinusitis with antibiotics, 4. Otoscopic examination - shows central
anti inflammatory drugs and decongestant perforation in the tympanic membrane with
pulsatile discharge coming out to external canal.
Page 393
Diagnosis is generally clinical. History with 3. Treatment of the focus of infection – Chronic
otological findings of central perforation is adenoiditis Tonsillitis, Deviated nasal septum
characteristic. Patient is advised to avoid risk factors and any sinus pathology.
in the form of avoiding excessive cold. Treatment is
4. The corrective surgery: The myringoplasty /
as mentioned above. Patient advised to keep ear dry
Tympanoplasty can be performed once the ear is
and avoid water going into the ear.
dry with perforation with no disease activity.
Treatment:
Indications of Tympanoplasty - There should be
1. Antibiotic treatment as per the culture and
(i) Well Sensorineural hearing preserved
sensitivity reports.
2. Regular ear cleaning and antibiotics ear drops in (ii) Eustachian tube should be patent
addition to oral/parental drugs. (Ampicillin
(iii) Stapes mobile
/Amoxicillin 500mg TDS x 5 days or
Amoxicillin + Clavulanic Acid 625 mg BD x 5 iv) Repeated attacks with no healing of disease.
days. Parental drugs. Inj. Cefotaxime 1gm IV
12 hourly x 5days.
Bibliography
1. Dhingra PL, Dhingra S, editors. In: Diseases of ear, nose and throat & head and neck surgery. 6th ed. New
Delhi: Elsevier; 2014.
2. Bhargava KB, Bhargava SK, Shah TM. A Short Textbook of E.N.T. Diseases. 10 th ed. Mumbai: Usha
Publications; 2014.
Further reading
1. Kazarika P, Nayak DR, Balakrishnan R. Textbook of Ear, Nose, Throat and Head& Neck Surgery Clinical
and practical Revised 2nd ed. 2009.
2. Indian Pharmacopoeia Commission. National Formulary of India (NFI). 4th ed. India: Government of India,
Ministry of Health and Family Welfare; 2011: pp 314.
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Page 394
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2. CHRONIC SUPPURATIVE OTITIS MEDIA
(CSOM)
i. Facial Nerve palsy
1. Definition:
ii. Labyrinthitis
It is a chronic inflammatory disease characterized by
foul smelling ear discharge with cholesteatoma iii. Meningitis
formation in atticoantral region. If attic involved, it
iv. Brain abscess - Extradural, Subdural abscess
is called as unsafe ear (infection may get routed to
nearby structures leading to complications. The v. Lateral sinus thrombosis
cholesteatoma is aggressive in nature and has got
vi. Mastoiditis
tendency of bone erosion leading to intracranial and
intratemporal complications. It is also called as vii. Petrositis
Atticoantral disease or unsafe type of CSOM.
4. Investigations:
2. Symptoms and signs: i. Oto microscopy
i. Usually scanty, intermittent, odourless mucoid ii. Aural swab for culture and anti bacterial
or mucopurulent discharge. If associated sensitivity test
infections foul smelling & continuous ear
iii. X-ray mastoids / CT-scan / MRI to confirm the
discharge, occasionally blood stained.
destructive pathology and spread of disease.
ii. Gradually increasing hearing loss- conductive Mastoid is usually sclerotic but may be
type. pneumatic with clouding of air cells.
iii. Perforation – Usually central iv. Pure tone Audiometry-It gives an assessment of
degree of hearing loss and its type
iv. May have associated polyp.
v. Investigations to assess the co-morbid
v. Patient may have:
conditions. (Biochemical & other Lab
a. Fever- Due to Acute Mastoiditis, Meningitis, investigations)
lateral Sinus thrombosis (fever chill and
rigors) 5. Treatment:
b. Headache- Due to Meningitis, Extradural
abscess 5.1 -At Level 1 & Level 2:
c. Vertigo, Tinnitus, Vomiting - Due to
i. Ear toileting to remove all discharge and debris.
Labyrinthitis, Brain abscess, Increased
Can be done by dry mopping or suction
intracranial tension, Meningitis
clearance under microscope. Irrigation with
d. Facial weakness or paralysis
normal saline (Not forceful with syringe). If
e. Post aural swelling due to Mastoiditis.
unresolved refer to higher centers.
ii. Ear drops: Antibiotic eardrops containing
Neomycin, Polymyxin, Chloromycetin or
Gentamycin. Combination with steroids can be
used to have local anti inflammatory effect.
iii. Systemic antibiotics: Are useful in acute
exacerbation in chronically infected ear.
Otherwise role of antibiotics is limited.
Fig 2.1 Showing Sub-total central perforation iv. Precautions: Patients are advised to keep water
out of the ear during bathing, hair wash or
3. Complications: swimming.
Page 395
v. Treatment of contributory factors like nasal Aims of modified radical surgery are
allergy, infected tonsils, adenoids
1. To make ear safe to patient by removing the
cholesteatoma by surgery.
2. To make ear dry and prepare a self cleansing
5.2 At Level 3: mastoid cavity
 Cholesteatoma being aggressive and destructive 3. To prevent complications of CSOM.
in nature-definitive management is surgery- in
the form of Tympanoplasty OR Modified 4. Establishing hearing mechanism of the ear
Radical Mastoidectomy (Reconstruction).
 Aim: Removal of disease.
Bibliography
Publications; 2014.
Further reading
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Page 396
3. ACUTE PAROTITIS -VIRAL/BACTERIAL
1. Mumps (Viral Parotitis) 2. Bacterial Parotitis
Caused by Paramyxovirus. Disease is contracted by 2.1. Definition –
droplet infection and fomites. Children are commonly
affected. Incubation period is 2 -3 weeks. Infection leading to Mechanical blockage of salivary
duct (stasis of salivary secretions coupled with
1.1. Symptoms & Sign- secondary infections), results in Bacterial Parotitis. It
is prevalent in debilitated patients.
 Parotid swelling - Unilateral or Bilateral
 Pain over gland, ear pain 2.2. Symptoms & signs –
 Low-grade fever
 Severe Pain
 Arthralgia
 Swelling over parotid
 Malaise
 Tenderness
 Headache
 Indurations of gland
 Erythema of skin and oral mucosa
 Fever.
2.3. Management–
 Appropriate antibiotics – Ampicillin /
Amoxycillin 500 mg three to four times daily
(25mg/kg/day for pediatric patients for 5 days)
 Adequate hydration
Fig 3.1 Showing unilateral and bilateral Parotitis
 Oral antiseptic gargles
1.2. Complication -  Good Oral hygiene
 Warm compression over gland
 Orchitis with painful and tender testis,
 Aseptic Meningitis or Meningoencephalitis may  Bimanual massage to milky purulent discharge /
occur with or without the salivary gland calculi from the gland
involvement,  Stone in the distal duct - can be manually
 Unilateral sensorineural hearing loss, expressed & removed by pushing in mouth
 Other Complications-Thyroiditis, Myocarditis, opening of gland
Nephritis and Arthritis.  Abscess drained out with a small incision.
1.3. Investigation -  Organized abscess to be confirmed by
Sialography, CT scan or USG. Needs open
 Haemagglutination inhibition test surgical intervention.
 Complement fixation test
 Surgical drainage: Elevation of anteriorly based
1.4. Treatment - flap over super facial parotid fascia, Parallel to
branches of facial nerve with placement of
 Supportive Measures - Bed rest, adequate
external drain.
hydration, Antipyretics
 Prevention –MMR (Mumps, Measles, Rubella)  Rule out tumor mass by CT/MRI before surgical
vaccine at 12-15 months of age excision.
Page 397
Fig 3.2 Parotid swelling in Acute Parotitis
Bibliography
2. Bhargava KB, Bhargava SK, Shah TM. A Short Textbook of E.N.T. Diseases. 10th ed. Mumbai: Usha
Publications; 2014.
Further reading
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Page 398
4. FURUNCLE
1. Definition:  Tragal cartilage area tenderness
Infection of root of hair follicle usually caused by  Otoscopy- swelling in ear canal
Staph aureus. This infection occurs in cartilaginous  Post auricular lymphadenitis (swelling)
ear canal.
4. Investigation:
Hb, CBC, Blood sugar & culture & sensitivity test
of discharge/pus.
5. Treatment:
5.1 Local:
Packing the ear with antibiotic ointment
Fig 4.1 Ear canal showing furuncle

5.2 Systemic:
 Antibiotics
2. Symptoms: Ampicillin/Amoxicillin 500 mg thrice daily
 Severe earache (25mg/kg/day) for pediatric patients for 5 days
 Movement of pinna painful or Amoxiclav 625 mg BD in adult for 5 days
 Blocking sensation  Analgesics (Diclofenac 50mg BD for 5 Days)
In case of Recurrent furunculosis: rule out Diabetes

3. Signs:
Bibliography
Publications; 2014.
Further reading
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Page 399
5. OTO-MYCOSIS
(mopping or suctioning)
1. Definition:
 Antifungal ear drops (Clotrimazole /
Fungal infection of ear canal caused by fungus like
Flucanozole 2 drops TID for 5 Days)
Candida albicans or Aspergillus Niger.
 Analgesics Tab Diclofenac 50 mg bid for 5
2. Symptoms & signs: days.
 Severe irritation and itching in the ear  Application of gentian violet, Treatment of
diabetes (If associated)
 Severe earache,
 Whitish wet paper like discharge (Candida), 4. Preventive:
 Black spores (Aspergillus) or combination of Keep ear dry, Avoid swimming in polluted water,
both fungi. Care in rainy season.
3. Treatment:
 Removal of fungal debris by ear toileting
Fig 5.1 Mixed fungal infections over the eardrum

Bibliography
Publications; 2014.
Further reading
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Page 400
6. NECK SWELLING
Differential diagnosis depends on swelling occupying 3. Soft: infection /inflammation
particular (Anterior & Posterior) triangle of neck.
4. Matted: Tuberculosis
1. Classification:  Pain:
Cervical lymph nodes: classified into 7 groups
o Present- acute inflammation
Level IA: submental
o Absent-granulomatous disease or malignancy
Level IB: submandibular
 Size: rapid increase –malignancy
Level II: upper jugular
Level III: middle jugular 3. Diagnosis:
Level IV: lower jugular  Blood investigations: CBC, ESR, HIV
Level V: posterior triangle  Cytology: FNAC (Fine Needle Aspiration

Level VI: pretracheal, prelaryngeal Cytology) Chest X-ray, Ultrasound
Level VII: mediastinal  CT/MRI
 Lymph node diagnostic excision biopsy
4. Treatment:
4.1 Antibiotics course for 7 to 14
days
Ampicillin / Amoxycillin 500mg thrice daily
(25mg/kg/day for pediatric patients for 5 days) /
Amoxyclav 625 BD 5 to 7 days and follow up
evaluation
Fig 6.1. Showing classification of neck nodes
according to levels
4.2 Surgical excision of neck
swelling
2. Symptoms and signs:
 Neck swelling-lymph node consistency: 4.3 Malignancy
Search for primary and treat accordingly, as neck
1. Stony hard: malignancy / metastatic
nodes appears secondary (Metastatic) to primary
2. Firm / rubbery: lymphoma malignant focus.
Bibliography
Publications; 2014.
Further reading
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Page 401
7. ATROPHIC RHINITIS
 Aims at maintaining nasal hygiene by removal
1. Definition: of crusts and decreasing putrefied smell due to
Chronic inflammation of nose characterized by
erosion & destruction.
atrophy of nasal mucosa and turbinate bones. The
 Nasal irrigation and removal of crusts – by
nasal cavities become roomy and full of foul-
retracted nasal douching with saline, glucose,
smelling crusts.
and glycerin solution.
 Nasal douching - The patient must be asked to
douche the nose at least daily with Normal
Saline or Alkaline solution [Sodium
Bicarbonate – 1part, Sodium biborate 1 part and
Sodium Chloride – 2 parts (Total 1 spoon
powder) mixed in 280 ml of lukewarm water]
thrice a day till crust disappears.
 25% glucose in glycerin: - After crusts removal
Figure 7.1 Atrophic Rhinitis nose painted with 25% glucose in glycerin twice
a day for 1 month.
 Potassium iodide can be prescribed orally to the
2. Clinical Symptoms and patient in an attempt to increase the nasal
signs: secretion.
 Commonly seen in females and starts around  Placental extract injected submucosally in the
puberty. nose has been attempted with varying degrees of
 Foul smell form nose success.
 Feeling of Nasal Obstruction 3.2. Surgical management:
 Formation of crusts in the nose i. Sub mucous injections of paraffin
 Epistaxis may occur after crusts removal ii. Teflon strips, and autogenous cartilage grafting
 Roomy nasal cavity iii. Wilson's operation - Sub mucosal injection of
 Anosmia 50% Teflon in glycerin paste.
 Atrophy of Nasal turbinates, nasal mucosa looks iv. Young's operation or Modified Young’s
pale and atrophied operation - This surgery aims at closure of one
 Saddle nose deformity (destruction of cartilage) or both nasal cavities by plastic surgery in rare
 Sometimes nasal septal perforation (erosion of cases.
v. Narrowing of nasal cavities by submucosal
cartilage)
injection of Teflon paste, insertion of fat,
cartilage or bone, or medial shift of the lateral
3. Management: wall of nose.
3.1. Conservative:
Bibliography
Publications; 2014.
Further reading
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Page 402
8. NASAL MYASIS
Nasal Myasis commonly known as maggots in the ii. Foul nasal discharge is present.
nose. It is an infestation of the nose by maggots iii. Cellulites of the nose and face may develop.
which are larvae of fly. Maggots are living foreign iv. Fever and toxemia may be present.
bodies in the nose.
1. Causes: 3. Treatment:
i. Removal of maggots by installing Liquid
 Poor hygiene,
paraffin may be used to stifle the worm. Liquid
 Leprosy, paraffin blocks or chokes the lung of the
 Atrophic rhinitis maggots, thereby killing them. The killed
 Other nasal diseases which forms crust with foul worms can easily be removed.
purulent discharge and loss of nasal sensation ii. Turpentine packs can be kept in the nose which
attracts flies to the nose. irritate the maggots. Nasal saline douching is
done for removal.
iii. Surgical procedure: nasal endoscopic complete
2. Clinical Features: removal of the worms & infected parts of nose.
i. Maggots are seen crawling in the nose. They
come out of the nose.
Fig 8.1 Adult house fly Fig 8.2. Stages of Development of Housefly Fig 8.3 Maggots in nasal cavity
Bibliography
Publications; 2014.
Further reading
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Page 403
9. FOREIGN BODIES IN NOSE
1. There are two types of 3. Investigation:
foreign bodies in nose i. Anterior Rhinoscopy gives site of foreign body
in the nose.
i. Non-living: Organic like seeds and grams.
Inorganic like beads, paper or buttons. ii. Nasal endoscopy will locate exact site of the
body.
ii. Living: Maggots.
iii. Xray will detect only radio-opaque foreign
iii. Iatrogenic: Cotton wool, pledgets or swabs may body.
be left behind accidentally.
iv. Commonest occurrence by mishaps in children, 4. Treatment:
age group 0-5 years (self insertion)
(i) Generally Blowing the nose or induction
sneezing may expel the foreign body.
2. Clinical Features:
(ii) Removal of foreign body by Eustachian tube
● History of insertion of the foreign body may be catheter, which is inserted behind the foreign
available from patient/pain in the nose, body, without destructing nasal mucosa &
bleeding. touching F.B. otherwise bleeding may obscure
● Blocking of the nose. visibility. It is performed under local
anaesthesia.
● Sneezing may be present.
(iii) Endoscopy: Under General Anaesthesia
● Unilateral Foul Smelling Blood Stained
Discharge – one should suspecte old foreign
body in the nose.
Fig. 9.1. Foreign body impacted in nose Fig. 9.2 Nasal polyp can be mistaken for foreign body in nose
Bibliography
Publications; 2014.
Further reading
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Page 404
10. DEVIATED NASAL SEPTUM
1. Introduction: 3. Investigation:
The septal deformities are of the following types: - History, examination of the nose by anterior
rhinoscopy & posterior rhinoscopy. X Ray PNS
i. Deviations are smooth deflections which are
waters view / CT scan PNS.
upper or lower, anterior or posterior. i.e. C-
shaped deviation.
4. Treatment:
ii. Spurs are isolated thickenings at the junction
of the bone and the cartilage. Required only if the patient has persistent or
recurrent symptoms due to the deviated septum or
iii. Thickening may result from trauma leading to blockage of nose. Permanent relief is obtained by the
overriding of the cartilaginous fragments, Submucous Resection of the Nasal Septum or
which grow later in double layers. Septoplasty sugery.
iv. Dislocation: The anterior edge of the septal 4.1. Sub mucous resection of nasal
cartilage may be displaced to one side causing
the widening of the columella of the nose. septum:
v. S Shaped Deformity. Indications for sub mucous resection of nasal septum:
vi. Bony posterior deformity of vomerine/  Marked septal deviation occurring behind the
ethmoid bone. vertical line passing between the nasal processes
of the frontal and maxillary bones. This
2. Clinical features: deviation must be the cause for the patient's
symptoms.
 Unilateral or bilateral blocking of the nose.
 Closure of septal perforations.
 Headache due to sinusitis.
 Source of grafting material.
 Recurrent Colds.
 To obtain surgical access in hypophysectomy,
 Epistaxis. and vidian neurectomy.
 Anosmia.
4.2. Septoplasty:
 External deformity associated with deviation of
Indicated as tailor-made operation without disturbing
the septum.
nasal mucosa of other nasal fossa, where only
obstructing part is removed. It can be associated with
Rhinoplasty surgery.
Fig 10.1 Nasal Septum deviation and its types
Page 405
Bibliography
Publications; 2014.
Further reading
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Page 406
11. NASAL OBSTRUCTION
 Radiological: X Ray PNS / CT PNS region
1. Introduction:
The common causes of Nasal obstruction are DNS, 4. Management:
Nasal polyps, Hypertrophied turbinate & Old nasal
foreign body like rhinolith. 4.1. Medical:
 Local nasal decongestants Xylometazoline 0.1
% 2 drops BID for 3 days,
2. Clinical feature:
 Nasal obstruction, nasal stuffiness, watery  Local nasal steroid spray like Fluticasone once
discharge if associated with polyp. daily, Antibiotics (Ampicillin / Amoxicillin 500
mg thrice daily / Amoxicillin + Clavulanic Acid
 Partial or total loss of sense of smell
625 mg BD (5 to 10 mg/kg of body weight for
 Headache, sinusitis, epistaxis, external nasal Paediatric patients for 5 days), Antihistaminic
deformity (Cetirizine 5mg BD for 7 days)
3. Investigations: 4.2. Surgical:

 History, examination of the nose by anterior  Nasal polypectomy
rhinoscopy, posterior rhinoscopy & functional  Turbinoplasty, Turbinectomy
nasal endoscopy (FESS).
 Septoplasty
 Cottles test used to check the nasal obstruction
is due to abnormal nasal valve.  Endoscopic sinus surgery
Fig 11.1 Hypertrophied turbinate Fig 11.2 Nasal polyp causing nasal obstruction
Bibliography
Publications; 2014.
Further reading
2. Indian Pharmacopoeia Commission. National Formulary of India (NFI). 4 th ed. India: Government of India,
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Page 407
12. TONSILLITIS
1. Acute tonsillitis 2. Chronic tonsillitis

1.1 Definition: 2.1 Definition:
It is acute infection/ inflammation of palatine tonsils. It is chronic inflammation/ infection of palatine
tonsils.
1.2 Pathological types: It is characterized by recurrent episodes of acute
a. Acute parenchymal tonsillitis tonsillitis. A history of 3-4 episodes of acute
b. Acute follicular tonsillitis tonsillitis in a year should be labelled as “Chronic
c. Acute membranous tonsillitis tonsillitis”
1.3. Clinical features: 2.2. Clinical features:

1.3.1 Symptoms- 2.2.1 Symptoms:
 Sore throat,  Recurrent history of sore throat, Odynophagia
and fever with symptom free interval between
 Difficulty in swallowing, the two attacks
 Fever, malaise, headache may be present,  Halitosis
 Pain may be referred to the ears.  Change of taste
1.3.2 Signs:  Dry cough: Hawking due to irritation in throat.

 Patient may look toxic and febrile.  Failure to thrive: Seen in children
 Tonsils are enlarged and congested; may be
studded with follicles or membrane. (Scanty pus 2.2.2 Signs:
may come out)  Tonsils may be enlarged (Parenchymatous type)
 Anterior pillars are congested or Fibrotic and small (Fibrotic type)
 Tongue is coated  Yellowish cheesy material is seen in tonsillar
crypts which oozes out when the tonsils are
 Jugulodiagastric lymph nodes are enlarged and pressed by tongue depressor.
tender.  Enlarged Jugulodiagastric lymph nodes.
 Occasionally, yellowish cystic swelling
1.4 Treatment: (retention cyst) may be seen on the surface of
 Bed rest, tonsil.
 Soft, bland & warm diet,  Redness of the anterior pillar
 Avoid cold, oily, spicy food,
 Antibiotics for 5-7 days: Amoxicillin 500mg-3 2.3 Investigation:
times/day, Amoxicillin with Clavulanic acid Hematological: Hb%, CBC, ESR, BT, CT, PT
X-ray neck lateral view for adenoiditis & X-ray chest
625 mg twice/day x 5 days,
for preoperative evolution.
 Anti-inflammatory analgesics to reduce pain,
fever and inflammation: Ibuprofen with
2.4 Treatment:
Paracetamol (200+325) mg 2 times/day x 5 days
 Tonsillectomy by dissection method under
 Antiseptic gargles General Anesthesia.
 Multivitamins orally BD x 5days.
Page 408
Fig. 12.2 Acute staphylococcal
Fig. 12.1 Multiple follicles on the medial pseudomembranous tonsillitis with unilateral
surface of both the tonsils and signs of hypertrophy of the right tonsil
acute inflammation
Bibliography
Publications; 2014.
Further reading
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Page 409
13. ADENOIDITIS
 Cervical lymphadenopathy
1. Introduction:
Inflammation of adenoids is called Adenoiditis.
2.4 Facial features: (Adenoid
Facies)
Adenoids are also called as nasopharyngeal tonsils. It
 Pinched Nose
is group of lymphoid tissue situated at the junction of
the roof and posterior wall of nasopharynx. Adenoids  Mouth Breathing
usually atrophy by the age of 13-14 (puberty).  Dribbling of Saliva
However, in some patients it may be hypertrophied  Flat nasal arch
and produce symptoms, then treatment is required.  Malar hypoplasia
 High arched palate
2. Symptoms:  Crowded and protruding teeth
Symptoms and signs occur due to the following:
 Elongated face
2.1 Due to nasal obstruction-  Dull’ idiotic’ appearance
 Mouth breathing  Loss of nasolabial fold
 Snoring  Short protruding upper lip
 Drooling of saliva
 Difficulty in breathing 3. Investigations:
 Change of voice X ray soft tissue nasopharynx: It shows enlarged
 Rhinitis and sinusitis adenoids and compression of airway.
4. Treatment:
2.2 Due to Eustachian tube 4.1 Medical Treatment
obstruction:
 Ear pain Acute infection is treated with:
 Retracted Tympanic Membrane and conductive  Antibiotics: Antibiotics of choice are-
hearing Loss Amoxycillin 500mg TID, Amoxycillin with
 Recurrent attacks of Acute Otitis Media & Clavulanic acid 625mg BD for 5 days.
 Anti-inflammatory agents like Ibuprofen 200mg
Chronic Otitis Media
BD for 5 days
 Serous Otitis Media in children  Nasal decongestants: Xylometazoline 0.05%
(Adult: 0.1%)
2.3 General symptoms and signs  Antihistaminic: Levocetrizine 5 mg OD for 5
 Recurrent sore throat days
 Dysphagia 4.2 Surgical treatment:
 Malnutrition Adenoidectomy under G.A.
 Mental dullness
 Nocturnal enuresis
Fig 13.1 Adenoids Fig 13.2 Adenoid faces
Page 410
Fig 13.3 Surgical removal of Adenoids
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Bibliography
Publications; 2014.
Further reading
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Page 411
14. PERITONSILLAR ABSCESS (QUINSY)
tonsillar region. Cervical Iymphadenopathy is
1. Introduction: commonly seen.
It is collection of pus in the peritonsillar space which
is in between the capsule of tonsil and the superior 4. Investigation:
constrictor muscle.
As mentioned in chronic tonsillectomy section.
It usually follows acute tonsillitis.
5. Treatment:
5.1 Medical management:
These are generally due to septicemia and resemble
any acute infection. Symptoms like fever, chills & IV antibiotics Inj. Ampicillin 500mg 12 hourly for 5
rigors, general malaise, body aches, headache, nausea days, IV fluids, and analgesics like Paracetamol 500
and constipation are present. Local symptoms like mg bid for 5 days, good oral hygiene
unilateral severe throat pain, odynophagia, muffled
thick speech like hot potato voice. Foul breath, 5.2 Surgical Management:
Ipsilateral earache, trismus.  Incision and drainage of abscess (I & D)
3. Examination findings:  Interval tonsillectomy
On examination tonsil, pillars & soft palate on the
involved side are congested and swollen, uvula is
swollen and edematous, bulging of the soft palate and
anterior pillars. Mucopus may be seen covering the
Fig 14.1 Site of incision for drainage of Fig 14.2 Inflamed peritonsillar space with
peritonsillar abscess. abscess
Bibliography
Publications; 2014.
Further reading
Page 412

Page 413
15. ACUTE PHARYNGITIS
 Ulcerative pharyngitis:
1. Definition: Ulceration and sloughing of the posterior
It is acute infection / inflammation of pharynx.
pharyngeal wall. It is rare and may occur in
immune compromised patients.
2. Etiology:  Granular pharyngitis:
Red granulations over the posterior pharyngeal
a. Infective wall. (due to hypertrophied lymphoid tissue)
b. Associated with Tonsillitis, Rhinitis, Sinusitis.
4. Treatment:
c. Associated with Gastro-oesophageal reflux.
 Bed rest and improvement of oral hygiene.
3. Clinical features:  Soft bland diet with plenty of fluids
 Antibiotics: Antibiotics of choice are.
3.1. Symptoms- Amoxicillin 500mg 3 times/day x 5,
 Sore throat or raw sensation in throat with Amoxicillin with Clavulanic acid 625 BD x
halitosis 5days.
 Fever, malaise  Antacids: Tab. Ranitidine 150 mg/Cap.
 Odynophagia (Pain during swallowing) Omperazole 20 mg daily in case of reflux.
 Dry, irritating cough  Anti-inflammatory agents like Diclofenac and
Paracetamol (50+325mg) BD x 5days.
3.2. Signs-  Antiseptic Gargles like Betadine or
 Catarrhal pharyngitis: Chlorhexidine.
Edema, congestion and inflammation of
posterior pharyngeal wall and soft palate
Bibliography
Publications; 2014.
Further reading

Page 414
16. HOARSENESS OF VOICE
1. Introduction: 4.1.1 Things to do
 Rest to the voice
Hoarseness is term used to describe changes in voice  Drink plenty of water
quality. It results from changes in vocal cords.
A hoarse voice is rough and unpleasant, and it results 4.1.2 Things to avoid
from Lesions of the vocal cords. The causes of  Tobacco
hoarseness may range from innocent Acute  Shouting
Laryngitis to Laryngeal Diphtheria and Malignancy.  Drinking alcohol
 Trying to talk excess when there is cold or
2. Evaluation of hoarseness: laryngitis
 Whispering loudly or for very long
In the absence of upper respiratory tract infection any
 Trying to change naturally speaking voice
patient with hoarseness persisting for more than two
weeks needs evaluation.
4.1.3 Voice therapy
3. Physical examination: Maladaptive vocal habit and techniques are replaced
with appropriate use of vocal mechanism.
i. Thorough head and neck examination. If not responded to this then surgery may be advised.
ii. Assessment of hearing acuity.
iii. Upper airway mucosa, tongue mobility. Cranial 4.2. For organic causes
nerve examination. Treatment of the cause, mostly surgical interventions,
iv. Laryngeal examination. followed by speech therapy
a. Indirect laryngoscopy
b. Flexible nasolaryngoscopy 4.3. For psychogenic causes
c. Strobolaryngoscopy Provide counselling on how to cope with emotional
v. Examination for signs of systemic disease such and stressful conditions.
Give speech therapy to patient.
as Hypothyroidism or neurologic dysfunction
such as Tremors or Parkinson’s disease.
4. Treatment:
4.1. For habitual dysphonia
Treatment is by prevention by easing vocal abuse.
Bibliography
Publications; 2014.
Further reading

Page 415
17. STRIDOR
5. May have difficulty in deglutition,
1. Definition: 6. Change in voice
It is an auditory manifestation of disordered
respiratory functions due to airflow changes within 4. Investigation:
larynx, trachea or bronchi.
 Xray neck lateral view,
It may be-
 X-ray chest,
1. Inspiratory- when obstruction is at the level of
supraglottis and above.  Direct laryngoscopy,
2. Expiratory- when obstruction is at the level  Bronchoscopy &
bronchioles.
3. Biphasic- i. e. Both during inspiration and  C.T.scan to find out cause & level of stridor.
expiration and obstruction is at the level of
trachea or sub glottis. 5. Treatment:
2. Types: 5.1. General measures:
1. Congenital 1. Humidified oxygen
2. Acquired 2. Steroids (Prednisolone up to 40mg/day x 7 days.
3. Antibiotics- Ampicillin 500mg TDS x 5days
3. General features of stridor: 4. Intubation or tracheostomy is indicated if stridor
is severe to relieve airways obstructions
1. Stridor is not a disease but a symptom or sign,
2. Noisy breathing which may be wheezing, 5.2. Surgical
crowing, whistling, croaking, sighing, rattling or
snoring, With the help of investigation, cause & level to be
3. Cough, find out & depends upon that cause, surgical
4. Hoarseness, intervention is needed.
Bibliography
Publications; 2014.
Further reading

Page 416
18. FACIAL PALSY (BELL'S PALSY)
 X-ray studies, blood test- CBC, ESR, blood sugar
1. Introduction: and serology
It is an Idiopathic condition leading to peripheral facial  Nerve conduction & excitability tests to monitor
paralysis or paresis, which is of acute onset. nerve degeneration
 Topodiagnosis - localize site of lesion
High Risk cases of Bell’s palsy are diabetics and
pregnant women. 5. Treatment:
2. Causes: 5.1 General –
Reassurance, pain relief by analgesics (Tab. Diclofenac
Viral infection due to herpes simplex, herpes zoster or 50 mg BD for 7 days), eye care, physiotherapy, massage
E.B. virus & other condition leading to external pressure of facial muscles, use of eye pads.
on facial canal.
Acyclovir - 200 - 400 mg 5 times a day for 5-7 days
5.2 Medical –
 Sudden onset  Steroid therapy: Prednisolone 1 mg/kg per day in
 Patient is unable to close his eyes completely a divided doses for 5 days, if paralysis recovers
with the dose of prednisolone, then it is tapered for
 Dribbling of saliva from angle of mouth (weakness next 5 days, if paralysis remains the same dose
of angular oris muscle) continued for next 10 days and thereafter tapered
in next 5 days
 Face becomes asymmetrical
Contraindications for Steroid therapy - Pregnancy,
 Epiphora - Tears flow down from the eye Diabetes, Hypertension, Peptic ulcer, Pulmonary
Tuberculosis and Glaucoma.
 Pain in the ear  Ascorbic acid 500 mg Once a day for 7 days
 Noise intolerance due to stapedial paralysis  Multivitamins –
Vitamin B1, B6, B12 1 b.i.d for 7 days
 Loss of taste due to involvement of chorda
tympani.
5.3 Surgical Treatment -
4. Investigation &Diagnosis:  If there are no signs of recovery within 7 days,
then opt for surgical intervention.
 It requires careful history, complete otological and
head and neck examination  Facial nerve decompression exploring fallopian
canal where facial nerve is encased to release
pressure.
Fig 18.1 Bell's Facial Palsy
Page 417
Bibliography
Publications; 2014.
Further reading

Page 418
19. SENSORINEURAL HEARING
LOSS AND ITS MANAGEMENT
Early detection of SNHL is important as measures
1. Sensorineural hearing loss can be taken to stop its progress, reverse it or to start
(SNHL) an early rehabilitation & interventions.
Result from lesions of the cochlea, VIII nerve &
central auditory pathways. It may be present at birth
2. Specific forms of hearing
(congenital) or start later in life (acquired). loss
1.1. The characteristics of 2.1 Inflammations of labyrinth
sensorineural hearing loss are: i. Viral labyrinthitis
ii. Bacterial
 A positive Renne test i.e. AC>BC. (Bone
iii. Syphilitic
conduction impaired)
 Weber test lateralized to better ear (better 2.2 Ototoxicity
hearing ear). i. Amino glycoside antibiotics - Neomycin,
 ABC test: Bone conduction reduced on absolute Kanamycin, Amikacin, Streptomycin, and
bone conduction tests. Dihydrostreptomycin are cochleotoxic drugs
with Selective destruction of outer hair cells
 More often involving high frequencies. ii. Patients particularly at risk are those having
 No gap between air and bone conduction curve impaired renal function.
an audiometry. iii. Diuretics- Frusemide and Ethacrynic acid
 Loss may exceed 60 dB. iv. Salicylates - Symptoms of salicylate ototoxicity

are tinnitus and bilateral sensory neural loss.
 Speech discrimination is poor. (Hearing loss particularly affecting higher
frequencies.)
 There is difficulty in hearing in the presence of
noise. v. Quinine - Ototoxic symptoms due to Quinine
are Tinnitus and Sensorineural hearing loss
1.2. Diagnosis: vi. Chloroquine - Effect is similar to that of
 History Quinine and permanent deafness can result.
 Duration of illness - sudden or slowly vii. Cytotoxic drugs - Nitrogen mustard, Cisplatin
impairment or since birth. and Carboplatin can cause cochlear damage.
 Severity of deafness viii. Miscellaneous - Erythromycin, Ampicillin,

Chloramphenicol, Ibuprofen, Indomethacin,
 Type of audiogram, whether loss is high Phenylbutazone, Tetanus antitoxin, Propranolol,
frequency, low frequency, mild Frequency or Propylthiouracil, Alcohol, Tobacco &
flat type. Marijuana also cause damage to the inner ear
 Site of lesion i.e. cochlear, retro cochlear or ix. Topical Eardrop - Chlorhexidine drop
central by BERA test. containing amino-glycoside antibiotics. E.g.
Neomycin, Framycetin & Gentamycin.
 Brainstem Evoked Response Audiometry
(BERA) helpful in profound sensorineural loss. 2.3 Noise Trauma –
1.3. Management: Hearing loss associated with exposure to noise has
been well known in boiler operators, iron &
coppersmiths & artillerymen. Lately, noise trauma
has assumed greater significance because its being an
Page 419
occupational hazard, the compensation asked for & iii. Vascular – Hemorrhage, Embolism or
the responsibilities thrust upon the employer & the Thrombosis of labyrinthine or Cochlear artery
employee to conserve hearing. High level of sound or their vasospasm.
pollution, use of speaker walls leads to Noise trauma. iv. Ear (otologic) - Meniere's disease, Cogan's
syndrome
TYPES
v. Toxic - Ototoxic drugs.
1) Acoustic Trauma-Very high sound decibel level vi. Neoplastic - Acoustic neuroma. Metastases in
for short duration cerebellopontine angle, carcinomatous
neuropathy.
2) Noise Induced Hearing Loss- Over period of
time 2.4.3 Management -
2.4 Sudden Hearing Loss  Bed rest.
 Steroid therapy- Prednisolone 40-60 mg in a
2.4.1 Definition: single morning dose for one week & then tailed
It is defined as Sensory neural hearing loss that has off in a period of 3 weeks.
developed over a period of hours or a few days. Loss  Inhalation of carbogen- (combination of CO2 &
may be partial or complete. Mostly it is unilateral. it O2) It increases cochlear blood flow & improve
may be accompanied by tinnitus or temporary spell oxygenation.
of vertigo.  Low molecular weight Dextran
 Hyperbaric Oxygen therapy
2.4.2 Etiology –
2.4.4 Prevention aspects-
Most often the cause of sudden deafness remains
obscure, in which case it is called the idiopathic  Immunization of child & ANC mothers.
variety.  Avoidance of ototoxic drugs.
 Use of driving safety gadgets.
i. Infection - Mumps, Herpes zoster, Meningitis,
 Ear infection prevention & treatment in time
Encephalitis, Syphilis, Otitis media.
ii. Trauma - Head injury, Ear operations, Noise  Avoiding sound pollution areas
trauma, Barotraumas, Spontaneous rupture of
cochlear membrane.
Bibliography
Publications; 2014.
Further reading

Page 420
20. VERTIGO
1. Definition: 2.2.2 Central Vestibular Disorder
Revolving around or spinning around. i. Vertebrobasilar insufficiency
ii. Posterior inferior cerebellar artery syndrome
2. Disorder of vestibular iii. Basilar migraine
system cause vertigo & is iv. Cerebellar disease- Cerebellum may be affected
divided into: by hemorrhage infraction, infection or tumours.
v. Multiple sclerosis - It is a demyelinating disease
2.1 Peripheral– affecting young adults. Vertigo & dizziness are
Which involve vestibular end organs & their first common complaints.
order neurons. The cause lies in the internal ear or the vi. Tumours of brainstem & floor of IV ventricle -
8thnerve. They are responsible for 85% of all cases of Gliomas, astrocytomas may arise from pons &
vertigo. midbrain, epidermoid cysts or teratomas may
arise from floor of IV ventricle.
2.2 Central –
vii. Epilepsy
Which involve central nervous system after the
entrance of vestibular nerve in the brainstem and viii. Cervical vertigo - Vertigo may follow injuries
involve vestibulo-ocular, vestibulo-spinal and other of neck 7-10 days after the accident
central nerves system pathways.
3. Investigations:
2.2.1 Peripheral Vestibular Disorders
i. Meniere's disease (endolymphatic hydrops) -It 3.1 Examination:
is characterized by trio of vertigo, fluctuating 3.1.1 History:
hearing loss, tinnitus with sense of pressure in
the involved ear. Vertigo is of sudden onset, History of dizziness, giddiness, deafness, tinnitus,
lasts for a few minutes to 24 hours otorrhoea, systemic & neurological symptoms. Past
history of Giddiness, Injury, Diabetes, Hypertension,
ii. Benign paroxysmal positional vertigo (BPPV) Medication and Surgery should be noted. History of
It is related to positional changes. Certain tobacco and alcohol consumption should be noted.
provoked position leads to attack of vertigo.
3.1.2 Otoscopy:
iii. Vestibular neuronitis
iv. Labyrinthitis  For attic perforation with cholesteatoma to be
rule out.
v. Vestibulotoxic drugs - Drugs like Gentamycin
& Amikacin cause ototoxicity by damaging the  Blood pressure measurement, CVS & CNS
hair cells of the inner ear. exam includes tests for co-ordination, gait, past-
pointing test, Romberg's test and corneal
vi. Head Trauma - Head injury may cause reflexes.
concussion of labyrinth, completely disrupt the
bony labyrinth or VIII nerve or cause a 3.2 Ear Function Test:
perilymph fistula.
(i) Hearing test tuning forks test, Audiometry etc.
vii. Perilymph fistula
(ii) Labyrinthine tests: Caloric test,
viii. Syphilis Electronystagmography (ENG)
ix. Acoustic neuroma - It has been classified in
peripheral vestibular disorders as it arises from 3.3 X-Ray
CN VIII within internal acoustic meatus Mastoid, cervical spine and skull
Page 421
position. (Dix Hallpike manoeuvre). It will
cause vertigo and nystagmus. Wait till vertigo
3.4 Lab investigations and nystagmus subside.
 CBC with Hb%
 Glucose tolerance test for Diabetes Mellitus  Position 2 - Head is now turned so that affected
 Serum cholesterol ear is up.
 V.D.R.L  Position 3 - The whole body and head are now
 Thyroid Function tests. rotated away from the affected ear to a lateral
recumbent position in a facedown position.
3.5 Electrocardiogram  Position 4 - Patient is now brought in a sitting
position with head still turned to the unaffected
3.6 CT Scan & M.R.I. of the head side by 45 degrees.
 Position 5- the head is now turned forward and
4. Management: chin brought down 20 degrees.
There should be a pause at each position till there is
4.1 Medical: no nystagmus or there is slowing of nystagmus,
before changing to the next position. After
 Reassurance regarding the nature of the disease, manoeuvre is complete, patient should maintain an
no jerks, avoidance of provocative posture upright position for 48 hours. Eighty percent of the
 Labyrinthine sedatives like Prochlorperazine patients will be cured by a single manoeuvre. If the
5mg BD for 7 days patients remain symptomatic, the manoeuvre can be
 Vasodilators like Cinnarizine 25/75 mg BD for repeated. A bone vibrator placed on the mastoid bone
7 days or vestibular sedatives like Betahistidine helps to loosen the debris.
8/16 mg BID for 7 days or for a long time.
 Vitamins like B1, B6 and B12 can be used in 4.3 General:
supplementary doses Smoking and alcohol should be avoided.
 Diuretics (Frusemide 20/40Mg for 3 to 5 days)
and low salt diet for reducing the tension of 4.4 Surgical:
endolymph.
i. Operations, which reduce the tension of
4.2. Labyrinthine Exercises are endolymph
helpful in regaining the ii. Vestibular nerve section.
confidence of the patient:
iii. Labyrinthectomy
4.2.1 The manoeuvre consists of five positions.
 Position 1 - With the head turned 45 degrees,
the patient is made to lie down in head hanging
Bibliography
Publications; 2014.
Further reading

Page 422
21. FRACTURE NASAL BONE
1. Introduction: 4. Investigation:
Two, all pieces of nasal bone present on nasal bridge  Imaging study like X-ray nose lateral view, X-
which usually get fractured in Head and Facial ray PNS, CT scan.
trauma, assault, RTA, sport or industrial accident.  Anterior & Posterior rhinoscopy
 Routine Biochemical & Serological Laboratory
2. Symptoms and Signs: Test.
 Preinjury photographs if available.
 History of Trauma
 Nasal deformity with swelling. 5. Management:
 Pain
 Bleeding nose 5.1. Medical:
 Nasal blockage  Head up position, cold compression to reduce
 Discoloration of nasal skin oedema.
 Suturing of open wound
3. Signs:
 Anti inflammatory drug (Tab. Diclofenac 50 mg
 Epistaxis (active or clots in nasal cavity) BD x 7 days).
 Crepitus on palpation over nasal bone area.
 Deformity  Antibiotics (Amoxycillin 500mg TID x 5 days
or Parenteral Amoxyclav 1.2gm I.V. 12 hourly)
 Oedema on and around nose
 Nasal obstruction. 5.2. Surgical:
 Associated traumatic injury
 Closed reduction under General Anesthesia with
 Black eye septal elevation.
 Open reduction with wiring in case of multiple
fractures.
Bibliography
Publications; 2014.
Further reading

Page 423
22. FRACTURE MAXILLA
1. Introduction: 5. Types of Maxillary fracture:

Maxillary bones are present on either side of nose &  Le fort I - Floating fracture
are part of skull bone. Fracture maxillary bone occurs
in Head and Facial trauma, assault, RTA, sport or  Le fort II – Midlevel / sub zygomatic fracture
industrial accident.  Le fort III - Craniofacial fracture at supra
zygomatic, zygomaticomaxillary complex
2. Symptoms: fracture or Tripod fracture.
 History of trauma
 Nasal deformity with swelling.
6. Management:
 Pain 6.1 Emergency care -
 Bleeding nose
 Airway maintenance,
 Nasal blockage
 Discoloration of nasal skin  Control of oral & nasal bleeding.
6.2 Medical Management -

3. Signs:
 Includes emergency care & stabilization of
 Epistaxis (active or clots in nasal cavity) general condition.
 Crepitus on palpation over nasal bone area.
 Anti inflammatory drug (Tab. Diclofenac
 Deformity
500mg BD x 7 days.
 Oedema on and around nose
 Nasal obstruction.  Antibiotics (Amoxicillin 500mg t.i.d. x 5 days
or Parenteral Amoxiclav 1.2 gm IV 12 hourly.
 Associated traumatic injury
 Black eye 6.3 Surgical-
Multi disciplinary approach with involvement of
4. Investigation: ENT surgeon, Maxillofacial surgeon &
 Imaging study like X-ray nose lateral view, X- Neurosurgeon may be needed depending upon types
ray PNS, CT scan PNS. & severity of fracture.
 Anterior & Posterior rhinoscopy
 Routine Biochemical & Serological Laboratory
Test.
Page 424
Figure 22.1 Flowchart of fracture involving Maxilla
History of Trauma to Face: Le fort I/ Floating fracture

Assault 1. Vitals
RTA 2. Check for ventilation/Circulation
3. Mobility of maxillary alveolar segment (floating
Gunshot wounds fracture)
Sports 4. Pain and tenderness while speaking or
Falls clenching
Industrial accidents 5. Ecchymosis or laceration in labial or buccal
vestibule
Any Other 6. Swelling and oedema of upper lip
7. Mal occlusion
8. Bilateral epistaxis
9. Bruising of palatal tissues (15-20% of cases)
10. On palpation tenderness over buttress area
Suspect Fracture Involving Maxilla 11. Percussion of teeth – cracked pot sound
Le fort II/ Pyramidal fracture/ Mid level

i. Zygomaticomaxillary fracture/ Subzygomatic fracture
complex # (tripod fracture) 1. Oedema mid third of face (Moon face) (Panda faces)
2. Paresthesia of cheek
Le Fort – I, II, III # 3. Bilateral circumorbital ecchymosis
ii. Zygomatic arch # 4. Bilateral subconjunctival hemorrhage
iii. Alveolar process of maxilla # 5. Dish face deformity
iv. Smash fractures # 6. Depressed nose
7. Epistaxis
8. CSF rhinorrhea
9. Limited ocular movement (Diplopia)
10. Mal occlusion
11. Inability to open mouth
12. Percussion of teeth – cracked pot sound
Le fort III/ Craniofacial dysfunction/

High level fracture/ Suprazygomatic
fracture
1. Oedema of face (Panda faces)
2. Bilateral periorbital edema
Emergency Care: 3. Bilateral circumorbital ecchymosis (Raccoon eyes)
1. Airway immediately evaluated for obstruction 4. Bilateral subconjunctival hemorrhage
5. Dish face deformity
6. Depressed nose, flattening of nose
If not maintaining SPO2 - ETT / Tracheostomy 7. Epistaxis
8. CSF rhinorrhea
If Cervical Spine fracture - No endotracheal intubation 9. Limited ocular movement (Diplopia, Enophthalmos)
10. CSF otorrhoea
Tracheostomy Rather than ETT
11. Mal occlusion – posterior gagging of occlusion
Cervical collar 12. Inability to open mouth
Control of oral or nasal bleeding by- 13. Mobility of fractured fragment at NF, FZ sutures
If active Anterior/ Posterior nasal bleeding -AN / PN 14. Tenderness over zygomatic bone, arch and FZ suture
Packing Ecchymosis at mastoid process (Battle’s sign)
1. Start Secured IV line for Fluids Replacement
Page 425
Bibliography
Publications; 2014.
Further reading

Page 426
23. PENETRATING NECK INJURY
1. Causes: 4. Immediate Treatment:
 Gunshot
 Securing Airway by neck stabilization &
 Stab endotracheal intubation if necessary
 Penetrating shrapnel with or without speed.  Maintaining Breathing
 Maintaining Circulation
2. Levels:
 This requires immediate intervention.
 Includes skin and platysma.
 Includes important structures like major 5. Investigations: any of these, which are
vessels (carotid & jugular vein), trachea, relevant to the case
esophagus, cranial & other nerves.
 CT neck
 Involvement of spine &vertebrae.
 Angiography
3. Look for  Laryngoscopy
 Dysphasia,  Bronchoscopy
 Hoarseness of voice,  GI scopy
 Oropharyngeal bleeding, 6. Treatment:
 Neurological deficit,
 Emergency medical intervention to maintain
 Hypotension, BP through IV fluid, airway maintenance
through plastic airway in mouth or intubation.
 Sub cutaneous emphysema  Surgical intervention includes Hemostasis of
 Air bubbles through wound & tracheal area. major bleeding vessels & operative
management for respective traumatized organ
& treatment of head injury component (If
associated with).
Page 427
Figur.23.1 Flowchart of Penetrating Neck injury
Investigations and surgical referrals
History of: Stab wound
i. Gunshot wounds Penetrating Platysma

ii. stab wounds
iii. penetrating debris e.g. glass or
shrapnel
Primary
survey:
Assess ABC
No airway Potential for

Airway compromise
compromise- airway intervention required:
continue with compromise: Call help and Prepare - for
primary survey Endotracheal surgical airway -
intubation tracheostomy or
Call help from cricothyroidotomy
Look for: ENT/Anesthesia

i. Dysphagia – Tracheal and/or
Consider for OT
esophageal injury Any of the following
ii. Hoarseness – Tracheal and/or 1. Vascular &/or spinal cord injury
esophageal injury (especially 2. Hypotension
recurrent laryngeal nerve) 3. Subcutaneous emphysema
iii. Oronasopharyngeal bleeding 4. Stridor /respiratory distress
– Vascular, tracheal, or 5. Hematoma (expanding)
6. Active external hemorrhage from the wound site
esophageal injury 7. Bruit/thrill
iv. Neurologic deficit – Vascular 8. Pulselessness/pulse deficit
v. Hypotension – Nonspecific; 9. Multi trauma
may be related to the neck
injury or may indicate trauma
elsewhere Soft sign
vi. Subcutaneous emphysema – Dysphagia CT angiography
Tracheal, esophageal, or Hoarseness neck/angiography
pulmonary injury Oronasopharyngeal
bleeding
vii. Air bubbling through the
Laryngeal and/or
Suspicion of airway
esophageal injury
Suspicion for esophageal injury consider
Hematoma (expanding) – injury consider Upper GI bronchofibrescopy/DL
Vascular injury scopy scopy
Active external hemorrhage or barium study or both

from the wound site –

Page 428
Bibliography
Publications; 2014.
Further reading

Page 429
24. BLUNT EXTERNAL LARYNGEAL TRAUMA
(FLOW CHART)

Page 430
Bibliography
Publications; 2014.
Further reading

Page 431
25.EPISTAXIS
 Duration & frequency
1. Definition:
 Site, Side, Type, Any medical disorder
It is defined as bleeding from inside the nose.
 Drug intake
2. Types: 4.2. First aid -
2.1 Anterior– Littles area compression- Pinch the nose with thumb
More common, site of bleeding is littles area, in and index finger for 2 min. & ask the patient to
children and young adults. breath orally.
2.2 Posterior– 4.3 Medical/Surgical Management

 In Anterior Epistaxis anesthetize the bleeding
Less common, site of bleeding is posterior superior
point and cauterize with bead of silver nitrate or
area, seen in adults.
coagulate with electro cautery
3. Causes:  Anterior Nasal packing
 Posterior Nasal Packing
 Endoscopic cauterization
3.1 Local –  If above measures fails, then ligation of vessels.
Injuries to nose, Vascular malformation, Fracture of o External carotid- after the origin of superior
maxilla, Fracture nasal bone, Nasal surgery, Acute thyroid artery
sinusitis, Rhinitis, Nasal diphtheria, Atrophic rhinitis, o Maxillary artery - approached through
Rhinitis sicca, Tuberculosis, Syphilis, Caldwell- Luc operation.
Rhinosporidiosis, Foreign body in nose like maggots, o Ethmoid artery ligation
Deviated nasal septum.
4.4 General Measures
3.2 Nasopharyngeal -  Sit up with back rest
Adenoids, Juvenile angiofibroma, Malignant tumors
 Record blood loss in spitting & vomiting
3.3 General causes -  Reassure
Hypertension, Leukemia, Hemophilia, Aplastic  Mild sedation
anemia, Cirrhosis of liver, Nephritis, patient with
Anti coagulant therapy, Influenza, Chickenpox,  Check vital signs
Malaria.  Maintain hemodynamic-blood transfusion if
required
4. Management:
 Intermittent oxygenation
4.1. Enquire about  Investigate & treat
 Mode of onset
Bibliography
Publications; 2014.
Further reading
Page 432

Page 433
26. PREMALIGNANT LESIONS OF THE ORAL
CAVITY
 Lip: Inspect and palpate inner and outer surfaces
1. Introduction: of the upper and lower lip.
Oral cavity cancer accounts for approximately 3% of  Buccal mucosa
all malignancies and is a significant worldwide health o Inspect and palpate buccal mucosa and cheek.
problem. Most oral malignancies occur as squamous o Inspect and palpate parotid duct to express
cell carcinomas (SCCs); Most of the oral SCCs saliva.
develop from premalignant conditions of the oral  Gingival and alveolar ridge: Inspect and palpate
cavity. The early detection of cancer is of critical gingival and alveolar ridge on facial and lingual
importance because survival rates markedly improve aspects.
when the oral lesion is identified at an early stage  Tongue
(early intervention) o Inspect and palpate dorsal and ventral surfaces
with accompanying retraction of the tongue
2. Types with gauze.
o Inspect and palpate lateral borders from
2.1 Leukoplakia anterior to posterior with manual retraction.
White patch or plaque  Floor of the mouth
o Inspect and palpate floor of the mouth.
2.2 Erythroplakia o Inspect and palpate submandibular ducts to
A fiery red patch with a soft, velvety texture express saliva.
 Hard palate: Inspect and palpate.
2.3 Proliferative verrucous  Soft palate and oropharynx: Depress the dorsal
leukoplakia surface of the tongue and inspect soft palate and
Proliferative verrucous leukoplakia (PVL) is a unique anterior oropharynx.
form of aggressive disease.  Salivary glands: Palpate the parotid,
submandibular, sublingual, and minor salivary
2.4 Palatal lesion of reverse glands. Ensure clear salivary flow.
smokers Extra oral
The palatal lesion of reverse smokers is unique to  Inspect the head and neck.
individuals who place the lit end of a cigarette inside  Palpate cervical lymph nodes and salivary
the mouth. glands
2.5 Oral submucousfibrosis (SMF) 4. Investigations:

It is a chronic progressive condition. In which normal  Biopsy of the lesion and histopathological
mucosa with blood supply is replaced by fibrous diagnosis is the gold standard investigation.
tissue leading to narrow mouth opening.
 Oral cytology
2.6 Other forms: Oral cytology describes a diagnostic technique
Lichen planus, discoid lupus erythematous, and used to sample oral tissue for histopathogical
epidermolysis bullosa. analysis. To obtain a tissue sample, the clinician
applies a stiff brush to the oral mucosa with
3. Work-up and the Early enough pressure to induce pinpoint bleeding,
which ensures a full-thickness or trans-epithelial
Detection of Oral Cancer: tissue sample. These cellular samples can then
The standard criteria for diagnosis and identification be analyzed by a variety of unique diagnostic
of oral lesions is histopathology analysis via the measures including cytomorphometry, DNA
procurement of a tissue sample by surgical biopsy. cytometry, and immunocytochemical analysis.
3.1 Oral cavity examination:
Page 434
Fig. 26.1 Leukoplakia of the buccal mucosa Fig 26.2 Submucous fibrosis involving the
retromolar trigone anterio tonsilar pillars
and soft palate on both sides
 
Fig 26.3 Leucoplakia of tongue Fig 26.4 Leucoplakia of Lips

Bibliography
Publications; 2014.
Further reading

Page 435
27. ACUTE UPPER AIRWAY OBSTRUCTION
dysphonia, aphonia, chocking, drooling
1. Introduction: gagging,
Upper airway consists of nose, nasopharynx,  Signs of hypoxemia and hypercarbia. Anxiety,
pharynx, larynx and trachea up to carina. Different confusion, lethargy and cyanosis may be
pathologies in this area can lead to acute airway present as the obstruction worsen
obstruction.  Powerful inspiratory efforts against an
obstruction may produce ecchymosis and
Obstruction here may be partial or complete. This is
subcutaneous emphysema.
also called as extra thoracic airway. The airway
collapses during inspiration and dilates during
expiration.
3. Management:
3.1. General measures:
2. Clinical presentation  Reverse hypoxia- 100% Oxygen or as close as
possible.
May be partial or complete
 IV access as soon as possible.
2.1. Complete upper air way  Continuous monitoring and observation.
obstruction:
 Universal chocking sign: patient is unable to 3.2 Airway management techniques
breath, speak or cough and may hold the 3.2.1 Airway manoeuvres
throat between the thumb and finger. i. Jaw thrust,
 Vigorous attempts at respiration with ii. Endotracheal intubation,
intercostals and supraclavicular retraction. iii. Oropharyngeal or nasopharyngeal airway may
 Raised Heart rate and raised blood pressure, be useful in the unconscious patient,
Patient becomes rapidly cyanosed. iv. If the patient is not immediately intubated,
 This is followed by diminished respiratory then give coma position i. e. Semi prone,
efforts, loss of consciousness, bradycardia, slightly head down.
and hypotension.
 Cardiac arrest. 3.2.2 Endotracheal intubation.
 Death is inevitable if obstruction is not
relieved within 3-5 minutes. Surgical airway:
 Indicated when endotracheal intubation not
2.2. Partial airway obstruction possible.
 May be stable or their may be progressive  Percutaneous transtracheal jet ventilation.
deterioration  Cricothyroidectomy.
 Signs and symptoms may be mild but as they  Formal tracheostomy under local anaesthesia
worsen patient develops inspiratory stridor, may be tried before emergency tracheostomy.
 Emergency tracheostomy rarely required.
Bibliography
Publications; 2014.
Further reading
Page 436
Ministry of Health and Family Welfare; 2011: pp 314

Page 437
28. DEAF MUTISM
1. Definition: 4. Investigation:
Deaf Mutism is the inability to acquire speech due to  Brainstem Evoked Response Audiometry
profound or high degree hearing loss (congenital or (BERA) - It is of value to find out the threshold
early acquired childhood) of sensory neural type in of hearing in infants, particularly the high risk
both ear. group & in the diagnosis of retro- cochlear
pathology.
 Oto acoustic emission (OAE)
2. Causes:  Audiometric examination
 Free field audiometry
2.1 Prenatal  Visual reinforce audiometry
i. Genetic Defect  Play audiometry
ii. Maternal Infection  Electrocochleography
iii. Drugs During Pregnancy  Impedance audiometry
1. Amino glycosides
 High-resolution CT scan
2. Quinine
3. Chloroquine
iv. Radiation to Mother in first trimester 5. Treatment:
v. Other factors: Nutritional deficiency, diabetes,
toxaemia & thyroid deficiency  Bilateral hearing aid
 Surgical interventions including Cochlear
2.2 Perinatal implant
i. Anoxia  Auditory training
ii. Prematurity  Language communication
iii. Birth injuries
iv. Neonatal Jaundice 6. Referral:
v. Ototoxic drugs
If deaf mutism is suspected after investigation, the
2.3 Post natal - child should be referred to a higher centre for
i. Genetic Cochlear implant.
ii. Non-Genetic
7. Prevention:
3. Identification of Deafness:
Vaccination to child, avoidance of ototoxic drugs,
 History regular antenatal checkup & care.
 Responses of hearing in child by investigations
Bibliography
Publications; 2014.
Further reading
Ministry of Health and Family Welfare; 2011: pp 314

Page 438
Ophthalmology
7. Ophthalmology
1 Lid 439
2 Dacryocystitis 441
3 Conjunctiva 443
4 Cornea / Ulcer 445
5 Sclera 448
6 Uveitis 450
7 Glaucoma 452
8 Cataract 456
9 Ophthalmitis 459
10 Retinal Detachment 461
11 Refractive Error 463
12 Diabetic Retinopathy 467
13 Ocular injuries 469
14 Ocular Emergencies 472
15 Pediatric Ocular Problems 474
16 Low Vision 478
17 Eye Banking 479
1. LID SWELLING
1. Stye (Hordeolum Externum) 2. Hordeolum Internum
1.1 Definition 2.1 Definition
It is an acute suppurative inflammation of the
It is an acute suppurative inflammation of the Zeis /
Meibomian glands.
Moll glands.
Figure 1.2 Hordeolum Internum

Figure 1.1 Stye
2.2 Symptoms
1.2 Etiology Pain, lid swelling and watering.
Bacterial- Staphylococcus
2.3 Sign
1.3 Symptoms A painful swelling at the lid margin.
 Pain
 Lid swelling
2.4 Treatment
 Ciprofloxacin 0.3 % eye drops six times per day for
 Watering
5 days
1.4 Sign  Tablet Ciprofloxacin 500mg (Systemic antibiotics)
twice daily and Tab. Diclofenac sodium 50mg BD
A painful swelling at the lid margin. (anti-inflammatory) for three days.
 The pus should be drained by incising it.
1.5 Treatment
 Hot fomentation 2-3 times per day. 3. Chalazion
 Ciprofloxacin 0.3 % (Antibiotic) eye drops. 1-2 3.1 Definition
drops six times per day for 5 days. It is a chronic granulomatous inflammation of the
Meibomian gland.
 At night time Ciprofloxacin eye ointment for 7
days.
 Tablet Ciprofloxacin 500mg (systemic antibiotics)
twice daily and Tab. Diclofenac Sodium 50mg bid
(anti-inflammatory) for three or four days.
 When pus points out it should be let out by pulling
the affected eye lash – Epilation.
Figure 1.3 Chalazion
Page 439
3.2 Etiology
 Uncontrolled Diabetes Mellitus in adults.
 Refractive errors.
3.3 Symptoms
Swelling of the lid and Watering.
3.4 Sign
Painless nodular swelling away from the lid margin.
3.5 Course
 Spontaneous resolution. Figure 1.4 Blepharitis
 If secondarily infected, then it is called as Internal
Hordeolum. 4.2 Causes
 It may burst through the conjunctiva.  Seborrhoeic Blepharitis due to dandruff at the base
 Very rarely a malignant change may occur of eye lashes.
(Meibomian carcinoma) especially in old age with a  Ulcerative Blepharitis because of infection by
history of recurrence. Staph. Epidermidis / Streptococci.
3.6 Treatment 4.3 Symptoms

 Incision and curettage under Proparacaine 0.5 % Itching / rubbing of eyelids.
eyedrop (local anesthesia.)
 In Marginal chalazion intralesional injection of 4.4 Signs
Triamcinolone 40mg/ml (Depot steroids): 0.1 to 0.2 Edema of lid margin, dandruff /ulcer at the root of eye
ml once may be helpful. lashes.
 Correction of refractive errors, if any.
4. Blepharitis 4.5 Treatment

 Clean the lid margin with warm water 2-3 times a
4.1 Definition day.
Inflammation of the lid margin is called as Blepharitis.  Chloramphenicol- Polymixin B combination
(Ocupol) eye oint. 3 times a day for 3weeks.
If a Chalazion recurs soon after removal or is rapidly growing in size or ulcerates, a biopsy must be done to rule
out any malignancy.
Bibliography
1. Kanski, Jack J. Clinical Ophthalmology: A Systematic Approach. Edinburgh: Butterworth-
Heinemann/Elsevier; 2007.
Further reading
1. Wong BJ, Hong BK, Samrao D, Kim GH, Rao NA. A 49-year-old man with unilateral, non-tender left
eyelid swelling. Digital Journal of Ophthalmology: DJO. 2014;20(1):15-19.
2. Sharma R, Brunette DD. Ophthalmology. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen's
Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Elsevier Mosby; 2009:
Chapter 69

Page 440
2. DACRYOCYSTITIS
ii. Tab. Ibuprofen 3 times a day (Non-Steroidal Anti
1. Acute Dacryocystitis Inflammatory Drug).
1.1 Definition: iii. Hot fomentation 3 times a day.
Acute Dacryocystitis is a suppurative infection in the
lacrimal sac caused by a blocked nasolacrimal duct. iv. Ciprofloxacin 0.3% eye drop one drop four times a
(NLD) day and Ciprofloxacin eye ointment at night time
for 5 days.
v. If there is a pus point, drainage of pus is required.
NO SYRINGING IS DONE IN ACUTE CASES OF
DACRYOCYSTITIS
1.8 Complications:
Acute conjunctivitis, corneal ulcers, lid abscess, orbital
cellulitis, cavernous sinus thrombosis.
1.9 Referral:
Figure 2.1 Acute Dacryocystitis When acute attack of Dacryocystitis is subsided, patient
is referred to higher centre for sac surgery (DCR) and
1.2 Pathogenesis: Fistulectomy, if required.
When the opening of NLD is blocked, tears and mucous
will remain within sac, forming a deposit that gets easily
infected. 2. Chronic Dacryocystitis:
2.1 Definition:
1.3 Microorganism:
Most commonly Staphylococcal infection and Chronic low grade inflammation of lacrimal sac is called
Streptococcal infection. as Chronic Dacryocystitis.
1.4 Stages:
i. Stage of cellulitis.
ii. Stage of lacrimal abscess.
iii. Stage of fistula formation.
1.5 Clinical features:

Acute onset, painful, red, hot, firm swelling over
lacrimal sac area.
Figure 2.2 Chronic Dacryocystitis
In severe cases there may be a pus point, which may 2.2 Pathogenesis:
burst Stricture formed due to chronic inflammation.
There is also Tear Lake, fullness, conjunctival Obstruction of lower end of nasal nasolacrimal duct
congestion (i.e. watering and redness of eyes.) caused by polyp or hypertrophied inferior turbinate.
1.6 Associated symptoms:
Fever, malaise. 2.3 Clinical Picture:
 Essential symptom is watering of eyes.
1.7 Treatment:  There may be swelling at lacrimal sac area
i. Tab. Ciprofloxacin 500mg twice daily initially for (Mucocele).
5 days.
Page 441
 Regurgitation test (on pressure over medial canthus
of eye i.e. over sac region) is positive (Muco-pus,
3. Congenital Dacryocystitis
pus). 3.1 Definition:
2.4 Treatment: Non canalization of nasolacrimal duct leading to
blockage of drainage passage may lead to Congenital
Topical Ciprofloxacin 0.3% eye drops four times a day.
Dacryocystitis.
Syringing with Ciprofloxacin 0.3% daily once for 5
days.
2.5 Complications:
Chronic intractable conjunctivitis, corneal ulcer,
ectropion.
2.6 Referral:
For sac surgery (Dacryocystorhinostomy or
Dacryocystectomy).
Figure 2.3 Congenital Dacryocystitis
2.4 Treatment: 3.2 Symptoms:
Topical Ciprofloxacin 0.3% eye drops four times a day.
Syringing with Ciprofloxacin 0.3% daily once for 5 Baby is brought with complaints of watering from
days. one/both eyes.
3.3 Signs:
2.5 Complications: Swelling at sac region, discharge on pressure over
Chronic intractable conjunctivitis, corneal ulcer, swelling.
ectropion.
3.4 Treatment:
Moxifloxacin 0.5 % eye drops 4 times a day.
2.6 Referral:
For sac surgery (Dacryocystorhinostomy or  Crigler Massage over sac region.
Dacryocystectomy).  If the block persists for more than 6 months
probing of nasolacrimal duct is done by
ophthalmologist under general anaesthesia.
Bibliography
Further reading
1. Srivastava S P. Dacryocystorhinostomy - Observation on 52 cases. Indian J Ophthalmol [serial online]
1958; 6: 78-9. [cited 2016 Jul 4]
Available from: http://www.ijo.in/text.asp?1958/6/4/78/40708
2. Sood N N, Ratnaraj A, Balaraman G, Madhavan H N. Chronic dacryocystitis - a clinico-bacteriological
study. Indian J Ophthalmol 1967;15:107-10


Page 442
3. CONJUNCTIVITIS
1. Definition: 2.1.6 To prevent spread of infection:
 Frequent hand washing.
Inflammation of conjunctiva is called as conjunctivitis.
 Avoid crowded places.
2. Types  Avoid sharing of handkerchief, towels, napkins,
It can be Infectious or Allergic. pillows etc.
Infectious conjunctivitis can be bacterial or viral. 2.2 Viral conjunctivitis
2.1. Mucopurulent/purulent 2.2.1 Definition:
(Bacterial) conjunctivitis Acute conjunctival inflammation caused by viruses.
2.1.1 Definition:
Acute purulent inflammation of conjunctiva.
Figure 3.2 Viral Conjunctivitis

2.2.2 Causative organisms:
Herpes simplex, Herpes zoster, adenovirus etc.
Figure 3.1 Conjunctivitis
2.2.3 Symptoms:
2.1.2 Causes: Acute redness of eyes, grittiness of eyes, watering from
eyes, photophobia.
Staphylococci, Streptococci, Pneumococci, Gonococci
etc. 2.2.4 Signs:
2.1.3 Symptoms: Local: Conjunctival congestion, follicular hypertrophy
with pre-auricular lymphadenopathy.
Acute redness of eyes, grittiness of eyes with muco-
purulent purulent discharge.
Systemic: Patient may have fever, Upper respiratory
2.1.4 Signs: tract infection.
Conjunctival congestion, mucopurulent / purulent 2.2.5 Treatment:
discharge (no diminution of vision, photophobia),
matting of eye lashes due to discharge. Usually self-limiting course.
2.1.5 Treatment:  Acyclovir 3% eye oint. 5 times a day for 14 days
with,
 Moxifloxacin 0.5 % eye drops two hourly for 7
 Prophylactic Moxifloxacin 0.5% eye drops four
days. times a day for 7 days with,
 Chloramphenicol 1% eye oint. At bed time for 7  Fluorometholone 0.02% eye drops four times a day
days. for 7 days.
 Dark goggles.  In case of Herpes Zoster Ophthalmicus refer to
Ophthalmologist immediately.
Page 443
To prevent the spread of infection
Prevention of spread of infection is equally
important as that of treatment
 Frequent hand washing to be done.
 Avoid crowded places.
 Avoid sharing of handkerchief, towels, napkins, 3. PTERYGIUM
pillows etc.
 AVOID USE OF STEROIDS (BOTH TOPICAL
AND SYSTEMIC).
2.3. Allergic conjunctivitis
2.3.1 Definition: Conjunctivitis caused as allergic
reaction to pollens, dust, etc.
Figure 3.4 Pterygium

Pterygium –
A Pterygium is a triangular sheet of fibro vascular tissue

which invades the cornea. Pterygia typically develop in
patients who have been living in hot climates and may
Figure 3.3 Allergic Conjunctivitis represent a response to chronic dryness and exposure to
2.3.2 Symptoms: the sun.
Recurrent attacks of redness, ropy discharge, irritation, Signs –
itching.
 The conjunctiva then overgrows the opacities
2.3.3 Signs: and progressively encroaches onto the cornea
Conjunctival congestion, mucoid discharge, papillary in a triangular fashion.
hypertrophy.
 Early cases show small, grey, corneal
2.3.4 Treatment: opacities near the nasal limbus.
 If there is secondary infection, use combination of
Tobramycin 0.3% & Fluorometholone 0.02% eye
drops, one drop 4 times a day for 15 days, along
Treatment –
Surgical excision is indicated either for cosmetic
with Carboxymethylcellulose 1% eye drops
reasons or in cases of progression towards the visual
(Lubricating eye drops) one drop 4 times a day for
axis. The excision of the conjunctival component
15 days.
followed by auto grafting or amniotic membrane
OR grafting
 Olopatadine 0.1% eye drops, One drop twice a day
for 1 week.
Bibliography
Further reading
1. "Conjunctivitis." UXL Complete Health Resource. 2001. [cited 2016 Jul 4]
Available from: http://www.encyclopedia.com/doc/1G2-3437000119.html
2. Protect Yourself from Pink Eye [Internet]. Centers for Disease Control and Prevention. 2014 [cited
2016 Jul 4]. Available from: http://www.cdc.gov/conjunctivitis/about/causes.html

Page 444
4. CORNEAL ULCER
1. Definition:
Corneal ulcer is defined as breech or
discontinuation of corneal epithelium with necrosis
of surrounding corneal tissue.
Figure 4.1 Hypopyon Corneal ulcer
2. Etiology of Corneal Ulcer:

Etiology of Corneal Ulcer
________________________________________________________________
NON - INFECTIVE
INFECTIVE
________________________________________________________
FUNGI VIRUSES
BACTERIA PROTOZOAS
Pathogens can invade intact corneal epithelium & can cause ulceration.
Infective agents:
N. Gonorrhoea, C. Diptherium, N. Meningitidis.
Page 445
NONINFECTIVE
Traumatic Post-Surgical Lacrimal Lids& Lashes
Neurological Immunological Dermatologic Nutritional
Others
Figure 4.2: Etiology of Corneal ulcer

 Anterior Chamber depth –Shallow (Indicates
3. Clinical features Perforation)
3.1 Symptoms:  Iritis

 Redness  Posterior synechiae
 Pain  Lens normal
 Watering / discharge  IOP Normal/ Raised
 Photophobia  Sac (Dacryocystitis)
 Diminution of vision
4. Investigations:
3.2 Signs:  Fluorescein Staining
 Lid Edema
 Corneal Scrapings
 Conjunctival Congestion
 Gram Staining
 Ciliary Congestion
 Giemsa Staining
 Corneal Ulcer
 KOH Mount
 Hypopyon
 Culture & Sensitivity
Page 446
 Systemic antibiotic: Tab. Ciprofloxacin
500mg BD for 5 days.
 Sac syringing
 Diclofenac Sodium 50mg BD (anti-
 Routing Investigation
inflammatory) for three or four days.
 Blood Pressure
 Refer the patient to Ophthalmologist
 Blood Sugar
5. Treatment: 6. Complications after
 Cleanliness perforation:
 Adherent leucoma
 Fortified topical antibiotic eye drops like
Amikacin 80mg/2ml.  Ant. Staphyloma
 Tobramycin – with a syringe, Inj 2ml of  Corneal fistula
Tobramycin (40mg/ml) directly into a 5 ml
bottle of tobramycin (0.3%) eye drop. Use  Pseudo cornea
within 14 days. keep in refrigerator.  Spread of infection to other ocular tissues
 Antibiotics: Topical Moxifloxacin 0.5% eye  Expulsion of the lens / vitreous
drops 2hrly.
 Expulsive choroidal hemorrhage
 Cycloplegics -Atropine sulphate 1% eye oint
twice a day.  Spontaneous evisceration
 Hot fomentation.  Endophthalmitis / Panophthalmitis
 Rest.
Bibliography
Further reading
1. Rohatgi J N. Bacteriology of corneal ulcer with special reference to hypopyon corneal ulcer. Indian J
Ophthalmol [serial online] 1967; 15:54-7. [cited 2016 Jul 4]
2. EyeRounds.org: Tutorials in Ophthalmology (Eye Physicians & Surgeons) [Internet].
Webeye.ophth.uiowa.edu. 2016 [cited 4 July 2016].
Available from: http://webeye.ophth.uiowa.edu/eyeforum/tutorials/INDEX.htm

Page 447
5. SCLERA
5. Scleritis
5.1 Definition
Scleritis is a granulomatous inflammation of the sclera.
Figure 5.1 Episcleritis

1. Episcleritis
It is a common, benign, self-limiting and frequently
Figure 5.2 Scleritis
recurrent disorder which typically affects young adults.
It is seldom associated with a systemic disorder and 5.2 Types
never progresses to a true Scleritis.
5.2.1 Anterior Scleritis
a. Non-necrotizing – diffuse or nodular.
2. Types of Episcleritis b. Necrotizing – with or without inflammation.
2.1 Simple Episcleritis – 5.2.2 Posterior Scleritis

It is characterized by sectoral or rarely, diffuse
redness. It usually resolves spontaneously within
5.3 Symptoms
1-2 weeks.  Unilateral mild discomfort
2.2 Nodular Episcleritis –  Tenderness to touch
It is localized to one area of the globe, forming a
nodule with surrounding congestion.  Watering
3. Symptoms 5.4 Associated systemic diseases
 Unilateral mild discomfort
About 45% of patients with Scleritis have associated
 Tenderness to touch systemic diseases like,
 Watering  Rheumatoid Arthritis
 Connective tissue disorders
4. Treatment  Miscellaneous conditions like relapsing
Polychondritis, Herpes Zoster.
 Mild cases –
Topical steroids, Ciprofloxacin 0.3% +
5.5 Treatment
dexamethasone 0.1% eye drops, one drop three  Oral NSAIDs – Flurbiprofen 100mg three times a
times a day or topical NSAIDs Ketorolac day for 5 days.
Promethymene eye drops 0.5% one drop three times
a day for one week.  Oral Prednisolone – 40-80mg a day tapered
according to response.
 Unresponsive recurrent cases – Systemic
Flurbiprofen 100mg three times a day.  Combined therapy with a NSAID and low dose
steroid.
Bibliography
Page 448
Further reading
1. Rohatgi J N. Bacteriology of corneal ulcer with special reference to hypopyon corneal ulcer. Indian J
Ophthalmol [serial online] 1967;15:54-7. [cited 2016 Jul 4]
2. EyeRounds.org: Tutorials in Ophthalmology (Eye Physicians & Surgeons) [Internet].
Webeye.ophth.uiowa.edu. 2016 [cited 4 July 2016].
Available from: http://webeye.ophth.uiowa.edu/eyeforum/tutorials/INDEX.html

Page 449
6. UVEITIS
1. Definition: 3.2 Intermediate uveitis

Inflammation of Uveal tract is known as 3.2.1 Symptoms:
Uveitis.
 Decrease in vision (usually slight blurring)
 Black spots in front of eyes (floaters)
3.2.2 Signs:
 Ciliary Congestion.
 Tenderness Over Ciliary Body.
 Snow Banking and Vitreous haze seen on
Ophthalmoscopy.
3.3 Posterior uveitis

3.3.1 Symptoms:
 No pain, Decrease in vision
 Black spots in front of eyes (floaters)
3.3.2 Signs:
Figure 6.1 Uveitis Vitreous haze, focal inflammatory lesions and macular
edema detected on ophthalmoscopy.
2. Causes:
 Auto immune 3.4 Panuveitis:
 Infective Symptoms and signs of both anterior and posterior
uveitis are present.
3. Classification:
Depending on the anatomical part of Uvea involved it is 4. Complications:
classified as  Complicated cataract
1) Anterior (Iridocylitis)  Secondary Glaucoma
2) Intermediate (Pars-Planitis)
3) Posterior (Choroiditis)  Cystoid macular edema
4) Panuveitis (all parts are involved)  Retinal Detachment
3.1 Acute Anterior Uveitis  Phthisis Bulbi (shrunken eye)
3.1.1 Symptoms:
5. Evaluation of a Case of
 Redness
Uveitis:
 Pain –dull-aching pain, more during night
 Watering  History
 Detailed history of previous episodes, treatment
 Photophobia (intolerance to light) and response to treatment.
 Decrease in vision (usually slight blurring)  History of associated systemic conditions like
Tuberculosis, Syphilis, HIV infection, Rheumatoid
3.1.2 Signs: Arthritis, Ankylosing Spondylitis, Malignancies,
Keratic precipitates and aqueous cells/flare can be seen Diabetes Mellitus etc.
on slit-lamp examination.
Page 450
5.1 Ocular examination:  X-ray chest, ESR and Monteux test to rule out
Tuberculosis.
 Visual acuity.  VDRL / TPHA – to rule out Syphilis.
 Pupillary reaction.  ELISA for HIV.
 Slit-lamp examination for keratic precipitates,
aqueous cells and flare.
 Dilated fundus examination for vitreous haze,
5.3 Treatment:
snow banking, chorioretinitis lesions, cystoid  Topical steroids – Prednisolone Acetate 1% eye
macular edema. drops (1hrly initially then tapered according to
response to treatment).
5.2 Investigations:  Cycloplegics –Atropine Sulphate 1% eye drops
TDS.
Depending on most likely cause in a particular case  Antibiotics and systemic steroids are usually not
following investigations may be required, required.
 Complete Blood Count
 Blood sugar levels
 Uveitis is a vision threatening condition. Refer the patient immediately on

suspicion of Uveitis.
 Long term use of steroids can cause Cataract and Glaucoma.
Bibliography
Further reading
1. Perkins, ES. Pattern of uveitis in children. Br J Ophthalmol. 1966;50:169–185.
2. Agrawal, R. V., Murthy, S., Sangwan, V., & Biswas, J. (2010). Current approach in diagnosis and
management of anterior uveitis. Indian Journal of Ophthalmology, 58(1), 11–19. [cited 2016 Jul 4]
Available from: http://doi.org/10.4103/0301-4738.58468

Page 451
7. GLAUCOMA
1. Introduction: -
 Second major cause of blindness.
 Often asymptomatic in early stage.
 Damage is irreversible.
 Effective treatment is available.
 IOP Depends on the balance between production
and removal of aqueous humour.
2. Definition:
Chronic progressive optic neuropathy caused by a
group of ocular conditions which lead to damage of Figure 7.1 Open-Angle Glaucoma
the optic nerve with loss of visual function.
Pathogenesis 5. Open-angle Glaucoma:

 Raised IOP (Intra Ocular Pressure)- mechanical The most common form of Glaucoma, accounting for at
changes - decreased axoplasmic flow - ganglion cell least 90% of all Glaucoma cases.
death – apoptosis.  It is caused by the slow clogging of the drainage
 Reduced optic nerve head perfusion – Ischemia. canals, resulting in increased intra ocular pressure
3. Classification  Has a wide and open angle between the iris and
cornea.
3.1 According to etiology
 Develops slowly and is a lifelong condition.
 Primary
 Secondary  Has symptoms and damage that are not noticed.
 Congenital- Present at birth.  It causes SLOW damage to the optic nerve causing
Infantile- present in first year life. gradual and irreversible loss of vision.
Juvenile- present in the late childhood.
 “Open-angle” means that the angle where the iris
meets the cornea is as wide and open as it should
3.2 According to Appearance of the be. Open-angle Glaucoma is also called primary or
Angle chronic glaucoma. It is the most common type of
Glaucoma.
 Open angle Glaucoma
 Closed angle Glaucoma a. Risk Factor:
 Combined mechanism Glaucoma  Age - 6th decade.
 Sex –Common in Female.
 Race – Common and more severe in Black.
4. Investigations: -  Family History and Inheritance –First degree
 IOP with Applanation / Schiotz Tonometer relative of patients with POAG (Primary Open
 SLE (Slit Lamp Examination) Angle Glaucoma) are at increased risk of
 Fundus Examination developing the disease.
 Gonioscopy  Refractive error- POAG is common in Myopia
 Visual –field testing
 OCT (Optical Coherence Tomography) b. Clinical features:
 Generally asymptomatic headache.
 Frequent changes in Presbyopic correction.
 Difficulty in dark adaptation.
 Scotoma (especially in inferior field). {Blindness
in particular sector}
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c. Signs:
 Intraocular pressure > 21 mmHg (Schiotz
Tonometer).
 Optic nerve head changes - C: D ratio > 0.5.
 Asymmetry between two nerve heads > 0.2.
 Narrowing/notching/pallor of NRR.
 Disc hemorrhages.
 Visual field defects.
 Defects in nerve fiber layer.
d. Management:
 Start Timolol Maleate 0.5% twice daily if patient is
not Asthmatic or not Hypertensive, according to
response.
 Start Latanoprost 0.005 % /Travoprost 0.004 %
(Prostaglandin analogues) one drop once daily in
the evening if patient is Asthmatic or Hypertensive,
according to response.
 Systemic Tab. Acetazolamide 250-1000 mg /day
orally.
 Surgical Treatment – Trabeculectomy
 Refer the patient to a Higher Centre for evaluation
and management.
6. Primary Angle Closure

Glaucoma Figure 7.2 Angle-Closure Glaucoma
a. Introduction: - c. Predisposing factors:

Angle-closure glaucoma, a less common form of  Short eye, Hypermetropia.
glaucoma:  Smaller corneal diameter.
 Is caused by blocked drainage canals, resulting in a  Shallow anterior chamber.
sudden rise in intraocular pressure.  Relative forward positioning of lens-iris
 Has a closed or narrow angle between the iris and diaphragm.
cornea. d. Clinical features:
 Develops very quickly.
 Has symptoms and damage that are usually very  Unilateral headache or brow ache.
noticeable.  Blurring of vision on the same side.
 Demands immediate medical attention.  Unbroken colored halos around lights during the
It is also called acute glaucoma or narrow-angle episode.
glaucoma. Unlike open-angle glaucoma, angle-closure  Gross diminution of vision.
glaucoma is a result of the closure of angle between the  Red eye.
iris and cornea.  Nausea, vomiting.
 Ciliary and conjunctival congestion, hazy cornea.
b. Definition:
 Vertically oval, mid dilated pupil.
Spectrum of conditions in which the peripheral iris  Stony hard eyeball (very high IOP).
moves forward to block the openings of the trabecular
meshwork at the angle, causing a rise of intraocular e. Treatment:
pressure.  Systemic - Intravenous Mannitol 20% 1-2 gm per
Kg over ½ an hr.
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 Tab. Acetazolamide, 250-1000mg per day in
divided doses should be given if the patient is not
nauseating or vomiting and can tolerate oral
medication.
 One drop of 2% Pilocarpine placed in the eye every
5 min till pupil constricts, then one drop QID.
 One drop of Timolol Maleate 0.5 % twice daily
7. Congenital Glaucoma
(Buphthalmos) Figure 7.4 Lens Induced Glaucoma
a. Definition:
a. Classification:
Glaucoma appearing between birth and the ages of 3-4
years.  Phacolytic glaucoma.
 Phacomorphic glaucoma.
 Phacoanaphylactic glaucoma.
b. Symptoms:
 Diminution of vision.
 Pain.
 Redness of eyes.
 Headache.
c. Signs:
 Decreased visual acuity.
 Conjunctival congestion.
Figure 7.3 Congenital Glaucoma
 Corneal oedema.
b. Pathogenesis:
 Anterior Chamber – shallow (Phacomorphic
 Failure / abnormal development of the trabecular
glaucoma).
meshwork.
 Angle remains closed by persistent embryonic  Flare, cells, sterile Hypopyon.
tissue.
 Pupil – sluggishly reacting to light.
c. Clinical features:
 Lens – mature or hyper mature Cataract.
 Enlarged eye.
 Hazy cornea - frosted glass appearance.  IOP – raised.
 Intolerance to light.  Fundus – Absent Glow.
 Corneal edema.
d. Investigations:
 Watering.
 Blue sclera.  Complete Blood Count.
 Iridodonesis.
 Blood Sugar Level estimation.
d. Management:
Urgent referral to higher center for Goniotomy /  Kidney Function Test.
Trabeculotomy.  Serum Electrolytes.
8. Lens Induced Glaucoma  Serology.

Definition:  B-Scan.
It is a type of Optic Neuropathy secondary to raised IOP
due to Cataractous lens (Hyper mature Cataract).
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e. Aims of Management: IV or systemic Acetazolamide – 250-1000 mg/day
till IOP reduces.
 To relieve pain.
f. Surgery:
 To minimize optic nerve, insult secondary to raised
IOP.  After controlling IOP.
 To remove the cause.  Extracapsular Cataract Extraction with PCIOL
implantation.
 To reduce the IOP – IV Mannitol (20%) – 1-2
gm/kg over 30 min.  Post-Operative – IOP monitoring.
 Visual damage in Glaucoma is irreversible hence early detection by regular screening is important.
 Once diagnosed, Glaucoma is lifelong, which needs continuous lifelong treatment and follow up.
 Treatment is aimed at preserving the vision.
Bibliography
Further reading
1. Perkins, ES. Pattern of uveitis in children. Br J Ophthalmol. 1966; 50: 169–185.
2. French, D.D., Margo, C.E. Glaucoma medications and mortality: a retrospective cohort study. Ann
Epidemiol. 2010; 20: 917–923.
3. Rhee DJ. Which therapy to use in glaucoma? In: Yanoff M, Duker JS, eds. Ophthalmology. 4th ed.
Philadelphia, PA: Elsevier Saunders; 2014: chap 10.23.
4. Gross RL. Current medical management of glaucoma. In: Yanoff M, Duker JS, eds. Ophthalmology.
4th ed. Philadelphia, PA: Elsevier Saunders; 2013: chap 10.24.

Page 455
8. CATARACT
A cataract is clouding of the lens of the eye, which
impedes the passage of light. Most cataracts are related
to ageing, although occasionally children may be born
with this condition, or cataract may develop after an
injury, inflammation or disease.
Risk factors for age-related cataract include Diabetes,
prolonged exposure to sunlight, tobacco use and alcohol
consumption. Vision Can be restored by surgically
removing the affected lens, and replacing it by an
artificial one.
Figure 8.3 Traumatic Cataract
Figure 8.1 Cataract

Figure 8.4 Complicated Cataract
1. Definition:
Any opacity of lens or its capsule whether congenital
or acquired is known as cataract.
2. Types of cataract:
2.1 Senile cataract
2.2 Traumatic cataract
2.3 Complicated cataract
2.4 Metabolic cataract
Figure 8.5
3. Stages of Cataract:
 Immature cataract
 Intumescent
 Mature cataract
 Hyper mature- Morgagnian
 Sclerotic
4. Clinical features:
 Painless progressive diminution of vision, glare,
black spots before the eyes, distortion of objects,
Figure 8.2 Senile Cataract polyopia.
 Complications of hyper maturity like Uveitis and
Lens dislocation, Glaucoma.
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5. Investigation: - 6.2.1 Bullous keratopathy
Corneal oedema due to corneal decompensation.
Managed in initial stage, by local hypertonic saline
 V/A, IOP, Syringing.
eye drops (four times a day and eye ointment at
 Blood Pressure, Blood sugar, ECG, Urine night) & oral tab Acetazolamide 250mg three times
routine. a day. If unresponsive, Keratoplasty is the
 A-scan. treatment of choice.
 Xylocaine sensitivity test.
 Physician fitness. 6.2.2 Posterior Capsular Opacification
It is the thick capsular opacification of posterior
6. Treatment: capsule after extra capsular cataract surgery. It can
be managed by Nd: YAG capsulotomy.
6.1 Surgery-
 Conventional Extra Capsular Cataract 6.2.3 Cystoid Macular Edema.
Extraction with Posterior Chamber Intra Ocular Relatively uncommon in uncomplicated
Lens Implant (PCIOL). phacoemulsification, occurs more often after the
 Manual Small Incision Cataract Surgery (SICS) complicated surgery. Peak incidence 6-10 weeks.
with PCIOL.
 Phacoemulsification with PCIOL 6.2.4 Post-Operative Endophthalmitis
a. Definition: -
6.1 Post-Operative Management – Refers to intraocular inflammation predominantly
involving the vitreous cavity and anterior chamber
as a result of post-operative intraocular colonization
 Topical – Steroid + antibiotic eye drops by microorganisms.
Ciprofloxacin 0.3% + Dexamethasone 0.1%
eye drops one drop six times a day for one b. Symptoms
week tapered every week up to six weeks &
topical NSAIDs, Ketorolac Promethymene eye
• Pain, Diminution of vision, redness and
watering of eye.
drops 0.5% one drop three times a day for two
c. Signs: -
weeks. Tropicamide 1% eye drops one drop at
night time for two weeks.  Decrease visual acuity.
 First follow up at end of the first week & final  Lid swelling.
follow up after 40 days for spectacle correction.  Discharge.
 Corneal edema.
 Conjunctival Chemosis.
6.2 Complications of cataract  A/C Reaction, Iritis, Corneal Haze,
surgery: Hypopyon, Circumcorneal congestion.
d. Risk factors:
• Post-operative Endophthalmitis.
 Early- Striate Keratitis, corneal edema, prolapse • Environmental factors: Improper OT
of iris, Hyphema, Anterior Uveitis, delayed fumigation, improperly cleaned OT.
formation of anterior chamber, early • Improper sterilization techniques.
Endophthalmitis, Toxic Anterior Segment • URTI in Surgeon / staff/ patient.
Syndrome(TASS). • Instrumentation with improperly autoclaved
 Late- Bullous Keratopathy, Cystoid Macular instruments.
edema, posterior capsular opacification, • Infection of Sac –Blepharitis.
secondary Glaucoma, Retinal Detachment, late • Open wound leak.
Endophthalmitis. • Poor patient hygiene.
• Poor compliance in putting post-operative
It is imperative for a Medical officer to recognize medicine.
late complications of cataract surgery. • Post-operative rubbing of eyes/ Trauma
Page 457
e. Types (onset)
Immediate Delayed
Within 24-48 hrs. 48-72 Hrs.
Complication: Complete loss of eye sight if no - Fortified Gentamycin eye drop every 15min.for 2
timely intervention done. hrs. then one hourly three days.
- Moxifloxacin 0.5% eye drops ½ hourly.
f. Treatment: - Cycloplegics – Atropine Sulphate 1% eye
It is an acute ophthalmic emergency ointment, eye drops.
- Start intrusive systemic and topical antibiotics. - Urgent referral to Ophthalmologist is required.
Bibliography
Further reading
1. What Are Cataracts? [Internet]. American Academy of Ophthalmology. 2014 [cited 2016 July 5]
Available from: http://www.aao.org/eye-health/diseases/what-are-cataracts
2. Cataract - EyeWiki [Internet]. Eyewiki.aao.org. 2016 [cited 2016 July 5].
Available from: http://eyewiki.aao.org/Cataract

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9. OPHTHALMITIS
1. Endophthalmitis: 1.3.2 Fungal
 Contaminated irrigating solutions.
1.1 Definition:  Contaminated IOLs, viscoelastics, poor OT
Endophthalmitis is the clinical term used to describe the Hygiene, hospital construction activities.
inflammatory response of the eye to ocular infection.
1.4 Symptoms
Patient presents with symptoms most commonly on the
second day after surgery.
 Pain
 Red
Figure-9.1: Endopthalmitis
Figure 9.2 Endophthalmitis with Purulent
Hypopyon
 Decreased vision.
Acc to aetiological agents  Hazy cornea.
Based on aetiological agents  Hypopyon.
 Post-operative Endophthalmitis is the most
Endophthalmitis common form.
 It comprises 70% of Infective Endophthalmitis.
Bacterial
Fungal Viral
Fungal
1.5 Management
Parasitic
 In established Endophthalmitis, antibiotics when
given orally or I.V., have poor penetration into the
vitreous cavity.
 Hence, intravitreal injections are treatment of
choice.
 Intravitreal injections bypass the blood retinal
barrier and rapidly achieve therapeutic levels at the
1.2 Types: sites of infection.
 Large majority follow cataract surgery, most
common surgical procedure (approx. prevalence
0.082%-0.1%)
 Post-operative Endophthalmitis is one of the most
dreaded complications of cataract surgery and
constitutes a true emergency.
1.3 Risk Factors

1.3.1 Bacterial
 Defects in sterilization of instruments.
 Contamination of tap water.
 Multiple dose fluids and drugs. Figure 9.3
Page 459
Late onset Endophthalmitis
May be due to infection by organism of low virulence
or fungi. Toxic reaction to Intra Ocular Lens (IOL)
may also present as late Endophthalmitis. An urgent
referral to ophthalmologist is required.
2. Panophthalmitis
2.1 Definitions: -
Refer to the inflammation of all coats of the eye
including intraocular structures. It can also extend
with the tissue surrounding the eyeball. Figure 9.5 Morganella morganii panophthalmitis
2.2 Symptoms of Panophthalmitis  Cornea is cloudy and edematous.

 Anterior chamber is full of pus.
 Eye pain.
 Vision is completely lost and perception of
 Burst opening of the eye ball.
light
 Protruding eyeball.
is absent.
Loss of Vision.
 Intraocular pressure is markedly raised.
2.3 Signs  Globe perforation may occur at limbus, pus
 Lids show a marked oedema and hyperaemia. comes out and intraocular pressure falls.
 Eyeball is slightly proptosed, ocular movements  Complications include:
are limited and painful. - Orbital cellulites
 Conjunctiva shows marked chemosis and ciliary - Cavernous sinus thrombosis
as well as conjunctival congestion. - Meningitis or encephalitis
2.4 Treatment
There is little hope of saving such an eye and the
pain and toxemia lend an urgency to its removal.
1. Anti-inflammatory and analgesics should be
started immediately to relieve pain.
2. Broad spectrum antibiotics should be
administered to prevent further spread of infection
in the surrounding structures.
3. Evisceration operation should be performed to
avoid the risk of intracranial dissemination of
Figure 9.4 Acute necrotizing Panophthalmitis infection.
Bibliography
Further reading
1. Barry P, Seal DV, Gettinby G, Lees F, Peterson M, et al. (2006) ESCRS Endophthalmitis Study
Group. ESCRS study of prophylaxis of Postoperative Endophthalmitis after cataract surgery:
Preliminary report of principal results from a European multicenter study. J Cataract Refract Surg
32(3): 407–410. doi: 10.1016/j.jcrs.2006.02.021
2. Endophthalmitis: Background, Pathophysiology, Epidemiology [Internet]. Emedicine.medscape.com.
2016 [cited 2016 July 5].

Page 460
10. RETINAL DETACHMENT(RD)
It is one of the major ocular disease conditions o Trauma
causing visual loss.
o Post-cataract vitreous incarceration
Predisposing factors
o Pars Planitis
 High myopia.
 Exudative RD
 Trauma.
 Family history of retinal detachment. 4. Prophylaxis
 Intraocular Surgery-Aphakia, Pseudophakia Indicated in retinal breaks
 Inflammation.  In Aphakic eyes.
 Peripheral Retinal degenerations (Lattice/ Snail  More than 1 clock hour of break.
track).
 Family history of RD.
1. Definition:  Any symptomatic tear.

Asymptomatic tears and holes can be observed.
It is a separation of neurosensory retina from retinal
pigment epithelium due to accumulation of fluid in 3 Modalities of prophylaxis.
the sub-retinal space through a retinal break, hole or a
tear.  Laser Photocoagulation on slit lamp or IDO
(Indirect Ophthalmoscope) with indentation.
2. Symptoms:  Cryotherapy at the break to seal it.
 Occurrence of flashes of light (Photopsia)
more serious in nasal field.
 Scleral buckling surgery for large tears(rarely).
 Floaters in the vision.
 Curtain/ Veil in front of eye in any portion,
5. Treatment:
more appreciated in lower field than upper. RD surgery can be done only by tertiary eye care
centers with infrastructure and trained personnel.
 Sudden significant loss of vision, if macula is
involved.
 A large bullous detachment. 6. Complications of long
standing RD
3. Types:  Uveitis.
 Rhegmatogenous RD.  Complicated cataract.
 Tractional RD.  Glaucoma.
o Diabetic Retinopathy  Phthisis bulbi.
In cases of high suspicion of Retinal Detachment, patient should be referred to tertiary eye care
centre because timely treatment has better chances of saving vision.
Page 461
Bibliography
Further reading
1. Retinal Detachment: Practice Essentials, Background, Pathophysiology [Internet].
Emedicine.medscape.com. 2016 [cited 2016 July 5].
2. Feltgen N, Walter P. Rhegmatogenous Retinal Detachment—an Ophthalmologic Emergency.
Deutsches Ärzteblatt International. 2014;111(1-2):12-22. doi:10.3238/arztebl.2014.0012.
3. Heimann H, Bartz-Schmidt KU, Bornfeld N et.al. Scleral buckling versus primary vitrectomy in
Rhegmatogenous retinal detachment: a prospective randomized multicenter clinical study.
Ophthalmology. 2007;114: 2142–2154.

Page 462
11. REFRACTIVE ERRORS
1.Introduction –
Normally, the rays of light entering the eye are brought
to a precise focus on the retina – the light sensitive layer
lining the back of the eye. When such a focus is not
achieved, a refractive error results and vision is not
clear.
When parallel rays of light from a distant object are
brought to focus on the retina with the eye at rest, is
called as Emmetropia (that is not accommodating).
Figure 11.2 Myopia

4.2Etiology:
 Axial lengthening of eyeball (1mm=3D).
 Curvature- abnormal curvature of cornea.
eg. Keratoconus (0.1=3D).
 Index myopia eg. Old age, Nuclear Sclerosis.
 Acquired Myopia due to trauma.
Figure 11.1 Emmetropia 4.3Types:

 Developmental.
2. Causes of Refractive Errors  Simple.
The eye’s ability to refract or focus light- sharply on the
 Pathological.
retina-is primarily based on three features.
4.3.1 Developmental Myopia:
1. The overall length of the eye.
 Abnormally long eyeball Myopia 10D.
2. The curvature of the cornea.
 Fundus - marked choroidal sclerosis,
3. The curvature of the lens inside the eye. hyperpigmentation and myopic crescent.
3.Types of Refractive Error  Usually stationary image.

4.3.2. Simple Myopia:
 Myopia.
 Commonest, progressive from childhood to adult,
 Hypermetropia. seldom exceeds 5-6D.
 Astigmatism.  Generally, stop progression by 21 year of age.
 Presbyopia.  Best corrected vision is 6/6.
 Fundus exam. Shows Myopic crescent, Tigroid
4. Myopia fundus and optic nerve degeneration with or
without retinal break.
4.1. Definition:
A Dioptric condition of eye in which parallel rays of 4.3.3. Pathological Myopia:
light from infinity come to focus in front of retina when  Essentially degenerative and progressive condition,
manifests in early childhood.
eye is at rest.
 The defect can reach up to 30D to 40D.
 The defect has strong heredity more common in
female than male.
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 Rapid increase in Myopia during puberty.
5.Hypermetropia
 Retinal evaluation is mandatory /compulsory.
4.4. Clinical feature:

 Inability to see the distant object and holding the
book close to the eye in simple Myopia.
 Eye strain and headache.
 Black spot in front of eye.
 In pathological myopia-eye unusually prominent
with slightly dilated pupil.
 Ophthalmoscopy reveals vitreous degeneration and Figure 11.3 Hypermetropia
opacity.
5.1. Definition:
 Chorio-retinal degeneration patches at posterior
Pole, choroidal sclerosis and Foster Fuchs spot at It is an error of refraction wherein parallel rays of light
macula, Posterior Staphyloma. coming from infinity are focused behind the retina with
accommodation at rest.
4.5. Complications:
5.2. Etiology:
 Retinal hemorrhage due to post vitreous  Axial
detachment.
 Curvature
 Lattice degeneration with retinal tear.
 Index
 Complicated Cataract.
 Posterior dislocation of lens
4.6. Treatment:  Aphakia
 Optical lens- concave lenses with slight under
correction. 5.3. Types:
 Contact lens.  Latent.
 Manifest- Facultative.
4.7. Surgery: - -Absolute.
Refractive surgery like RK, PRK, ICR, LASIK 5.4. Clinical feature:
 Low degree- no symptoms.
4.8. Other important aspects
 High degree-eye strain, headache.
Avoid contact sports where chances of blunt trauma are
more  Latent convergent squint in young.
 Low vision aid- in pathological Myopia LVA is  Presbyopia develops at an early age.
helpful. Glasses or contact lens does not improve
 Predisposed to angle closure glaucoma.
the vision.
 Genetic counseling.  Fundus may show features of pseudopapillitis.
 General health-nutritional diet.
 Increased chances of acute angle closure (Risk of
 Outdoor activity.
Angle Closure Glaucoma).
 Near work in good illumination.
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5.5. Treatment: 6.4. Clinical features:
 Optical lens- convex lens.  Small Astigmatism – Often asymptomatic.
 Contact lens.  Severe symptom in hyperopic astigmatism where
accommodation brought in play to overcome
5.6. Surgery - hyperopia.
Laser, Thermal Keratoplasty, LASIK, Phakic
intraocular lenses  Irregular astigmatism is caused by corneal scar,
penetrating injury to eye, Keratoconus.
6. Astigmatism 6.5. Treatment:
 Cylindrical glasses.
 Contact lens.
6.6. Surgery:
LASIK, Photo astigmatic Keratectomy, Incisional
correction (LRI), IOL, Conductive Keratoplasty,
Corneal transplantation.
7. Presbyopia:
Figure 11.4 Astigmatism
6.1. Definition:
Astigmatism is condition wherein refraction varies in
different meridian of the eye hence the point of focus
cannot be formed on retina.
6.2. Etiology:
 Curvature Astigmatism- most common with
corneal curvature.
 Index Astigmatism- inadequacies of refractive Figure 11.5 Presbyopia
index of lens in different sector.
6.3. Types: Normal aging process, when near images can’t be

 With the rule. focused on the retina due to reduced accommodative
ability.
 Against the rule.
The focus is behind the retina as in hyperopia.
i. Regular
If initially Emmetropic: Person begins to hold reading
ii. Irregular material farther away and distance vision is unaffected.
If initially hyperopic: Presbyopia occurs earlier.
Corrected with a convex lens for reading (bifocal).
.
All refractive errors should be detected and treated in childhood by regular school health
checkups and should be fully corrected.

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Page 465
Bibliography
Further reading
1. Refraction and Refractive Errors Information Page | Patient [Internet]. Patient.2016 [cited 2016 July 5].
Available from: http://patient.info/in/doctor/refraction-and-refractive-errors
2. McCarty CA. Uncorrected refractive error. Br J Ophthalmol. 2006 May;90(5):521-2
3. Mohan M. National Survey of Blindness-India. NPCB-WHO Report. New Delhi: Ministry of Health
and Family Welfare, Government of India; 1989
4. Murthy G, Gupta SK, John N, Vashist P. Current status of cataract blindness and Vision 2020: The
right to sight initiative in India. Indian J Ophthalmol [serial online] 2008; 56:489-94. [cited 2016 Jul 5]

Page 466
12. DIABETIC RETINOPATHY
1. Introduction: 5. Systemic Evaluation
India has become the Diabetic capital of the world.  Control of systemic risk factors is the cornerstone
There is a high incidence of Diabetic Retinopathy (DR), in management of DR.
among patients who are suffering from Diabetes
Mellitus for duration of more than 15-20 years. Early  Glycemic control: Besides Blood Sugar Level,
diagnosis and intervention is crucial in dealing with this HbA1c levels more than 7.0 % is a known risk
malady. Incidence and severity is more in type I (IDDM) factor.
than type II (NIDDM).  Hypertension more than 130/90mmHg.
2. Classification:  Increased Triglycerides, cholesterol. Decreased
HDL.
 Smoking, Sedentary life style.
6. Diagnosis
 Symptoms: decreased vision, floaters.
 On examination.
Figure 12.1NPDR (Non Proliferative)  Visual acuity.
 IOP.
 Neovascularization of iris.
 Gonioscopy: Neovascularization of the angle.
 Dilated fundus examination.
7. Fundus:
 Veins dilated and tortuous.
 Dot and Blot hemorrhages.
Figure 12.2 PDR (Proliferative)  Hard exudates.
Maculopathy (Clinically Significant)
 Cotton wool spots.
3. Risk Factors:  Micro-aneurysms.
1. Advanced Diabetic Eye disease.
2. Vitreous hemorrhage.  NPDR stage.
3. Traction RD.  New vessels and traction bands seen.
4. Neovascular Glaucoma.  PDR stage.

4. History  Vitreous hemorrhage and traction RD complicates
the picture.
 Duration of Diabetes.
 Maculopathy runs as a distinct disease entity with
 Control of Diabetes. maximum visual defect.
 Other systemic illness.  Fundus Fluorescein Examination (FFE).
 F/H/O severe vision loss due to DR.
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 Iodine based dye is injected into the 8.3 PDR:
antecubital vein and fundus pictures taken and
digitally analysed.  Pan Retinal photocoagulation.
 Leaks and ischemic areas can be picked up.  Intra vitreal injection of VEGF inhibitors
 Optical Coherence Tomography: i. Bevacizumab
ii. Ranibizumab
 Non-invasive retinal tissue pictures
 Vitrectomy may be needed for Vitreous
hemorrhage, Tractional RD.
8. Treatment:
8.1 NPDR : 9. Prevention:
 Intensive glycaemic control immediately after
 Periodic observation. diagnosis of DM leads to lessen the
complications.
 Antioxidants.
Today Telemedicine has taken sophisticated
 Control of Diabetes. technology to the rural masses yet the cornerstone is
increasing awareness in public.
8.2 CSME:
 Focal/ Grid photocoagulation
 Fundus examination with dilated pupil must be done for all newly diagnosed Diabetic patients and
thereafter atleast once a year.
 A tight glucose control from the beginning has more long term benefits as compared to a tight control
many years after diagnosis or after an end organ damage.
Bibliography
Further reading
1. Singh R, Ramasamy K, Abraham C, Gupta V, Gupta A. Diabetic retinopathy: An update. Indian
Journal of Ophthalmology. 2008;56(3):179-188.
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Page 468
13. OCULAR INJURIES
 Decrease /Loss of vision.
1. Introduction :
 Inability to open the eye.
Eye can get injured by chemicals, heat, radiation and
mechanical trauma. Ocular injuries are emergencies and b. Signs:
treatment in first few hours can affect the visual
prognosis.  Severe Blepharospasm (forceful closure of lids).
 Conjunctival congestion.
2. Type of Injuries :-
 Raised IOP.
 Chemical.
2.1.4. Diagnosis:
 Mechanical injuries.  History of the chemical causing injury should be
elicited.
2.1. Chemical injuries :-  Examination is difficult because of severe
Common chemicals causing injuries are, Blepharospasm.
 Ocular examination should be done under surface
Alkalis –lime, ammonia, sodium hydroxide, cement,
anaesthesia and if required sedation (especially in
detergent soaps.
children).
2.1.5 Immediate treatment:
 Removal of any particulate matter (with special
attention to lime pest/powder).
 Simple treatment is WASH-WASH-WASH the
eye with water.
 Continuous irrigation with one bottle of normal
saline over a period of 30 minutes.
 Topical Ciprofloxacin 0.3% + Dexamethasone
0.1% eye drops-one drop 4 times a day.
Figure 13.1 Alkali burn  Topical Atropine sulphate 1% eye drops one drop
twice daily.
Acids –Hydrochloric, Sulphuric, Acetic acids (vinegar),
Toilet cleaners.  Tab Ibuprofen 400mg twice daily for pain relief.
2.1.1 Alkali burn: Alkalis can penetrate through  Tablet Acetazolamide 250mg. (carbonic anhydrase
cornea causing severe inflammation. They cause inhibitor) one tablet four times a day.
occlusion of limbal vessels causing ischemia and After primary care patient should be referred to
necrosis of ocular surface. Necrosed tissue is sloughed ophthalmologist for further management.
off causing ulceration and healing by granulation tissue
giving rise to abnormal adhesions between lid and ocular Prevention: Keep Limestone /Chuna and other sources
surface (symblepharon), severe dry eye, vascularized of Chemical Ocular Injuries away from the reach of
opaque cornea and even phthisis bulbi. children.
2.1.2 Acid burn: Coagulates the ocular surface tissue
but usually does not penetrate inside the eye. Acids can 2.1.6. Medical management at higher centre
cause limbal ischemia, severe dry eye, vascularized includes
corneal opacities.  Assessment of limbal ischemia.
2.1.3 Clinical features:  Topical steroids - Ciprofloxacin 0.3% +
a. Symptoms: Dexamethasone 0.1% eye drops-one drop 4 times a
 Distressing pain. day first 7 days.
 Watering from eyes.
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 Topical lubricating eye drops -
Carboxymethylcellulose 1% eye drops one drop 4
times a day for 15 days.
 Prevention of symblepharon formation by
symblepharon ring.
 Surgical treatment in the form of amniotic
membrane transplant, limbal stem cell grafting or
Keratoplasty.
2.1.7 Complications: Figure 13.2 Symblepharon and corneal opacity
 Dry eye
 Corneal ulcer  Immediate Copious irrigation with normal
 Lid scarring saline minimizes the damage.
 Symblepharon
 Phthisis bulbi (shrunken eye)  Use protective glasses at work place
(Prevention better than cure!)
2.2 Mechanical Injuries :
Figure 13.3 Ocular trauma classification
Mechanical eye injury
Closed globe injuies Open globe injuries
Contusion
Laceration Rupture
Superficial foreign body Perforating injry
Intraocular foreign body

Lamellar laceration
Penetrating injury
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2.2.1. Superficial foreign bodies Examine the cornea (stain with sterile fluorescein strip
Common extra ocular foreign bodies are particles of if necessary) to locate the foreign body.
dust, coal, emery, steel, lime particle, grain of corn, husk
of seeds, wing/ mouth part of insects, caterpillar hair, 2.2.3. Treatment:
thorns etc.  Removal of foreign body.
 Conjunctival foreign body can be removed by
Patient gives history of foreign body in the eye. cotton bud or irrigation.
 Corneal foreign body should be removed by
cotton bud or 26 G needle (hold the needle
tangent to cornea to avoid perforation) under
surface anaesthesia of eye with 4% xylocaine
or Paracaine eye drop.
 Ciprofloxacin eye drop0.3 (Antibiotic) four
 Homatropine 2% eye drops three times a day for
4 days in case of corneal foreign body.
 Eye pad for 24 hrs.
 Follow up to rule out infection.
Figure 13.4 Foreign bodies
2.2.2. Symptoms:
 Redness. If patient gives history of foreign body but it is not
 Pain (pricking). found on examination, suspect intraocular foreign
 Watering. body and carefully examine for wound of entry.
 Forceful closure of lids.
Anaesthetize the eye with 4% xylocaine eye drops/

proparacaine eye drops (0.5%).
Examine the conjunctiva by everting/double everting the
upper lid.
 Immediate Copious irrigation with normal saline minimizes the damage.

 Take precaution by using protective glasses at work places. (Prevention is always better than cure).
Bibliography
Further reading
1. Ocular Injury- AAPOS [Internet]. Aapos.org. 2016 [cited 2016 July 5].
Available from: http://www.aapos.org/terms/conditions/136
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14. OCULAR EMERGENCIES
1. Ocular conditions requiring 3. Common Causes Of Acute
emergency ophthalmological Red Eye
consultation.
 Trauma -Ruptured Globe
 Lid Lacerations.
 Chemical injuries.
 Endophthalmitis.
 Angle Closure Glaucoma.
 Severe Uveitis.
 Corneal Ulceration.
 Acute Vision Loss.
 Optic Neuritis. Figure 14.1 Conjunctivitis
 Orbital cellulitis.
 Conjunctivitis (with mucopurulent /purulent
 Lens induced Glaucoma. discharge)Subconjunctival hemorrhage (painless).
 Corneal ulcer.
 Acute iridocylitis (dull aching pain and slight
2. Common causes of sudden blurring of vision).
diminution of vision:  Endophthalmitis (severe pain with Diminution of
Table-14.1:Common causes of sudden vision).
diminution of vision  Panophthalmitis (severe pain, proptosis, with
painful ocular movements).
Painful diminution of Painless diminution  Orbital cellulitis (severe pain, proptosis, with
painful ocular movements).
vision of vision
 Acute congestive  Vitreous

Glaucoma hemorrhage
 Chemical injuries  Retinal Detachment
 Mechanical injuries  Central retinal
 Endophthalmitis artery occlusion
 Panophthalmitis  Ischemic central
retinal vein
occlusion
 Optic Neuritis
 Malingering
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
Bibliography
Further reading
1. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007 Sep 15;76(6):829-36.
2. Eye Emergencies [Internet]. Healthline. 2016 [cited 2016 July 5].
Available from: http://www.healthline.com/health/eye-emergencies#Overview

Page 473
15. PAEDIATRIC OCULAR PROBLEMS
 Corneal scarring (scarring of the outer eye
1. Introduction :- because of vitamin A deficiency & trauma).
Out of 45 million people worldwide who are blind, around
 Cataract – forms 39 per cent of all childhood
1.4 million are children under 16years of age. The vast
blindness.
majority of childhood blindness happens before the age of
 Infections -
five – a period when 75 per cent of learning is through
 Ophthalmia neonatorum.
sight.  Congenital Dacryocystitis.
 Blepharitis.
2. Why is childhood blindness a  Squint.
priority?  Ocular Trauma.
There are several reasons why stakeholders believe that
 Congenital and Developmental Cataracts.
eliminating childhood blindness is a priority. Leukocoria.
 There are an estimated 500,000 new cases each year  Congenital anomalies
of childhood blindness – roughly one per minute.
3.1 Ophthalmia neonatorum
 Blindness in children is often preventable if
communities and parents become aware of the
causes.
 Without early intervention for cataract blindness,
children may go blind permanently.
 Blinding conditions increase child mortality – up to
50% of children who become blind die within two
years.
 90% of children who are blind don’t go to school.
 Eliminating childhood blindness will lead to a greater Figure 15.1 Ophthalmia neonatorum
reduction in the number of “blind years”
experienced by adults. 3.1.1. Definition:
3. Causes of childhood blindness: Conjunctivitis occurring during 1st month after birth.
 Refractive errors. 3.1.2. Mode of presentation, differential

diagnosis & treatment:
(For details please refer to refractive error topic).
Table 1: Ophthalmia neonatorum - mode of presentation, differential diagnosis and treatment
Time of onset Differential diagnosis Treatment
Within the first 48 hrs Neisseria Gonorrhoeae Inj. Ceftriaxone IM,
Gentamycin / Moxifloxacin eye drops 1hrly

(till discharge decreases), followed by 4 times a
day for 7 days.
Bacitracin eye oint. 4 times a day for 7 days.
Chemical Wash the eyes, Erythromycin eye oint 4 times a
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Time of onset Differential diagnosis Treatment
day for 3 days
48 hrs to 72 hrs Other bacteria Gentamycin /Tobramycin eye dops two hourly
for 7 days.Neomycin-Bacitracin eye oint 4
5-7 days Herpes Simplex Virus(HSV II) Acyclovir eye oint 5 times a day for maximum
14 days.
>1 week Chlamydia Trachomatis(D-K) Erythromycin eye oint./Chloramphenicol eye

oint. 4 times a day for two weeks.
3.2. Squint : 3.2.1 Definition:

It is a condition where the eyes do not look in the same Malalignment of visual axes is called as squint. It can be
direction. Whilst one eye looks forwards to focus on an Esotropia/Exotropia or vertical malalignment i.e.
object, the other eye turns either inwards, outwards or hypertropia or hypotropia.
downwards. A child with a squint may stop using the
affected eye to see with. This can lead to visual loss 3.2.2 Types of Squint :-
called Amblyopia, which can become permanent unless  Esotropia – An eye that turns inwards.
treated early in childhood. Treatment involves patching
 Exotropia - An eye that turns outwards
the good eye, to force the use of the affected eye.
 Hypertropia - An eye that turns upwards.
Sometimes surgery is needed to correct the appearance
of a squint. Squints are common and affect about 1 in 20  Hypotropia - An eye that turns downwards.
children. Most squints develop before preschool age,  Constant – The squint present all the time.
usually by the time a child is three years old. Sometimes  Intermittent – The squint comes & goes.
squints develop in older children, or in adults  Manifest squint – The affected eye turns when the
eyes are open and being used.
 Latent squint – The eye turns only when it is
covered or shut, but looks fine when the eye are
open.
 Concomitant squint – The angle (degree) of the
squint is always the same in every direction that
you look.
 Incomitant squint – The angle of squint can vary
according to direction
Figure 15.2 Esotropia
3.2.3 Symptoms:
Squint(deviation of eye), diminution of vision
3.2.4 Signs:
Squint, diminution of vision, Amblyopia (lazy eye).
3.2.5 The aims of treatment of squint are :-
 Preserve or restore vision.
 Straighten the eyes.
Figure 15.3 Exotropia
 Restore binocular vision.
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3.2.6 Treatment: As the child does not complain of any poor vision, the
tumor may remain undetected. The most common way
 Refractive correction. of presentation is a white reflex (Leukocoria) behind the
 Amblyopia treatment. pupil. It may also present as squint (crossed eye), poor
 Exercises and if necessary surgical correction is vision, painful red eye, inflammation of the tissue
done. (before 10 yrs. of age to have binocular surrounding eye, protrusion of the eye ball (proptosis)
vision). etc. The aim of treatment in retinoblastoma, in order of
Evaluation of the squint by ophthalmologist at the priority, is to save the life, eye sight and cosmesis of the
earliest is must. child. There are many treatment modalities for this
3.3. Leukocoria: tumor.
3.6 Retinopathy of Prematurity :

The most important determinant of any ROP
management program is an effective screening strategy.
3.6.1 Whom to screen for ROP:
 All infants born below 1750 grams birth weight
must undergo screening and all infants between
1750 grams and 2000 grams must be screened in
Figure 15.4 Leukocoria
case of any risk factor.
3.3.1 Definition:  All infants born below 34 weeks of gestation must
White pupillary reflex is called as Leukocoria. undergo screening and all infants between 34-36
weeks must be screened in case of any risk factor.
3.3.2Common Causes:
 Congenital Cataract. 3.6.2. When to start screening:
 Retinoblastoma.  All babies must be screened not later than 30 days
 Retinopathy of Prematurity. of life or 4 weeks after birth.
 Toxoplasma /Toxocara Endophthalmitis.
 Persistent Hyperplastic Primary Vitreous.  Babies born < 1200 grams or < 28 weeks must be
screened by the 2nd – 3rd week of life.
3.4. Congenital Cataract: 3.6.3. Treatment:
It is clouding or opacity of the normally transparent lens  Laser Photocoagulation.
inside the eye. Babies are sometimes born with cataracts
as a result of an infection, injury, or poor development  For advanced stages like retinal detachment
before they were born, or they may develop during surgical treatment is required.
childhood.
3.7 Congenital anomalies:
It is very important to treat this condition as soon as
possible to get the best results. The treatment options 3.7.1 Ptosis:
and the timing of surgery will be decided by the
Ptosis refers to drooping of an upper eyelid of one or
ophthalmologist, based on the following factors:
both eyes. The droop may be barely noticeable, or the lid
 Age of the child. can descend over the entire pupil. Surgery usually is the
 Density of cataract. best treatment for drooping eyelids. Children born with
 Whether cataract involves one eye or both eyes. moderate or severe ptosis require treatment in order to
get proper vision for subsequent development of child.
Failure to treat ptosis can result in Amblyopia.
3.5 Retinoblastoma:
All these are potentially vision threatening conditions
It is the cancer of the eye in children. It originates from which need immediate referral to
the retina, the light sensitive layer, in eye. It is the ophthalmologist.Every time the when the baby is
commonest tumor of the eye in childhood brought for immunization look for pupillary reflex.
Page 476
Bibliography
Further reading
1. Moore A. Pediatric ophthalmology. In: Fundamentals of clinical ophthalmology. London: BMJ Books;
2000.
2. R. Pitts Crick, Niels Kaj Jerne, Peng Tee Khaw. Textbook of Clinical Ophthalmology. A Practical
Guide to Disorders of the Eyes and Their Management. 3 rd Edition. World Scientific Publishing Co Pte
Ltd; 2003

Page 477
16. LOW VISION
Low vision is a reduced level of vision that cannot be

fully corrected with conventional glasses. It is not the
2. Causes
same as blindness. Unlike a person who is blind, a  Although low vision can occur at any stage in
person with low vision has some useful sight. life, most of people develop low vision because
However, low vision usually interferes with the of eye diseases.
performance of daily activities, such as reading or
driving. A person with low vision may not recognize  Common causes of low vision, particularly with
images at a distance nor able to differentiate colours older adults, include Macular Degeneration,
of similar tones. Glaucoma, and Diabetic Retinopathy.
You are legally blind when your best corrected
central acuity is less than 20/200 (perfect visual 3. Tests and Diagnosis
acuity is 20/20) in your better eye, or your side vision
is narrowed to 20 degrees or less in your better eye. 1. Refraction (to assess your vision and
People who are legally blind may still have some determine the prescription for your glasses, if
useful vision. If you are legally blind, you may glasses may be of any use).
qualify for certain government benefits. It is
2. Visual field (to assess your peripheral vision).
estimated that approximately 17 percent of people
over the age of 65 are either blind or have low vision.
4. Treatment and Drugs
1. Symptoms  Optical devices to help you adapt, such as
magnifiers, telephones, or closed-circuit
 Difficulty in recognizing objects at a distance
(street signs or bus signs). televisions.
 Difficulty in differentiating colors (particularly  Adaptive non-optical devices, such as large-

in the green-blue-violet range). print cookbooks and talking watches.
 Difficulty in seeing well up close (reading or  Occupational Therapy.

cooking).
Bibliography
Further reading
1. Dickinson C. Low vision: principles and practice. Edinburgh: Butterworth-Heinemann; 1998.

Page 478
17. EYE BANKING
Eye bank collects, evaluates and distributes the eyes 8. Only the transparent section of the eyes called
donated by the donors. All eyes donated are
cornea is taken out and not the complete eye
evaluated using strict medical standards.
ball.
1. Functions of eye bank: 9. A small quantity of blood will be drawn to rule
out communicable diseases.
Those donated eyes which are found unsuitable for
10. Anyone can pledge eyes.
transplantation are used for valuable research and
medical education purpose in the eye bank. 11. The eyes can be pledged to any eye bank
preferably the nearest one.
1. Availability of trained staff round the clock at
Eye donation center in all District hospitals & 12. The identities of both the donor and the
all Eye bank to attend the calls. recipient remain confidential.
2. Evaluate and provide quality corneas to corneal
surgeons. 13. One pair of eyes gives vision to TWO corneal
3. Enable corneal research using eyes unsuitable blind people.
for grafts to find newer techniques, improve
preservation methods and train corneal 14. Eyes donated to the Eye-Bank that are not
surgeons. medically suitable for transplant may be used
4. Increase public awareness about eye donation
for medical research and education purposes.
and eye banking.
2. Eye donation: 2.2. Process of Eye donation

Pledging for eye donation procedure:
2.1 Important aspects of eye
donation : 2.2.1 Eye donation can be done in either of
these two ways.
1. Eyes are to be donated only after death.
1. She/he can walk in to a nearest Eye Bank and
2. Eyes must be removed within 4-6 hours after
PLEDGE their eyes for donation. For this, a
death. pledge form needs to be filled, signed by a
witness (can be your relative/friend) and given
3. In case of death, nearest eye bank should be
back to the eye bank. At the time of donor’s
informed immediately. death, his/her relative/friend, who was a witness
for the pledge form or any other family
4. Eyes must be removed only by a trained doctor.
member/friend who had the knowledge that the
5. The eye bank team may remove eyes at home of person who passed away intended to donate the
eyes, should call the nearest eye bank. One
the deceased or at a hospital. important aspect to be noted here that it is not
6. Eye removal process is simple and takes only 10 sufficient if a person pledges for donating
his/her eyes after the death, his/her relatives and
to 15 minutes. friends should be well informed and be well
7. Eye removal does not lead to any disfigurement aware to call the nearest eye bank, for donating
the eyes after their death.
in eye.
2. After death, a relative or a friend of the
deceased person can inform the eye bank and
Page 479
tell them that they wish to donate the eyes of  The donor's family receives a certificate of
their bereaved folk. appreciation from the eye bank.
 The eyes are taken to the eye bank and
2.2.2. Donation procedure: evaluated by trained staff.
If there is an unfortunate death occurs of one of your  Eyes are preserved in a solution of Optisol GS
family member/close relative/close friend, pick up and refrigerated. This solution contains
the phone and dial to the nearest eye bank. Please chemicals and drugs that are needed to keep the
note that this should be done WITHIN 6 hours of the living cells of cornea healthy and functional.
death.  Tests are carried out and the report is sent to the
Give the eye bank officials the location of the house corneal surgeon
along with a landmark so that they can come and
collect the eyes as quick as possible. These eyes will  The eyes are used for a corneal transplant
give a new vision to two blind people. operation within 72 hours, but with present day
availability of special storage media the eyes
can be stored for a longer time before being
2.2.3. Important points to be taken care after
transplanted.
a person's death, before eye donation:
 The recipient is chosen from the eye bank's
After the death of a person, call the nearest eye bank waiting list and called for corneal transplant.
within SIX HOURS of the death of the person.  Neither the patient knows whose cornea is used
for him, nor the relatives of the donor know
 Switch off fans & keep AC on, if you have one. who has received the cornea. This information
is strictly confidential.
 Close the eye lids gently and keep a moist cloth
over the eyes.
• Periodic follow-up of the recipient is done over
 Raise head with a pillow. the time to ensure that the graft is successful.
2.2.4 What happens after eye donation?
Bibliography
Further reading
1. Rao GN. What is eye banking? Indian J Ophthalmol [serial online] 1996; 44:1-2. [cited 2016 Jul 5]
2. India. Directorate General of Health Services. Ministry of Health and Family Welfare. Standards of
Eye Banking in India. New Delhi: MoHFW; 2009.

Page 480
Surgery
8. Surgery
1 Abdominal Pain 481
2 Wounds & Abscess Management 484
3 Head Injury 486
4 Chest Injury 488
5 Abdominal Injury 492
6 Gangrene 494
7 Burns 496
8 Dressings 498
9 Breast 500
10 Congenital Anomalies 504
11 Venous Thromboembolism 509
12 Varicose Veins 511
13 Genito Urinary Disorder 513
14 Ano-rectal diseases 515
15 Tracheostomy 519
16 Urinary Catheterization 521
17 Triage 526
1. Abdominal Pain
 Stabilize the patient & shift the patient for surgical
1. Introduction intervention after stabilization patient or after
Acute is a term used synonymously for a condition that
primary treatment.
needs immediate intervention
3. Biliary Tract & Pancreas:

3.1. Presentation:
 Colicky pain in right upper abdomen, dyspepsia,
nausea/vomiting
 Occasional jaundice
3.2. Investigation:
 Routine investigation: CBC, ESR
 USG Abdomen
 Serum amylase estimation.
Figure 1.1: Acute causes  Serum lipase / LFT
Abdominal Pain can be due to various organs 3.3. Treatment:
involved with underlying causes & patient will
 Analgesics like Aceclofenac 50 mg BD,
present accordingly.
Dicyclomine 20 mg BD
 Antibiotics - Cefotaxime 1 gm I.V. BD, Gentamycin
2. Gastric & Duodenal ulcer: 80 mg I.V. BD
 Metronidazole - 500 mg I.V. BD
2.1. Presentation: Stabilize the patient and as per diagnosis- biliary
 Burning pain at the epigastric region referred to stone/ Pancreatitis patient may be referred for expert
back worsened (gastric ulcer) or relieved by intake management to surgical hospital as early as
of food (duodenal ulcer) possible.
 Dyspepsia, nausea/vomiting, occasionally 3.4. Acute epididymo-orchitis /
haematemesis/melena.
 Complication – with aggravation / progression of Pyocele
illness may cause perforation Acute epididymo-orchitis is an infection in epididymis,
testes & spermatic cord & manifests as acute Pain in
2.2. Investigation: Scrotum may be associated with fever. When infection,
 Routine investigation (Hb, CBC, Urine) pus in tunica vaginalis, it is called as Pyocele.
 X-ray shows gas under diaphragm in perforation 3.4.1 Symptoms -
 Gastroscopy - Pain is scrotal area.
 USG Abdomen - Erythema, in local area.
2.3. Treatment: - Difficulty is walking due to pain.
2.3.1 Drugs- - Fever
 Ranitidine 150 mg BD or Omeprazole 40 mg BD 3.4.2 Investigation
and alike drugs on empty stomach for 15 to 30 - USG Scrotum
days. - CBC shows leukocytosis
 Intestinal motility regulators Domperidone 5 to 10 3.4.3 Treatment:
mg BD after meals for 15 to 30 days a) Antibiotics
 Liquid antacids b) Inj. Cefotaxime 1 gm IV 12 hourly.
Inj. Metronidazole 500 mg IV / 8 hourly.
2.3.2 If perforation is diagnosed Inj. Diclofenac 50 mg /IM 8hourly.
 NBM, RT aspiration c) Magnesium sulfate dressing:
 I.V. fluids – RL, DNS, D 5% 5000-6000 cc in 24 d) Surgical intervention – Surgical intervention is
hrs. to stabilize the patient required if conservative treatment does not give
 Antibiotics Cefotaxime 1 gm I.V. BD, Gentamycin relief. Pyocele has to be drained for relief.
- 80 mg I.V. BD,
 Metronidazole - 500 mg I.V. TDS
Page 481
4. Small & Large Intestine: 5.1. Sign & symptoms
Abdominal pain from loin to groin on one side or both
4.1. OBSTRUCTION sides in flank & back. Pain is associated with burning
4.1.1 Presentation: micturition, nausea, vomiting, fever & chills. Patient
 Severe pain, vomiting complains of haematuria. Stone size is not associated with
 Distension of abdomen severity of pain.
 Constipation
5.2. Investigations
4.1.2 Investigation:
 Routine investigation (CBC, KFTs & LFTs)  Haemogram
 X-ray standing - Shows multiple gas-fluid levels (>  Urine- m/e, c/s
4 levels significant).  Renal profile (KFT + Serum Calcium)
4.1.3 Treatment:  X-ray (KUB)
a) NBM, Ryle’s Tube aspiration  USG abdomen (KUB)
b) I.V. fluids – RL, DNS, Dextrose 5% (Adult 5000-  IVEU (Intravenous Excretory Urogram)
6000 cc) in 4 to 6 hrs. to stabilize patient
c) Antibiotics Cefotaxime 1 gm I.V. BD, Gentamycin 5.3. Treatment
- 80 mg I.V. BD,  Analgesics- Inj. Diclofenac 50 mg/IM
d) Metronidazole - 500 mg I.V. BD
 Antibiotics- Inj. Ampicillin
e) Stabilize the patient & shift patient for surgical
500 mg IV /6 hourly.
intervention after primary treatment.
 Inj. Gentamycin 80 mg. IV/12 hourly. 3 to 4 days
 IV Fluids -Ringer lactate, DNS,
4.2. PERFORATION Dextrose 5%
4.2.1 Presentation:  Catheterization SOS
 Severe pain in abdomen, vomiting Give the treatment to stabilize the patient and / or refer
 Distension of abdomen, constipation the patient to higher surgical unit.
 On examination Tender G/R
6. Acute Appendicitis
The acute appendicitis is essentially a surgical condition
 Routine investigation
& can be defined as pain of sudden onset in right lower
 X-ray standing - Shows gas under diaphragm abdomen with fever with or without vomiting, nausea.
 USG abdomen Obstruction in lumen is cause for Acute appendicitis.
4.2.3 Treatment: 6.1. Presentation:

a) NBM, RT aspiration
b) IV. fluids – RL, DNS, Dextrose 5% (Adult 5000-  Pain at first starts around the umbilicus or
6000 cc) in 4-6 hrs to stabilize patient epigastrium and later it shifts to the right iliac fossa.
c) Antibiotics Cefotaxime 1 gm I.V.BD, Gentamycin  Sudden disappearance of pain without improvement
80 mg IV BD, of general condition means gangrene and
d) IV Metronidazole 500 mg BD perforation.
e) Stabilize the patient & shift patient for surgical  Anorexia, Nausea and Vomiting
intervention after primary treatment  Fever
 Tachycardia and it is proportionate to temperature
5. RENAL & URETERIC except in cases of gangrene, perforation and
COLIC generalized peritonitis.
It’s type of pain caused due to irritation or obstruction by  Tenderness in right iliac fossa /guarding and rigidity
stone, in kidney or ureter itself. It is repeated spasmodic
pain of longer or shorter duration till cause is removed 6.2. Investigation:
i.e. stone removal or expulsion.  Routine Haemogram (CBC & WBC is increased)
Renal pain most of the time is located in lumbar or back  KFT
region. Ureteric pain is typical colic, mild or severe in
 Urine examination
nature radiates from lumbar to scrotal region. It is
 CECT abdomen
invariably associated with haematuria (micro/
macroscopic)  X- ray abdomen, abdominal Sonography
 CT abdomen with contrast
Page 482
7. Obstructed Inguinal Hernia
6.3. Treatment: It is due to obstruction / retention of Abdominal
6.3.1 Conservative Treatment visceral organs in hernia sac.
Appendicitis with signs of localization Patient presents with- non-reducible Inguino-scrotal
 Rest in a hospital swelling, pain in, distension of repeated vomiting. In
late stages fever, septicemia.
 Nil by mouth
 Analgesics- Inj. Diclofenac 50 mg/IV 8 hourly 7.1. Investigations:
/SOS.  Routine Haemogram
 Antibiotics- Inj. Ampicillin 500 mg IV/6 hourly.  X-ray standing position - shows multiple gas fluid
Inj. Gentamycin 80 mg IV/12 hourly. levels
Inj. Metronidazole 400 mg IV/8 hourly.  USG pelvis
 IV Fluids - Ringer lactate, DNS, Dextrose 5%  No cough impulse.
 If patient is responding/ improving, give above 7.2. Treatment:
treatment for 5 to 6 days  NBM, Ryle's tube aspiration, head low position
 IV Fluids - Ringer lactate, DNS, dextrose 5%
6.3.2 Surgical Treatment
 Analgesics- Inj. Diclofenac 50 mg / IV
If during the conservative treatment there is evidence
 Antibiotics- Inj. Ampicillin 500 mg IV/6 hourly.
of gangrene, perforation, generalized peritonitis or
Inj. Gentamycin 80 mg / IV/12 hourly.
abscess formation, operation is indicated. If patient
Inj. Metronidazole 400 mg / IV /8 hourly.
starts deteriorating with conservative line of treatment,
then patient may be posted for emergency  Try to reduce the hernia, if not possible, then after
appendectomy. stabilization of patient within 4 to 6 hours shift the
Emergency appendectomy is contra indicated when patient for further needful surgical intervention at
diagnosis is appendicular mass. higher center.
Bibliography
1. Bailey H, Love M. Bailey & Love's Short Practice of Surgery. Ed: Williams NS, Bulstrode CJK
O’Connell PR. 26th edition. Florida: CRC press; 2013: 880.
2. Das S. A Manual of Clinical Surgery. 11th edition. S. Das’s publication; 2015:650
Further reading
1. Wein AJ, Kavoussi LR, Partin AW, Peters AC. Campbell Walsh Urology. 10th edition. Elsevier;
2011:704
2. McAninch J, Lue TF. Smith and Tanasho’s General Urology. 18th edition. McGraw Hill Professional,
2012: 768
3. Townsend Jr CM, Beauchamp RD, Evers Bm, Mattox KL. Sabiston Textbook of Surgery. 19th
edition. Elseviers, 2012: 2152
4. Brunicardi F, Hunter JG et al. Schwartz’s Principles of Surgery. 10th edition. McGraw Hill Education;
2014: 2069.
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Page 483
2. WOUNDS AND ABSCESS MANAGEMENT
From the earliest times the healing of wounds has contamination, wound infection, to be done by
been the central problem in surgical practice. This secondary suturing, skin grafting.
applies equally to the wounds of warfare and human
assault, to the wounds of accidents, and to the 3.3.1 Suture Material:
wounds which the surgeon makes deliberately in the  Non-absorbable -linen, silk, nylon, proline,
course of surgical operations. ethilone
The breach in the surface of the body, the skin,  Absorbable- cat gut, vicryl
exposes the deeper tissues to the danger of bacterial
infection (sepsis), and this danger persists until the 3.3.2 Suture Types:
healing process has restored an intact surface.  Simple - single or continues
 Mattress - single or continues
1. Commonly occurring  Tension sutures - when there is requirement of
forced alignment of wound edges
injuries can be open or
3.4 Supportive treatment to the
closed.
associated injury/illness as
 Abrasions, bruises required- fracture site
 Contusions
 Lacerated wounds
stabilization etc.
 Penetrating wounds 4. Abscess
 Incised
 Crush wounds 4.1 Clinical features:
 De-gloving injury- wounds with skin loss An abscess is a tender mass generally surrounded by
 Vascular injuries a colored area from pink to deep red. Abscesses are
often easy to feel by touching. The middle of an
2. Observe for abscess is full of pus and debris which leads to
fluctuation test positive.
2.1 Three 'B'
Painful and warm to touch, abscesses can show up
 Bleeding any place on your body. The most common sites are
 Breathing in your armpits (axillae), areas around your anus and
 Breaks (fracture) vagina (Bartholin gland abscess), the base of your
spine (pilonidal abscess) around a tooth (Dental
2.2 Wound Contamination abscess) and in your groin. Inflammation around a
hair follicle can also lead to the formation of an
2.3 Concealed bleeding (internal) abscess; which is called a boil (furuncle).
3. Management: 4.2 Treatment

3.1 Cleaning of wounds Unlike other infections, antibiotics alone will not
3.2 Debridement of dead or usually cure an abscess. In general, an abscess must
open and drained in order for it to improve.
devitalized tissue Sometimes draining occurs on its own, but generally
3.3 Suturing of wounds it must be opened by a doctor in a procedure called
 Wound healing may be primary intention- this is incision and drainage (I&D)
brought about by joining together the edges of Other risk factors for abscess include exposure to
the wounds by sutures, clips, adhesive materials dirty environments, exposure to persons with certain
 Secondary intention - when the wound edges are types of skin infections, poor hygiene, and poor
not brought together as there is - skin loss, gross circulation.
Page 484
Seek immediate medical attention for any puncture
wounds, especially if associated with some debris in
4.3. Drugs: it
 Antibiotics - Cap. Ampicillin 500mg QID 4 to 5 4.5. Important points

days or
Once treated, the abscess should heal
Tab. Ciprofloxacin 500mg BD 4 to 5 days or
Many people do not require antibiotics
Tab. Cefadroxil 200mg BD 4 to 5 days
The pain often improves immediately and subsides
 Symptomatic treatment by analgesic, anti- more each day
inflammatory drugs
Wound care includes wound repacking, soaking,
 Supplementary/supportive – Vitamin C 500 OD washing, or bandaging for about 7 to 10 days. This
3 to 4 days usually depends on the size and severity of the
abscess
4.4. Prevention After the first two days, drainage from the abscess
Maintain good personal hygiene by washing your should be minimal to none. All sores should heal in
skin with soap and water regularly 10-14 days.
Take care to avoid nicking yourself when shaving Synonyms and Keywords
your underarms or pubic area
Abscess, abscesses, boils, carbuncles, furuncles, hiler
adenitis, suppurative, pilonidal abscess, pustules, and
white heads.
wounds, associated medical conditions of patients
On steroids or chemotherapy
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

Page 485
3. HEAD INJURY
Head injuries comprises of injuries to skin, skull,
intracranial organs with vessels, in combination or 2.1 Intra-cerebral hemorrhage - in
singly.
the brain substance it is usually
Skull is the protective bony cage/vault for brain.
Though it is not a perfect fit considering weight & associated with lacerations in
volume of brain which may in turn leads to injury to brain.
the brain by inclusive of skin & vault or singly by 2.2 Subarachnoid- in the pre
mere inertia to brain & its membrane. The brain is
suspended by superior cerebral veins from above, and arachnoids mesh.
antero - posteriorly to the membranes and laterally by 2.3 Extradural Hemorrhage:
attachments of dural process causing direct impact
injuries to site - coupi injuries or indirectly to the Extradural - Outside the dura between dura and
opposite side of skull called counter coupe injuries. periosteum of inner table of skull associated with
fracture of skull.
1. Injuries can be classified It is an injury causing blood accumulation between
grossly as skull & dural membrane. This causes pressure effects
on brain & its functioning. It causes phase of
 Concussion
unconsciousness with period of apparent recovery
 Contusion
between two periods of unconsciousness, which is
 Laceration known as lucid interval.
Treatment: Craniotomy and immediate surgical
1.1 Cerebral Concussion: evacuation
It is distortion and displacement of brain substance 2.4 Subdural Hemorrhage:
minimally. Producing sudden loss of consciousness
Subdural under the dura, but outside the arachnoids
on sensory & motor paralysis with variable duration
matter: It is usually from the veins causing blood
from seconds to minutes. There is a complete
accumulation beneath the dural membrane.
recovery in this injury.
Classification: Acute < 3 days, Sub-acute 4 -21 days,
1.2 Cerebral Contusion: chronic >21 days
Treatment: Craniotomy and immediate surgical
In this injury distortion, displacement is of severe evacuation.
nature along with injury to brain matter- neural
fibers, this additional sliding movement between gray
& white matter in to producing damage to nerves & 3. Signs & Symptoms:
axons.  Vomiting
 Bleeding - ENT
1.3 Cerebral Laceration:  Convulsions
 loss of consciousness, disorientation
In this injury internal changes are same but the brain
surface is actually torn. Clinically causing prolonged 4. Clinical Examination
unconsciousness which leads Intracranial  Examine level of consciousness, reaction and
Hemorrhage. size of pupils: Cranial nerve examination, Spine
examination DTR/Planters
2. Intracranial Hemorrhages:  Blood pressure, pulse, respiratory rate
There are four anatomical types of intracranial 5. Investigations:
hemorrhages
 Routine investigations
 Skull X-ray AP & Lateral
 CT-Scan Plain and CECT
 MRI
Page 486
o Inj Diclofenac 3cc IM slowly
6. Management:  Catheterization
It depends upon the site, severity of injury, general  Maintenance of air way, throat & nasal suction
condition of the patient & other relevant  Control of bleeding
complications.  Care of associated injuries
 Nil by mouth: RTA  Oxygen inhalation with mask, SOS intubation /
 IV fluids, RL, D-10% 4000-5000 ml tracheostomy
 Drugs  Management of shock
o IV Mannitol 100 cc / BD  After stabilization, patient to be shifted to
o Inj. Phenytoin 200-600 mg / day or higher center for expert neurosurgical
o If convulsions than Inj. Sodium Valproate management as early as possible.
400-2000 mg / day
o Inj. Cefotaxime 1gm / BD
o Inj. Gentamycin 80 mg / BD
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

Page 487
4. CHEST INJURY
Chest injury is common in road accident, fall from
height, stab injury
7. Common injuries:
Common injuries we come across which need primary
1. Chest wall treatment to stabilize the patient are:
 Fractured ribs
 Flail chest 7.1. Fracture Ribs:
 Fractured sternum 7.1.1 Clinical presentation
 May be single or multiple, simple or compound.
with or without Pneumothorax. Patient may
2. Pleura: present with - pain, difficulty in breathing in a later
 Pneumothorax stage sometimes inability to take breath secondary
 Tension Pneumothorax to Pneumothorax,
 Traumatic haemothorax  On examination: Tachycardia, Tachypnea
7.1.2 Diagnosis & management
3. Lung:
 Pulmonary contusion Patient needs to be investigated by X-ray chest
 Pulmonary laceration  Analgesia
 Breathing
4. Mediastinal structures:  Strapping
 Ruptured thoracic aorta 7.2. Flail Chest
 Ruptured bronchus 7.2.1 Clinical presentation
 Ruptured diaphragm
This type of injury is commonly seen in accidents due to
 Blunt injury to the heart
multiple rib fractures causing paradoxical movement of
 Haematopericardium chest wall. Resulting in to respiratory insufficiency &
retention of pulmonary secretions.
5. Penetration injuries: 7.2.2 Diagnosis & management
 Bullet
 Stab wounds to the chest To be diagnosed by X-ray Chest
Patient needs following treatment.
6. Early Treatment:  Propped up position
 Relief of pain – analgesics Inj. Diclofenac stat TDS  Oxygenation by mask
 Stabilization of the chest wall- strapping  Chest wall stabilization by strapping
 Removal of pleural blood or air -Simple aspiration,  Tracheostomy – SOS
air tapping by needle, ICD  IPPV
 Removal of tracheo-bronchial secretions
 Tracheostomy 7.3. Traumatic Pneumothorax:
 Oxygen administration by mask 7.3.1 Clinical presentation
 NBM It is a trapped air in pleural cavity due to penetrating
 IV Fluids - Ringer lactate, DNS, dextrose 5% wounds to chest wall, pleura and or lungs. It may be
 Antibiotics- associated with haemothorax.
- Inj. Ampicillin 500 mg. IV/6 hourly.
- Inj. Gentamycin 80 mg. IV/12 hourly. 7.3.2 Diagnosis & management
- Inj. Metronidazole 500 mg IV/8 hourly. a) To be diagnosed by X-ray Chest - evidence of
 Blood transfusion in massive haemothorax fracture ribs, lung collapse black radiolucent chest
 After stabilization, patient to be shifted to higher cavity area on injured sides. Sometimes air fluid
center for expert management within 4-8hrs level in Haemo/ Pneumothorax.
b) Patient needs ICD as above / IPPV
Page 488
7.4. Tension Pneumothorax: 8.2. PREPARATION
8.2.1. Requirements for Chest Tube Insertion
7.4.1 Clinical presentation
procedure:
A tension Pneumothorax develops when there is a one-
way valvular leak of air into the pleural cavity. Air  Chlorhexidine or povidone-iodine solution
rapidly accumulates, compressing the lung, and urgent  Sterile towels and drapes
treatment is required, as it is a life threatening  Sterile sponges
emergency.  2% Lidocaine without epinephrine (40 ml)
 10-ml syringe
7.4.2 Diagnosis & management  18-, 21-, and 25-gauge needles
X-ray chest  Mayo scissors
 Standard tissue forceps
To be diagnosed and treated as above in addition patient
 Towel forceps
needs.
 Needle holder
a) Simple needle aspiration to release tension  0-Silk suture with cutting needle
b) ICD with under water seal  Scalpel handle and no. 10 blade
 Chest tubes (24, 28, 32, and 36 French)
7.5. Haemothorax:  Chest tube drainage system with NS
7.5.1 Clinical presentation  2-in. adhesive tape
 Sterile gowns and gloves, masks, caps
An accumulation of blood in the pleural cavity can occur
from injury to the muscles in the chest wall, lung, heart
or great vessels. There may also be a Pneumothorax in
association.
Patient may be presented with pain, breathlessness,
shock. On examination there are signs of pleural
collection with lack of breath sounds & dull percussion
note.
7.5.2 Diagnosis & management Figure 4.1: Inter-coastal Drainage tube
a) To be diagnosed by X-ray Chest of fluid level

8.3. Pneumothorax / Haemothorax
ICD insertion procedure:
b) Patient needs following treatment with ICD
8.3.1 Part Preparation
 Blood transfusion SOS  Parts shaved and prepared
 After stabilization of the patient as and where  Consent taken which should be valid and in written
required as per condition of injury & patient to be  Parts painted and draped
shifted to higher center in ALS transport vehicle.  Position: Semi recumbent (45%) on a backrest
Turn the patient's head on the opposite side
8. INTERCOSTAL
DRAINAGE (ICD) 8.3.2. Anesthesia: LA
8.3.3. Site:
8.1. Indications for Chest Tube
 2nd inter costal space, mid-axillary line for
Insertion: pneumothorax.
 Pneumothorax
 7th inter costal space, in the mid-axillary line for
 Hydropneumothorax Haemothorax.
 Haemothorax
 Empyema
Page 489
Cut skin, Subcutaneous tissue. Split the muscles with
artery forceps, till the pleura is reached. Keep the
inter costal tube ready - Malecot's catheter or Portex
ICD tube. Keep the underwater drain and drainage
tube ready. Plunge the artery forceps into the pleura.
The ICD tube mounted on another long & blunt
artery forceps in thrust into the pleura along the
direction of opposite shoulder.
8.3.3. Position the ICD tube: Figure 4.4: Intercostal Tube fixation
All the holes of the tube should be in the pleural
cavity
8.4. POST INSERTION:
8.3.4. Fix the ICD tube with a skin stitch: 8.4.1 X-ray chest watch for complications:
 Air bubbles are seen coming out and a column of  Not draining (check for kinking)
fluid moving with respiration. Blood is seen
 Organ injury (lung, liver, spleen, heart, vessel) –
coming out and a column of fluid moving with
careful insertion
respiration in Haemothorax.
 Indication for Surgery
 Clinically, the patient improves: The tachypnoea  Surgical emphysema (small hole and good
settle. Respiratory sounds are heard. Chest X-ray suturing)
shows lung expansion.  Infection (sterile technique)
8.3.5 Inter costal drain is removed when the
lung is expanded completely and air 8.5. Safety features:
column movement absent  First tube connecting drain to drainage bottles
X-ray Chest shows full expansion, Column of fluid must be wide to decrease resistance
in the IC drain stops moving.
 Volume capacity of this tube should exceed ½ of
patient’s maximum inspiratory volume (otherwise
8.3.6 Removal: water may enter chest)
Cut the skin stitch, pull the IC drainage tube out
 Volume of water in bottle should exceed ½ of
and give immediate strapping (Vaseline gauze
patient’s maximum inspiratory volume to prevent
airtight)
in drawing of air during inspiration
 Drain should always stay at least 45cm below heart
level (prevention of removed fluid or water
refluxing into patient)
 Clamp drain when moving
 Water level above tube in another bottle
determines the amount of suction applied before
air drain through tube (safety suction limiting
device).
Figure 4.2: Site for Lidocaine Infiltration
Figure 4.3: Intercostal Tube insertion
Page 490
Bibliography
2. Das S. A Manual of Clinical Surgery. 11th edition. S. Das publication; 2015:650
Further reading
2011:704
2012: 768
2014: 2069.
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Page 491
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5. ABDOMINAL INJURIES
It has only muscle layers protecting the internal  Cold clammy extremities
organs anteriorly and laterally.  Restlessness
 Breathlessness
1. Blunt Trauma  Sweating
Occurs when the offending agent is blunt and wide  Altered level of consciousness
area of contract occurs at the time of impact. Severity  External injuries
of the injury depends on the force of the offending 3.2. Stabilize the hemodynamically
agent. Most commonly it effects to injury of spleen
unstable patient first, investigate
2. Penetrating trauma later.
Occurs when injured by sharp instruments and the 3.3. Cardiothoracic, head and
depth and direction of the wound is more important spinal injuries get priority over
than the size of the wound. Most commonly it effects
to Small bowel.
Abdominal and other skeletal
and surface injuries.
2.1. Cause: Refer patient immediately for emergency surgery
 Accidents (Traffic, industrial and disasters) & expert managements.
 Falls 3.4 Blood transfusion if blood loss
 Assaults
 In children (child abuse, bicycling, swimming,
or in shock.
etc) 3.5 Treatment
2.2. Investigation  NBM, RT aspiration
 The history of the traumatic event is important  IV Fluids - Ringer lactate, DNS, Dextrose 5%
in determining the nature and severity of the  Analgesics - Inj. Diclofenac 50 mg/IM.
intra-abdominal organ injury.  Antibiotics-
 X-ray abdomen standing  Inj. Ampicillin 500 mg IV /6 hourly OR Inj.
 USG abdomen and CECT Cefotaxime 1 gm/BD.
 Inj. Gentamycin 80 mg IV / 12 hourly.
3. Presentation & Management  Inj. Metronidazole 500 mg IV/ 8 hourly.
3.1 Life saving measures such as 4. Proceed in the following
ABCDE order for haemodynamically
 Airway patency
 Bleeding control stable patient:
 Circulation maintenance  Complete clinical examination
 Breathlessness  Plain X-ray - Erect or left lateral position
 Deformity (cervical stabilization and fracture  Diagnostic peritoneal tapping
immobilization) should be done first before  Ultra sound (CECT)
transport to the hospital.  Abdominal CT
- Examine head to toe thoroughly on arrival of
the trauma patient to identify the entire If there is progression in illness/detected internal
injuries. Categorize patient immediately into injury, patient to be shifted for further expert
treatment to higher center.
hemodynamically stable or unstable.
- Haemodynamically unstable patient will have
the following features
Page 492
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

Page 493
6. Gangrene
1. Definition: Dry gangrene: Treat the cause
 Macroscopic death of the tissues with superadded Wet gangrene:
putrefaction.
 Rest pain is an ominous symptom and usually  Stabilize the patient hemodynamically.
requires revascularization because this form of
 Requires urgent assessment and shift the patient as
advanced ischemia generally progresses to tissue
required for further surgical treatment.
loss. Patients with Diabetes or Renal failure are
more susceptible to the development of ischemic  Exclude Diabetes by repeated Blood Sugar
pedal ulcers. estimation.
Two Types of Gangrene
 Dry gangrene usually results in patients with 3. Fournier's Gangrene
chronic critical limb ischemia without infection or Idiopathic Gangrene of scrotal skin
without any other complicating factors like
diabetes, osteomyelitis etc. It is characterized by 3.1 Clinical features:
dry shrivelled appearance, with clear line of  Common in young apparently healthy individuals.
demarcation and no foul smell.  Sudden appearance of scrotal inflammation - red
 Wet gangrene is characterized by no clear line of swollen, very painful. Patient is toxic with fever,
demarcation, foul smell, purulent discharge, prostration
evidence of proximal spread in form of skip areas  Within one/two days, extensive gangrene of the
scrotal skin occurs resulting in sloughing of the
scrotal skin exposing the testicles. In few, the
gangrene can involve skin of the penis, anterior
abdominal wall, medial side of thigh, perianal
region. In such situations, it is described as perianal
phlegm
 Luckily, the testis does not get involved in
Fournier’s gangrene because of thick tunica
albuginea.
3.2 Treatment
Figure 6.1: Dry Gangrene Figure 6.2: Wet Gangrene  Antibiotics- -Inj. Cefotaxime 1 gm/BD.
-Inj. Gentamycin 80 mg. IV/12 hourly 12-24 hrs.
-Inj. Metronidazole 500 mg. IV/8 hourly.
2. Treatment:  IV Fluids - RL, DNS 5000-6000 ml
 Analgesics- Inj. Diclofenac 50 mg/IM
 Antibiotics- Inj. Ampicillin 500 mg. If there is no regression in ischemic changes and when
extensive debridement is required, shift patient to
IV/6 hourly. OR
higher surgical center.
Inj. Cefotaxime 1gm. IV/12 hourly 3- 4 days
* Exclude Diabetes by blood sugar levels. When
Inj. Gentamycin 80 mg. IV/12 hourly. granulations occur, skin grafting is needed if raw area
is large, if small wound can be sutured by
Inj. Metronidazole 500 mg. IV/8 hourly.
approximating the skin edges of the wound.
 IV fluids -Ringer lactate, DNS, dextrose 5% 5000-
6000 ml
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Bibliography
Further reading
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7. Burns
1. Introduction:
A common surgical emergency. Children and females
are more vulnerable in India. Commonest are accidental
scalds due to hot water or oil in children and stove burst
or suicidal/ homicidal burns in females.
Clinically burns can be classified as follows:
 Burns >10% in children and >25% in adults
require Intravenous fluid therapy. In addition,
certain specific cases as shown in figure 1
preferably need to be managed in Burn Centres.
 In adults, Rule of Wallace or rule of 9 is
applicable.
 In Paediatrics, head is large hence rule of 9 is
not applicable.
3. Treatment:
3.1. Medical:
 Reassure the patient.
 Burn surface calculation using Wallace rule of '9'
and Calculate fluid requirement according to Figure 7.1: Calculation of Burns percentage
Parkland Formula and administer. Strictly monitor
patient’s intake and urine output after
catheterization. If the burn surface area exceeds
35%, consider keeping the patient NBM and put
Ryle’s tube anticipating paralytic ileus to avoid
aspiration.
 Investigations:
- CBC
- ABG
- BSL
- KFTs
3.2 Dressing:
3.2.1 Open – Figure 7.2: Burn Surface Area = Burn percentage
Wounds to be cleaned with distilled water and
antiseptic lotion, apply antiseptic
ointment/creams – Furacin, Silver sulfadiazine
+Chlorhexidine etc.
3.2.2 Close –
Deep burns need close dressing by autoclaved
bandage after completion of procedure
mentioned above or use Tulle Gras (Bactigras
or Sofra Tulle) of Silver sulfadiazine +
Chlorhexidine, Povidone-Iodine etc.
Page 496
3.3 Proper antibiotics coverage  Endotracheal intubation SOS Tracheostomy in
 Burn patients should be given antibiotics like Inj. patients with airway and breathing difficulty
Cefotaxime 1gm BD or 3rd generation HNF.
Cephalosporins.  Escharotomy incisions may be required for
 Inj. Gentamycin 80 mg BD circumferential deep burns involving the
extremities or the chest.
 IV Metronidazole 500 mg 8 hourly etc. for 7 to 8
days keeping in view the condition of the patient.  Daily needful dressing under aseptic precaution
 Adequate oral hydration
3.4 Other 4. When to refer:
 Venesection may be required in case if peripheral  All patients requiring special burn centre care as
lines are all collapsed. Preferably Venesection is listed earlier.
done at the ante cubital fossa. But if not possible  Patients in septicemia shock
due to extensive burns, then long Saphenous vein
can be cannulated for administering fluids.
Bibliography
Further reading
2011:704
2012: 768
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Page 497
8. Dressings
 Normal saline
1. Aim of wound dressing:  Hydrogen peroxide
In an open wound which is being allowed to heal by
secondary intention, or is being prepared for a  EUSOL
delayed reconstructive procedure, the requirements 4.2 Dressing material
are prevention of desiccation of the surface, removal  Cotton gauze / pads / bandage
of excess wound exudates, protection from physical  Hydrocolloid dressings
damage and reduction of risk of infection  Paraffin / non adhesive gauze (BACTIGRAS)
 Collagen granules
2. Types of wound dressing:  Adhesive strips
2.1 Occlusive (covered)
In most cases, occlusive wound dressings are 5. Types of wounds and
preferable since they prevent bacterial
contamination, keep the wound moist and
dressings:
provide a cover over the wound allowing normal 5.1 Clean open wounds:
activities. Such wounds require simple cleaning with
2.2 Non occlusive (open) normal saline followed by a light dressing with
non-adherent gauze such as Bactigras / plain
Non occlusive wound dressing may be used in
paraffin gauze. Adherent dressings such as plain
special cases of clean granulating wounds,
cotton gauze should be avoided as they tend to
burns, dry escharotic where the patient is well
damage the granulation tissue on dressing
informed and educated regarding keeping the
change.
wound clean and local hygiene.
5.2 Clean sutured wounds:
Electively sutured clean wounds require only a
3. Indications for wound light dressing of cotton gauze. The treating
dressing: doctor may or may not place a layer of
 The primary determinant of the need for a antiseptic ointment over the wound (e.g.
dressing is the depth and degree of bacterial povidone iodine, soframycin). Repeat dressings
contamination of the wound. are not required.
 Superficial clean wounds are best managed by 5.3 Contaminated sutured wounds:
infrequent dressing. Contaminated wounds require thorough
 Deep clean wounds are best managed by cleaning with copious amounts of normal saline.
immediate suturing and light dressing (for If the degree of contamination is high, this
physical protection only ) should be followed by hydrogen peroxide. The
 Contaminated / Dirty wounds are best managed wound should then be irrigated with an
by surgical debridement / wash followed by antiseptic solution and covered with cotton
regular wound dressing gauze. Dressing change may be performed at 24
 All electively sutured surgical wounds DO NOT hours and is primarily to assess the presence of
require regular wound dressing. At most they a collection or infection in the wound. The
require a light dressing for physical wound presence of either should prompt removal of
protection. some or all the sutures converting the wound
into an open contaminated wound. Such wounds
may also require systemic cover of antibiotics
4. Dressing components: depending on the degree of contamination.
4.1 Antiseptics and wound 5.4 Contaminated open wounds:
cleaning solutions Such wounds require regular (daily) dressing.
 Povidone iodine Irrigation with hydrogen peroxide should be
 Cetrimide performed followed by normal saline to decrease
 Glacial Acetic acid 10% - infected greenish the physical contamination of the wound.
wounds (pseudomonas) Antiseptic solution irrigation should then be
performed. Such wounds tend to discharge, so a
Page 498
bulkier dressing with more absorbent gauze may performed with hydrogen peroxide, followed by
be required. normal saline and antiseptic solution. The
5.5 Dirty wounds: covering cotton gauze should be soaked in
Such wounds are characterized by presence of normal saline or EUSOL. Dressing changes
slough, necrotic tissue, eschar or frank need to be frequent and may have to be repeated
gangrene. These wounds require initial surgical thrice daily. The covering material should
debridement for removal of gross necrotic tissue ideally be kept moist with saline / EUSOL. The
and debris. Debridement may have to be wounds with surrounding cellulitis, edema
repeated. Depending on the degree of slough, should be covered with Magnesium sulfate
this may be performed bedside or may require dressings. It absorbs the fluids, reduce edema
an OT and anesthesia. The dressing should be and pain. Large granulating wounds should be
sent for Skin grafting.
Bibliography
2. Das S. A Manual of Clinical Surgery. 11th edition. S. Das publication; 2015:650
Further reading
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Page 499
9. BREAST
 Both axillae should be examined for palpable
1. Common presentations lymph nodes ensuring the anterior, medical
1.1. Lump: posterior and apical nodes. The size, numbers and
 Any new discrete lump (Mass) in breast or axillae fixity should be recorded
 New lump (Mass) in pre-existing Modularity  Note that clinical assessment of axillary nodes may
 Asymmetrical Modularity that persist after one or not reflect their pathology status. For TNM staging
two menstrual cycle it is important.
 Abscess or breast inflammation which does not  The supraclavicular and infra-clavicular fossa and
settle after treatment cervical region should also be examined for
 Recurrent mass/swelling palpable lymph nodes
1.2. Pain:  Any other symptomatic regions should be
examined as required for signs for metastatic
 If associated with a lump (mass)
diseases
 Unilateral persisting pain in postmenopausal
 All examination findings must be recorded in
women
sketch or written form, as part of good clinical
1.3. Nipple Discharge: practice and for medico legal reasons
 Blood stained discharge  Initial assessment, investigations and staging of
 Persistent single duct discharge breast symptoms should be notified.
1.4. Nipple retraction or distortion /
nipple eczema 3. Benign Breast Conditions
1.5. Skin retraction of long duration  Fibro-adenoma
 Cyst
 Duct Papilloma
 Fibroadenosis or Fibrocystic disease of Breast.
4. Inflammatory conditions
 Abscess (Acute Mastitis)
 Fistula
5. Other conditions (Non-
malignant)
5.1. Fat necrosis
Figure 9.1: Signs of Breast Cancer Fat necrosis following trauma can occur. Small cancer
may clinically and radiologically mimic fat necrosis.
2. Examination of breast: Treatment is by reassurance or excisional biopsy.
Some key steps:
 The patient (naked to the waist) is examined in the 5.2. Mastalgia (Breast pain):
presence of a female attendant  Can be symptom in malignancy of breast in less
 With patient sitting – note change in contour, skin than 10%
tethering, nipple tethering, arms above her head  Chest wall disease should be excluded
 Tethering of lesion to the chest wall  Intra-abdominal (gall stones) intra-thoracic
 Examination of axillary tail with flat of hand (cardiac, pleural) pain may all present as breast
 Lump should be assessed for size (measured by pain.
calipers) shapes, consistency, tenderness, mobility  Exclusion of significant breast pathology,
and fixity to the overlying skin/ underlying chest reassurance and non-steroidal drugs can provide
wall, skin changes in the form of edema (peau symptomatic relief.
d'orange
Page 500
5.3. Gynaecomastia: 6.2.2 N-regional lymph nodes
 Pubertal Gynaecomastia N0- No palpable homolateral axillary nodes
 Gynaecomastia secondary to drugs therapy liver
disease testicular tumors hyperthyroidism renal N1 – Mobile homolateral axillary nodes
disease should be excluded. N2- fixed homolateral axillary nodes or matted
N3- Homolateral supraclavicular and infra-clavicular
6. Malignant lump (cancer): nodes + internal mammary and/or edema of arm.
6.1. Definition: 6.2.3 M – Metastasis
The risk of developing distant metastasis increase with
tumor size. Early breast cancer is defined as the M0 - No distant metastasis
condition in which tumor is confined to the breast, size 2 M1 - Distant metastasis
cm with obvious no metastasis.
6.3. Screening for breast cancer:
 Beneficial in women over 30 + years age
 Can detect smaller tumor with lower mass of
lymph node, metastasis
 Early detection of breast cancer. By examination
and mammography reduces morbidity in screened
patients.
Figure 9.2: Metastatic spread of Ca Breast
6.2 T.N.M. classification

T-primary tumor N-nodes M-metastasis
6.2.1 T – Primary tumor mass Figure 9.3: Breast Self-Examination
This classification is internationally accepted and widely
used to describe the extent of the tumor, regional nodes 6.4. High Risk factors:
and metastasis.  Strong family history of Breast or Endometrial
T0 - No demonstrable tumor cancer
 Carcinoma of Contra-lateral Breast
Tis - Carcinoma in situ  A history of intra-ductal papilloma
T1 - Tumor diameter 2cm or less without fixation  Childless women and those conceiving after 30
years of age
T2 – 2 cm to 5 cm without fixation  Breasts with dense parenchyma with prominent
T3 - Tumor greater than 5cm duct patterns (fatty breasts with minimal
connective tissue elements are at risk)
T4 - Extension of a tumor of any size to skin or chest
wall.
Page 501
6.5. Diagnosis of breast cancer: 6.6. Investigation:
6.5.1 Physical examination of breast (Clinical-  Biopsy, Tru-cut needle biopsy of the lesion for
examination of breast fortnightly) histopathological evidence
 Estrogen, Progesterone / Hormonal receptor status
 MRI spine for Metastasis in the vertebras.
 USG Liver for secondaries.
6.7. Treatment:
6.7.1 Aim:
 To reduce morbidity and extend 5-year and 10-
year survival rates.
 To conserve the breast, if possible
Figure 9.4: Symptoms of breast cancer  To achieve the control of disease.
6.5.2 FNAC (fine needle aspiration cytology) by
23G needle: 6.7.2 Treatment options:
 Surgical management (MRM, BCT, QUART)
 Radiotherapy
 Chemotherapy
 Hormonal therapy
7. Surgical management:
7.1 Surgical management includes
 Modified radical mastectomy (Patey’s)
 Radical mastectomy (Halstead) not done
commonly
 Breast conservative procedure (Quadrantectomy,
Figure 9.5: FNAC Aspiration cytology lumpectomy, wide local excision)
 Simple mastectomy for ulcerated, foul smelling
6.5.3 Imaging methods/ mammography lesion of breast (toilet mastectomy)
 Breast reconstruction cosmetic surgeries-after
complete removal
7.2 Radiotherapy:
 Pre-operative – for tumor mass
depletion/regression
 Post-operative – as advised by Surgeon
7.3 Hormonal therapy:
 Tab. Tamoxifen 100 mg BD
7.4 Chemotherapy: CMF regime, will achieve
25% reduction in the risk of relapse over 10 -15 years.
Figure 9.6: Mammography
Bibliography
Further reading
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Page 503
10. Congenital Anomalies of G.I.T
1. Most common anomalies are: 1.1.3. Diagnostic evaluations:
 Apparent at birth.
i. Cleft Lip or Cleft Palate
ii. Hernias  Examining the palate
iii. Esophageal Fistula  Prenatal diagnosis after 13-14 weeks when the soft
iv. Anorectal malformations tissue of the fetal face can be visualized.
1.1.4. Why CP more serious than CL?
1.1 Cleft Lip (CL) or Cleft Palate  It interferes more with feeding and breathing, more
(CP) difficult to repair.
CL and CP are facial malformations that occur during
embryonic development and they are the most common 1.1.5. Therapeutic Management
congenital deformities of the head and neck. They may The management of CL involves the cooperative efforts
appear separately or more often together. of a multidisciplinary health care team.
1.1.1 Definition:  Pediatrics

a) Cleft Lip: It is a congenital fissure in the upper lip.  Plastic surgery
b) Cleft Palate: It is a midline fissure of the palate that
results from failure of the two sides to fuse.  Speech/ language pathology
 Audiology
 Nursing and social work
1.1.6. Management is directed toward:
 Closure of the clefts, Surgery can be done after 6
months of age with Hb more than 10 gm and baby
weight more than 10 kg.
 Prevention of complications.
 Facilitation of normal growth and development in
the child.
1.1.7. Prognosis:
Figure 10.1: (A) Unilateral cleft lip, (B) Unilateral Even with good anatomic closure most children have:
cleft lip and jaw, (C) Bilateral cleft lip with cleft
palate and (D) Isolated cleft palate  Some degree of speech impairment.
 Inefficient functioning of the muscles of the soft
1.1.2 Important feature of Cleft Lip & Cleft palate and nasopharynx.
Palate
 Small notch  Improper tooth alignment.
 Extending into the base of the nose.  Varying degree of hear loss.
 Unilateral or bilateral.
 Improper drainage of the middle ear.
 CL/CP may involve the soft and hard palate.
 One or both sides.  Recurrent Otitis media with scarring of the
tympanic membrane.
 Unilateral clefts are nine times more common than
bilateral clefts.
 60% to 80% of children born with cleft lip and
palate are male.
Page 504
1.1.8. Nursing consideration 1.2. Hernias
It is important for nurse to emphasis not only the
infant’s physical needs but also on the parent’s It is a protrusion of a portion of a visceral organ through
emotional needs. an abnormal or normal opening. Commonly seen
hernias are:
 CL or CP reduces the infant’s ability to suck,
interferes with compression of the areola.  The diaphragm,
 Feeding is best with the infant’s head in upright  The Abdominal wall, or
position.  The inguinal canal.
 Large, soft nipple with large holes have been
1.2.1. Diaphragmatic Hernias
advised and used.
Protrusion of Abdominal organs through opening in
 Large syringe with soft rubber tubing can be diaphragm.
used.
 With some infant spoon feeding works best
 Breast pump may be useful to stimulate the
letdown reflex.
1.1.9. Postoperative care for CL:
 Elbow restrains are used to prevent the infant
from rubbing or disturbing the suture line.
 Older infants who roll over will require a jacket
restraint to prevent rolling on the bed and
rubbing the face on the sheet.
 Adequate analgesia is required to relieve pain. Figure 10.2: Congenital Diaphragmatic Hernia
 Clear liquids are offered when the infant has a) Symptoms

fully recovered from anesthesia.  Mild to severe respiratory distress
 The suture site is carefully cleansed.  Tachypnea, cyanosis, dyspnea
 Absent breath sound.
 A thin layer of antibiotic ointment may be  Shock
applied. b) Diagnosis:
 Gentle aspiration of mouth and nasopharyngeal  Symptomatic
secretions.  X ray chest
c) Treatment
 An upright infant position.  Supportive treatment of respiratory distress (Use
1.1.10. Postoperative care for CP: of endo-tracheal intubation, oxygenation).
 Lie on the.  Prophylactic antibiotics (Ampicillin 50 mg/kg)
 Surgical reduction of hernia and repair of defect.
 Feeding by bottle, breast or cup. d) Nursing care:
 Oral packing, it is usually removed after 2 to 3 Preoperative:
days.  Resuscitation, maintain suction, oxygen.
 IV fluids
 Elbow restrains.  Positioning head up.
 Instruct the parents to keep the restrains at home  Administer medication
until palate is healed (2 to 6 weeks). Post-operative:
 Carry out routine postoperative care and
 Mild sedatives may be prescribed. observation.
 Soft food after discharging the patient as per
advice of surgeon.
Page 505
1.2.2 Hiatus Hernia:
Protrusion of stomach through esophageal hiatus.
a) Symptoms:
 Dysphagia, vomiting,
 Bleeding (haematemesis)
b) Management:
 Conservative management – maintaining
Posture.
 Surgical repair
Figure 10.4: Umbilical Hernia
1.3 Esophageal Fistula

The esophagus instead of being an open tube from the
throat to the stomach is closed at some point. A fistula is
common between the trachea and esophagus.
1.3.1. Clinical manifestation:
 Excessive salivation.
 Coughing, choking, cyanosis,
 Apnea
 Abdominal distention.
Figure 10.4: Types of Tracheoesophageal Fistula

(TEF)
1.3.2. Nursing alert:1
Any infant who has an excessive amount of frothy
saliva in the mouth or difficulty with secretions and
Figure 10.3: Hiatal Hernia unexplained episodes of cyanosis should be suspected
of having an EA / TEF and referred immediately for
1.2.3 Umbilical Hernia medical evaluation.
Weakness in Abdominal wall around umbilicus, 1.3.3. Therapeutic Management:
incomplete closure of Abdominal wall allowing
intestinal contents to protrude through opening.  Maintenance of patent airway.
a) Investigation:  Prevention of pneumonia.
USG abdomen
b) Symptoms:  Surgical repair of the anomaly.
 Noted by inspection and palpation.  Avoid oral intake, start IV fluids.
 High incidence in premature.
c) Management  Removal of mouth secretion by suction.
Surgical repair  Broad spectrum antibiotic therapy.
 Gastrostomy and repair of the TEF.
Page 506
1.3.4. Nursing role: Investigation:
 Invertogram will detect type of anomaly: Low or
 Nursing responsibility for detection of this High.
malformation immediately after birth. Diagnosis:
 After feeding the infant swallows, but  There is no anal opening.
suddenly coughs and the fluid return through
 The nurse is unable to insert the thermometer.
the nose or mouth, report immediately.
 No passage of meconium.
 The infant placed in incubator oxygen is  Later on abdominal distention and pain occur.
administered.
Treatment:
 Intermittent or continuous suction of nose. High anomaly will require immediate colostomy
while for low anomaly Local incision and Dilatation
 Oral fluids are withheld, the fluid intake met will be required.
by IV fluids or Gastrostomy. Postoperative care:
1.3.5. Postoperative care:  The anal area should be kept dry and clean.
 The infant is returned to radiant warmer or  If a colostomy has been done the skin around the
incubator. wound must be clean and apply colostomy clean
dressing.
 The Gastrostomy tube is connected to gravity
 The excoriations of skin occur around Colostomy
drainage until the infant can tolerate feeding. area due to digestive enzymes from intestinal
 Tracheal suction with extreme caution to avoid juices leaking from the side of bag. To prevent
injury to the suture line. this aluminum paint should be painted on the skin
 The initial attempt at oral feeding to make sure around the Colostomy site.
that the infant can swallow without choking.
 Oral feedings are begun with sterile water,
followed by frequent small feeding of formula.
 Infants are usually not discharged until they
are taking oral fluids well and the Gastrostomy
tube is removed.
1.4. Anorectal malformations
 Abnormal development of genitourinary and
pelvic organs.
 The rectum and urinary tract separate
completely by the seventh week of gestation. Figure 10.6: Imperforate anus repair
a) Imperforate anus
Is the most common congenital anomaly of
GIT in newborn.
Figure 10.5: Imperforate anus
Page 507
Bibliography
Further reading
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Page 508
11. Deep Vein Thrombosis
History and physical examination are therefore
1. Introduction: unreliable in the diagnosis of DVT. In addition,
Despite increased awareness and use of prophylactic symptoms and signs generally associated with DVT,
modalities, DVT and pulmonary embolism (PE) such as extremity pain and/or swelling, are
remain important preventable sources of morbidity nonspecific. DVT of the leg is complicated by the
and mortality. The incidence of DVT ranges between immediate risk of pulmonary embolus and sudden
5 and 9 per 10,000 person-years in the general death.
population, and the incidence of VTE (DVT and PE
combined) is approximately 14 per 10,000 person-
years. 3. Investigations:
Color Doppler will confirm the diagnosis.
The more common acquired risk factors include
advanced age, hospitalization and immobilization,
hormone replacement and oral contraceptive therapy, 4. Treatment:
pregnancy and the recently postpartum state, prior
VTE, malignancy, major surgery, obesity, nephrotic 4.1 Antithrombotic Therapy:
syndrome, trauma and spinal cord injury, long-hour Antithrombotic therapy may be initiated with IV or
travel (>6 hours), varicose veins, antiphospholipid SC Unfractionated Heparin, SC Low molecular
syndrome, myeloproliferative disorders, and weight Heparin, or SC Fondaparinux (a synthetic
polycythemia. Heritable risk factors include factor V pentasaccharide). This initial therapy usually is
Leiden; Prothrombin 20210A gene variant; continued for at least 5 days, while oral vitamin K
antithrombin, protein C, and protein S deficiencies; antagonists are being simultaneously administered.
and dysfibrinogenemias. Patients are at risk of The initial therapy typically is discontinued when the
developing a post thrombotic limb and venous international normalized ratio (INR) is ≥2.0 for 24
ulceration. hours
Hemorrhage is the primary complication of UFH
therapy. The rate of major hemorrhage (fatal,
intracranial, retroperitoneal, or requiring transfusion
of >2 units of packed red blood cells) is
approximately 5% in hospitalized patients undergoing
UFH therapy (1% in medical patients and 8% in
surgical patients). For patients with UFH-related
bleeding complications, cessation of UFH is required,
and anticoagulation may be reversed with protamine
sulfate. Protamine sulfate binds to UFH and forms an
inactive salt compound. Each milligram of protamine
neutralizes 90 to 115 units of heparin, and the dosage
should not exceed 50 mg IV over any 10-minute
period. Side effects of Protamine sulfate include
Figure 11.1: Deep Vein Thrombosis Hypotension, Pulmonary edema, and anaphylaxis.
2. Clinical Evaluation Most patients who receive therapeutic LMWH do not

require monitoring. Patients who do require
Early in the course of DVT development, venous
monitoring include those with significant renal
thrombosis is thought to begin in an area of relative
insufficiency or failure, pediatric patients, obese
stasis, such as a soleal sinus vein or immediately
patients of >120 kg, and patients who are pregnant.
downstream of the cusps of a venous valve in the axial
calf veins. Isolated proximal DVT without tibial vein
thrombosis is unusual. Early in the course of a DVT,
there may be no or few clinical findings such as pain
or swelling. Even extensive DVT may sometimes be
present without signs or symptoms.
Page 509
4.2 Vitamin K antagonists: Virchow’s Triad
Includes Warfarin and other Coumarin The factors described by Virchow are important
derivatives, are the mainstay of long-term in development of venous thrombosis these are:
antithrombotic therapy in patients with VTE.
Warfarin therapy usually is monitored by  Endothelial injury (Vascular injury)
measuring the INR, Vitamin K antagonist may
 Stasis or turbulence of blood flow
be started on the same day as the initial para-
enteral anticoagulant, usually at doses ranging  Hyper- coagulability of blood.
from 5 to 10 mg. Smaller initial doses may be
needed in older and malnourished patients, in
those with liver disease or congestive heart
failure, and in those who have recently
undergone major surgery and depends on liver
function, diet, age, and concomitant
medications.
Bibliography
Further reading
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Page 510
12. Varicose Vein
Patient usually has Cosmetic concerns
Symptoms of tiredness & heaviness in legs and
itching and even leg ulcer
3. Etiology and Risk Factors

Female sex, Pregnancy (especially multiparity),
pelvic tumors, family history,
4. Complications:
 Ankle edema, Ankle flare, Pigmentation, Venous
eczema, Venous ulcer, Profuse Hemorrhage,
Superficial Thrombophlebitis, Equinous
deformity, Calcification.
 Deep vein thrombosis:
One of the important etiology as well as
complication of varicose veins. It presents
clinically as swollen woody calf, pain, ankle
edema and redness. Patient may have fever.
Figure 12.1: Varicose veins
1. Introduction: 5. Investigations:
Varicose veins are dilated, tortuous and elongated Doppler ultrasound is most ideal for complete
superficial veins of the lower limbs. Most develop in evaluation.
the tributaries of the greater and lesser saphenous
veins, which are usually dilated but rarely varicose 6. Treatment:
themselves.
6.1. Management options at glance
 Age old disease known since Hippocrates,
Mentioned in Ebers Papyrus in 1550.  Bisguard’s exercise– Heel raises at least 4 times
every day.
 Incidence - F>M, Prevalence 10–23% in men
 Compression stockings – For early varicosities
30–40% in women
without complications. Types of stocking are
 Skin changes – 5%, Active ulcers – 0.5%. - Below/Above knee
- Mid-thigh
1.2 Types:
 Primary Varicose Vein: (More Common, 6.2. Surgical treatment
congenital predisposition, decreased number of  Flush ligation at sapheno-femoral junction with
defective valves) stripping of long Saphenous Vein.
 Secondary Varicose vein: Less common,  Perforator ligation – Sub facial.
dysfunction of valves, trauma, DVT, AV fistula.
6.3. Others
1.3 Risk Factors: Female sex, pregnancy, family  Sclerotherapy - Ultrasound-guided foam
history, prolonged standing & obesity Sclerotherapy for short segments or recurrent
varicosity.
 Radiofrequency ablation (Closure®),
 Endo Venous Laser Ablation.
 Ambulatory phlebectomy or a Combination of
these treatments.
Page 511
7. Do’s and Don’ts: 8. Instructions to patient:
 In case the varicosity starts bleeding do not panic,  Life style changes, follow Bisguard’s exercises
immediately lie down flat on the ground and raise daily, use of compression stocking through the day
the bleeding limb above the heart level and apply can be removed at night. While sleeping ask the
Compression. patient to raise the foot end of the bed to aid
venous return
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.
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Page 512
13. GENITO-URINARY DISORDERS
1. PARAPHIMOSIS 2.3. Treatment:
 I.V. fluids - Ringer lactate, DNS, dextrose 5%
1.1 Clinical features:  Analgesics- Inj. Diclofenac 50 mg/I.M.
 Antibiotics-Inj. Ampicillin 500 mg 12 - 24 hrs
It is a condition in which the contracted foreskin cannot
I.V/6 hourly.
be retracted over the glans (phimosis). It is forcibly
retracted back off the glans and cannot be pulled  Inj. Gentamycin 80 mg I.V./12 hourly.
forwards again. The tight band causes obstruction of  Inj. Metronidazole 400 mg. I.V./8 hourly
venous returns followed by swelling of the distal
foreskin and glans. It can occur at any age. Condition is If not relived after stabilization of patient to be referred
very painful & if not taken care may cause to surgical center.
Ischemic/Pre-gangrenous changes.
3. EPIDIDYMO-ORCHITIS
Clinical features: It is an inflammatory & infective condition affecting
 Difficulty in micturition. epididymis and testis
 Ballooning of prepuce during micturition
 Edema, Erythema and tenderness of the prepuce 3.1. Patient present with:
and presence of purulent discharge
 Scrotal pain
 Inability to retract the foreskin
 Testicular swelling
 Low grade fever with chills
1.2 Treatment: 3.2. Investigation:
Technique of Reduction- Parts shaved & prepared
Patient in OT Parts painted & draped. Local anesthesia  Routine investigation
2% Xylocaine infiltrated at the root of the Penis.  USG Scrotum - Doppler study
 Manual compression and reduction 3.3. Treatment:
 By giving multiple needles punctures over  Analgesics tablet Acelofenac 10-20 mg/ BD OR
swollen & edematous foreskin of penis and Dicyclomine 50 mg/ BD
squeezing it to drive out the edema fluid followed  Antibiotics- Ofloxacin 400 mg/ BD for 5 to 7 days
by mechanical reduction by pulling it to normal OR Cefodoxime 200 mg/ BD 5 to 7 days.
position.  Anti-inflammatory- Serratiopeptidase -5 to 10 mg/
 Dorsal slitting at 12' O clock position and TDS 5 to 7 days
reduction.  Ibuprofen 200-400 mg/ TDS 5 to 7 days
Reduction of the paraphimosis is followed by a course  Scrotal support for 2-3 weeks
of antibiotics. And after 8-10 days perform
Circumcision (at surgical center).
2. TORSION TESTIS:
It is a condition caused by the twist of suspended testis.
2.1. Patient presents with

Sever scrotal pain of sudden onset referred to lumbar
region Vomiting, fever, Scrotal swelling with gross
tenderness up to the cord
2.2. Investigation:
 Routine investigation
 USG Scrotum - Doppler study - shows decreased
blood flow & also viability of the testis.
Page 513
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

 
Page 514
14. ANO-RECTAL DISORDERS
 Gangrene
1. Hemorrhoids  Suppuration
Hemorrhoids are clumps dilated veins occurring in  Portal pyemia
relation to the ano-rectal junction (commonly known
as piles) 1.5 Treatment: -
1.1. Classification: 1.5.1 Conservative management:
 Dietary improvement – high fiber diet
1.1.1. By descent  Avoid straining at defecation
Grade 1- Bleeding 1.5.2 Active Surgical Treatment

Grade 2- Protrusions with spontaneous reduction  Sclerotherapy
Grade3- Protrusions regressing with manual  Banding
reduction
 Photo coagulation
Grade4- Irreducible protrusions
 Hemorrhoidectomy
1.1.2. By Location
1.6 Postoperative care
 External: arise from inferior hemorrhoidal
Table 1: Post-Operative Care and Complication
plexus, and are covered by modified squamous
epithelium occurs below pectinate line.
 Internal: arise from superior hemorrhoidal
plexus, also above pectinate line. Post-Operative care Post-Operative
 Interno-external- when both are present. Complication
1.2 Clinical Features

1.2.1 Symptoms:  Watch for Early
 Bleeding, bright red and painless, frequent bleeding  Pain acute retention
bleeding may lead to anemia  Sitz bath twice of urine
 Prolapse daily in the  Reactionary
 Pain on prolapse postoperative Hemorrhage (24
 Mucus discharge period hrs)
 Pruritus / itching  Analgesics  Constipation
 Stool softeners Late
and laxatives  Secondary
1.3 Investigations:
 Avoids digital hemorrhage (24 hrs)
 Direct Visualization
rectal examination  Anal stricture
 Digital Rectal Examination in the early  Anal fissure
 Proctoscopy postoperative  Fecal incontinence
 Basic investigation (Hb, CBC, Urine) periods
 Blood grouping and RH typing
 USG (Associated portal hypertension)
 Colonoscopy
1.7 Important note:-
1.4 Complications: -  Surgery is for failure in conservative
 Profuse hemorrhage management or in severe cases
 Fibrosis  Colonic carcinoma to be ruled out
 Thrombosis (colonoscopy)
 Infection
 Pyelophlebitis  Anemia to be corrected pre-operatively (Blood
transfusion if required)
 Ulceration
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 Muco-cutaneous bridges should be preserved Ointment to relax anal sphincter and improve
during surgery to prevent anal stenosis blood flow like Diltiazem / Nifedipine cream /
glyceryl trinitrate ointment
 Conservation treatment preferred in pregnant  Sitz bath
ladies and elder.
 High fiber diet
2. Anal Fissure 2.5.2 Surgery: -
2.1. Definition:  Anal dilatation under GA
Anal fissure is an ulcer or a crack in the canal or anal  Fissurectomy
verge that may extend from muco-cutaneous junction
to dentate line. Anal fissure is of particular concern if 3. Pilonidal Sinus
it is acute because the degree of patient discomfort,
pain and disability are extremely high.
A pilonidal sinus is a depression in the skin or small
The type of fissure is acute and chronic. pit that occurs at the bottom of the tailbone (coccyx)
and can become infected and filled with pus. Once
 Acute anal fissure is a deep tear through the skin infected, the technical term is pilonidal abscess.
of the anal margin extending into the anal canal. Pilonidal abscesses look like a boil at the bottom of
There is little inflammatory indurations or the tailbone, just above the crack of the buttocks. It is
edema of its edges. There is accompanying more common in men than in women. It usually
spasm of the anal sphincter muscles. happens in young people up into the fourth decade of
 Chronic anal fissure is characterized by life.
inflamed indurate margins, and a base 3.2 Treatment:
consisting of either scar tissue or the lower 3.2.1 Medical treatment
border of the internal sphincter muscle. Chronic  Antibiotics (Cap. Ampicillin 500 mg TDS x
anal fissure does not heal with conservative 5 days)
measures.
 Analgesics (Tab. Diclofenac 50 mg BD x 5
days)
2.2. Symptoms: - 3.2.2 Surgery
 Pain during the defecation and / or after  Anal dilatation under GA.
defecation  Fissurectomy
 Slight bleeding / streaking
4. Anorectal abscess
2.3. Examination: -
 Acute fissure – Pain during per rectal 4.1 Definition:
examination with or without palpatory mucosal Anorectal abscess is a collection of pus in the area
abrasion of the anus and rectum.
 Chronic fissure – Skin tag fibrosed ano-rectal
mucosa 4.2 Causes
 Common causes of anorectal abscess include:
2.4. Investigations: -
 Blocked glands in the anal area
Basic investigation – Hb, CBC, Urine
 Infection of an anal fissure
Colonoscopy  Sexually transmitted infection
 Deep rectal abscess may be caused by intestinal
2.5. Treatment: - disorders such as Crohn's disease or
2.5.1 Conservative Management diverticulitis.
Laxatives – Cremaffin 30ml at bed time / stool 4.3. Risk factors

bulking agents -
 Anal sex
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 Chemotherapy drugs used to treat cancer 4.6. Treatment: -
 Diabetes 4.6.1 Analgesics-
 Inflammatory bowel disease (Crohn's disease Inj. Diclofenac 50 mg/IM BD/ SOS
and ulcerative colitis) 4.6.2 Antibiotics-
 Use of medications such as Prednisolone. Inj. Ampicillin 500 mg. I.V. / 6 hourly. 5 days
Inj. Gentamycin 80 mg. I.V. / 12 hourly.
 Weakened immune system (such as from
HIV/AIDS) Inj. Metronidazole 400 mg. I.V. /8 hourly.
The condition may occur in infants and toddlers who 4.6.3 Treatment involves surgery, open and drain
are still in diapers and who have a history of anal the abscess, patient may be shifted at surgical
fissures. center.
4.4. Symptoms 4.6.4 Post-operative care
 Swelling around anus and constant throbbing After surgery patient needs warm sitz baths sitting in
pain, fever are the most common symptoms. a tub of warm water) this may help to relieve pain,
Pain with bowel movements may be severe. reduce swelling and make the abscess easier to drain.
Other symptoms may include: - Drained abscesses are usually left open and have no
o Constipation stitches.
o Discharge of pus from the rectum Patient should be advised to take stool softeners,
practice good hygiene and eat a soft or liquid diet
o Fatigue and general malaise until the abscess has healed.
o Fever night sweats, and chills
4.7. Possible complications
o Lump or nodule, swelling, redness,
 Anal fistula
tenderness at edge of anus
 Sepsis
o Painful, hardened tissue  Continuing pain
In infants, the abscess often appears as a swollen, red,  Problem keeps coming back (recurrence)
tender lump at the edge of the anus. The infant may  Scars
be fussy and irritable from discomfort, but there are
usually no other symptoms. 4.8. Prevention: -
 Prevention or prompt treatment of sexually
4.5 Investigations transmitted diseases may prevent this cause of
A rectal examination may confirm an anorectal anorectal abscesses. Use condoms during
abscess. intercourse, including anal sex, to prevent such
infections.
A procto sigmoidoscopy may be done to rule out  Frequent diaper changes and proper cleaning
other diseases. during diaper changing will help to prevent both
Rarely, you may need a CT scan, MRI or ultrasound fissures and perianal abscesses in infants and
to determine where the pus collection is located toddlers.
Bibliography
Further reading
2011:704
Page 517
2012: 768
2014: 2069.
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Page 518
15. Tracheostomy
1. Introduction 5. Inner Cannulas

Tracheostomy is one of the most common surgical The inner Cannulas should be used at all times in the
procedures performed in the ICU and is the airway of ICU. They serve to extend the life of the
choice for patients requiring mechanical ventilation tracheostomy tubes by preventing the buildup
for more than 2 weeks. secretions within the tracheostomy. The inner
cannulas can be easily removed and either cleaned or
2. Procedure replaced with a sterile, disposable one. Disposable
Patient’s neck is extended and the surgical field is inner cannulas have the advantage of quick and
exposed from the chin to several inches below the efficient changing, a decrease in nursing time,
clavicle. This area is prepared and draped and decrease risk of cross-contamination, and guaranteed
prophylactic antibiotics are administered at the sterility. The obturator should be kept at the bedside
discretion of the surgeon. A vertical or horizontal at all times in the event that reinsertion of the
incision may be used; however, a horizontal incision tracheostomy is necessary.
will provide a better cosmetic result. The platysma
muscle is divided in line with the incision and the 6. Humidification
strap muscles are separated in the midline. The One of the functions of the upper airway is to
thyroid isthmus is then mobilized superiorly or is moisten and humidify inspired air. Since
divided as needed to access the trachea. In the event tracheostomy bypass the upper airway, it is vital to
of a low-lying cricoids cartilage, dissection on the provide patients who have tracheostomy with warm,
anterior wall of the trachea helps to mobilize the humidified air. Humidification of inspired gases will
trachea out of the mediastinum, and also the use of a prevent complications in patients with tracheostomy
cricoids hook will elevate the trachea to expose the Failure to humidify the inspired gases can obstruct
second or third tracheal ring. Following identification the tube by inspisated secretions, impair mucociliary
of the second or third tracheal ring, a vertical clearance, and decrease cough.
tracheostomy is created or a tracheal flap (Bjork flap)
is fashioned to create a fistulous tract by suturing the 7. Suctioning
tracheal mucosal flap to the skin in the incision Patients with tracheostomy frequently have increased
amounts of airway secretions coupled with decreased
3. Postoperative Care ability to clear them effectively. Keeping the airways
The care of a tracheostomy tube after surgery is clear of excess secretions is important in decreasing
important. Highlighted below are some specific the risk of lung infection and airway plugging.
issues that all intensivists need to know when caring Suctioning is frequently required in patients with
for patients with tracheostomies. poor or ineffective cough. Suction techniques should
remove the maximal amount of secretions while
4. Wound and Dressing Care causing the least amount of airway trauma. Routine
Daily examinations of the stoma are important in suctioning, however, is not recommended.
identifying infections or excoriations of the skin at
the tracheostomy site. In addition, keeping the wound 8. Tracheostomy Tube
clean and free of blood and secretions is very
important, especially in the immediate post
Changes
tracheostomy period. Dressing changes should be Tracheostomy tubes do not require routine changing.
performed at least twice a day and when the dressings In general, the tube only needs to be changed under
are soiled. Some authors recommend cleaning the the following conditions: (a) there is a functional
stoma with 1:1 mixture of Hydrogen Peroxide and problem with it, such as an air leak in the balloon; (b)
sterile saline. When changing dressings and tapes, when the lumen is narrowed due to the buildup of
special care is needed to avoid accidental dislodging dried secretions; (c) when switching to a new type of
of the tracheostomy tube. tube; or (d) when downsizing the tube prior to
decannulation. Ideally, a tracheostomy tube should
not be changed until 7 to 10 days after its initial
placement. The reason for this is to allow the tracheal
Page 519
stoma and the tract to mature. Patients who have their  Cardio respiratory arrest (uncommon)
tracheostomy tube changed before the tract is fully  Tracheo-laryngeal injury (uncommon)
mature risk having the tube misplaced into the soft  Crushed airway from dilatational tracheostomy-
tissue of the neck. If the tracheostomy tube needs to uncommon
be replaced before the tract has had time to mature,
the tube should be changed over a guide, such as a
suction catheter or tube changer.
9.2. Intermediate Complications
(from day 1 to day 7)
9. Complications of  Persistent bleeding
 Tube displacement
Tracheotomies  Tube obstruction (mucus, blood)
 Major atelectasis
9.1. Immediate Complications (24  Wound infection/cellulitis
hours)
 Tube displacement 9.3. Late Complications (>day 7)
 Arrhythmia  Tracheo innominate artery fistula
 Hypotension  Tracheomalacia
 Hypoxia/hypercapnia  Tracheal stenosis
 Loss of airway control  Necrosis and loss of anterior tracheal cartilage
 Pneumothorax  Tracheoesophageal fistula
 Pneumomediastinum  Major aspiration
 Acute surgical emphysema  Chronic speech and swallowing deficit
 Major hemorrhage  Tracheo cutaneous fistula
 Bacteremia
 Esophageal injury (uncommon)
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

Page 520
16. URINERY CATHETERZATION
1. Indication:
Urinary catheterization is done when a person is unable
to urinate using a toilet, bedpan, urinal, bedside
commode or when accurate urinary output is required.
Red rubber
Figure 16.1: Diagrammatic presentation of

Urinary Catheter assembly
2. Types of catheters:
2.1 Condom catheter:
Consists of a soft plastic or rubber sheath, tubing,
and a collection bag for the urine. The sheath is Latex
placed over the penis and the collection bag is
attached to the leg. Collects urine when there is no
need for catheter insertion.
2.2 Straight catheter:
Is used when the catheter is to be inserted and
removed immediately.
2.3 An indwelling catheter:
Also known as Foley catheter, is left inside the
bladder to provide continuous urine drainage.
2.4 Suprapubic catheter:
It is a type of indwelling catheter. The supra-pubic
catheter is inserted into the bladder through a
surgical incision made in the Abdominal wall, right
above the pubic bone.
2.5 3-way catheter: Silicon
For continuous bladder irrigation (CBI) is a type of
indwelling catheter. Irrigate the bladder to prevent Figure 16.2: Types of Catheter
obstruction (i.e. bleeding)
Page 521
Figure 16.3: Catheterisation
Straight Condom
Suprapubic Indwelling
3. Sizes & Subtypes: 3.3 Coude (French for elbowed)

catheters have a 45° bend at the
tip to allow easier passage
through an enlarged prostate
"Council tip" catheters have a
small hole at the tip which allows
them to be passed over a wire
Figure 16.4: Balloon retainer 4. Caring for a Person with an

3.1 Most common sizes are 8 F to Indwelling Urinary Catheter:
28 F.  The catheter tubing is secured loosely to the
person’s body near the insertion site using a catheter
3.2 1 F is equivalent to 0.33 mm = strap or adhesive tape
.013" = 1/77" of diameter.  Securing the tubing to the person’s body prevents
the catheter from being accidentally pulled out
during repositioning
 The drainage bag is then secured to the bed frame at
a level lower than the person’s bladder.
Page 522
5. Emptying Urine Drainage 7.3. Important aspects
Bags:  Arrange equipment
 Urine measured at the end of each shift or every 4  Wash hands

hourly in ward, every hourly in ICU.  Provide privacy
 Urine drainage bags should also be emptied if they  Raise bed, stand on left side of bed if right handed
are full. (right side if left handed)
 Leg bags need to be emptied frequently because  Water proof pad under client
they are smaller, and hold less urine.
 Position & drape client
6. Quantity:
 Be sure to monitor urine output
 Amount
 Characteristics (color, clarity, sediment,
haematuria, odor) Figure 16.5
 Less than 30 ml/hr of urine indicates a problem
7. Catheter Insertion:
7.1. Equipment:
(check packages and expiry dates)
Figure 16.6
 Catheter tray (with drapes, fenestrated drape,
cotton balls, swab holder, bowl) 7.4 Position
7.4.1 Female: dorsal recumbent (supine with knees
 Catheter 14-16 Fr (for women) 12 Fr for young flexed) or Sims position (side-lying with upper leg
girls flexed at knee and hip)
 16-18 Fr (for men)
 Sterile drainage tubing with collection bag
 Correct size syringe (check catheter balloon)
 Sterile water Figure 16.7
 Cleansing solution: Chlorhexidine 4%, Povidone
7.4.2 Male: supine position
Iodine 10%
 With disposable gloves, wash perineal areas
 Lubricant anaesthetic jelly
Anatomy:
 Sterile gloves
 Specimen container
 Tape to anchor tubing
7.2. Assess
 Review physician’s order and understand purpose
of inserting catheter
 Assess client (last urination, level of awareness,
understanding)
 Palpate bladder
 Identify meatus and assess skin integrity
 Identify potential difficulties (i.e. enlarged
Figure 16.8: Male urinary tract
prostate)
Page 523
7.4.5 Men: retract foreskin, hold penis below glans,
maintain position of hand, with forceps clean in
a circular motion from meatus down to base of
glans, repeat three more times
Figure 16.9: Female External Reproductive tract Cleaning of part Draping

7.5 Procedure: Figure 16.13 Figure 16.14
7.5.1 Anaesthetic Lubricant jelly
7.5.2 Apply sterile drapes keep gloves sterile
women: under buttocks and fenestrated over
perineum
men: over thighs and fenestrated over penis
7.5.3 Place sterile tray and contents between legs
7.5.4 Cleanse meatus:
Catheter in situ
Figure 16.15
7.4.6 Women:
With non-dominant hand, expose meatus, maintain
Position of hand, clean with forceps, wipe from front to
back, each time take new cotton ball for each swipe, far
labial fold, near and directly over meatus
7.6 Insertion:
 Hold end of catheter loosely coiled in dominant
hand, place end of catheter in tray
 Insert catheter:
Women: Ask client to bear down as if to void,
insert 5 to 7.5 cm or until urine flows, then
advance another 2.5 to 5 cm
Men: Hold penis perpendicular, ask client to bear
Figure 16.10: Cleaning of part down, insert 17 to 22.5 cm or until urine flows,
Figure 16.11: Male Urethra then advance to bifurcation
Figure 16.12: Catheter in situ
 Collect specimen if indicated
 Allow bladder to empty unless policy restricts (800
to 1000 ml) Pelvic floor blood vessels may become
engorged from the sudden release of pressure,
Page 524
leading to possible hypotensive episode. This may 7.9. Document:
also cause painful bladder spasms.
 Report and record type and size of catheter
 Inflate balloon with amount indicated (10 ml)
 Amount of fluid used to inflate balloon
 If client complains of pain, aspirate solution and
 Characteristics of urine, amount, reason for
advance catheter further and inflate
catheter, specimens, client’s response
 Gently pull to feel resistance
 Attach catheter to collection bag and attach to bed
8. Procedure for removal:
frame below bladder  Deflate the bulb completely with syringe
 Anchor catheter (thigh if appropriate and coil  If bulb cannot be deflated, then
tubing on bed and attach to mattress)
 Cut the one-way valve
7.8 Evaluate:  Puncture the channel with needle
 Palpate bladder
 Go on puncturing from distal most end to most
 Assess comfort proximal end
 Characteristics and amount of urine  USG guided suprapubic needle puncturing of the
bulb
 Inflate further till it gets busted.
Bibliography
1. Townsend Jr CM, Beauchamp RD, Evers Bm, Mattox KL. Sabiston Textbook of Surgery. 19th edition.
Elseviers, 2012: 2152
Further reading
2014: 2069.
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Page 525
17. TRIAGE
 Gathering information at point of triage.
1. Introduction:  Perform initial assessments at point of triage.
It is the method of quickly identifying the victims  Triage process should be completed within five
who have immediately life threatened injuries & have minutes.
the best chance of surviving. 4.1 Important steps
The process in which: The right patient in the right
4.1.1 Start System:
place at right time to receive the right level of care.
Classification is based on
Triage involve a dynamic equilibrium between needs
 Respiration
and resources
 Perfusion
Needs= Number of wounded and types of wounds  Mental Status
Resource = Infrastructure and equipment at hand &
competent personnel present 4.1.2 Shift
 Identify and remove
2. The Triage Team  Select those severely injured
 The dead
 Triage team leader – coordinator  The slightly injured
 Clinical triage officer  The uninjured
 Head nurse, matron; chief organizer 4.1.3 Sort:

 Nursing groups Categorize the most severely injured based on:
 Life-threatening conditions (ABC)
3. Triage Documentation:  Anatomic site of injury
3.1 General information  Red Cross Wound Score
 Treatment available in terms
Name, age, gender, chief complaints, history of past  Serious wounds: resuscitation and immediate
illness, mechanism of injuries, past medical and surgery
surgical history, allergy to food or drug and current  Second priority: need surgery but can wait
medication, date of last tetanus immunization, last  Superficial wounds: ambulatory management
menstrual period for female age 11 to 60 years
 Severe wounds: supportive treatment
3.2 Vital sign- temperature, Pulse,
B.P & respiration etc. 5. Categorization:
3.3 Level of consciousness 5.1 Category i) (Red): Resuscitation
and immediate surgery
3.4 Visual inspection for
Patients who need urgent surgery lifesaving and have
deformities, laceration, a good chance of recovery. (E.g. Airway, Breathing,
bruising, rashes etc. Circulation: tracheostomy, haemothorax,
hemorrhaging abdominal injuries, peripheral blood
4. Triage Process vessels)
Page 526
Figure 17.1
Figure 17.4
Figure 17.2
Figure 17.5
5.2 Category ii (Yellow): Need
surgery but can wait 5.3 Category iii (Green): Superficial
Patients who require surgery but not on an urgent basis.
wounds (no surgery, ambulatory
treatment)
A large number of patients will fall into this group. (e.g.
non-haemorrhaging Abdominal injuries, wounds of Patients with wounds requiring little or no surgery. In
limbs with fractures and/or major soft tissue wounds, practice, this is a large group, including superficial
penetrating head wounds GCS > 8.) wounds managed under local anesthesia in the
emergency room or with simple first aid measures.
Figure 17.3
Figure 17.6
Page 527
5.4 Category iv (Black): Very severe Example:
 Cardiac Arrest
wounds (no surgery, supportive  Airway Obstruction
treatment)  Hemorrhage with shock
 Complicated Delivery
Patients with such severe injuries that they are unlikely  Seizures
to survive or would have a poor quality of survival.  Asthma
 Acute Bleeding or Acute Pain
The moribund or those with multiple major injuries  Depressed Level of Consciousness
whose management could be considered wasteful of
scarce resources in a mass casualty situation. 6.2.3 Urgent: Category 2 Colour Code YELLOW
Those conditions that are serious and if not treated in
timely manner are likely to become critical. Time
needed serious illness or injury that must be attended to,
but wait upto two hrs.
Example:
 Complex long bone fractures

 Bleeding Controlled with a pressure dressing
 Acute psychiatry problems
 High fever with another vital signs stable
6.2.4 Not Urgent: Category 3 colour code GREEN
Figure 7
Condition that can wait without likelihood of
6. Hospital Triage Setting: deterioration. Time needed, condition can wait for more
Doctor performs daily triage on a routine basis every day than 2 hrs.
in emergency department.
Example:
6.1 Aim:  Minor lacerations which requires sutures
It is to identify those patients who have the highest  Minor joint trauma requires x-ray for diagnosis
degree of compromise for the purpose of providing rapid  Chronic conditions that are stable such as
care to sickest patient first. preexisting skin rashes.
6.2.5 Category 4 colour code Black
6.2 Hospital Triage System Dead to be honored and to be taken care as marked in
end session, if not possible by assigned agency earlier.
i. Emergent
ii. Urgent 7. Conclusions:
iii. Non Urgent
iv. Deceased  Triage is method of quickly identifying victims who
have immediately life threatening injuries AND
6.2.1 Emergent: Category 1 Colour Code RED who have the best chance of surviving.
Those patients that are life threatening but likely to be  Key elements of the START Triage Systems are:
amenable to rapid intervention. Respiration, Perfusion and medication.
 Reverse Triage is used for mass casualty incidents.
Time required treatment immediately or within 15 to 30
minutes.
Page 528
Bibliography
Further reading
2011:704
2012: 768
2014: 2069.

Page 529
Orthopaedics
9. Orthopaedics
1 Infections in Orthopaedics 530

2 Arthritis 533
3 Congenital Disorders 535
4 Metabolic Disorders of Bone 537
5 Regional Conditions 538
6 Common Spine Disorders 541
7 General fracture management 543
8 Poly Trauma 547
9 Pelvic Injury 549
10 Fractures of upper limb 550
11 Fractures of lower limb 555
12 Dislocations 558
13 Ligamentous injuries 561
14 Spinal trauma 562
15 Mangled Extremities (Amputation) 566
16 Common Fractures in children 568
17 Bone Tumors 569
1. INFECTIONS IN ORTHOPEDIC
Infections of bone are difficult to treat due to precarious
blood supply. Most common is Haematogenous spread.
1. Osteomyelitis
1.1 Classification:
Based on duration and mechanism of Infection
Duration:
 Acute
 Sub-Acute
 Chronic
Mechanism:
 Exogenous – Open fracture, Surgery or contagious
 Haematogenous Fig. 1.1: X-RAY SHOWING OSTEOMYELITIS OF
TIBIA
1.2 Factors increasing susceptibility
to Infection:
 Patient dependent factors are nutritional and
immunological status.
 Surgeon dependent factors are skin preparation,
operation room, environment and prophylactic
antibiotic therapy
1.3 Most Common Organism:
 Staphylococcus aureus
1.4 Type:
1) Acute
2) Sub-Acute
3) Chronic
1.5 Most Common Site:

Around Knee and Hip (in Paediatric cases)
Fig. 1.2: INFLAMMATION OF SKIN
1.6 Clinical Features:
 Pain and swelling
1.8 Imaging studies:
 X-Ray
 Constitutional symptoms
 Computed Tomography (CT)
 Warm to touch
 Radionuclide scanning
 Restricted movements
 MRI
1.7 Laboratory studies:
 HB, TLC, DLC & ESR
 Aspiration of fluid (>50000wbc/cu.mm.)
 Gram Stain sensitivity (30%)
 Culture sensitivity (90%)
 Blood Culture
Page 530
1.9 Treatment: 2.3 Agent:
 Mycobacterium Tuberculosis
1.9.1 Medical Therapy(Conservative)-
Immobilize the joint with splint for pain relief

Antibiotic therapy of Osteomyelitis.
Treat with intravenous Antibiotics for 3 to 6 weeks
Cephalosporin and Aminoglycosides.
Paediatric dosage: -
 Inj. Cefotaxime 750 mg twice a day for 3 to 6
weeks.
 Inj. Amikacin 250 mg/ Inj. Gentamicin 20 mg IV
twice a day for 3 to 6 weeks.
Adult Dosage: -
 Inj. Cefotaxime 1500 mg IV twice a day for 3 to 6
weeks.
 Inj. Amikacin 500mg / Inj. Gentamicin 40mg IV Fig. 1.3: PICTURE OF DESTRUCTION OF SPINE
twice a day for 3 to 6 weeks.
Treat for at least 3 weeks with IV Antibiotics initially

and then shift to oral for another 3 weeks.
Antibiotics should be used in accordance with Antibiotic
protocol of Institute.
NSAIDs such as Tab. Diclofenac sodium 50 mg thrice a

day along with Antacids until Inflammation subsides and
supportive treatment such as multivitamins.
1.9.2. Surgical therapy-

 Debridement
 Sequestrectomy
 Saucerization
 Sinus tract excision
2. Tuberculosis of Bone
Bone is most common extra pulmonary site of Infection Fig. 1.4: CROSS SECTION OF KOCH SPINE
of Mycobacterium Tuberculosis.
 Mono articular
2.1 Source:  History of Night cries, Loss of weight, Anorexia
Always secondary.  Decreased joint movement
 Wasting of muscles
2.2 Site:  Pain and Tenderness
Most common site is spine followed by hip and  Cold abscess
Knee. Commonly occurs in first three decades
of life
2.5 Investigations:
 HB, TLC, DLC & ESR
 X-ray early De-calcification & Late Joint
destruction
Page 531
 Confirm diagnosis by biopsy or culture and 2.6.2 Operative-
start treatment.
1) Capsulotomy
 MRI
2) Synovectomy
2.6 Principles of Treatment: 3) Curettage
1) General Support Protein rich diet & Haematinics. 4) Excision
2) Chemotherapy-Anti-tuberculous treatment as per
RNTCP CAT-II. 2.6.3 Abscess-
1) Incision and drainage.
2.6.1 Local Treatment- 2.7 Complication of Bone Infections:
Bed rest and Traction in acute and early stages,
 Pathological fracture
Splints and braces.
 Non-union / Mal union
.  Para-paresis in spinal tuberculosis
Bibliography
1. Maheshwari J. Essential Orthopaedics. 4th edition. New Delhi: JP Medical Ltd; 2012
2. Miller MD, Thompson SR, Hart J. Review of Orthopaedics. 6th edition. Elsevier Health Sciences.
3. India. Ministry of Health and Family Welfare. Standard Treatment Guidelines. The Clinical
Establishment (Registration and Regulation) Act 2010, MOHFW. [cited 2016 July 5]
Available from: www.clinicalestablishments.nic.in/WriteReadData/822.pdf
Further reading
1. Tuli SM. Tuberculosis of skeletal system.
2. Moon MS. Tuberculosis of the spine. Controversies and a new challenge in Spine 1997: 1791-1797
3. Jain AK. Tuberculosis of the spine: a fresh look at an old disease. J Bone Joint Surg. 2010:
Jul;92(7):905-13.
4. Jain. Treatment of tuberculosis of the spine with neurologic complications. Clin Orthop Relat Res.
2002 May; (398):85-92.
5. Rajasekaran S. The problem of deformity in spinal tuberculosis. Clin Orthop Relat Res. 2002
May;(398):75-84.
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Page 532
2.ARTHRITIS (JOINT DISEASES)
b) Local Hydrocortisone Acetate Injection 40 mg
1.Osteoarthritis Intra articular once. Dosage can be repeated after
It is degenerative disease of joint which commonly 2-3 months as and when needed (under aseptic
involves Knee, Hip and Ankle joint. precautions).
c) Surgery (joint replacement).
Primary Osteoarthritis is degenerative process without
any precipitating factors.
Secondary Osteoarthritis is mostly due to Trauma, 2. Ankylosing Spondylitis
Infection and avascular necrosis. Chronic progressive inflammatory disease of
1.1 Clinical Features: sacroiliac joints and the axial skeleton, having
insidious onset affecting young patients age less than
40 years.
 Pain
 Swelling
 Restricted range of movements 2.1 Clinical Features:
 Backache
1.2 Investigations:  Restricted movements of spine and hip
 Morning stiffness, improvement with exercise,
 X-ray of involved joint
persistence for more than 3 months
2.2 Extra Articular Manifestations:

 Acute iritis
 Pericarditis
 Aortic incompetence
 Subluxation of atlanto-axial joints
2.3 Investigations:
 Haemogram
 HLA B27
 X-ray, Pelvis and Spine
Fig. 2.1: X-RAY SHOWING SEVERE
OSTEOARTHRITIS CHANGES 2.4 Diagnostic Criteria:
HLA B27 positive and X-ray picture showing
1.3 Treatment: bamboo spine and ankylosed SI and hip joints.
a) NSAIDS - 2.5 Treatment:
1) Tab. Diclofenac sodium 50 mg Thrice a day a) Conservative Management-
for 1 week and SOS later Or 1) Rest.
2) Tab. Indomethacin 25 mg thrice a day for 1 2) NSAIDS.
week and SOS later Or NSAIDs cause hyperacidity hence antacids such
3) Tab. Ibuprofen 400 mg Thrice a day for 1 as Cap. Omeprazole 20 mg or Tab. Pantoprazole
week and SOS later 40 mg once a day should be given.
NSAIDs cause hyperacidity hence antacids 3) Physiotherapy / back exercise.
such as Cap. Omeprazole 20 mg or Tab. 4) Occupational therapy.
Pantoprazole 40 mg once a day should be 5) General preventive measures like genetic
given. counseling.
4) Local application of Diclofenac Sodium Gel b) Physiotherapy -
4-5 times per day.
Page 533
Fig. 2.2: X- RAY SHOWING BAMBOO SPINE IN ANKYLOSING SPONDYLITIS

Bibliography
Further reading
1. Garrett S, Jenkinson T, Kennedy L, Whitelock H, Gaisford P, Calin A. A new approach to defining
disease status in Ankylosing spondylitis: The Bath Ankylosing Spondylitis Disease Activity Index. J
Rheumatol. 21 (12): 2286–91.
2. Jiménez-Balderas FJ, Mintz G. Ankylosing spondylitis: clinical course in women and men. J
Rheumatol. 20 (12): 2069–72.
3. Khan MA. (2002). Ankylosing spondylitis: The facts. Oxford University Press.
4. Reveille JD. Major histocompatibility genes and Ankylosing spondylitis. Best Practice & Research
Clinical Rheumatology. 20 (3): 601–609.

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Page 534
3. CONGENITAL DISORDERS
1. Congenital Torticollis (Wry

2.2 Various splints include:
neck)
 Von Rosen splint
 Usually due to contracted sternocleidomastoid  Pavlik harness
muscle.  Triple diapers
 Head tilted towards and chin rotated away from  Craig splint
affected side.
 A firm swelling at junction of mid and distal 3rd
of the muscle may be felt. 2.3 Treatment:
 Associated with congenital anomalies in cervical 2.3.1 Age 1 - 3 Years-
spine.
 Treatment includes stretching exercises, if Initially closed reduction is tried. If it doesn’t give
deformity persists for 2 years surgical correction the needed result, then surgical correction is opted.
lengthening of sternocleidomastoid muscle. Surgery is planned after a period of traction. If the
 Early identification and immediate child is more than 18 months only surgical
implementation of treatment gives good results. procedures can help.
Earlier the treatment, better are the results.
The methods are
1) Removal of the interposed soft tissue from the
2. Congenital Dislocation of joint.
2) Innominate osteotomy.
Hip (CDH) 3) Femoral osteotomy.
If displacement of femoral head from its normal
position within the Acetabulum is found at birth. It is 2.3.2 More than 3 Years-
regarded as CDH or Developmental Dysplasia of the Preliminary traction followed by open reduction.
Hip (DDH).
The methods are
2.1 Clinical Features: 1) Removal of limbus.
 More common in females 2) Salter innominate osteotomy.
 Asymmetric groin folds 3) Pemberton pericapsular osteotomy of ilium.
 Shortening of limb 4) Rotation osteotomy of femur.
 Ortoloni and Barlow tests - Performed to test the
vulnerability of the Hip to dislocate and relocate 2.4 Complications:
within the acetabulum.  Avascular necrosis of femoral head.
 Telescopy test - Performed with Hip and Knee  Neglected cases develop painful instability of hip
flexed in 90 degree and axial force applied to the and degenerative arthritis in later life.
thigh and the greater trochanter movements in
 Persistent dislocations presenting in adulthood
relation to the ASIS (Anterior Superior Iliac
with OA can be treated with total hip
Spine) are seen.
replacement Arthroplasty.
 X-ray shows broken Shenton's line
 Head lying outside the acetabulum Congenital Clubfoot
 Dysplastic acetabulum / femur 3. Congenital Talipes Equino
 Early identification and immediate
implementation of treatment gives good results – Varus (CTEV)
Good physical examination
- Plane Radiography
- Ultrasonography
Page 535
3.1 Etiology: Methods
Unknown but mostly attributed to mechanical causes. 1) French
2) Ponseti method produces best results which
 Germ plasm defect and primary soft tissue
comprises correction of deformity in order of
abnormalities.
CAVE (Cavus, Adduction, Varus & Equinus) with
 Features are usually obvious at birth.
serial castings followed by Tendo-Achilles-
 Foot is twisted and turned inwards so that it faces tenotomy and retention of correction in Steinbeck
postero-medially. shoes till walking age.
 Foot is plantar flexed, inverted and adducted at
forefoot. The leg muscles are smaller and heel cord
3.2.2 Surgical correction-
is tight and associated internal tibial torsion may be
Should be opted for in cases that have failed
present.
conservative line of management.
a) Soft tissue procedure

1) Closed Tendo Achilles Tenotomy.
2) Lengthening of medial and posterior structures.
3) Talonavicular reduction and maintenance.
Methods
1) Turco
2) Carroll
3) External fixator correction
4) JESS: Less than 7 years
5) Ilizarov: More than 7 years upto 12 years
b) Bone procedures
Fig. 3.1: CLINICAL APPEARANCE OF
Done in case of deformity that has persisted for
BILATERAL IDIOPATHIC CTEV BEFORE
more than 3 yrs.
TREATMENT
 In addition to posteromedial release lateral column
3.2 Treatment: shortening and / or medial column lengthening
3.2.1 Conservative- procedures can be done.
Aim of treatment is to produce and maintain a painless  Late / relapsed cases.
supple plantigrade foot. Preferably should be started Options
within a day or two after birth. Manipulative correction  Soft tissue and bone procedures with tendon
and maintenance in cast. transfers, gradual correction using Ilizarov method.
 Neglected cases can be treated by triple
arthrodesis.
Bibliography
Further reading
1. Aegerter, Kirkpatrick. Orthopedic Diseases – Physiology, Pathology and Radiology.
2. Canale ST, Beaty JH, Elesvier M. Campbell’s Operative orthopedics.
3. Roberts L. Orthopedics in Infancy and Childhood.
4. Kulkarni GS. Text Book of Orthopedics and Trauma.
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Page 536
4. METABOLIC DISORDERS
 Increased thoracic kyphosis
1. Osteoporosis
Osteoporosis is defined as abnormally porous bone 1.5 Treatment:
and its strength is less than normal for a person of a) Physiotherapy.
that age and sex. b) Bisphosphonate,
Alendronate 70 mg once weekly given with full
1.1 Clinical features: glass of water before breakfast (in severe cases)
 Bone pain for 3 months.
 Fractures c) Vitamin D 1000IU/ day for 3 months.
 Kyphosis d) Calcium - both diet and drug
 Weakness Tab. Calcium carbonate 500 mg twice a day for
 Fatigue 2-3 months and can be extended later.
e) Hormone replacement therapy in selected
1.2 Investigations: cases.
f) Calcitonin Nasal spray (200 IU/day) once a
 X-ray week for 3 months minimum, Injectable
 Special investigations (if needed) include Calcitonin for limited use.
 DEXA Scan g) If and when combination of Calcium and
Vitamin D is available, it should be used.
1.3 Diagnosis:
SD > 2.5 below the average for premenopausal
1.6 Secondary Osteoporosis:
women for that population group.  Nutritional
 Endocrine
1.3.1 X-ray features:
 Drug induced
 Loss of trabecular definitions.  Malignant disease
 Thinning of cortices.  Identify the cause and treat it accordingly
 Correct the nutritional deficiency
1.4 Primary osteoporosis:  Correction of hormonal imbalance
Physiological bone depletion that normally
accompanies ageing and loss of gonadal activity. 1.7 Surgery:
1.4.1 Post-Menopausal Osteoporosis  Vertebroplasty & Kyphoplasty –in presence of
 Complaints of back pain neurodeficit.
Bibliography
Further reading
2. Canale ST, Beaty JH, Elesvier M. Campbell’s Operative orthopedics.
Ions
Page 537
5. REGIONAL CONDITIONS
 Tardy-ulnar nerve palsy may be present - treated
1. Peri Arthritis Shoulder with anterior transposition of ulnar nerve.
(Frozen Shoulder)  Gross deformity – supracondylar osteotomy.
Significant restriction of both active and passive
shoulder motion.
3. Cubitus Varus
 Inward deviation of forearm at elbow.
1.1 Clinical Features:  Most common cause is Malunion of
Night pain, inability to reach overhead and reach supracondylar fracture.
away from the body.  Change in arc of motion with hyper extension
and restricted flexion.
1.2 Investigations:  Deformity needs – supracondylar osteotomy.
 X-ray
 Blood - rule out metabolic causes
4. De Quervain's Disease
 Ultrasound (Dynamic ultra sound) Chronic constrictive tenosynovitis of abductor
 MRI (Thickness of the capsule and synovium pollicis longus and extensor pollicis brevis.
>4mm) to rule out other pathology
1.3 Treatment: Diffuse pain at distal end of radius laterally,
a) Supportive - Diathermy, Ultrasound, TENS. tenderness and painful movements of thumb.
b) Medications
 Finkelstein's test positive.
1) Tab. Diclofenac sodium 50 mg thrice a day for
1 week and SOS later Or 4.2 Treatment:
2) Tab. Indomethacin 25 mg thrice a day for 1
week and SOS later Or a) Early - splint wrist and thumb in full extension.
3) Tab. Ibuprofen 400 mg thrice a day for 1 week b) Anti-inflammatory drugs.
and SOS later 1) Tab. Diclofenac sodium 50 mg thrice a day
NSAIDs cause hyperacidity hence antacids such for 1 week and SOS later Or
as Cap. Omeprazole 20 mg or Tab. Pantoprazole 2) Tab. Indomethacin 25 mg thrice a day for 1
40 mg once a day should be given. week and SOS later Or
c) Intra- articular steroids. – Inj. Hydrocortisone 3) Tab. Ibuprofen 400 mg thrice a day for 1
acetate 40 mg once every 3 months. week and SOS later.
d) Physiotherapy -Stretching exercises. NSAIDs cause hyperacidity hence antacids such
e) Manipulation under general anaesthesia (if as Cap Omeprazole 20 mg or Tab. Pantoprazole
symptomatic > 6 months). 40 mg once a day should be given.
f) Surgical Release (If not response to above c) Local administration of Inj. Hydrocortisone 40
treatment). mg once every 3 months.
Open or Arthroscopic release at specialized d) Later soft - tissue release can be done.
centers.
5. Carpel Tunnel Syndrome
2. Cubitus Valgus
Most commonly found in IT professionals and
 Outward deviation of forearm at elbow.
students. Median nerve is involved.
 Normal carrying angle is 100 in male and 150 in
females.
2.1 Causes: It is caused by entrapment of medial nerve in carpel
tunnel. Also seen in malunited lower end radius
 Nonunion fracture of lateral condyle of
fractures and in pregnant women.
humerus.
 Destruction of lateral condyle due to sepsis.
Page 538
Tinel’s sign – It is reproduction of tingling sensation 7.2.1 Medical treatment-
in palm and wrist by tapping over the course of 1) Tab. Diclofenac sodium 50 mg thrice a day
nerve. for 1 week and SOS later Or
5.2Treatment: week and SOS later Or
3) Tab. Ibuprofen 400 mg thrice a day for 1
5.2.1 Conservative-
week and SOS later
NSAIDs
NSAIDs cause hyperacidity hence antacids such
1) Tab. Diclofenac sodium 50 mg thrice a day for 1
as Cap. Omeprazole 20 mg or Tab. Pantoprazole
week and SOS later Or
40 mg once a day should be given.
2) Tab. Indomethacin 25 mg thrice a day for 1 week
4) Local Steroids. – Inj. Hydrocortisone acetate
and SOS later Or
40 mg once every 3 months.
3) Tab. Ibuprofen 400 mg thrice a day for 1 week
and SOS later.
NSAIDs cause hyperacidity hence antacids such as 7.2.2 Surgical release
Cap. Omeprazole 20 mg or Tab. Pantoprazole 40 mg 8
once a day should be given. 8. Avascular Necrosis of
Or
5.2.2 Surgical Release Femoral Head
Death of bone due to gradual vascular impairment or
6. Tennis Elbow sudden infarction. Clinically there is pain in groin,
radiates to thigh and knee, local tenderness, limitation
 Lateral epicondylitis due to repetitive stress of movements, loss of abduction and internal
Injury rotation, preserved flexion.
 Commonly seen in house wife’s and players:
6.1 Treatment: 8.1 Radiological Features (X-rays):

 Stage1- Pre radiologic stage – no radiologic
6.1.1 Medical treatment-
findings.
1) Tab. Diclofenac sodium 50 mg thrice a day
for 1 week and SOS later Or  Stage 2- Osteoporosis, sclerotic cystic areas.
2) Tab. Indomethacin 25 mg thrice a day for 1  Stage 3- Partial collapse, flattening of femur
week and SOS later Or head, increased density and deformity of head.
3) Tab. Ibuprofen 400 mg thrice a day for 1  Stage 4 -Secondary deterioration of the articular
week and SOS later. cartilage.
NSAIDs cause hyperacidity hence antacids
such as Cap. Omeprazole 20 mg or Tab. 8.2 Other Investigations:
Pantoprazole 40 mg once a day should be  Radio-isotope scanning
given.  MRI – most sensitive to detect ischemic
4) Local Steroids. – Inj. Hydrocortisone acetate necrosis
40 mg once every 3 months.  Bone-marrow pressure measurements
Supportive splints.
 Intramedullary venography
 Core biopsy of femur head
6.1.2 Surgical release-
8.3 Treatment:
7. Golfers Elbow a) Early – Bed rest, traction, weight reduction,
7.1 Clinical features: withdrawal of steroid and alcohol.
Medial epicondylitis which is due to repetitive stress. b) Stage 2 - Core decompression of head, muscle
Injury commonly seen in house Wife’s and Players. pedicle bone grafting.
c) Stages 3 & 4 - Osteotomy and replacement
arthroplasty.
7.2 Treatment:
Page 539
Knee
Plantar Fig. 5.1: BILATERAL GRADE 4 AVASCULAR NECROSIS OF FEMUR HEAD
1) Tab. Diclofenac sodium 50 mg thrice a day

9. Plantar Fasciitis / Calcaneal for 1 week and SOS later Or
Spur 2) Tab. Indomethacin 25 mg thrice a day for 1
week and SOS later Or
9.1 Clinical Features: 3) Tab. Ibuprofen 400 mg thrice a day for 1
 Pain in both heels week and SOS later.
 Unable to bear weight NSAIDs cause hyperacidity hence antacids
 Tenderness over medial tuberosity of calcaneum such as Cap. Omeprazole 20 mg or Tab.
X-ray - lateral view of calcaneum may show Pantoprazole 40 mg once a day should be
spur given.
9.2 Investigation: c) Local Steroids-
X-ray Calcaneum lateral view to rule out spur Blood 1) Inj. Hydrocortisone acetate 40 mg once
sugar to rule out diabetes. Every 3 months.
2) Surgical release.
9.3 Treatment: d) Ultrasound therapy
a) Soft sole pad in the heel
b) Medical-
Bibliography
Further reading
2. Canale ST, Beaty JH, Elesvier M. Campbells Operative orthopedics.

Page 540
6. DISORDERS OF SPINE
If you see any of the red flags refer urgently to higher
1. Lumbar Spondylosis center with surgical facility.
1.1 Clinical Features: 2. Cervical Spondylosis
Low back ache is a very common problem faced in
day to day life. Not all of them, are caused by disc It is a degenerative condition of the cervical spine
pathology. Clinical features suggestive of disc occurring over 50 years of age. Involves the
pathology include backache associated with para intervertebral discs, posterior intervertebral joints.
spinal spasm, stretch pain and leg pain. Commonest at C5 - C6.
1.2 Investigation: 2.1 Clinical Features:

 Pain and stiffness.
1) X-rays lumbosacral spine AP  Radiating pain to shoulder or downwards on the
outer aspect of the forearm and hand.
1.3 Treatment:  Giddiness on and off.
a) Rest.  On examination there is loss of normal cervical
b) Medical management. lordosis and limitation in neck movements.
1) Tab. Diclofenac sodium 50 mg thrice a day for  Tenderness over the lower cervical spine or in
1 week and SOS later Or the muscles of the paravertebral region.
week and SOS later Or 2.2 Investigations:
3) Tab. Ibuprofen 400 mg thrice a day for 1 week X-ray cervical spine AP and Lateral
and SOS later.
NSAIDs cause hyperacidity hence antacids 2.3 Treatment:
such as Cap. Omeprazole 20mg or Tab. a) Rest.
Pantoprazole 40mg once a day should be b) Medical management.
given. 1) Tab. Diclofenac sodium 50 mg thrice a day for
1 week and SOS later Or
4) Local Application of Muscle relaxant gel such 2) Tab. Indomethacin 25 mg thrice a day for 1
as Diclofenac sodium gel. week and SOS later Or
c) Education about proper back posture – 3) Tab. Ibuprofen 400 mg thrice a day for 1 week
maintenance of lumbar lordosis with erect and SOS later.
posture or lumbar pillow. NSAIDs cause hyperacidity hence antacids
d) Physiotherapy interferential therapy, traction such as Cap. Omeprazole 20 mg or Tab.
e) Epidural steroid Injections. Pantoprazole 40 mg once a day should be
given
1.4 Operative Indications: Local Application of Muscle relaxant gel such
as diclofenac sodium gel.
 Cauda Equina syndrome - especially with bowel c) Education about proper Neck Posture.
and bladder involvement. d) Physiotherapy, interferential therapy, Cervical
 Patients with persistent pain not relieved by traction.
conservative measures for 6 - 8 weeks.
 Unilateral leg pain extending below knee that 3. Kyphosis
has lasted at least 6 weeks.
 Discectomy is performed usually by posterior It is a posterior curvature of the spine.
approach and patients will have good post- Types
Operative pain relief. i. Smooth rounded kyphosis
 Scheuermann’s disease
1.5 Watch for Red Flags Signs: ii. Angular kyphosis
 Bowel-bladder involvement.  Tuberculosis spine
 Hypoesthesia around anus.  Traumatic
Page 541
4. Scoliosis 4.3 Investigations:
 Radiography of the whole spine
4.1 Definition:  Degree of the curve is measured by the Cobb’s
Scoliosis is defined as lateral curvature of the spine. angle
Scoliosis is named according to the level and side to  Skeletal maturity by the fusion of the iliac
which the main convexity of the curve is directed. apophysis (Risser sign) is an indicator of end of
growth of spine
The common patterns are,
i. Thoracic scoliosis 4.4 Treatment:
ii. Thoraco-lumbar
a) Mild cases – Conservative with serial custom
iii. Cervico-thoracic scoliosis (depending upon the
made braces.
site of primary curve)
b) Moderate cases - Spinal and breathing exercise
4.2 Clinical Features: with correction by Milwaukee Brace.
c) Severe cases - Cobb’s angle > 40 deg. surgical
Rib hump, Prominence of posterior chest wall. Test
correction with instrumentation and Fusion
done to decide whether deformity is mobile or rigid.
carried out with cancellous bone graft.
Make the patient lie in the lateral position on the
concave side. Curvature is diminished in mobile
cases.
Fig. 6.1: SCOLIOSIS OF DORSO – LUMBER SPINE
Bibliography
Further reading
2. Canale ST, Beaty JH, Elesvier M. Campbells Operative orthopedics.

Page 542
7. GENERAL FRACTURE MANAGEMENT
1. Definition
Disruptions of bone tissue are called fracture; visible
6. Management includes
disruption of articular cartilage is also called fracture a) Conservative management for closed fracture
(Chondral fracture). and Type I - open fracture for which closed
manual reduction tried and patient put on
2. Types of fractures appropriate Plaster of Paris splint for 3 - 4
weeks.
i. Closed fracture and Open fracture
b) Surgical management.
ii. Incomplete fracture or Greenstick fracture and
Complete fracture 6.1 Initial management of open
iii. Linear fractures - Transverse, Oblique
iv. Spiral, Comminuted (more than two fragments). Injuries:
v. Segmental fracture, fracture with bone loss and  Record vitals, start lifeline, I.V. fluids, I.V.
Impacted fracture Antibiotics, Analgesics.
vi. Stress fracture  Immediately debride the wound of contaminated
vii. Pathological fracture wound, devitalized tissue. Look for 4 C’s,
Consistency, Colour, Contractility, Circulation.
3. Gustilo-Anderson  Irrigate copiously with saline: – Type I – 3L
classification of open saline, Type II – 6 L saline, Type III – 9 L
saline.
fracture  Enlarge the wound if necessary for adequate
 Type I Open fracture with wound < 1cm Bone debridement.
is not exposed.  Remove contamination in the medullary canal.
 Type II Wound > 1cm without extensive soft  If wound can be closed, suture the surgically
tissue damage / skin flaps avulsion. created wound, put loose stitch for other
 Type III A Open fracture with extensive soft wounds over a drain if necessary. If closure is
tissue damage, but with adequate soft tissue not possible, leave the wound open.
coverage of bone. It also includes segmental
fracture, comminuted fracture with laceration < 7. Complications
1cm.
 Type III B Extensive soft tissue loss with 7.1 Acute:
periosteal stripping with bony exposure.  Shock
 Type III C Open fracture with an arterial Injury  ARDS
that require immediate repair regardless of size  Thrombo-embolism
of the wound.  Neuro-vascular Injuries
 Crush syndrome
4. Clinical features  DVT
 Pain 7.2 Chronic:

 Swelling  Delayed union, Non-union, Malunion
 Inability to use the affected limb  Growth disturbances
 Deformity  Joint stiffness
 Crepitus  Volkmann’s ischemic contracture
 Abnormal mobility  Myositis Ossificans
 Loss of transmitted movement  Post-traumatic arthritis
 Avascular necrosis
5. Investigations 7.3 Peculiar to Open fractures are:
 Routine X-ray AP and Lateral view
 Infection
 Special views if necessary
Page 543
 Tetanus
 Gas gangrene
13. Joint stiffness
 Osteomyelitis Due to inappropriate fracture immobilization, intra
 Hypovolemic shock articular fractures, periarticular adhesion of soft
tissues, capsules and muscle contractures.
8. Crush Syndrome
13.1 Treatment:
Severe crush Injury of limbs and muscles results in
release of myoglobin leading to renal failure. a) Physiotherapy.
Treatment is managing acute renal failure and b) Exercises.
Maintain hydration. c) Manipulation under anesthesia
d) Surgical excision and lengthening of
9. Compartment Syndrome contractures.
 It is due to ischaemic necrosis of structures of

anterior compartment of fore-arm / legs. 14. Myositis Ossificans
 It is defined by the following signs (6 P’s). It is a reactive lesion (ossification) occurring in
a. Pain soft tissues and in stripped periosteum followed
b. Pallor by trauma and ill-advised massage.
c. Paraesthesia
d. Paralysis 14.1 Treatment:
e. Pulselessness a) Drugs:
f. Positive Passive stretch Low dose Indomethacin (25 mg TDS) for 1
month.
9.1 Treatment: b) Mobilization and ROM excision till pain free
joint range.
Emergency surgical decompression by fasciotomy.
15. Fractures of Necessity
10. Delayed union
For these fracture, surgery is always necessary.
Union is considered delayed, when healing has not
advanced at the average rate for the location and the  Lateral humeral condyle fracture
type of fracture, usually 3 - 6 months. Conservative  Femoral neck fracture
management with functional cast for additional 4 - 12  Distal tibial epiphysis fracture
weeks or ORIF with appropriate implant with or
without bone grafting. 16. Physeal Injuries
Salter and Harris classification of Physeal Injuries.
11. Non-union
 Type– I Epiphyseal separation through
A diagnosis of Non-union is justified either by
physis only with or without displacement.
clinical or X-ray findings which show healing has
 Type–II Triangular metaphyseal spike
ceased, minimum of 9 months elapsed since Injury
attached to separated epiphysis. (Thurston
and the fracture shows no visible progressive signs of
Holland sign.)
union for 3 months.
 Type–III Physeal separation with fracture
Time period – through the epiphysis into the joint. If there is
displacement joint incongruity occurs.
 Fracture of long bone - 6 to 9 months
 Type–IV Fracture through the metaphysis,
 Fracture of neck of femur – 3 months
physis, epiphysis.
 Type–V Compression fracture of the physis
12. Malunion producing growth arrest, diagnosed
A malunited fracture is one that has healed with the retrospectively.
fragments in a non - anatomical position. Corrective  Type–VI Bruise or contusion to the periphery
osteotomy with internal or external fixation with or of the physis producing growth disturbances.
without bone grafting.
Page 544
I II III IV V
Epiphyseal Fracture through Fracture through Fracture of Epiphyseal Damage to the
slip only Epiphyseal plate with The Epiphyseal and shaft, crossing Epiphyseal plate
Triangle of shaft Extending into the Epiphyseal
Attached Epiphyseal plate plate
Fig. 7.1: EPIPHYSEAL INJURIES
16.1 Management:
Details of splinting and transport of trauma patient
Majority of children’s fracture are treated are mentioned in treatment of individual fractures.
conservatively. Few fractures require open reduction
and internal fixation or closed pinning. 18.2 Preparation of Cast/Slab
17. Open fractures in Children Application:
It is essential to prepare the patient and all necessary
Frequent and vigorous debridement with irrigation material and equipment before beginning the
and adequate stabilization of fracture will reduce the processes of fracture reduction and cast application.
rate of non-union and secondary infection. Rarely
after closed reduction Haematogenous osteomyelitis Required materials
occurs at the fracture site. 1) Examination couch or Table
18. Splintage and Transport of 2) 2-4 rolls 150 mm padding
Trauma Patient 3) 8-9 Plaster of Paris(POP) rolls, 150 mm wide
4) Bucket with cool water
18.1 Guidelines:
5) Pillows to support casted leg
1) Immobilize one joint above and below.
2) Usage of readily available materials such as 6) Aprons to protect team members and patient
umbrella, Plaster of Paris, folded paper, wooden 7) Paper to cover the floor
stick.
3) Splintage should neither be too tight or too
loose. Everything must be assembled and ready before
4) Do Not transfer patient unless his vitals are beginning the procedure.
stabilized.
Page 545
Fig. 7.2: MATERIALS FOR APPLYING SLAB/CAST
18.3 Method: position and applied over dorsal or ventral surface

with cotton padding and bandage.
Slab is prepared by overlaying of Plaster of Paris
rolls of adequate length and layers to splint the Cast is cylindrical application of Plaster of Paris rolls
fracture along with adjacent joints in anatomical over adequate cotton padding over the fractured limb
in anatomical position.

Bibliography
Further reading
1. Bucholz RW, Williams L, Wilkins. Rockwood and Green’s fractures in adults. 6th and 7th edition.
2. Canale ST, Beaty JH, Elesvier M. Campbell’s Operative orthopaedic. 11th edition.
3. Chapman MW, Williams L, Wilkins. Chapman’s Orthopaedic surgery. 3rd edition.


Page 546
8. POLYTRAUMA
1. Definition 2.4 Golden Hour:

 Injury severity score (ISS) 16 or above First one hour after injury, with three-fold increase in
 Systolic blood pressure below 80 mm Hg mortality for every 30 minutes.
 Glasgow coma score less than 15
 Higher fluid resuscitation requirements 3. Follows ABCDE
 Chest, head, abdominal organ Injuries  Airway
 Fractures of more than one long bone  Breathing
 Circulation
2. Stage of Care  Disability
 Exposure
2.1 Acute Resuscitation Period:
(1-3 hours) 4. Initial Management of
 From the first point of contact with medical
service to the control of acute life threatening
patient in Shock
conditions. a) Direct control of obvious bleeding by direct
 Rapid systemic assessment to identify life pressure - (preferable), tourniquet clamping of
threatening conditions. blood vessels
 Then Airway, Breathing, Circulatory (ABC) b) Large-bore intravenous access
support should be made. This involves airway 1) Ringer lactate infusion
control, Thoracocentesis, rapid control of 2) Blood replacement as indicated, by serial
external bleedings, vigorous fluid and blood haematocrit estimation and blood pressure.
replacement therapy. c) Traction with Thomas Splints or extremity
 Then complete diagnostic checkup if there is no splints to limit hemorrhage from unstable
acute life threatening situation. fractures.
2.2 Primary Stabilization Period: d) Consideration of angiography or immediate
operative intervention for Hemorrhage control.
(upto 48 hours)
 From the control of acute life threatening 4.1 Haemorrhagic Shock:
situation and complete stability of Respiratory,
Haemodynamic and Neurologic symptoms.  Diagnosed by Hypotension, Tachycardia, seen
in patients with large open wounds, active
 Here acute management of fractures associated
bleeding, Pelvic and / Femoral fractures and
with arterial injuries and acute compartment
Abdominal or Thoracic trauma.
syndrome are managed.
 In the absence of open hemorrhage bleeding
 Fractures are temporarily stabilized with
into voluminous space (chest, abdomen, pelvis,
external fixators and compartments.
thigh) must be ruled out.
2.3 Secondary Regeneration Period:  This may require Peritoneal lavage,
(2 - 10 days) Angiography, CT, MRI.
 In this, general condition of the patient is  Managed by aggressive fluid replacement, blood
stabilized and monitored. transfusion, Angiographic embolization
 Systemic inflammation and multiple organ operative intervention, fracture stabilization, etc.
dysfunction syndrome are managed.
 Tertiary reconstruction and rehabilitation period
4.2 Blood Replacement:
(weeks to months) after trauma.  Fully cross matched blood is preferable
 Necessary surgical procedures.  In case of life threatening situations ‘O’-
 Definitive treatment of complete mid-phase negative blood can be used.
fractures.  Warming of blood prior to administrations
 Specialized procedures to achieve fracture prevents Hypothermia
correction or joint reconstruction.
Page 547
 Monitor coagulation factors, Platelets and d. Rectal tone and sensation.
Calcium levels.  GCS = Eye opening score + Verbal (intubated
or non-intubated) score + Motor score.
 GCS if < 13, systolic BP < 90, RR< 10 / min or
5. Indications for Immediate > 30 / min warrants Emergency trauma care.
Surgery
 Hemorrhages secondary to Liver, Splenic renal 6. Radiographic Evaluation
parenchymal injury –Laparotomy.
 X-rays of Skull, pelvis, spine and Extremities
 Aortic, Caval or Pulmonary vessel tears –
 Ultra sound abdomen
Thoracotomy.
 CT, MRI
 Depressed skull fracture or acute intracranial
hemorrhage – Craniotomy.
Assess the concomitant Injuries such as head Injuries,
 Disability (Neurologic Assessment). thoracic Injuries, and genitourinary Injuries and refer
a. Assess level of consciousness by GCS. the patient to higher centers for tertiary care
b. Pupillary response sensation. management.
c. Motor response in all extremities.
Pelvic Fracture
Bibliography
Further reading
1. Bucholz RW, Williams L, Wilkins. Rockwood and Green’s fractures in adults. 6th and 7th edition.
2. Canale ST, Beaty JH, Elesvier M. Campbell’s operative Orthopaedic. 11th edition.
3. Chapman MW, Williams L, Wilkins. Chapman’s Orthopaedic surgery. 3 rd edition


Page 548
9. PELVIC INJURIES
f) If it is > 2.5 cm – external fixation or Open
1. Introduction reduction and Internal fixation.
 It is an emergency in Orthopaedics which g) If there is unstable fracture with vertical
involves multispecialty intervention. displacement, then treat with ORIF.
 Mode of Injury. h) If Haemodynamically unstable, then stabilize
a. High energy injuries the Pelvis with external fixator at the casualty
b. Crush injuries itself without shifting the patient and follow the
c. Impact injuries above steps.
 Associated with complications and other
fractures. 4. Associated Complications
and Treatment
2. Clinical Features
a) Shock-blood transfusion and fluid replacement.
 Pain and Tenderness at affected site b) Embolisation of bleeding Pelvic vessels.
 Range of movements painful (intervention radiology)
 Shock c) Urethral rupture - diagnosed by blood in
 Intra-abdominal / Urethral / Vascular injuries Urethra, Perineal hematoma, Distended bladder,
managed by Urologist.
3. Management d) Bladder rupture-extravasation of urine-Urologist
and Surgeon.
a) Evaluate ABCDE and stabilize the patient. e) Bowel and intra-abdominal injuries are
b) Evaluate for other associated injuries Head, managed by General surgeon.
Chest, Abdomen and Spine. f) Thrombosis - DVT prophylaxis, vascular
c) If Haemodynamically stable, assess opinion must be obtained.
radiologically with X-ray pelvis AP view, inlet g) Post-operative-
and outlet view. If there is no or minimal 1) Infection rate (0-25%) managed accordingly
displacement, treat conservatively with strict 2) Thrombo-embolism
bed rest and analgesics. 3) Pin tract infection
d) If there is displacement with anterior opening 4) Death inevitable in certain situations
type (unstable Fracture) then assess the
displacement.
e) If it is < 2.5 cm – treat conservatively.
Bibliography
Further reading
1. Bucholz RW, Williams L, Wilkins. Rockwood and Green’s fractures in adults. 6 th and 7th edition.
2. Canale ST, Beaty JH, Elesvier M. Campbell’s operative orthopedic. 11th edition.
3. Park K. Textbook of Preventive and social medicine. M/s Banarsidas Bhanot Publishers. 20th edition.
2009.
4. Chapman MW, Williams L, Wilkins. Chapman’s Orthopedic surgery. 3rd edition.
5. Global status report on road safety: time for action. WHO, Geneva. 2009
www.who.int/violence_injury_prevention/road_safety_status/2009

Page 549
10. FRACTURES OF UPPER LIMB
a) Investigation -
1. Mode of Injury  X- ray of hand Antero posterior and oblique view
a. Fall on outstretched hand
b. Road Traffic Accident
b) Treatment -
c. Associated Poly Trauma
1) Primary Stabilization in anatomical position with
the help of available splinting material.
2. Type of Fracture 2) Closed or open reduction and internal fixation with
1. Fracture of Hand: 'K' wire.
i. Fracture of the base of the first Metacarpal
ii. Fractures of the other Metacarpal bones A. Rolando Fracture
iii. Fractures of the Phalanges It is a common extra articular fracture of base of first
metacarpal bone.
2 Fractures around Wrist: a) Investigation -
i. Fracture of the Scaphoid bone  X-ray of hand Antero-posterior, Lateral and
ii. Fractures of other Carpal bones Oblique views.
iii. Dislocations of the Carpal bones b) Treatment -
iv. Fracture of the lower end of the Radius (Colles' and 1) Primary stabilization in anatomical position with
Smith's) the help of available splinting material.
v. Galeazzi fracture – dislocation 2) Closed or open reduction and internal Fixation
vi. Fracture – separation of the lower Radial epiphysis with 'K' wire ORIF by K wire.
vii. Fracture of the shafts of the forearm bones 3) External fixation
4) Mini fragment ‘T’ plate fixation
3 Fractures around Elbow: 2.1.2 Fracture of the other Metacarpal Bones
i. Fracture of the head and neck of the Radius
ii. Fracture of the upper end of the Ulna with a) Investigation -
dislocation of the head of the radius (Monteggia  X-ray of hand Antero-posterior and Oblique
fracture – dislocation) views.
iii. Fracture of the Coronoid process b) Treatment -
iv. Fracture of the Olecranon process 1) Primary stabilization in anatomical position with
v. Fractures of the Epicondyles and Condyles the help of available splinting material.
vi. Supracondylar fracture 2) Conservative - Cock up splint.
3) Surgical - Close or Open reduction and internal
4 Fracture of the Humerus: fixation with K wire or mini plate.
i. Fracture of the Shaft 4) External fixation for compound (open) fracture.
ii. Fracture of the Greater tuberosity
iii. Common Fracture of Proximal Humerus/ Fracture 2.1.3 Fractures of the Phalanges
of greater tuberosity a) Symptoms -
Pain & Swelling and bony deformity with loss of
5 Fractures of the Shoulder Girdle: active movements.
i. Fractures of the Clavicle b) Signs -
ii. Fractures of the Scapula Tenderness at Fracture site along with Crepitus and
Abnormal Mobility.
c) Investigation -
2.1 Fracture of Hand: X- ray of hand AP and Oblique views.
2.1.1 Fractures of base of the first metacarpal- d) Treatment-
Bennett’s Fracture 1) Primary stabilization in anatomical position with
Intra-articular fracture through base of first Metacarpal the help of available splinting material.
bone in which the fractured shaft is displaced laterally 2) Conservative - Buddy strapping, POP slab, finger
due to unopposed pull of APL. (Abductor Pollicis splints
Longus)
Page 550
c) Investigations -
 X-ray of the wrist in AP, lateral and
oblique views.
 CT Scan
d) Treatment -
1) Primary stabilization in anatomical (glass
holding) position with the help of
available splinting material.
2) Conservative – Manipulative reduction
Fig. 10.1: FINGER SPLINT under anaesthesia and plaster
immobilization.
3) Surgical – K (Kirschner) wire or JESS (Joshi's 3) Surgical – operative replacement of carpal
External Stabilization System) fixator. bones.
e) Complications -
 Avascular necrosis
2.2 Fractures Around Wrist:  Osteoarthritis
2.2.1 Fracture of the Scaphoid bone-  Injury to median nerve
It is common in young adults usually caused due to fall
on outstretch hand, often overlooked. 2.2.4 Fracture of the lower end of the
a) Symptoms – Pain, Swelling and Restriction of radius
wrist movement.
b) Signs – Tenderness in anatomical snuff box and A. Colles' fracture - It is a fracture of the lower
impairment of wrist movement. end of Radius at metaphyseal region which
c) Investigations - X-ray of wrist in AP, lateral and manifests in bent fork deformity due to dorsal
two oblique projections. and radial displacement of the distal fragment.
d) Treatment - Primary stabilization in anatomical
(glass holding) position with the help of available B. Smith's fracture – It is reverse of the Colles'
splinting material. fracture with ventral displacement.
1) Conservative - Plaster immobilization usually
till 2 to 3 months. a) Symptoms -
2) Surgical – Closed or open reduction and internal Pain, Swelling and bony deformity of the
fixation with a special compression screw. wrist with loss of active movements
e) Complications: b) Signs -
The incidence of complications is high. Tenderness at fracture site along with or
 Delayed or non-union without Crepitus and abnormal mobility
 Avascular necrosis c) Investigation -
 Osteoarthritis  X-ray of forearm with wrist AP and
Oblique views.
2.2.2 Fractures of other carpal bones-  X-ray Wrist in Ulnar deviation.
These are less common serious fractures. The d) Treatment -
treatment is conservative management with plaster 1) Primary stabilization in anatomical (glass
immobilization. holding) position with the help of available
2.2.3 Dislocations of the carpal bones- splinting material.
Complete dislocation of the wrist is very uncommon 2) Close reduction and plaster immobilization.
and incomplete carpal dislocation involve one or more 3) Close reduction with K wire fixation.
of the carpal bones and are as follows: 4) Close reduction with K. wire fixation and
1) Dislocation of lunate bone. external distractor application.
2) Perilunar dislocation of the carpus. 5) Open reduction and internal fixation with
a) Symptoms – Pain, Swelling, Deformity and multiple K wires, plate and screws.
restriction of movement of the wrist joint.
b) Signs – Tenderness and Loss of anatomical
position of wrist and hand.
Page 551
2.2.5 Galeazzi fracture – dislocation- d) Treatment:
It is the fracture of radial diaphysis at the 1) Primary stabilization in anatomical position by
junction of middle and distal third of the shaft applying gentle axial traction and splinting with
with associated disruption of distal radio ulnar the help of available material. (moulded splints,
joint. folded newspaper, card board or wooden plank)
a) Symptoms - 2) Splintage.
Pain, Swelling, Deformity and Shortening of
the forearm.
b) Signs -
Bony Deformity & Tenderness, Crepitus &
Pain aggravated by passive stretching of
wrist.
c) Investigation -
X- ray forearm with Elbow and Wrist in AP
and lateral projection.
d) Treatment –
1) Primary stabilization in anatomical
position by applying gentle axial traction
and splinting with the help of available
material. (moulded splints, folded
newspaper, card board or wooden plank)
2) Surgical
 Mostly needed for prevention of
Malunion
 Open reduction and internal fixation
with plate and screws Fig. 10.2: SPLINTAGE FOR FRACTURE
RADIUS/ULNA AND LOWER END OF
2.2.6 Fracture – separation of the lower HUMERUS
radial epiphysis-
It is seen in children before Physeal fusion in 3) Conservative - Closed reduction and plaster
which the epiphysis is fractured and separated application under anaesthesia, mostly in children.
from the metaphysis and results into gross 4) Surgical –
deformity, if not treated adequately. The clinical  Closed reduction and internal fixation with
features and management are same as that of elastic (in children) or rigid intramedullary nails.
fracture of lower end of radius in adults except  Open reduction and internal fixation with plates
surgical intervention which is rarely needed. and screws.
 External fixator application in case of open
2.2.7 Fracture of the shafts of the forearm fractures.
bones-
The forearm bones, radius and ulna get fractured 2.3 Fractures Around Elbow:
either single or both and are very common 2.3.1 Fracture of the head and neck of the
Injuries which result into gross deformity and radius-
functional restriction, if not treated. One of the commonest fractures of the upper limb
in young adults.
a) Symptoms- a) Symptoms -
Pain, Swelling over forearm and bony Pain and Swelling on lateral aspect of Elbow and
deformity. restriction of movement.
b) Signs - b) Signs –
Tenderness, Crepitus, Abnormal mobility Sharp local Tenderness and impaired
with or without signs of compartment movements. (Flexion of elbow and pronation and
syndrome. supination)
c) Investigation -X-ray of the forearm with c) Investigations –
wrist and elbow in AP and lateral projections X-ray of elbow joint with forearm in AP and
lateral projections.
Page 552
d) Treatment - Complications -
 Injury to the Brachial artery leading to
1) Primary stabilization in anatomical position
Volkmann's ischaemic contracture in delayed or
(flexion at elbow and mid prone position of
neglected cases.
forearm).
2) Conservative – in case of slight damage to the  Injury to median nerve
radial head and neck with plaster  Malunion
immobilization.
3) Surgical - 2.3.6 Supracondylar fracture-
 Open reduction and internal fixation in case a) Clinical features -
of severe damage to the radial head and neck. Pain, Swelling and Deformity.
b) Investigation -
 Excision of radial head in severely damaged
X-ray Elbow, AP and lateral views.
and displaced fractures.
c) Treatment -
2.3.2 Fracture of the upper end of the ulna 1) Conservative – plaster immobilization.
with dislocation of the head of the radius 2) Surgical - Closed or open reduction and internal
(Monteggia fracture – dislocation)- fixation with K wires or cancellous screws.
This is uncommon Injury with characteristic 2.4 Fracture of Humerus:
displacement, the ulna is angled forwards and the 2.4.1 Fracture of the shaft-
head of radius is dislocated forwards which is a) Clinical Finding -
obviously seen on clinical and X-ray examinations. Pain and Swelling over arm abnormal mobility,
Clinical features are same as the forearm fractures. crepitus.
b) Investigation -
a) Treatment - X-ray of arm with shoulder & elbow AP and Lat.
1) Accurate fracture reduction is essential. It is c) Treatment –
seldom possible to reduce both the dislocation 1) Splintage
and fracture by closed method.
2) Open reduction and internal fixation with plate
and screws is essential.
2.3.3 Fracture of the coronoid process-

The Coronoid process is seldom fractured unless in
association with posterior dislocation of the Elbow.
2.3.4 Fracture of the olecranon process-

The Olecranon process is fractured by a fall on the
point of the elbow usually in adults.
Clinical feature same as fractures above with distinct
disruption of three-point bony relation of the Elbow.
Fig. 10.3: SPLINTAGE OF FRACTURE OF
(It is a triangle formed by the tip of Olecranon and
HUMERUS
the two epicondyles) 2) Surgical – Closed nailing by
a) Treatment - - Rush nail
The treatment depends upon the type of fracture i.e.
- Ender’s nail Children
plaster immobilization in case of crack fracture,
- Flexible nail
internal fixation for fracture separation and excision
- Humerus Inter locking Nail.
in case of comminuted fracture.
- Open reduction and internal fixation with plate
& screws.
2.3.5 Fractures of the condyles and - External fixator
epicondyles Watch for wrist drop. (radial nerve injury pre and
Condylar fractures are relatively uncommon, but post reduction)
often troublesome and occur mainly in children.
a) Symptoms - Pain, Swelling and Restriction of
movement of the elbow.
b) Signs -
 Marked tenderness and widening of the Elbow.
 Disruption of the three-point bony relation.
Page 553
2.4.2 Fracture of Surgical Neck Humerus
a) Clinical Finding -
 Pain and Swelling over Shoulder
 Painful movements of Shoulder
 Crepitus, Tenderness
b) Investigation -
X-ray shoulder AP and Lateral view (special
views if needed)
c) Treatment –
1) Conservative immobilization
2) Surgical – K wire fixation
Buttress plating Fig. 10.4: FIGURE OF 8 BANDAGE
2.4.3 Common Fracture of Proximal Humerus/

b) Investigation -
Fracture of greater tuberosity - X-ray Shoulder AP
a) Clinical Finding - c) Treatment -
 Pain and Swelling over Shoulder.  Conservative – Figure of '8' bandage. (Clavicle
 Painful movements of Shoulder. brace)
 Crepitus, Tenderness.  Surgical - Closed reduction and K wire fixation
b) Investigation - for fracture of lateral end and open reduction and
X-ray Shoulder AP & CT Scan internal fixation with plate and screws for mid
c) Treatment - shaft fractures.
1) Conservative – Arm to chest strapping.
2) Surgical –Cancellous screws or plate 2.5.2 Fracture of Scapula -
fixation. a) Clinical -
3) Primary shoulder replacement. Pain and Swelling over shoulder painful
movements of shoulder.
2.5 Fractures of the Shoulder b) Investigation -
X-ray Shoulder AP
Girdle: c) Treatment - Shoulder immobilization
2.5.1 Fracture of Clavicle -
a) Clinical Finding -
 Pain and Swelling over shoulder.
 Bony Deformity
 Crepitus, Tenderness
Bibliography
Further reading
1. Bucholz RW, Lippincott Williams L, Wilkins. Rockwood and Green’s fractures in adults. 6 th and 7th
edition.
3. Chapman MW, Williams L, Wilkins. Chapman’s Orthopaedic surgery. 3 rd edition.

Page 554
11. FRACTURE OF LOWER LIMB
1. Mode of Injury
1) Road Traffic Accident
2) Associated Poly Trauma
2. Type of Fracture
i. Fracture Upper End Femur
 Intra capsular
 Extra capsular
 Femur head fracture
ii. Fracture Shaft Femur.
iii. Fracture Lower End Femur.
 Intra articular
Fig. 11.3: STEP 3 BUDDY STRAPPING
 Extra articular
iv. Fracture Patella
v. Fracture Upper End Tibia
vi. Fracture shaft Tibia
vii. Fracture around Ankle joint
viii. Fracture of bones of foot
Splinting of Lower Limb Injuries
Fig. 11.4: ALTERNATE METHOD OF

SPLINTING
3. Fracture Neck of Femur
(Intra-capsular)
Introduction-
Fracture neck of Femur more common in old age due to
Fig. 11.1: STEP 1 TRACTION Slip and fall.
3.1 Classification According to the
site of fracture:
 Subcapital
 Transcervical
 Basicervical
Usually caused by trivial fall in the elderly due to
presence of Osteoporosis, however metastasis from
malignancies can also lead to the pathologic fractures.
The aim of treatment is to achieve union of

the fracture and a durable hip joint
Fig. 11.2: STEP 2 LIMB SPLINTING
afterwards
Page 555
3.2. Principles of management i) Severe Tenderness and Swelling around hip
region.
include: ii) Shortened and externally rotated lower limb.
iii) Inability to do straight leg raising.
3.2.1 Osteosynthesis
i. Screws, Moore’s Pins etc.  Investigations:
ii. DHS, Blade Plate. i) X-ray of pelvis with both hips in AP view and
iii. Internal Fixation + Fibular Grafting. affected Hip in Axial view
iv. Muscle pedicle Graft + Internal Fixation. ii) CT Scan
3.2.2 Osteotomy  Treatment:

i) Pauwels valgus osteotomy i) Conservative – Initial traction and
ii) Mc Murray’s osteotomy immobilization in NRB (Non Rotatory Boot)
in Undisplaced fracture
ii) Surgical -
3.2.3 Arthroplasty
o Closed reduction and internal fixation with
 Hemiarthroplasty
Dynamic Hip Screw and plate (DHS)
 Total Hip Replacement o Proximal Femoral Nail (PFN)
 Excision Arthroplasty o Intramedullary Hip Screw
o Dynamic Condylar Screw (DCS)
4. Trochanteric Fractures For sub trochanteric fractures a DCS is the implant of
choice after closed or open reduction. Other
(Extra-Capsular Fracture modalities like PFN, Angled blade plate,
Reconstruction nail or Modified Kuntscher nail may
Neck Femur) also be used as per the preference of the surgeon.
4.1 Fracture of Greater Trochanter
This is isolated fracture of greater trochanter due to
fall on the side of Pelvis, usually minimally displaced 5. Fracture Shaft of Femur
and managed with pelvic stripping and non-weight Fractures of the shaft of the femur are mostly due to
bearing. high-energy trauma.
4.2 Fracture of Intertrochanteric
Region: 5.1 Types of Femoral Shaft
Intertrochanteric Hip fractures are more common in Fractures:
road traffic accidents in young adults and domestic  Type I - Spiral or transverse (most common)
fall in elderly.  Type II – Comminuted
4.3 Fracture of Sub Trochanteric  Type III – Open
Region:
Occur between lesser trochanter and a point 5 cm 5.2 Investigations:
distally and are seen as independent entities or as an X-ray shaft Femur with X-ray of Pelvis and Knee for
extension of intertrochanteric fractures. associated injuries.
4.4. Classification
4.4.1 Trochanteric fractures are classified 5.3 Treatment:
according to Boyd and Griffin 5.3.1 Conservative management-
classification Conservative management of fractures in children in
Spica cast or with skeletal traction.
4.4.2 Sub trochanteric fractures are
classified according to Seinsheimer 5.3.2 Surgical management-
 Kuntscher nail for Isthmic fractures
classification
 Interlocking Nailing in comminuted fractures
A. Clinical features:
 Plating for lower third fractures
 Symptoms - Pain, Swelling, Bruising,
shortening of the limb and inability to stand or  Plating of shaft Femur fracture in children
walk. Blood transfusion if needed and correct hypovolemic
shock.
 Signs -
Page 556
6. Fracture of Tibia/Fibula 7. Fracture Calcaneus
6.1 Introduction: 7.1 Mode:
Mostly due to road traffic accident Fall from height.
6.2 Signs /Symptoms: 7.2 Sign /Symptoms:
 Pain, Swelling, Tenderness  Swelling, Oedema, Pain, Tenderness.
6.3 Investigation: 7.3 Investigation:
 X-ray of Tibia along with X-ray of knee and  X-ray of heel
ankle joint.  CT scan for intra articular fractures.
6.4 Treatment: 7.4 Treatment:
6.4.1 Conservative - In Undisplaced fracture,  Conservative (Boot Cast). Strict non-weight
closed reduction and above knee cast for 12 weeks. bearing till fracture heals.
 Intra-articular fractures of Calcaneus involving
6.4.2 Surgical – Displaced fracture, Interlock nail sub-talar joint should preferably treated with
or plating depending on fracture anatomy. restoration of anatomical fracture geometry is
must.
Bibliography
Further reading
edition.

Page 557
12. DISLOCATIONS
Loss of Alignment of joint surfaces which should be 1.5 Treatment:

treated as emergency.
 Reduction – Traction – Counter Traction,
Abduction, Extension, External rotation –
1. Shoulder Dislocation Reduction.
Most common dislocation.  Stimson – Sedation and prone position with 5 lbs.
weight
1.1. Types  Surgery
i. Anterior
ii. Posterior  Irreducible dislocation
iii. Inferior (Luxatio erecta)  Displaced fracture dislocation with ORIF
1.6 Complications:
 Recurrent dislocation
 Axillary Nerve and Artery injury
 Brachial plexus injury
 Stiffness
2. Elbow Dislocation
Most common- Posterior Dislocation of Elbow
2.1 Mechanism:
 Posterior - Elbow Hyperextension, Valgus stress,
Arm Abduction, Fore-arm Supination.
Fig. 12.1: X-RAY PICTURE OF SHOULDER
 Anterior-direct force over posterior fore-arm with
DISLOCATION
Elbow in Flexed position.
1.2 Mechanism: 2.2 Clinical Features:

 Most commonly indirect / direct violence  Gross instability
 Posterior dislocation is common in Electric shock  Swelling
and Convulsions.  Three-point bony relation altered
 Associated Injuries - Radial head and Coronoid
1.3 Clinical Features: Fracture
1.3.1 Anterior- 2.3 Investigation:
 Patient comes with injured shoulder in Abduction
 X-ray Elbow AP and Lateral
and External rotation.
 Closed manual reduction under GA, followed
1.3.2 Posterior-
with above Elbow posterior slab 90-degree
 No striking deformity, Shoulder in Abduction
Flexion.
and Internal rotation.
1.3.3 Luxatio erecta- 2.4 Operative Indications:
 Salute position Abduction forward elevation.  Re-dislocation
 Severe Pain, Neuro vascular deficit, more with  Non-concentric Reduction
latter two.  Surgery: Open reduction and repair of soft
1.4 Investigation: tissues, Hinged external fixation, pinning
 X-ray  Neurovascular Injury
AP, Scapular view, Axillary view, CT scan  Femoral head fractures
 Heterotopic ossification
 Recurrent dislocation
 Thromboembolism
Page 558
2.5 Complications: 4. Knee dislocation
 Loss of motion
 Neurologic compromise  Mode of Injury: high energy / low energy
 Vascular Injury  Hyperextension with or without Varus / valgus
 Compartment syndrome
 Re-dislocation
 Myositis Ossificans
3. Hip dislocation
3.1. Types of dislocation:
3.1.1 Posterior-
Posterior dislocation is the most common type of
dislocation. Occurs mainly due to dash board Injury.
3.1.2 Anterior- Fig. 11.2: X-RAY PICTURE OF KNEE

Anterior dislocation occurs because of blow to the DISLOCATION
back in squatting position.
3.1.3 Central dislocation- 4.1 Clinical features:

Occurs due to direct blow over the trochanter  Gross knee distortion is present
 A neurovascular examination must be done
3.2. Clinical Features:
3.2.1 Posterior- 4.2 Investigations:
 Limb in flexion, adduction, internal rotation, limb  First reduce the dislocation
shortening  Then take X-rays AP and lateral, 45-degree
 Sciatic nerve Injury oblique, patellar sunrise views
3.2.2 Anterior-  MRI
 Limb in flexion, abduction, external rotation,  Arthroscopy
limb lengthened  Assess the ligament Injuries
 Injury to femoral nerve.
4.3 Treatment:
3.3 Investigation: a) Immediate closed reduction, avoid direct pressure
over the popliteal fossa after reduction, splint at
 X-ray.
20 - 30 degrees of flexion.
 Hip AP and lateral.
b) Operative indications:
 CT, MRI. o Unreduced, residual soft tissue interposition
o Open Injuries, ORIF with ex-fix.
3.2 Management: o Reconstruction of ligaments at later setting.
a) Resuscitate, CPR attempted with in-line traction
with patient lying supine, under general 4.4 Complications:
anesthesia.
 Limited range of movements
b) Methods used are the classical Watson-jones,
 Ligamentous laxity and instability
Bigelow and reverse Bigelow, Allis, Stimson
gravity method.  Vascular compromise
c) Maintain it with skeletal traction.  Nerve traction Injury
d) If irreducible, nonconcentric, ipsilateral neck
Fracture or Acetabular Fracture then open
reduction is done.
3.5 Complications:
 Osteonecrosis
 Post-traumatic osteoarthritis of the joint
Page 559
Bibliography
Further reading
edition.
3. Chapman MW, Williams L, Wilkins. Chapman’s Orthopaedic surgery. 3rd edition.

Page 560
13. LIGAMENTOUS INJURIES
1. Mode of Injury 4. Treatment

Indirect, Twisting or Bending Forces on the Knee. a) Initial management with Brace/Splint and
NSAIDs
2. Clinical Features b) Conservative management with Bracing and
 Pain, Swelling, Tenderness, Loss of range of Physiotherapy
motion and Positive Patellar Tap. Bracing for 2 weeks followed by MRI
3. Investigations c) Operative: Arthroscopic ligament repair.
 X-ray of associated joint and MRI
Bibliography
Further reading
edition.

Page 561
14. SPINAL TRAUMA
Table 1: ASSESSMENT OF MOTOR FUNCTION
1. Spinal Cord Injury (SCI)
It is an insult to the Spinal Cord resulting in a change, Diaphragm C3-5
either Temporary or Permanent, in its Normal Motor,
Shrug shoulders C4
Sensory or Autonomic Function.
Deltoids/elbow flexion C5
Extend wrist C6
Extension of elbow/ flexion of
C7
wrist
Abduct fingers C8
Active chest expansion T1-T12
Hip flexion L2
Knee extension L3-4
Ankle dorsiflexion L5-S1
Ankle plantar flexion S1-2
Fig. 14.1: HEAD TO TOE STABILIZATION IN
CASE OF SPINAL INJURY ON SPINE BOARD Table 2: ASSESSMENT OF SENSORY
FUNCTION
2. Optimal Diagnostic Criteria, Deltoid area C5

Investigations, Treatment & Thumb C6
Referral Criteria Middle finger C7

Little finger C8
2.1 Rural/ Sub District Hospital:
Optimal Standards of Treatment in Situations where Nipple T4
technology and resources are limited. Xiphoid T8
2.1.1 Clinical Diagnosis- Umbilicus T10
After the ABC has been taken care of, the patient is Symphysis T12
gently log rolled and whole of the Spine is Palpated for
Tenderness or a palpable step-off deformity. Anterior thigh L2
Neurogenic shock, Incontinence of Bowel, Bladder
Anterior knee L3
and Penile erection indicate severe spine Injury. A
careful and detailed Neurological examination is then Antero-lateral ankle L4
performed and meticulously documented. nd
Dorsum of great and 2 toe L5
2.1.2 Frankel’s grades- Lateral side of foot S1
Spinal Cord Injury is most commonly graded using
Frankel’s grades (A to E). Posterior calf S2
A: Complete Motor and Sensory loss
B: Sensation only present below lesion Perianal sensation S2-5
C: Sensations present and Motor function is
present but useless
D: Motor useful but not normal
E: No neurological deficit.
Page 562
After the motor and sensory examination, presence Day care might be needed for situations like
of sacral sparing may be noted by voluntary Rectal Debridement of bed sores.
Sphincter tone and toe flexor contractions. Presence
of Sacral sparing indicates a better neurological 2.1.6 Referral criteria-
prognosis. i. The patient should be Hemodynamically
stable and fully resuscitated at the time of
Although spinal shock is over by 24 hours, rarely it referral.
may be prolonged. A positive Bulbocavernous reflex ii. All the patients who need surgery (indications
or a positive anal wink indicates the end of spinal discussed in the next section) need to be
shock. If no motor or sensory function can be referred to a specialized tertiary care centre.
documented at this stage, a complete spinal cord iii. The decision of need for surgery can only be
injury is present. made by an experienced Spinal surgeon either
2.1.3 Investigations- Orthopedic or Neurosurgeon. In absence of
All patients with suspected spinal Injury should have these all patients with proven or suspected
radiographic evaluation. spine injury should be referred to a higher
center.
a) Initial screening can be done by conventional
Antero-posterior and Lateral X-rays. The Cervical
spine radiographs must include the C7-T1 junction to
2.2 At District Hospital
be considered adequate 2.2.1 Clinical Diagnosis-
iv. As described above (in situation 1)
- Additional Open-mouth views should be done to
evaluate odontoid Injury. 2.2.2 Radiographic evaluation of patients
- Whole spine should be evaluated with a patient of with spinal Injury-
spinal Injury. i. Initial screening can be done by conventional
Antero-posterior and Lateral X-rays.
b) The patient should be referred for advanced ii. Additional open-mouth views should be done
diagnostic modalities only when the patient is to evaluate Odontoid Injury.
stable: iii. Special views like Swimmer’s view and
i. CT Oblique views can be done to see junctional
ii. MRI areas.
iv. CT scan of the whole spine should be done if
in presence of clinical suspicion but fractures
2.1.4 Out Patient care- cannot be demonstrated on X-rays or if
A secondary hospital is expected to provide junctional areas are not visualized.
outpatient care to the Spinal cord injury patients who v. MRI should be done to evaluate Ligamentous
may be referred back from specialized centers after injury, Spinal cord injury.
definitive treatment. This may be in form of a vi. In patients with pre-injury morbidities such as
i. Physiotherapy for passive mobilization of all Ankylosing.
joints and active exercises for muscles. vii. For Stiff spine, CT and MRI should be done to
ii. Teaching of clean intermittent catheterization rule out occult instability even if X-rays are
iii. Counselling of the patient and attendants normal.
iv. Care of bed sores viii. Whole spine should be evaluated with a
patient of Spinal injury
2.1.5 Day Care-
Page 563
Fig. 14.2: X-RAY VIEW OF CERVICAL SPINE TRAUMA Fig. 14.3: MRI OF SPINE TRAUMA
2.2.3Treatment: Standard Operating procedure No clinical evidence exists to definitively recommend

(a) On arrival in Emergency room: the use of any Neuro protective pharmacologic agent,
including Steroids, in the treatment of Acute Spinal Cord
injury to improve functional recovery. However high
 Once the patient with a potential Spinal injury dose Methyl-Prednisolone may be used as per NASCIS
reaches the emergency, the patient should be
III recommendations (Methylprednisolone: Bolus dose
transferred off the backboard onto a firm padded
of 30 mg/kg of body weight over 15 minutes, followed
surface while maintaining spinal alignment. A
by a 45-minute pause, and then a 23-hour continuous
baseline skin assessment can be performed at the
infusion of 5.4 mg/kg/hr., (If patient presents between 3
time of shifting the patient from spine board to
and 8 hrs., give the above steroid infusion for total of 48
hospital bed. Adequate number of personnel should
hrs.) if the patient presents within 8 hours of injury. The
be employed for Logrolling during patient
risk of complications as Infection, Sepsis, Respiratory
Repositioning, Turning and Transfers.
complications and Gastrointestinal Hemorrhage should
be kept in mind while administering steroids. It is
basically a treatment option, not standard care.
Once initial Resuscitation is done, complete a
comprehensive tertiary trauma survey in the patient with
potential or confirmed Spinal Cord injury.
In the patient with acute Spinal Cord injury,
particularly higher Cervical injury, assess frequently
and early document any evidence of Traumatic Brain
injury (TBI) in the form of Loss of consciousness and
post traumatic Amnesia.
Screen for Thoracic and Intra-abdominal injury in all
patients with spinal cord injury.
Perform early stabilization of extra spinal fractures.
Fig. 14.4: LOG ROLLING WHILE EXAMINING & Perform this surgery as early as possible to facilitate
early Rehabilitation and Concomitantly with any
SHIFTING OF SPINAL INJURY PATIENT required Spinal Stabilization if the patient is medically
stable.
Page 564
(b) Out Patient (c) Day Care
Outpatient care is needed for non-surgically treated Referral criteria:

patients on Ambulatory care and Surgically treated Surgically treated patients may be referred back to
patients. This will include: secondary hospitals for Physiotherapy and care of
Back, Bladder and Bowel.
Prescription of appropriate Orthoses physiotherapy
services, Counselling: Social, Physiotherapy,
Vocational
Bibliography
Further reading
edition.
4. Sekhon LH, Fehlings MG. Epidemiology, demographics and pathophysiology of acute spinal cord
injury. Spine 2001: 26: S2–12.
5. Amar AP, Levy ML. Pathogenesis and pharmacological strategies for mitigating secondary damage in
acute spinal cord injury. Neurosurgery 1999: 44:1027–39.
6. Transfer to definite care. In advanced trauma life support for doctors’ student course manual. American
college of surgeon, Chicago. 8th edition. 2008:269-76.
7. Aebi M, Arlet J, Webb J. AO Spine manual. Thieme publishers.
8. Practice Management Guidelines for the Screening of Thoracolumbar Spine Fracture. The Journal of
Trauma, Injury, Infection and Critical Care. Volume 63:3-709.
9. Trauma practice guidelines of the Eastern Association for the surgery of trauma (EAST). Identifying
Cervical Spine Injuries following Trauma. [cited 2016 July 6]
Available from: www.east.org


Page 565
15. MANGLED EXTREMITIES (AMPUTATION)
1. Introduction 4. Standard treatment protocol
 Traffic is increasing day by day and so are road
for management of Mangled
traffic accidents. extremities at RH/SDH/DH
 Most of RTA involve trauma to extremities to
varying level.  No Delay in receiving the patient and starting
treatment.
2. At PHC/Sub Center level  Multi-systemic approach
 Patient should be examined according to ATLS
 Follow ATLS guidelines of A B C D E protocol of ABCDE.
 After stabilization of patient, examine for other  Look for signs of poly trauma, involvement of
associated injuries such as Pelvis and Spine Head injury, Spine or Abdominal and Pelvic
which are common in poly trauma injuries.
 If such injuries are present, then refer the case to
higher center without any delay. 4.1 Informed consent:
 If absent, then grade the injury according to
MESS (Mangled Extremity Severity Score)  Two surgeons should certify that the limb needs
which is useful for decision making regarding amputation.
definitive surgical treatment (Salvage or  Consent of the patient (if conscious and co-
Amputation of the limb) and refer the patient to operative) should be taken.
the higher centre.  Consent of relative should be taken if patient is
non responsive.
3. Before Referring  Detailed informed consent in their local
language should be taken.
 Wash the wound primarily with Normal Saline,
Iodine solution and Hydrogen Peroxide till all 4.2 Pre-operative care:
visible contamination in removed.
 Stop any active bleed with help of Compression  Pain management
bandage or Tourniquet  Clinical assessment
 Avoid excessive handling of injured limb to  Decision making
avoid neurovascular complications  Discharge planning
 Infuse IV fluids and Blood  Record keeping
 Inject first dose of higher Antibiotics
 Give Inj. TT. O.5 ml intra muscular 4.3 Peri operative care:
Things to be done Before Referral  The scheduling of operations
 Inform the concern center about MESS score  Operation undertaken
and expected time of arrival of patient  Antibiotic prophylaxis
 Arrange for proper transport  Thrombo prophylaxis
 Make sure that patient will be
Hemodynamically stable during entire
4.4 Post-operative care:
duration of transport.
 Pain management
 Wound care
 Rehabilitation
Page 566
Bibliography
Further reading
edition.


Page 567
16. COMMON FRACTURES IN CHILDREN
o Epiphyseal injury around Hip and Knee

1. Common fractures Closed reduction and Immobilization in
Mode – Fall on out- Stretched hand splints
o Surgical treatment – Open reduction and
 Lower end Radius treated by closed reduction internal fixation with multiple cancellous
 Greenstick fracture both bone Forearm screws or mini DHS plate
requires Closed reduction under General  Fractures around hip Surgical treatment
anesthesia o Shaft femur
 Supracondylar fracture Humerus Depending Undisplaced – Conservative
on classification either Closed reduction or Displaced
closed reduction with cross k-wire or Open o Shaft tibia
reduction Undisplaced – Conservative
 Fracture Lateral Condyle Humerus requires Displaced – Surgical in the form of Closed
Open reduction or Open reduction and internal fixation with
 Fracture Clavicle treated by Figure of 8 either elastic nails or plate and screws.
bandage
 Fractures of lower limb
Bibliography
Further reading
1. Bucholz RW, Williams L, Wilkins. Rockwood and Green’s fractures in Children. 6 th and 7th edition.

Page 568
17. BONE TUMORS
Primary Neoplasms of the skeleton are rare,  Complications: - Bursitis, Neuropathy,
amounting to only 0.2% of the overall human tumour limitations of movement, Malignant
burden. However, children are frequently affected transformation (chondrosarcoma) occur rarely
and the etiology is largely unknown. Significant  X-ray: - Bony growth made up of mature
progress has been made in the histological and cortical bone and marrow. Cartilaginous gap not
genetic typing of bone tumours. Furthermore, visible.
advances in combined surgical and chemotherapy  Treatment: - Excision including Periosteum
have led to a significant increase in survival rates
even for highly malignant neoplasms, including 1.1.3 Fibrous Dysplasia-
Osteosarcoma and Ewing sarcoma. Normal bone is replaced by fibrous tissue.
Erodes the cortices of bone from within.
1. Primary bone tumors  Thin layer of sub - periosteal bone forms around
the mass, so bone appears expanded. Site- upper
1.1 Benign Tumors: end of Femur, Tibia, Ribs.
1.1.1 Osteoid Osteoma-  Mono-ostotic one bone is affected. Poly-ostotic
True benign tumor of bone many bones are affected.
 Age group: - 5 - 25yrs  Clinical features: - Pain, Deformity, Pathologic
 Commonest site: - Diaphysis of long bone. e.g. fractures.
tibia.  X-ray: - Ground glass appearance.
 Clinical features: - Night pain, relieved by  Treatment: - Curettage and bone Grafting.
Salicylates. 1.1.4 Osteoclastoma (Giant Cell Tumor)-
 Pathology: - Consists of a Nidus surrounded by
dense Sclerotic bone Common bone tumor with variable growth
 X-ray - Zone of sclerosis surrounding a nidus potential
 Treatment: - Complete excision of Nidus with  Age group: - 20 - 40 years
Sclerotic bone.  Site: - starts in Epiphysis and extends into
 Prognosis - Good Metaphysis
 Commonly lower end of Femur, upper end of
1.1.2 Osteochondroma- Tibia
Commonest Benign tumor of bone, arises from  Pathology
adjoining Epiphysis to Metaphysis  Cell of origin is uncertain
 Age group: - Adolescents  Tumor consists of undifferentiated spindle
 Clinical features: - Painless swelling around a  Cells with multinucleated giant cells
Joint, Sessile or Pedunculated  Clinical feature: - Swelling, Vague pain
 Multiple site involvement is called Diaphyseal  X-ray
Aclasia o Lytic expansile lesion
o Eccentric location
o Soap bubble appearance – Pathognomonic.
Page 569
Fig. 16.1: SOAP BUBBLE APPEARANCE OF GIANT CELL TUMOUR
 Excision with reconstruction  Occurs most often in distal Femur, may also be
 Curettage with or without supplementary in the Humerus, Tibia, and Ulna
procedures like chemical Ablation,  Develops on surface of bone and progresses
Cryotherapy, PMMA implantation slowly
 Amputation: aggressive tumors, recurrence  Treatment
 Radiation: tumor involving vertebrae a) Surgery
b) Tumor Resection, possible Amputation
1.2 Primary malignant bone c) Inter-Scapulothoracic surgery
tumors: d) Hemipelvectomy
e) Chemotherapy
1.2.1 Osteogenic Sarcoma-
 Usually in males aged 10 to 20 1.2.3 Chondrosarcoma-
 Occurs most often in Femur, but also in Tibia  Usually in males ages 30 to 50 years
and Humerus  Occurs most often in Pelvis, proximal Femur,
 Occasionally in Fibula, Ileum, Vertebra or ribs and Shoulder girdle
Mandible  Develops from Cartilage and grows slowly
 Tumor arises from bone-forming Osteoblast and  Usually Painless, locally recurrent and invasive
bone-digesting Osteoclast  Hemipelvectomy
 Treatment  Surgical resection (ribs)
a) Surgery  Radiation and / or Chemotherapy
b) Radical Tumor resection
c) Mega Voltage Radiotherapy and / or
Chemotherapy or combination of both. 1.2.4 Multiple Myeloma-
It is the most common primary malignancy of bone
1.2.2 Parosteal Osteogenic Sarcoma- having short duration onset and aggressive in nature.
 Usually in females ages 30 to 40
Page 570
Age of occurrence – commonly around 60yrs. 2%
less than forty.
2. Metastatic bone tumors:
 The most common bony malignancies are
Clinical features: Metastatic Carcinomas
 Bone pain  Metastatic lesions represent the most common
cause of pathology fractures due to a Neoplasm
 Weakness
 Usually are multiple but can be solitary
 Weight loss
 The most common primaries are Breast,
 Anemia
Prostate, Lung, Kidney and Thyroid, in that
 Thrombocytopenia
order
 Peripheral neuropathy
 Renal metastasis is quite vascular and have cold
 Hypocalcaemia
bone scans
 Renal failure
Clinical features:
It manifests in pathological fractures commonly in
spine followed by Ribs and Pelvis.  Patients with known primary malignancy
presents with symptoms suggestive of
Laboratory studies: Secondaries in bone
 Urine - Bence Jones Protein present in 30% of  Bony pain, commonest site is spine
cases  Pathological fractures most common in spine
 Blood - Very high ESR, A/G ratio reversal
 Serum electrophoresis - Abnormal spike in Investigation:
Gamma Globulin region in 90% cases  X-ray - Majority are Osteolytic, few are
Treatment: Osteoblastic. e.g., Male- Prostatic Secondaries,
Female- Breast Secondaries
a) Chemotherapy – Melphalan is the drug of  Blood - High ESR, elevated serum Calcium,
choice elevated serum Acid Phosphatase in Prostatic
b) Given in combination with Vincristine, Secondaries
Prednisolone and sometimes
Cyclophosphamide. Cycles are repeated 3 - 4 Treatment:
weeks for 6 - 12 cycles a) Symptomatic relief of Pain and prevention of
c) Splintage of diseased part pathologic fractures
d) Radiotherapy- Useful in case of Neurological b) Chemotherapy
compression c) Radiotherapy
e) Surgical intervention in advanced tumors

Bibliography
Further reading
1. Puri A, Agarwal MG. Current concepts in Bone and soft tissue tumours. Paras Medical Books Pvt.
Ltd. 2007.
3. Campbells. Operative orthopedics.
4. Coombs R, Friedlande G. Bone Tumour Management. Butterworths.
5. Roberts L. Orthopedics in Infancy and Childhood.
6. Kulkarni GS. Text Book of Orthopedics and Trauma.


Page 571
Anaesthesia
10. Anesthesiology
1 Introduction: General Protocol of Anaesthesia 572
2 Protocol of Difficult Air way 581
3 Pre – Anaesthesia Checkup Protocol 583
4 Conduct of Anaesthesia 585
5 Complications of Anaesthesia 586
6 Regional Anaesthesia – Clinical Protocol 588
7 Cardio Pulmonary Resuscitation 590
8 Anaesthesia Obstetric Protocol 593
9 Spinal Anaesthesia 597

1. INTRODUCTION
noxious stimuli with different inhalational and
1. Definition intravenous drugs.
Anesthesia is the reversible state of unconsciousness
with amnesia, analgesia and unresponsiveness to
2. Types of Anesthesia
GENERAL
Types of Anaesthesia
General (GA) Regional Total Intra Monitor

Intravenous Venous Anaesthesia
Anaesthsia Regional Care
(Short GA)
Anaesthesia (MAC)
with mask (G1 A)
Stand By
or without mask
Central Nerve Block Local Localized or

Neuroaxial selective
block nerve block
With
With PNS/USG Without PNS/USG PNS/USG
Sub Arachnoid Epidural Caudal Epidural Combined Spinal

Spinal Block Blocks Block Epidural Block
Fig. 1.1: ANAESTHESIA GENERAL PROTOCOL
Page 572
3. Pre-Anaesthetic Checklist
a) Check function of high vacuum suction g) Check gas supplies, both cylinder, pipeline &
machine. circuit.
b) Check reserve oxygen supply. h) Check oxygen supply failure alarm & oxygen
c) Check function of breathing system. flush.
d) Check vaporizer. i) Check oxygen nitrous oxide ratio.
e) Check absorber if in use. j) Mechanical ventilator.
f) Inspect equipment for k) Waste gas scavenging system.
 Endotracheal intubation l) Check reserved gas supply.
 Intravenous infusion m) Apply and check monitoring system &
 Resuscitation cautery, circuit and tourniquet.
n) Set appropriate alarm level.
l) Magill’s forceps (Adult & Pediatric), Scissors,

4. Recommended minimum Ampoule cutter, Torch, Thermometer.
essentials in Operation m) IV sets, Micro Sets, Blood sets, three-way IV
extension tube & central line.
theatre n) IV fluids crystalloids RL, DNS, D5 and
Colloids plasma expanders.
4.1 Minimum Essentials Required: o) For Difficult Airways fiber optic boogie, LMA
a) Continuous supply of oxygen via central (Classic & Pro Seal), I-gel, Tracheostomy, tube,
pipeline or jumbo cylinders. percutaneous tracheostomy set, Combitube and
b) Anesthesia machine with two oxygen and one all size Stylet (flexible & Rigid).
nitrous oxide input connections. p) Disposable spinal needles 23, 24, 25, 26, 27,
c) One small oxygen cylinder mounted on Boyles Epidural set 16, 18.
other than jumbo or central line and nitrous q) Radiant warmer/blanket, heating mattress, fluid
oxide cylinder along with cylinder valve opener warmer.
should be there. r) Postoperative recovery room with oxygen
d) Boyle’s machine should have Hypoxic and supply and monitors.
alarm safety system. s) BP apparatus & Stethoscope.
e) Working suction machine (Foot driven and t) Vaporizers-(Goldman) Halothane & Isoflurane
Electric) with all connectors, tunings, and u) Capnography – To monitor End Tidal Carbon
suction around the tip and exhaust fans. dioxide (ETCO2) Where laparoscopic surgeries
f) Multi-parameter (Pulse Oximeter, NIBP, ECG, are done.
ETCo2). New Born resuscitation kit
g) Defibrillator (Adult & Paediatric).
h) OT table with tilting facility.  Weighing scale.
i) Adult (Bain) & Pediatric (JR) Circuit.  Paediatric resuscitation kit with all masks &
j) Set of oral and nasal Airways – sizes 00, 1, 2, 3, LMA & Stylet.
4.  Flexible smooth rubber cord for tourniquet to
k) Silicon bag with all sizes of masks & cuffed and secure IV line.
plain Endotracheal Tubes. Working  Central line (cava fix, double & triple Lumen).
laryngoscope with 5 sizes of blades.  Glucometer, peak flow meter, height scale &
refrigerator (for blood sample).
Page 573
4.2 Emergency Medicine Kit:
Chart No. 1.1: EMERGENCY MEDICINE KIT

Injections  Metoprolol  Nebulizer
 Hydrocortisone  Hemolock
 Atropine
 Dexamethasone  Botroclot
 Glycopyrrolate
 Potassium chloride  Naloxone
 Adrenaline
 Calcium gluconate  ECG Lead
 Noradrenaline
 Soda bicarbonate
 Dopamine Tablets
 Magnesium 25% & 50%
 Dobutamine
 Mannitol  Nifedipine
 Mephentermine
 Tranexamic acid  Captopril
 Ephedrine hydrochloride 
 Dextrose 25% & 50% Sorbitrate
 Phenylephrine 
 Insulin Atenolol
 Vasopressin
 Deriphyllin
 Prostaglandin
 Aminophylline
 Isoprenaline
 Amiodarone.
 Digoxin
 Xylocard 2%
 Esmolol
 Furosemide (Lasix)
 Propranolol
4.3 Doses and Indication for Emergency Drugs:

Chart No. 1.2: EMERGENCY DRUGS & DOSES
Drug Indication Dose
Sodium bicarbonate Acidosis 2-4 m eq/kg
Atropine Bradycardia 0.03 mg/kg
Naloxone Narcotic depression 5-10 mcg/kg
Calcium gluconate Low perfusion 0.6 ml/kg
Epinephrine Asystole 5 mcg/kg of 1:1000 solutions.
4.4 Various Types of Anesthesia Drugs:

Chart No. 1.3: ANAESTHESIA DRUGS
A. Premedication D. Inhalational Anaesthetic Agent
1. Anticholinergic a) Halothane
a) Inj. Glycopyrrolate b) Isoflurane
b) Inj. Atropine c) Sevoflurane
2. Antacid d) Desflurane
a) Inj. Ranitidine
b) Inj. Pantoprazole
3. Antiemetic E. Reversal Agent
a) Inj. Metoclopramide
b) Inj. Ondansetron a) Inj. Neostigmine
c) Inj. Granisetron F. Obstetric Drugs
4. Opioids
a) Inj. Pentazocin (Fortwin) a) Inj. Oxytocin
b) Inj. Methyl ergometrine
Page 574
b) Inj. Butorphanol c) Inj. Prostaglandin F2 alpha
c) Inj. Fentanyl d) Inj. Magnesium Sulphate
5. Benzodiazepines
a) Inj. Diazepam F. Spinal Anaesthesia drugs
b) Inj. Midazolam a) Inj. Lignocaine (heavy) 5 %
b) Inj. Bupivacaine (heavy) 0.5%
G. Local Anesthetics
a) Inj. Lignocaine 2%
b) Inj. Lignocaine 2% with Adrenaline
B. Induction Agents c) Inj. Bupivacaine 0.5%
a) Inj. Thiopentone Sodium d) Inj. Bupivacaine 0.25% preservative free

b) Inj. Propofol e) Inj. Rocuronium 0.75%
c) Inj. Ketamine
H. Other Drugs
a) Inj. Tramadol
C. Muscle Relaxants b) Inj. Diclofenac
c) Diclofenac Suppository
Depolarizing Muscles Relaxants. d) Inj. Buprenorphine
a) Inj. Suxamethonium e) Inj. Dexmedetomidine
Non- Depolarizing Muscles Relaxants f) Inj. Clonidine
g) Inj. Bupivacaine 0.5% heavy
a) Inj. Pancuronium
h) Lignocaine Jelly 2%
b) Inj. Vecuronium
c) Inj. Rocuronium
d) Inj. Atracurium
4.5 Doses of Intravenous Anaesthesia Agents:

Chart No. 1.4: INTRAVENOUS AGENTS IN ANAESTHESIA
DRUG DOSE REPEAT DOSE/ INFUSION RATE
Thiopentone 5-6 mg/kg 2 mg/kg
Propofol 1-3 mg/kg 0.2-1 mg/kg
Ketamine 1.5-2 mg/kg 40 mcg/kg/min
Fentanyl 0.025-2 mcg/kg 4-10 mcg/kg/hr (Infusion)
Alfentanil 5-10 mcg/kg 05-10 mcg/kg/min (I)
Sufentanil 0.1 mcg/kg 0.01 mcg/kg/min) (I)
Succinyl Choline 2 mg/kg 4-10 mg/min (I)
Pancuronium 0.08 mg/kg 0.02 mg/kg
Atracurium 0.5 mg/kg 4-12 mcg/kg/min (I)
Vecuronium 0.08-0.1 mg/kg 0.12-2 mcg/kg/min (I)
Rocuronium 0.6 mg/kg 9-12 mcg/kg/min (I)
Diazepam 0.1-0.3 mg/kg
Page 575
Midazolam 0.5-0.1mg/kg
Flumazenil 0.1-0.5mg
Neostigmine 0.05 mg/kg
Adenosine 0.1 mg/kg
Digoxin 15-20 mcg/kg
Diltiazem 0.15-0.35 mg/kg
Benadryl 1 mg/kg
Furosemide 1-2 mg/kg
Mannitol 0.25-1 mg/kg
Esmolol 100-300 mcg/kg/min (I)
Dopamine 5-15 mcg/kg/min (I)
Dobutamine 7-15 mcg/kg/min (I)
NTG 1-1.5 mcg/kg/min (I)

15 mg/kg (loading) (I)
Amiodarone 5 mg/kg/hr. (maintenance)
KCL 0.5 mEq/kg/hr. (I)

Sodium 40-100 mcg/min (I)
Nitroprusside
Atropine 0.01 mg/kg
Glycopyrrolate 4 mcg/kg
Dexamethasone 0.1 mg/kg
Paracetamol 15 mg/kg
Diclofenac sodium 1.5 mg/kg
Neostigmine 0.05 mg/kg
Noradrenaline In titrated dose
4 mcg per mL
Bitartrate
Labetalol 20 mg IV push over two minute In titrated dose
Hydrochloride 40-80 over 2 - 10 minute
Page 576
5. Adrenaline Doses
Chart No. 1.5: ADRENALINE DOSES BY AGE
Adult: Paediatric: Neonatal:
1 mg 0.01 mg/kg (0.1 ml/kg) IV or 0.01 mg/kg to 0.03 mg/kg (0.1-0.3
intraosseous ml/kg)
Repeat Q 3-5 min
Maximum dose 1 mg IV/IO or 10 IV, intraosseous, or umbilical
Higher IV doses NOT recommended
mg ET repeat Q 3-5 min
Repeat Q 3-5 min
ET dose 2 to 2.5 mg
No Higher IV doses. ET dose 0.1
Higher IV doses NOT recommended
Drip 1-10 mcg/min mg/kg (ten times IV dose)
ET does 0.1 mg/kg (ten times IV
Strong preference for IV/IO!
dose)
Drip 0.05-1 mcg/kg/min
6. Important Aspects of Anaesthesia

Chart No. 1.6: TEN GOLDEN RULES OF ANAESTHESIA
1 Do an adequate preoperative assessment
2 Nil by mouth for six hours
3 Put patient on a tipping table
4 Check your machine and cylinders before you start
5 Keep a suction instantly ready
6 Keep patient’s airway clear
7 Be ready to control patient’s ventilation
8 Have a vein open
9 Check patient’s pulse and blood pressure
10 Always have someone who can apply cricoid pressure in emergency
Chart No. 1.7: BREATHING CIRCUITS

Jackson Rees circuit Use for neonate & children less than 25kg
Bain Circuit Most commonly used circuit weight more than 25 kg
7. Airway
Chart No. 1.8: ORAL AIRWAYS
Formula for size of ETT
Neonate 2.5 or 3
Children < 6 years age/3 + 3.5
Page 577
Children > 6 years age/4 + 4.5
Adult female ET Tube number 7 or 7.5
Adult male ET Tube number 8.5 or 9
8. Grading of Patients & Fluid Requirements
8.1 Grading of Patient:

Chart No. 1.9: GRADING
ASA 1: ASA 2: ASA 3:
A Normal Healthy A patient with severe systemic disease that limits
Patient with only surgical A patient with mild systemic
activity but is not incapacitating (Disease is not
Condition Disease (like, HTN, DM etc.
under control with treatment but not life
under control with treatment)
threatening)
ASA – American Society of Anesthesiology
8.2 Fluid Requirement for Children:

Chart No. 1.10: FLUID REQUIREMENT FOR CHILDREN
Weight (kg.) Hourly Fluid Requirement
<10 4 ml/kg
11-20 40ml + 2ml/kg > 10
>20 60ml + 1ml/kg> 20
9. Monitoring Standards
Chart No. 1.11: MONITORING STANDARDS
ESSENTIALS:
STRONGLY RECOMMENDED:
1) Continuous presence of qualified Anesthesiologist
1) Temperature
2) Oxygen supply failure alarm
2) End – tidal Carbon dioxide
3) Observation of reservoir bag & chest expansion
3) Monitoring of neuromuscular
4) Ventilator disconnect alarm
blockade
5) Oxygen analyzer of inspired gases
6) Pulse oximetry
7) Electrocardiogram
8) Non-invasive arterial blood pressure
Page 578
10. Fasting Guidelines
Chart No. 1.12: FASTING GUIDELINES

Ingested Minimum Fasting
material Period (h)
Clear Liquids 2
Breast Milk 4
Infant formula 6
Non-human Milk 6
Light Meal 6
a) These recommendations apply to healthy patients of all age group who are undergoing elective procedure.
b) Clear liquids: water, fruits without pulp, carbonated, beverages, tea & black coffee.
12.2 Advantages:
11. Operation Theatre
Solution has broad spectrum of Antimicrobial
Cleaning Protocol activity, effective against HIV, HBV and other
 Do not use Broom inside Operation Theatre pathogenic bacteria, viruses, molds and spores. It is a
non-toxic, eco-friendly. It liberates nascent oxygen
 Do Fogging after infected case and enter in
having strong oxidizing effect.
register
 In between the two cases, clean O.T. 12.3 Procedure:
1) Remove linen, instrument sets and used a) For 350 sq. ft. OT take 1000 ml (1lt) water in
material. tank and add solution in that.
2) Clean surface, wipe with Bacillocid solution. b) Keep fumigation machine on floor.
c) Keep machine near to door so after fumigation
3) Mop the floor (ideally with Lysol 3% or you can easily switch off machine.
Bacillocid) d) Daily mopping of OT is compulsory with
solution.
12. Operation Theatre e) Please cover all electric equipments, digital and
Fumigation Protocol (Power water resistance equipment (C arm monitor
microscope etc.) with cloth or plastic sheet.
Jet and Auto Mist) f) Empty the machine tank and use balance
solution.
12.1 Fumigation agents g) Do not run (power jet) machine continuously
For O.T. fumigation 20% aqueous solution of more than 35 minutes and total one hour in a
Hydrogen Peroxide 11 % and Silver Nitrate solution day; keep 4 to 6 hours of interval in between two
0.01% should be used. For 1000 cu. ft. Take 400 ml running.
clean water and add 80 ml. of fumigant solution – h) Do not operate machine in presence of patient
Hydrogen Peroxide 11 % + Silver Nitrate 0.01 % and do fumigation in vacant room only.
solution in a fogging machine. Keep the room / OT
closed for 60 min. Mop the flooring with clean floor
soaked in the same solution.
Page 579
13. Biomedical Waste Management
Chart No. 1.13: SEGREGATE BIOMEDICAL WASTE
Yellow Bag Red Bag White (Translucent) Blue Bag Black Bag
Human Anatomical Waste Contaminated Waste Waste sharps Glass General waste
including Metals
Human tissues, Organs & body Waste generates from Broken or
parts disposable items such Needles, Syringes discarded and
as tubing, bottles, IV with fixed needles, contaminated
Soiled waste
tubes & sets, catheters, Scalpels, blades or glass
Items contaminated with blood, urine bags, syringes any other
Metallic Body
body fluids like gloves, (without needle). contaminated sharp
Implants
dressings, plaster casts, cotton object that may cause
swabs & bags containing puncture & cuts
residual or discarded blood &
blood components
Microbiology, Biotechnology
& other clinical laboratory
waste
14. Universal Precaution for Health Care Workers in Operation

Theatre
a) Proper hand washing before and after contact f) Dispose all sharps in puncture proof container.
with each patient and handling patient’s
specimens. Do not leave sharps on bed or beside g) Avoid spills of blood & body fluids, If it occurs,
cover it with absorbent material like gauze over
of patient.
which 1 % solution of sodium hypochlorite
b) Use of PPE i.e. gloves, mask, gowns and should be poured and left for 10-15 minutes
protective eye-wear. (ideal 30min). Clean the area with a bleach mop.
c) Prevent needles stick injuries with other sharp Wash and dry the mop.
instrument. h) Proper segregation and disposal of Bio-Medical
d) DO NOT BEND OR RECAP NEEDLES. waste.
e) In case of needles stick injuries or cuts, wash the i) Immunization (for Hepatitis B).
area properly with water and soap and Contact
for post exposure prophylaxis treatment.
Bibliography
1. Cole F. Pediatric formula for Anesthesiologists. AMA J Dis child. 1957-94: 672-3
Further reading
1. Miller RD. Miller’s anesthesia. 7th edition. Philadelphia: Elsevier Churchill Living store. 2009


Page 580
2. DIFFICULT AIRWAY ALGORITHM
Assess the likely hood and clinical impact of basic incubate-(CVCI) Emergency surgical airway
management problems: In case of difficult Intubation (i.e. Cricothyrotomy) may be necessary if the
and difficult Ventilation awake intubation should be patient is hypoxic.
carried out. In case you cannot ventilate, cannot
Fig. 2.1: INTRODUCING LARYNGEAL MASK AIRWAY
Page 581
Fig. 2.2: LARYNGEAL VIEW OF AIRTRAQ VIDEO LARYNGOSCOPE
Bibliography
1. Gabbott DA, Baskett PJ. Management of airway and ventilation during resuscitation. Br J Anesth.
1997: 79; 159-71.
2. Cormark RS, Lesane J. Difficult tracheal intubation in obstetrics anesthesia. 1984: 39; 1105–11
3. Kristein A. Pioneer of direct laryngoscope Anesthesia 1986: 41; 42–5.
4. Brain AI, Verghese C, Addy EU, Kapila A. The intubating laryngeal mask, Development of a new
device for intubation of the trachea. Br. J. Amaesth. 1997: 79; 699–703.
5. Samsoon GLT, Yound JRB. Difficult Tracheal intubation: A retrospective study Anesthesia. 1987: 42;
48 –90.
Further reading
1. Martin F, Buggy DS. New airway equipment opportunities for enhanced safety. Br J Anesth. 200: 102;
734–8.
2. Bannister PB, Mac Beth RG. Direct laryngoscopy and tracheal intubation. Lancet 1944: 1: 651 –4.
3. Roberts JT. Clinical management of the Airway. Philadelphia PA. WB Saunders Company. 1994.
4. Adewale L. Anatomy and assessment of the pediatric airway. Pediatric anesth. 2009: 19 (suppi I): 1– 8.
5. Radev R. Prevention of aspiration syndrome in general anesthesia. Khirurgiia Sofia. 1989: 42 (4): 37–
42.
6. Swadia VN, Patel MG. Our preliminary experience with LMA C – Track Indian Journal Anesth 2009:
53: 312–7.
7. Channa A. Video laryngoscopes Saudi Journal. Anesth 2011: 5 (4): 357–9.
8. LMA Track Instruction manual Singapore. The Laryngeal Mask Company Limited. 2006 .

Page 582
3. PRE-ANAESTHESIA CHECK UP PROTOCOL
l) History of Dentures, braces, crown, loose
1. Pre Anaesthesia Checkup teeth, implanted Pacemaker, implanted cardiac
(PAC) Defibrillator, Prosthetic Heart valve,
Pre anesthetic checkup should be carried on prior day Orthopedic implant, Organ recipient.
of surgery to avoid unnecessary postponement of m) History of STD, Drug resistance.
patients. n) History of Anesthesia with due Allergy history
of Headache after anesthesia, Awareness
1.1 Following history should be during anesthesia, transfusion reaction,
admission to ICU after surgery, any
asked: complication after anesthesia.
a) High blood pressure, Diabetes, Asthma, Heart
Disease, Stroke, Cough and Cold in the past 2 2. Following history should be
weeks.
b) History of Shortness of breath, Difficulty in asked
breathing on lying flat, Difficulty in breathing a) Investigations as advised by Surgeon and
on climbing stairs, Chest pain, Palpitation, Anesthetist.
Chronic cough. b) ASA: (American Society of Anesthesiologist)
c) History of Cardiac illness such as heart failure, Assessment of patient in terms of
heart valve problem, high cholesterol level, I/II/III/IV/V/VI/E with additional risk factor.
RHD, CHD or Cardiac arrest. c) Do proper systemic examination of
d) History of Respiratory problems such as Cardiovascular system, Respiratory system,
Chronic Bronchitis, Allergic rhinitis, Snoring, CNS.
Tuberculosis, Lung cancer, Chest infection or d) Evaluate the patient’s airway – Thyromental
Pneumonia. distance (If < 3finger – anticipated difficult
e) History of Neurological problems such as intubations), dentition, mouth opening.
Epilepsy, Fainting, Coma, Paralysis, Chronic
Headache, Dizziness, Parkinsonism, Brain
Tumor.
f) History of Muscle or Bone problems such as
3. Consent
Osteoporosis, Neck pain or Neck stiffness, Informed consent of patient should be taken before
Difficulty to open mouth, Spine problem, surgery which means consent given to a proposed
congenital muscle disease. specific intervention, without any force, undue
g) History of Kidney problem such as dialysis. influence, fraud, threat, mistake or misrepresentation,
Gastric problem such as Heartburn, Reflux, and obtained after disclosing to the person giving
Jaundice. consent adequate information including risks and
h) History of Blood or Endocrine problems such benefits of, and alternatives to, the proposed
as Anemia, receipt of blood transfusion, intervention in a language and manner understood by
prolonged bleeding, Thalassemia, Sickle cell such person with no binding to consent after being
anemia, Thyroid disease. informed. Consent should be attested by staff nurse
i) History of Allergy. of ward. There should be common consent for
j) History of Medications such as Diabetes, surgery and anesthesia unless it is essential to take
Hypertension, Asthma, Psychotropic drugs, consent for anesthesia separately.
Steroids.
k) History of Smoking, Alcohol, Addictive drugs,
BOH.
Bibliography
1. Kumar A, Mullick P, Prakash S, Bharadwaj A. Consent and the Indian Medical Practitioner.
Publication of Indian Society of Anaesthesiologist. 2015: 59 : 11 : 695-700. [Cited 2016 July 7]
Available from: www.ijaweb.org
Page 583
Further reading
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
Page 584
4. CONDUCT OF ANAESTHESIA
e) Keep Glucometer and short acting regular
1. Anesthesia can be conducted insulin ready for intra-operative use.
taking 5’P’s into f) Assess target organ function and monitor
accordingly.
consideration
They are: -
2.3 Obstetric patients:
a) Prepare operation theatre ready for emergency
a) Pre –operative Assessment of Patients. LSCS.
b) Patients Preparation. b) Follow Anti-Eclamptic regimens for patients
c) Preparation of Operation Theatre. with pregnancy induced hypertension.
d) Premedication. c) Verify the availability of blood.
e) Plan of Anesthesia. d) Keep the difficult intubation kit ready.
e) Take care of prophylactic measures to treat
2. Anesthesia to different aspiration (Mendelson Syndrome).
f) Keep the Infant resuscitation bag, smaller
groups of patients endotracheal tubes, laryngoscope, suction
apparatus, infant radiant warmer, oxygen hoods
2.1 Hypertensive Patients: & emergency drugs for resuscitation.
a) Advise to take all anti-hypertensive drugs early
in the morning of surgery. 2.4 Trauma Patients:
b) Avoid ACE inhibitors on the day of surgery to a) Stabilize the patients taking into consideration
avoid intra operative fall in BP. ABC (Air, Breathing & Circulation) of
c) Keep anti-hypertensive drugs like resuscitation.
Nitroglycerine, Nifedipine and Metoprolol b) Stabilize the cervical spine (with collar for
ready. suspected C-spine injuries).
d) Keep volume expanders like colloids ready. c) Place the intercostal drainage for chest injuries.
d) Splint to the fractured site.
2.2 Diabetic Patient: e) Assess the GCS (Glasgow Coma Score).If<8,
intubate for airway protection.
a) Advice to skip the morning doses of Insulin and
f) Transport the patient to referral center with
Oral hypoglycemic.
portable ventilator, oxygen cylinder, ambu bag
b) Check fasting blood sugar, urine ketones and
on standby.
serum electrolytes on the morning of surgery.
c) Place the Diabetic patients first in the list of Inform the patient`s details to referral center prior to
surgery. or during transport.
d) Specific care of the patients with autonomic
disturbances.
Bibliography
1. HMIS (Health Management Information System) TNHSP. Standard Treatment Guidelines. A manual
for Medical Practitioners. Tamil Nadu Health Systems Project (TNHSP), Health and Family Welfare
Department, Government of Tamil Nadu.
Further reading


Page 585
5. COMPLICATIONS OF ANAESTHESIA
During General Anaesthesia
CARDIOVASCULAR RESPIRATORY NEUROLOGICAL THERMAL

PERTURBATIONS
 Hypertension  Pulmonary  Convulsions
 Hypotension aspiration  Delayed Recovery  Hypothermia&
 Arrhythmias  Hypoxia  Nerve palsies Shivering
 Myocardial Ischemia  Hypercarbia
 Cardiac arrest  Bronchospasm
Fig. 5.1: COMPLICATIONS OF ANAESTHESIA

c) Keep Flumazenil (antidote for Benzodiazepine)
1. Management of common & Naloxone (antidote for Opioids) ready to
complications during manage complications of over dosage.
General Anaesthesia 1.6 Nerve Palsies:
a) Position the patient appropriately to prevent
1.1 Aspiration: pressure on the nerves.
a) Follow appropriate fasting guidelines. b) In prone position – avoid pressure on eyeball
b) Administer anti-aspiration prophylaxis like H2 and avoid over – abduction of arms to prevent
blocker, Proton pump inhibitors, Brachial Plexus injury.
Metoclopramide. Ondansetron, Granisetron. c) In lateral decubitus position, keep axillary roll
c) Intubate by rapid sequence technique in full beneath axilla to prevent Brachial Plexus injury.
stomach patients. d) In lithotomy position, care must be taken to
1.2 Hypercarbia: avoid injury to the lateral popliteal nerve.
a) Ventilate appropriately as Hypoventilation is the
commonest cause. 1.7 Hypothermia and Shivering:
a) Increase theatre temperature (21-degree C for
1.3 Hypertension: adults & 28-degree C for children).
a) Maintain good plane of anaesthesia. b) Use warm intravenous fluids.
b) Use opioids for adequate pain relief. c) Use warm blankets and forced air warming to
1.4 Hypotension: combat hypothermia.
a) Manage blood loss appropriately. d) Use IV Dexamethasone or IV Pentazocin or IV
Tramadol to treat shivering.
b) Preload the patient adequately before spinal
anaesthesia.
1.8 Pulmonary Edema:
1.5 Post-Operative Apnoea:
a) Commonly due to over dosage or sensitivity of
Barbiturates, Opioids and inhalational agent and
inadequate reversal.
b) Titrate the doses of opioids. Use appropriate
dose to avoid respiratory depression. Give
adequate sedation to obese and geriatric patient.
Page 586
PULMONARY EDEMA
Assist breathing as needed oxygen
Take blood pressure Begin working on IV line Cardiac monitor
Is arrhythmia the cause?
cause
Due to Bradycardia? Due to tachyarrhythmia?
Bradycardia Algorithm Tachycardia Algorithm?
Sublingual Nitroglycerin 0.4 mg

Inj. furosemide 0.5-1 mg/kg IV
Propped position
Consider also:
Albuterol aerosol
positive airway pressure
Not responding?
Nitroprusside 0.1-5 mcg/kg/min
OR
Nitroglycerin 120-20 mcg/min
Consider intropic
support
Still in distress?
Consider intubation
Systolic BP>100? Systolic 70-100 or signs of shock?

Dobutamine 2-20 mcg/kg/min Dopamine 5-15 mcg/kg/min
Fig. 5.2: PULMONARY EDEMA
Bibliography
1. HMIS (Health Management Information System) TNHSP. Standard Treatment Guidelines. A manual
for Medical Practitioners. Tamil Nadu Health Systems Project (TNHSP), Health and Family Welfare
Department, Government of Tamil Nadu.
Further reading
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Page 587
6. REGIONAL ANAESTHESIA
1. Indication 6. Treatment of over dosage
For the production of local anesthesia. Treatment of patient with toxic manifestations
consist of arresting convulsions assuring
2. Dosage and Administration adequate ventilation with oxygen, if necessary
The dose is adjusted according to the response by assisted or controlled ventilation
of the patient and site of administration. (respiration) if convulsions occur they must be
treated rapidly by intravenous injection of
3. Contraindications Thiopentone 100 to 200mg. Alternatively,
Hypersensitivity is known to anesthetics of the Diazepam 5 to 10mg may be used and Intra-
Amide type. Solution containing Adrenaline is lipid (1.5 mg/kg body weight.).
contraindicated for anesthesia of Fingers, Toes, Once convulsions have been controlled and
tip of Nose, Ears and Penis. Bupivacaine is adequate ventilation of the lungs ensured, no
contraindicated for IV regional anaesthesia. other treatment is generally required. If
Hypotension is present. However, a vasopressor,
4. Precautions preferably one with inotropic activity, e.g.
Shock, heart block, known drug sensitivity, Ephedrine 15 to 30 mg should be given
Liver disease, Kidney disease, Epilepsy, intravenously in diluted from titrated dose.
impaired Respiratory function.
Anxiety or slight twitching, a small intravenous
5. Adverse Reaction dose of Inj. Diazepam may be given carefully
Over dosage may cause CNS reaction. and slowly; Oxygen should also be given. In
Numbness of tongue, light-headedness severe circulatory depression barbiturate such as
Dizziness, and Blurred vision, Tremors, Thiopentone is contra-indicated when
followed by Drowsiness, Convulsions, convulsion has developed. Cardiovascular
Unconsciousness and possibly respiratory arrest. collapse is treated with vasopressors & plasma
Cardiovascular reactions of over dosage include infusion, Inj. Intralipid.
Hypotension and Myocardial depression.
Concentration dependent adverse reactions for Lignocaine

Plasma con. Mcg/ml Adverse reactions
4 Light-headedness, tinnitus, circumoral numbness
6 Visual disturbance
8 Muscle twitching
10 Convulsions
12 Unconsciousness
20 Respiratory arrest
24 Circulatory depression
Chart No. 6.1: DRUG TOXICITY OF LIGNOCAINE
7. Local Anesthetics:
Methaemoglobinaemia may be treated by the a) Inj. Lignocaine 2 % (3 to 4 mg/kg body
intravenous administrations of 1% solution of weight).
Methylene blue in a dose of 1mg/kg. b) Inj. Lignocaine hydrochloride (2%) with
Page 588
Adrenaline (5 to 7 mg/kg body weight).
( 0.75%) or Inj.
12. Explanatory Footnotes on
c) Inj. Ropivacaine
Bupivacaine (0.5 %). Above Protocol
12.1 Local Anesthetics:
8. Sedation For consistency, 0.75% Ropivacaine is
Inj. Midazolam 0.05 mg/kg and Inj. Ketamine primarily used for blocks, with a dose of 20 -40
0.5 mg/kg and Inj. Propofol infusions in 25-75 ml depending on the type of block. Ropivacaine
mcg/kg/min range and deep sedation (50 to 100 results in 12-24 hours block duration. 2%
mcg in drip for deep sedation). Lignocaine for 3-4 hours duration. Mixing a
short acting and long acting local anaesthetic
9. Interscalene together appears to significantly decrease the
Success rate in posterior Interscalene (Cervical duration of the block.
PVBs) approach is more than anterior-lateral
approach. 12.2 Adjuncts:
a) Clonidine: 50-100 ug for an average of 3-
10.Supraclavicular/ 6 hours increased duration.
b) Epinephrine and Clonidine: Increase
Infraclavicular duration of regional block.
Inferior-posterior quadrant of plexus for c) Inj. Dexamethasone: 4 mg to 8 mg dose
Supraclavicular Block and Infra Clavicular as it may result in very prolonged blocks.
Block near posterior cord. d) Bicarbonate: Dose is 1 mEq/10ml, in
Bier Block.
11. Sciatic (Infragluteal)
Infragluteal approach is more comfortable to
patients than Classic Labat approaches.
Bibliography
1. Phillips BB. Campbell’s operative orthopedics. 12th edition, London: Churchill Living stone Elsevier
2012.
2. Winnie AP, Inter scalene brachial plexus block. Anesth Analg. 1970: 49(3): 455-66.
3. Graft BM, The cardio toxicity of local anesthetics. The place of Ropivacaine Curr. Top Med Chem.
2001:1:207-14.
4. Kulenkampf O. Anesthesia of the brachial plexus Zentra/b/Chir. 91:38:1337-40.
5. Cavino BG, Vassallo HL. Local Anesthetics Mechanism of action and clinical use. Grune and Jt.
Ratton. New York. 1976: 97.
6. Rosenberg PH. ASRA lecture Intra venous regional anesthesia Nerve block by multiple mechanism.
Reg. Anesth. 1993: 18: 1-5.
Further reading
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
Page 589
7. CARDIO PULMONARY- RESUSCITATION
(CPR)
CPR consists of a series of maneuvers by which children, perform cardiac massage if HR<60/min
oxygenated blood supply to brain and vital organs is with signs of poor perfusion.
maintained during cardiopulmonary arrest (CPA) i.e.,
cessation of respiration and circulation. In children, 3.1.2 Airway-
CPA is not sudden but end result of long period of Clear airway cleaning like blood, secretions, foreign
hypoxemia secondary to inadequate ventilation, particles (suction if available).
oxygenation or circulation. Therefore, prompt Prevent posterior displacement of tongue due to
management of these is essential to prevent CPA, the muscle relaxation during CPA, by head tilt and chin
outcome of which is poor. or jaw thrust (may use an airway if available).
Head tilt: Put a hand at forehead and tilt head back
1. Diagnosis of Cardiac arrest to sniffing or neutral position in an infant and little
more in older children and adults. (Caution: In a
a) Absence of pulse in major arteries (carotid or patient with suspected cervical spine injury head tilt
femoral in older children and femoral or should be avoided)
brachial in infants as carotid is difficult to Chin lift: Put finger of other hand under bony part.
palpate due to short neck). Jaw thrust: Place 2-3 fingers under each side of
b) Absence of heart sounds on auscultation. lower jaw at its angle and lift jaw upward with the
c) A systole / ventricular fibrillation on ECG. elbow resting on the surface on which victim is
lying.
2. Respiratory arrest 3.1.3 Breathing-
Determine the absence of breathing. Give mouth to
Absence of respiration on looking (absent chest mouth / nose / mask / airway breath (may use bag and
movements), listening (absent air flow on bringing mask if available). Inhale and then make a seal
ears in front of mouth) and feeling (absent air flow on around the mouth and nose together in infant and seal
keeping hands in front of mouth or nose). mouth only in older children and adults (nose
pinched with the hand used for head tilt) to exhale
3. Levels of CPR smoothly. Rate of breaths should be 20/min for
infants, 15/min in older child and 10-12/min in
There are two levels of CPR: adults.
a) BLS (Basic life support) the elements of CPR Rescuer should stand or kneel at the side of the
provided without additional equipment, skill patient so that his hips are on a level with the victim’s
and speed are more essential. chest.
b) ACLS (Advanced cardiac life support) Use of
equipment and drugs for assisting ventilation or In a newborn 2 thumbs are positioned side by side on
circulation. sternum just below the nipple line, with fingers
encircling chest and supporting the back and
3.1 Basic Life Support: compress sternum by 0.6 – 1.2 cm (120/min).
In an infant put index finger at the intersection of
Call for help; position the victim supine on firm flat
inter mammary line and sternum. Use 2 – 3 fingers
surface with head level with the heart. As per New
(index, middle and ring) to compress sternum by 1.5
AHA 2014 Guidelines ABC (Airway – Breathing –
– 2.5 cm (100/min) and do not lift the finger when
Circulation) changed to CAB (Circulation - Airway –
compression is released. Two thumb – encircling
Breathing) and chest compression and rescue breath
hands technique can also be used.
ratio is 30:2.
In children (1-8 years) use heel of hand on lower half
3.1.1Circulation- sternum with long axis of heel same as long axis of
Determine the absence of pulse after 2 breaths sternum and compress 2.5 – 3.5 (100/min) In adults
(rescue breaths). External cardiac massage if the heel of one hand is placed on the lower sternum
Asystole and unresponsive to rescue breaths. In and the other hand placed on top of the first. The
elbows should be locked in position with the arms
Page 590
straight and the shoulders over the hands. Sternum should be used as soon as IV access is achieved
should depress by 3.5 – 5.0 cm and the rate of (Intracardiac route is not desirable).
compression should be 80 to 100/min. (CAUTION:
Do not exert pressure on the ribs, costal cartilages or b) Inj. Lignocaine
xiphoid).
Indication: Ventricular tachycardia or fibrillation
3.1.4 Combination of ventilation and Cardiac non responsive to recurs after defibrillation.
massage - In adults: Initials bolus dose is 1.5 mg/kg.
If both cardiac and respiratory arrest – Compression: Additional bolus of 0.5-1.5 mg/kg can be given 5-10
ventilation = 30:2 in adults and children > 8; Children minutes during CPR up to a total dose of 3 mg/kg.
and infants 1-8 years = 5:1; Neonates =3:1. In children: Inj. 1 mg/kg IV stat followed by
infusion at 20-50 mcg/kg/min.
3.2 Advanced Cardiac Life Support
(ACLS): c) Inj. Amiodarone
Indication: Refractory shock with ventricular

If ACLS facility is available, shift the patient to
fibrillation (as an alternative to or after failure of
ACLS as soon as possible. If this is not available then
Lignocaine).
continue cardiac massage till spontaneous HR is
In adults: Initially 300 mg rapid infusion in 20-30 ml
more than 60-80/min and continue Endotracheal
intubation with IPPV till adequate respiratory efforts saline followed by 150 ml over 10 minutes followed
are present (good chest movement, no cyanosis or by 1 mg/min for up to 0.5 mg/kg/day.
shock). For ALCS proceed in the following order;
d) Inj. Atropine
3.2.1 Procedures-
Indication: Vagally mediated bradycardia during
ECG monitoring (if available) intubation, HR<80 or asystole in an infant and
a) If ventricular fibrillation – defibrillation. symptomatic bradycardia with AV block in any child.
b) In adults, first shock at 200 Joules; if the first is Dose and route: 0.02 mg/kg bolus (not <0.1 mg or>
unsuccessful then a second shock at 200-300 0.5 mg for a child and 1.0 mg for an adult) This dose
Joules. If both fail, additional shocks at 300- may be repeated after 5 minutes for a maximum total
360 Joules are given. dose of 1.0 mg for a child and 2.0 mg for an adult.
In children, 2 Joules / kg and can be repeated a e) Inj. Naloxone
few time (if does not revert to normal rhythm).
Continue cardiac, massage in the meantime. Indication: Narcotic overdose or poisoning and
c) All patients require oxygen (100%) because even newborn resuscitation (if mother has been given
with best CPR, only a fraction of the cardiac Morphine or Pethidine during labour).
output is provided and also there are other Dose and route: 0.1 mg/kg IV.
factors causing ventilation perfusion mismatch.
d) Establish IV line as early as possible to give f) Inj. Sodium Bicarbonate (NaHC03)
drugs and fluids and intubation of trachea Not required routinely as it can cause Alkalosis later
should be done to continue artificial ventilation. and worsen respiratory acidosis by releasing CO2 in
inadequate ventilation.
3.2.2 Drugs are used in the following order if Indication: Hyperkalemia, significant metabolic
indicated- acidosis (pH<7.2) or prolonged CPR.
In adults and in children: Inj. Sodium bicarbonate 1
a) Inj. Adrenaline mEq/kg stat and 0.5 mEq/kg every 10 minutes in
protracted resuscitation.
Indication: Asystole symptomatic bradycardia
unresponsive to ventilation. g) Inj. Calcium
In adults: 1 mg IV every 3 – 5 minutes.
In children: 0.1 ml/kg of 1: 10,000 solution (0.01 Indication: Not used routinely now a day unless
mg/kg) IV, intra-osseous or 0.1 ml/kg of 1:1000 there is Hyperkalemia, Hypocalcaemia or Calcium
solution by endotracheal tube followed by several channel blocker toxicity.
positive pressure breaths. Can be repeated every 5 Dose and route: In children, 0.5 ml/kg of Calcium
minutes by either route. IV route is preferred and gluconate IV. In adults, 10 ml to be given as a slow
infusion under ECG monitoring.
Page 591
h) Inj. Glucose  Treat the underlying pathology causing CPA.
Indication – Hypoglycemia
Dose and route: - 0.5-1 g/kg IV. Try to get ABG, 3.2.3 Monitoring-
serum electrolytes and blood sugar (dextrose stick
Pulse should be palpable and chest expansion should
/glucometer) – post resuscitation care.
be seen during effective CPR, blood pressure, Sp02,
 Maintain mechanical ventilation for several ET CO2 (In intubated patient and if facility
hours to ensure adequate oxygenation and available), ABG should be monitored during and
ventilation. soon after CPR.
 Look for and treat seizures.
 Inj. Mannitol 0.5 -1 g/kg IV if raised intracranial 3.2.4 Termination of CPR-
tension.
 Maintain temperature, fluid and electrolyte If asystole persists for >10 minutes after CPR has
balance and ABG. been performed, ventricular fibrillation eliminated,
and confirmed, adequate ventilation provided and
 Treat shock with fluids, Dopamine, Dobutamine
appropriate medications given.
and adrenaline infusion as required.
3.2.5 Summary of CPR-
Chart No. 7.1: CPR GUIDELINES FOR HEALTH CARE PROVIDERS
(Method, compression rate, and ventilation to compression ratio)

Adult Child Infant Newborn
(<8 yr) (< 1 yr)
Lone If known asphyxia arrest, 5 5 cycles of CPR Ventilation priority,
Rescuer cycles unless sudden compressions for HR<60,
Priority CPR witnessed collapse
Compression 1-hand 2-thumbs 2-thumbs
method Or Or 2-fingers or 2-fingers
2-hands 2-Hand If single for access to
Rescuer umbilical vein
Compression Rate 100/min 100/min 100/min 200/min

Ratio of 30:2 until intubated. 30:2 until intubated. 30:1
compressions to 8-10 breaths/min 8-10 breaths/min
ventilations After ET. After ET.
Use of AED Immediate AED Immediate AED Consider No
Consider 5 cycles 5 cycles CPR if >4-5Min Recommendation
CPR if > 4-5 min Unwitnessed Arrest. (for infant &New Born)
Unwitnessed arrest
Bibliography
1. Resuscitation official Journal of the European Resuscitation council.
2. American heart Association Guidelines. CPR ECC 2010: 1-25.
Further reading

Page 592
8. ANAESTHESIA OBSTETRIC PROTOCOL
1. Orientation 3. Antacid Prophylaxis
Labour room and the operation theatre should be All patients for elective Caesarean Section must
connected with each other. All the anaesthetic receive oral antacid premedication. If the patient
equipment’s and preparations should be ready 24/7 posted for an emergency Caesarean Section then
days apart from it. Laryngoscopes with stubby handle consider IV Metoclopramide 10 mg or Inj.
and McCoy blade should be available. NICU and Ondansetron 4 mg or IV Ranitidine 50 mg. Emptying
prenatal ICU should be on the same floor. Emergency the stomach with a large orogastric tube, keep it until
drugs and plasma expanders (e.g. Hetastarch & patient anaesthetized and up to extubation.
Voluven) should be present in the O.T. Blood and
blood products should be available at nearest possible 4. Regional Anaesthesia for
place. Anesthesiologists should check for anaesthesia
machines, defibrillator, Oxygen, other equipment’s Caesarean Section
and the required drugs.
4.1. Advantages:
The avoidance of the hazards of aspiration of gastric
2. Labour analgesia with contents and failed intubation during general
Epidural technique anaesthesia. A reduction in blood loss /
thromboembolism/absence of Neonatal depression.
2.1 General Aspects: Postoperative analgesia may be provided using spinal
or epidural opioids.
a) Proper pre-operative evaluation with
counselling of the patient and the relatives. 4.2. Disadvantages:
b) Explaining the procedure and its advantages and
disadvantages. Hypotension can occur due to aorto-caval
c) Secure broad gauge I.V. cannula with starting compression despite the use of left uterine
I.V. with crystalloid for preloading. displacement and seemingly adequate preload.
d) Epidural catheter inserted with standard
technique in lateral or sitting position under 4.3. Nausea and vomiting:
aseptic precautions at L3-L4 OR L4-L5 space. The incidence of this is often related to hypotension
No CSE should be performed above L1 level. and hence should be treated immediately. Nausea
e) The catheter should not be more than 2 to 3 cm following a regional block is an indication of the B.P.
inside the epidural space. Check for any fluid fall. Consider giving 100% oxygen and legs up
coming out of the catheter. position before IV Ephedrine. Use Oxytocin for
f) Can give the analgesic dose of local anaesthetic uterine contraction.
agent, preferably 0.125% of Bupivacaine about
8 ml with 2 mcg / ml of fentanyl can be given. Diclofenac:
g) The dose can be repeated as per the patient’s Do not administer Diclofenac to those allergic to
demand. The patient should be NSAIDs. Do not give it to unstable asthmatics. Also
hemodynamically monitored closely till the end avoid in those with renal dysfunction, peptic ulcer
of delivery. disease and severe pre-eclampsia especially if
h) If intervention needed, then continue the oliguria or thrombocytopenia.
epidural anaesthesia with higher conc. of
Bupivacaine i.e. 0.5% around 8 to 10 ml. can 5. General Anaesthesia for
be given for LSCS.
Caesarean Section
5.1 Pre-operative assessment:
2.2 Complications:
Thorough pre-operative assessment.
a) Epidural-Bloody Tap
b) Patchy action or unilateral block a) Antacid prophylaxis.
c) Subdural Block b) NBM status.
c) Informed consent from relatives.
Page 593
d) Make arrangement for blood and blood Don't panic! Place you thumb against the hub of the
products. Touhy needle, relax and think. You have 2 options:
e) Patients should be transferred to theatre in left a) Can give 0.5% Bupivacaine 2 – 2.5 c.c
lateral position. intrathecally and do LSCS under spinal
f) Administer Sodium citrate prior to pre- anaesthesia.
oxygenation. b) Insert epidural catheter intrathecally.
g) IV access 18G or 20G cannula. Approximately 2cms should be threaded into
h) Position of the mother supine on the table with the subarachnoid space.
15 degree left lateral tilt with slight head up. c) Remove the Touhy needle and insert at a
i) Pre-oxygenate the mother using 100% oxygen different level. Don't perform a CSE. Intrathecal
for 3 minutes unless there is severe maternal catheter - top up only by the Anaesthetist. You
and fetal emergency. can administer either: 1ml 0.25% Bupivacaine +
j) ECG, NIBP and pulse Oximeter during pre- 15-25µg of Fentanyl as regular top up. Or 0.5 -
oxygenation and ETCO2 is switched on. 2ml of standard LDM as regular top up. After
k) Perform RSI using Thiopentone 5-6 mg/kg and delivery remove catheter as usual. If epidural in
Suxamethonium 1.5mg/kg. Intubate after situ treat as normal Intrathecal epidural, but
adequate action of Suxamethonium. each top-up to be given by Anaesthetist under
strict aseptic conditions.
Please remember - Patients die from
prolonged attempts to intubate leading to 8. Central Neural Block
hypoxia and from unrecognized oesophageal
intubation and not from failure to intubate. 8.1. Indications:
"If in doubt, take it out" Ensure that the ETT is Labour analgesia. Anticipated difficult or operative
correctly placed by observing the Capnograph trace delivery (e.g. multiple pregnancy, breech, premature
and by listening to breath sounds. Give Atracurium foetus), Obstetric disease (e.g. pre-eclampsia),
when Suxamethonium action wears off. Maternal disease (e.g. specific cardiac, respiratory or
neuromuscular disease), Surgery during pregnancy.
5.2 Intubation Hints:
Optimize the patient's position. A smaller ETT is 8.2. Contraindications:
often needed in obstetrics. An unexpected invisible This list contains both
larynx is often due to incorrectly applied cricoid a) Absolute contraindications- Patient Objection,
pressure. And short stubbed laryngoscope or polio Local Sepsis, Coagulopathy.
blade. An anterior larynx just out of reach of the ETT b) Relative contraindications- Hemorrhage with
can usually be cannulated with a well lubricated hypovolemia, Raised intracranial pressure,
gum-elastic bougie. Some forms of anticoagulant therapy, Disease
of the nervous system, Gross spinal deformity,
6. Anticoagulation and Systemic sepsis, Severe foetal distress.
regional anaesthesia 8.3. Central Neural Block - Special
a) The incidence of epidural haematoma is less
Considerations
than 1: 100,000. a) Low Platelet Count: A platelet count of
b) NSAIDS are not a contraindication to CNB. <50000 is an absolute C/I to a regional block.
c) Enoxaparin 40mg SC post-operatively. b) Enoxaparin /L MWH: Many patients at risk
d) If the woman is on antenatal of venous thrombosis are on daily sub
thromboprophylaxis. a) Enoxaparin should be cutaneous Enoxaparin.
stopped 12 hours prior to performing CNB. b) c) Unfractionated Heparin (UH): If UH has
Epidural catheters should be removed 2 to 4 been given, wait 4-6 hours before siting an
hours prior to administration of Enoxaparin. epidural block. Remove the epidural catheter
e) Heparin a) Heparin should be stopped 4 hours at least 4 hours after the last dose of UH.
prior to attempting neuraxial blockade or d) Aspirin: Patients on aspirin can have a
removal of epidural catheters. b) Unfractionated regional block. A bleeding time is not
Heparins should not be administered for 2 to 4 required.
hours after catheter removal. e) Pre-eclampsia (PIH): Patients with mild to
moderate PIH should have a recent (within 24
7. Management of a Dural tap hrs.) platelet count before a regional block.
f) Maternal Pyrexia: Administer antibiotics.
Page 594
g) Haematological Disorders: The most own group as soon as possible. However,
common type of patient presenting for for patients with severe haemorrhage,
regional blockade are Haemophilia Carriers uncross matched group O, Rh negative can
and patients with Von Willebrand's Disease. be lifesaving.
h) HIV: HIV is not a Contraindications to a iii. The principles of intelligent management are:
regional block nor indeed to a blood patch. While blood is gushing out it is useless and
Standard high risk precautions should be taken wasteful to give clotting factor or platelet
when instituting a block. Consider double replacements. Once surgical haemostasis has
glove protection / eye protection / do not been more or less achieved, continued oozing
resheath needles when performing a block. may be due to blood clotting factor
i) Prolapsed Intervertebral Disc (PIVD) deficiencies. Further blood samples should be
Epidural or spinal analgesia / anaesthesia are sent for coagulation screen and platelet count.
not contraindicated. iv. If there is massive blood loss the MASSIVE
j) Harrington Rods / Spinal Instrumentation TRANSFUSION PROTOCOL should be
Many of these patients have severe scoliosis instigated. This will ensure that FFP is
with consequent cardiorespiratory available and platelets are ordered. While FFP
compromise. The surgical site should be can up to a point be issued "blind" as already
avoided. The epidural needle should be mentioned, the possibility of low platelets or
advanced towards the convexity of the curve. DIC may need different blood components for
k) Multiple Sclerosis (MS) MS is a CNS their correction. This can only be identified by
demyelinating disease with an incidence of laboratory testing.
1:10,000. It is a disease of relapse and v. A pressure bag system is essential in order to
remission. infuse fluids rapidly.
vi. Use a blood warmer as soon as possible.
vii. Blood filters are NOT needed and will slow
9. Placenta Previa down transfusion.
9.1. Anaesthetic management: viii. Early use of CVP monitoring and direct
arterial pressure monitoring.
a) Ensure adequate IV access (2x 14 or 16G ix. Think ahead to order blood and blood
cannulae). products in plenty of time.
b) Two anesthetists preferable if Grade 4, previous x. Use the Hemocue (available in Theatre) to aid
Previa or previous LSCS; this is mandatory if estimation of transfusion requirements.
proceeding under regional (see below). f) Measure the patient's temperature.
c) Manage major hemorrhage according to g) Additional Calcium is rarely needed and only if
guidelines. there is evidence of a calcium deficiency. 10%
d) Anaesthetic technique – considerations. calcium chloride is preferable to calcium
gluconate.
9.2. Action: h) Treatment of the cause may involve delivery of
baby and placenta, repair of lacerations and
a) Ensure adequate airway / conscious level. Give administration of Oxytocin (Ergometrine; 15-
high flow oxygen. methyl PGF2α [Carboprost - Hemabate]; PGE2
b) At least 2 peripheral lines will be needed of not [Misoprostol].
less than 14- 16G. If the decision is made to set i) All patients with more than moderate continuing
up invasive monitoring, it must not interfere haemorrhage need proper monitoring of pulse
with resuscitation. rate, CVP, blood gases, and urinary output as
c) Prevent Aorto-caval compression. well as dedicated care by the midwifery and
d) Take at least 20ml of the patient's blood for: medical staff. Serious consideration should be
i. Blood grouping / cross matching given to the potential advantages of transfer to
ii. Full blood count an HDU.
iii. Coagulation studies (including fibrinogen /
FDP's if abruption or other cause of DIC
suspected).
e) Blood Transfusion
i. Order a minimum of 4 units of blood.
ii. All patients should be given blood of their
Page 595
Bibliography
1. Jadon A. Complication of regional and general anesthesia in obstetric practice. Indian Journal
Anesthesia. 2010:54:415-20.
2. Yeon SB, Sng BL, Sia ATH. Anesthesia lower segment, Caesarean Section changing perspectives.
Indian Journal of Anesthesia. 2010:54:409-1.
3. Journal of Obstetric Anesthesia and critical care JOACC. Jul–Dec 2013/Vol 3/Issue 2/2013:3:104-7.
4. Anaemia and pregnancy. Anesthetic implication Indian Journal Anesthesia. 2010:54:380-6.
5. International Journal of Obstetric Anesthesia. www.obstetanesthesia.com.
6. Grewal A. Indian Journal of Anesthesia.
7. Obstetric Anesthesia Resident Guide October 2008.
8. Practical Guidelines for Obstetric Anesthesia.
9. Obstetric Anesthesia Guidelines pdf. Nottingham University Hospital – 2014.
10. Resuscitation official Journal of the European Resuscitation council.
11. American heart Association Guidelines. CPR ECC 2010: 1-25.
Further reading


Page 596
9. SPINAL ANAESTHESIA
incidence of headache than conventional cutting edge
1. Definition needle.
Spinal anesthesia is produced by introducing a
Hyperbaric or hypobaric or Isobaric anesthetic into Preexisting neurological deficit has to be documented
cerebrospinal fluid in the subarachnoid space result in i.e. Diabetic neuropathy, Hanson’s disease, Traumatic
to loss of sympathetic tone, sensation and motor neuropathy
function.
2.3 Drugs used for Spinal
Sympathetic block is 2-3 segments higher than the
sensory and the motor block 2-3 segment lower than anesthesia:
the sensory block. a) Inj. Lignocaine 5% solution
Position – 1) Sitting 2) lateral b) Inj. Bupivacaine 0.5% solution
c) Inj. Ropivacaine 0.75% solution with adjuvant-
1) Inj. Clonidine 2) Inj. Buprigesic
2. Approach - Median and Par
median 2.4 Advantages:
2.1 Saddle block given in sitting a) Economical.
position by Hyperbaric b) Minimum equipment required.
c) Control hypotension and bradycardia reduces the
anesthetic drug: bleeding at the site of surgery.
Spinal cord usually ends at the level of L2 in adult d) Less respiratory infection.
and L3 in children. e) Less incidence of thromboembolic and
pulmonary complication.
Important land mark is that line joining the top of the f) Useful in sickle disease / trait and in Diabetic
iliac crest corresponds to L4-5. patient (Less stress related hyperglycemia).
2.2 Practical implication: 2.5 Contraindications:
While administering spinal anesthesia spinal needle 2.5.1 Absolute-
pierce 1) Skin 2) Subcutaneous fat 3) Supraspinious
& Interspinious ligament 4) Ligamentum flavum 5) Allergy to local anesthetics, Local infection at needle
Epidural space 6) Dura 7) sub arachnoid space. insertion, Increased intracranial pressure (herniation
of brain stem)
Patient is adequately prepared, with the procedure
fully explained, has reliable intravenous access, is in a 2.5.2 Relative-
comfortable position and resuscitation equipment is
Hypovolemia, Anticoagulation treatment, Systemic
immediately available.
sepsis, Neurological diseases- Multiple sclerosis,
To be done under all aseptic precaution. Read the Tabes dorsalis, Syringomyelia, Amyotrophic lateral
label. sclerosis, Tumors of the spine, Airway compromise,
Low back pain and peripheral neuropathies,
Patient should be well hydrated and NVM at least 6 Haemorrhagic CSF.
hrs.
Strict intraoperative vital parameters monitoring is 2.6 Complications:
mandatory. Height of analgesia is directly 2.6.1 Peri-operative-
proportional to curvature of spinal column and
volume of drug, specific gravity, force and rate of Hypotension due to vasodilatation and bradycardia
injection, barbotage technique. due to increased vagal tone as a result of sympathetic
blockade, Respiratory insufficiency due to intercostal
Small bore needle makes smaller hole in the dura i.e. blockade, poor anaesthesia because of loculations of
separate Cauda filum and are associated with a lower arachnoid.
Page 597
2.6.2 Post- Operative- Inj. Ephedrine 30 mg (6mg/cc) Inj. Phenyl
epinephrine, Inj. Noradrenaline, Infusion. (titrated)
Headache due lo leakage of CSF or aseptic
inflammatory reactions, Urinary retention, Backache, 2.7.1 Total Spinal -
Infection. - Meningism, Arachnoiditis, Transverse
Needs to be quickly recognized and treat patient will
myelitis or the Cauda equine syndrome with varying
be initially unable to talk louder than a whisper and
patterns of neurological impairment and sphincter
will stop breathing. These patients have to be
disturbances. Para-paresis and rarely paraplegia due to
intubated and ventilated until the local anaesthetic
the ‘‘anterior spinal artery syndrome’’i.e. prolonged
effect wears off and also maintain the hemodynamic
vasospasm of the anterior spinal artery by the
stability.
vasoconstrictor adjutants or due to prolonged
uncorrected hypotension. 2.7.2 Headache post dural puncture headache
(PDPH)-
2.7 Treatment:
Encouraged to drink water, give intravenous fluids to
Hypotension – Nausea and vomiting may be the first maintain adequate hydration, strict bed rest,
sign of hypotension. Give adequate I.V. Fluid, Paracetamol, Aspirin or Codeine tea, coffee, epidural
Oxygen by mask, increasing the patient’s circulating blood patch, Tab. Samaritan.
volume is by raising their legs, Vasopressors drug -
Bibliography
1. Choi PT, Galinski SE, Takeuchi L, Lucas S, Tamaya C, Jadal AR. PDPH is common complication of
neuroaxial blockade in parturient.
2. Baumgarten RK. Should caffeine become the first line of treatment for post dural puncture headache.
3. Ornberry EA, Thomas TA. Posture and Post spinal headache: A controlled trial in 80 obstetric patients.
Br J Anesth. 1988: 60: 195.
4. Spencer SL, Medunald SB. Current issues in Spinal Anesthesia. 2001: 94: 888-908.
5. Morgan P. The role of Vasopressors in the management of the hypotension induced by Spinal and
epidural anesthesia. Canadian Journal of Anesthesia. 1994:41(5) 404-413.
6. Crichley LA. Hypotension Sub arachnoid block and the elderly patient Anesthesia. 1996: 51: 1139-
1143.
7. Current issues in Spinal Anesthesia. 2001: 94: 888 – 906
8. Clark RB, Thompson DS, Thompson CH. Prevention of spinal hypotension associated with cesarean
section Anesthesiology. 1976: 45: 670 – 74
Further reading
2. Anesthetic Protocol 2013 NHS Lothian
3. MacFie J. Issue in Professional Practice Guidelines for implementation of enhanced recovery
protocols. Association of surgeons of Great Britain and Ireland. 2009.
4. Blom RL, Van Heiji M, Bemelman WA. Initial experience of an enhanced recovery protocol.
5. The Good anesthetist standard of practice for career grade anesthetists. The Royal College of
anesthetist, London 2010. [Cited 2016 July 7]
Available from: www.rcoa.ac.uk/document-store/the good-anesthetist
6. World Journal Surgery: 2013, Oct i 37 (10): 2372-8, doi: 10.1007/S00268-013-2135-1 ERAS –
Protocol
7. Indian Journal of Anesthesia. 2014:58:385-7.
8. Anesthesiology Clinics. [Cited 2016 July 7]
Available from: www.journals.elsevierhealth.com

Page 598
Pathology
11. Pathology
1 Introduction 599
2 Haematology 600
3 Serology 611
4 Biochemistry 614
5 Histopathology 615
6 Cytology study 616
7 Blood Bank 617
8 Normal Lab Values 620
9 Laboratory tests performed at PHC/RH/SDH/DH 626
1. INTRODUCTION
The Pathology department basically deals with

diagnosis of disease by means of various types of
3) Section III –
tests performed on body fluids, blood and tissues. Biochemistry Section:
It is divided into 4 sections: It deals with different types of biochemical tests
to detect functions of liver, kidneys, lungs, heart
etc.
1) Section I –
Haematology Section: 4) Section IV –
In which the blood, urine and stool examination
done to detect any abnormality like anemia, Histopathology &
leukemia, renal infection and bowel infection Cytopathology:
and infestation
In this section mainly tissue cell morphology is
2) Section II – studied to detect infection / tumor in body.
Serology Section:
It deals with the rapid terms to detect M.P.,
Typhoid, V.D., RC H.I.V. etc. along with blood
culture to detect Typhoid etc.

Page 599
2. HAEMATOLOGY SECTION
Blood is one of the most common specimens studied in
1. Specimen Collection: laboratories. Blood will clot within few minutes after it
is removed from the body unless an anticoagulant is
Every specimen must be accompanied by a request used.
slip, which should indicate date, patient’s full name,
age and sex, hospital identification number, name of 1.1.1. Whole Blood: Blood with anticoagulant is
referring doctor, provisional diagnosis, kind of called whole blood.
specimen, laboratory services and equipment, exact
time the specimen was obtained and the name of the
1.1.2. Plasma: Fluid portion of unclotted blood is
called plasma and is obtained from anticoagulated
person who collected the specimen with signature. It is
blood.
necessary that the request slip be complete and clearly
written. Incomplete information may lead to total loss 1.1.3. Serum: Fluid portion of clotted blood and is
of the report. obtained from clotted blood, which is collected without
Specimens should be processed as early as possible. any added anticoagulant.
Temporary storage in refrigerators is advisable except
for C.S.F. and specimens submitted for bacteriological
1.2. Anticoagulant:
cultures. Urine and other body fluid should be The anticoagulant prevents the blood from clotting.
processed as early as possible (before 2 hrs.) as delay Most of anticoagulants remove calcium which is one
causes disintegration of cells and loss of morphology. of factor required for coagulation.
1.1. Blood:
Table 1: Various types of bulbs & its uses
Sr. Type of bulb Content (Anticoagulant) Used for

No.
1 EDTA Na and K salt of EDTA Routine Haematological work
2 Trisodium Citrate Sodium Citrate ESR
3 Heparin Heparin PCV, Osmotic Fragility test
4 Double Oxalate mixture NH4 and K Oxalate CBC, Blood Group
5 Sodium Fluoride Na Fluoride and K Oxalate Sugar
1.3. Vacutainers: 1.3.2. GREY Cap: Sodium fluoride + Pot oxalate

for glucose estimation
These are plastic tubes with coloured cap with capacity
of3-5ml blood used in laboratory now a day. These
may be with or without vacuum (The small glass 1.3.3. PURPLE Cap: Potassium EDTA for CBC,
bottles can also be used for sample collections after it Hb, TLC, DLC, PBS (Peripheral Blood Smear),
is properly prepared). The colour of the cap indicates Reticulocyte count, ESR
the presence of anticoagulant present inside the tubes.
The label is attached with the tube for patient’s
identification. Following are the types and uses.
1.3.4. LIGHT BLUE Cap: 3.2% Sodium Citrate
1.3.1. RED Cap No chemical for serum separation for coagulation studies (PT, APTT, TT, FDP, D-
(Biochemistry and Serological test) Dimer, Factors – VIII & IX assay)
Page 600
2. Hemoglobin Estimation 2.2. Principle –
When blood is added to N/10 HCL, Hb is converted to
2.1. SAHLI`S (Acid Haematin) brown coloured acid Haematin. The resulting colour
Method – after dilution is compared with standard brown glass
This method used in small laboratories at PHC level. reference blocks of Sahli’s haemoglobinometer.
Table 2: Haemoglobin estimation according to Sahli's method
Sr.
Test Name Methods Normal Value Interpretation
No.
1 Haemoglobin a) Sahli’s Method Male 13-18gm/dl Mild Anaemia up to 10gm%
b) Hemocue Method Female 12-16.5gm/dl Mod. Anaemia up to 8 gm%
c) Cell counter Method Pregnancy 11-14gm/dl Severe Anaemia below 7gm%
Raised Hb- Polycythaemia
Table 3: WHO classification for Anaemia
Population Non –Anaemia Anaemia (Haemoglobin in grams per litre)

Mild Moderate Severe
Children 6 - 59 months of age 11 or higher 10 - 10.9 7 - 9.9 Lower than 7
Children 5 - 11 years of age 11.5 or higher 11 – 11.4 8 - 10.9 Lower than 8
Children 12 - 14 years of age- 12 or higher 11 – 11.9 8 - 10.9 Lower than 8
Non-pregnant women (15 years of 12 or higher 11 – 11.9 8 - 10.9 Lower than 8
age and above)
Pregnant women 11 or higher 10 – 10.9 7 - 9.9 Lower than 7
Men (15 years of age and above) 13 or higher 11 – 12.9 8 - 10.9 Lower than 8
3. Leucocyte count: 3.2. Automated Differential

Leucocyte Counting:
3.1. Peripheral blood smear: This system is able to replace manual differential
Preparation and staining of peripheral blood film is leucocyte count to a great extent. When any abnormal
performed for doing total leucocyte count (TLC) and cell count or abnormal morphology of cells in seen,
differential leucocyte count (DLC). this system shows a flagging thereby suggesting a
visual count mandatory in such cases.
Page 601
Figure 3: Various types of White blood cells
Sr.
No.
2 Total Leucocyte Manual by counting 4000-11000 cells / Cu mm Raised TLC in Viral, Bacterial
Count (TLC) Infections, & Leukemia
Cell counter method
Decreased TLC - Septicemia,
Enteric fever, Aplastic Anemia.
3 Differential Cell Counter Polymorphs 40-65% Raised in Acute Bacterial
Leucocyte Infections.
Count (DLC) Manual by staining Lymphocytes 20-35% Raised in chronic infection like
Slides tuberculosis, leprosy
Eosinophils - 2-4% Raised in worm infestation,
allergic skin infection, Tropical
Eosinophilia.
Monocytes - 2-8% Raised in viral infection
Basophils - 0-1% Raised in Leukemia
erythrocytes in a given interval of time is the ESR

4. Estimation of erythrocyte (erythrocyte sedimentation rate).
sedimentation rate (ESR): Stages in the ESR – three stages in the ESR can be
observed: -
4.1. Principle: i. In the initial 10 minutes, there is rouleaux
When well mixed anticoagulated blood is allowed to formation.
stand undisturbed in a vertical tube the erythrocytes ii. For about 40 minutes, sedimentation occurs at a
tend to sink to the bottom. Two layers are formed the constant rate.
upper plasma layer and lower one of red blood cells. iii. Sedimentation slows in the final 10 minutes as
The length of fall of the top of the column of cells pack at the bottom of the tube.
Page 602
Sr.
No.
4 ESR Wintrobe Tube Method Male 0-10 mm at 1 hr. Raised in chronic infection like
Westergren Tube Method Female 0-20mm at 1 hr. Tuberculosis, Leprosy, Chronic
anemia.
4.2. Interpretation or clinical 6. Clotting time:

significance of ESR:
The whole blood clotting time is one of the simplest,
ESR is markedly elevated in monoclonal blood protein
imprecise, methods to determine the efficiency of the
disorders, such as Multiple Myeloma or
clotting process. Many conditions can disrupt the
Macroglobulinemia, Polyclonal Hyperglobulinemia,
pathways that produce a clot, including hereditary
due to inflammatory disease and in
disorders, liver disease and drugs that interfere with the
Hyperfibrinogenemia. Moderate elevations are seen in
normal function of platelets and coagulation factors.
active inflammation such as Rheumatoid Arthritis,
Chronic infections such as Tuberculosis, Collagen
disease and Neoplastic disease. Although ESR is a METHODS:
nonspecific phenomenon, this indicates the presence i. Capillary tube method
of an active disease. If patient is improving ESR tends
ii. Lee and white method
to fall. It provides an index of progress of diseases
such as TB, Rheumatoid Arthritis. It is also a useful
screening test in routine examination. An elevated ESR Normal Range for clotting time 5-10 minutes.
occurs as an early feature in Myocardial Infarction.
ESR is especially low in (0-1mm) Polycythaemia, 7. Prothrombin Time:
Hypofibrinogenemia, CHF, and Sickle cell anaemia.
PT test is an indicator of the efficiency of common
5. Bleeding time: pathway and extrinsic coagulation pathway, in which
This test measures the time taken for blood vessel preformed thromboplastin is added to the test plasma
constriction and platelet plug formation to occur. No in the presence of calcium and the time taken for
clot is allowed to form, so that the arrest of bleeding clotting of plasma is noted. The main factors involved
depends exclusively on blood vessel constriction and in the pathway are V, VII, X, II and I. Deficiency of
platelet action. This is one of the most important any one of them leads to prolongation of PT. The PT
preliminary test for bleeding disorders and test is used to monitor patients taking certain
preoperative investigation in patients going for medications (e.g. Control of anticoagulant therapy) as
surgery. well as sensitive to the presence of Heparin in blood
The duration of bleeding from a standard puncture and to low fibrinogen levels.
wound of the skin is a measure of the function of
platelets as well as the integrity of the vessels wall.
Commonly used methods are: Duke’s Method & Ivy's
Method.
Bleeding time is prolonged in:

i. Thrombocytopenia (Dengue Fever) - DIC
(Disseminated Intravascular Coagulation)
ii. Acute Leukaemia - Von Willebrand’s disease
iii. Aplastic Anaemia - Aspirin intake
Page 603
Sr.
No.
5 Bleeding Time Duke's Ivy's Method 1-5 min Raised in Coagulation defect,
B.T. vasculo-toxic snakebite, rat
poisoning, Hemophilia ITP.
6 Clotting Time Capillary method 4-9 min
C.T.
7 Prothrombin Time Quick’s method or 12-16 sec
P.T.
Semi-automated 12-16 sec Raised P.T. (factor no. II V, VII, &
coagulometer X)
8. Tests for Sickle Cell Anaemia

Sickle cell test is done for all ANC patients, for all Initially the patients are screened by Solubility test. If
population in tribal area & also done for all patients of Solubility test comes positive, then it is confirmed by
severe anaemia. Hb Electrophoresis.
Sr.
No.
8 Sickle cell Anemia Solubility test or Sickle  (HbS) Present & less than
Hemoglobin 40% is sickle cell trait or
Electrophoresis test or
(HbS) is carrier
HPLC method normally absent
 HbS more than 40% is
sickle cell disease
Laboratory Tests
1. Routine screening tests (in any haematology 8.1. Sickling test
laboratory) Na – Metabisulphite is used
2. Definitive or special tests (in reference laboratory)
Cells form sickle shape under low Oxygen tension
Laboratory testing
3. Screening tests Homozygotes – 1 hour at 37 ºC
4. Sickling test
Heterozygotes – longer time
5. Solubility test
Figure 2 Sickling Test showing sickle cell
Page 604
8.2. Solubility Test  Working solution: 10 ml of stock solution + 0.1g
Na – dithionate just before use
 Reagents: Phosphate Buffer (pH 7.1)
 Procedure: 20 µl RBCs (washed) + 2ml working
 Stock solution: KH2PO4 – 125 g solution
K2HPO4 – 217 g
 Read after 10 minutes
Saponin – 2.5 g
DW– 1 litre
Figure 3 Solubility Test
8.3. Confirmatory Test by i. Diagnosis and management of renal or urinary

diseases.
Electrophoresis
Confirmatory test for HbS after Hb electrophoresis ii. The detection of metabolic or systemic disease
not directly related to the kidneys.
Reason: Sensitivity is 93% compared to HPLC
iii. Microscopic examination of the sediment may
 Cannot differentiate between HbAS & HbSS indicate the kind of lesion present or the state of
activity of a lesion.
 Preliminary test in remote area but confirmation
must be done by HPLC or Hb electrophoresis. (3) 9.1. Collection of Urine: -
9. URINE EXAMINATION For routine work 15 ml or more is preferred and it
should be collected in a clean container, after properly
The urine examination is referred to as a liquid tissue cleaning the external genital area to avoid vaginal
biopsy of the urinary system. secretions and cellular debris of the urethral meatus.
It is useful in -
Page 605
9.2. Specimen Evaluation:
This includes proper labelling (name, date and time of Results: Faint Green-Trace
collection), proper specimen, proper receptacle, storage Green+
condition, preservative (Thymol, formaldehyde if
added). Greenish Blue++
9.3. Physical Examination: Blue+++

Following parameters are looked for: Deep Blue++++
i. Quantity 9.5. Microscopic Examination:
ii. Colour Examination of urinary sediment – the specimen
should be examined while fresh since casts begin to
iii. Appearance lyse within 1 to 3 hrs. Mix the specimen well. Take 10
iv. Character ml of urine in centrifuge tube, centrifuge at 2000
rotation /min for 5 minutes. Remove the supernatant.
v. Odour
Place a drop of sediment of slide and put a cover slip.
vi. Specific gravity Examine under both low power & high power.
Cells – RBC, WBC, Epithelial cells.
9.4. Chemical examination
i. Test for Proteins Cast - Hyaline, granular, epithelial, WBC cast, RBC
cast, Fatty, waxy.
ii. Reducing Substances in Urine (Urine for Sugar)
Crystal and amorphous chemical deposits.
iii. Ketone Bodies
Miscellaneous – Mucus, spermatozoa, bacteria, yeast,
iv. Bile Pigments parasite.
v. Bile Salts Compare the urine strip results with the colour on
bottle.
9.4.1 Benzidine Test (for occult blood)
Table 1: Urine Examination
Finding Interpretation
A ROUTINE EXAMINATION
1 Physical examination
1.1 Colour- Yellow/Reddish Yellow in Hyperbilirubinemia, Red in Hematuria
1.2 Appearance - clear/turbid Turbid in UTI, Nephrotic syndrome, Preeclampsia, Eclampsia.

2 Chemical Examination
2.1 Albumin - +/- UTI, Nephrotic syndrome, Preeclampsia, Eclampsia
2.2 Sugar - +/- Diabetes, Hyperglycemia
2.3 Ketone bodies - +/- Present in Starvation, Diabetic Ketoacidosis.
2.4 Bile salts & Bile pigment - +/- Present in Hyperbilirubinemia,
B MICROSCOPIC EXAMINATION
1 No of RBCS / HPF Hematuria, renal calculi, normal menses
Page 606
2 No. of Pus cells/ HPF UTI
3 No. of Epithelial cells /HPF Normally present
4 Casts - Present /Absent Nephropathy
5 Crystals - Present / Absent Present in Calciuria (Oxalate, Phosphate, Urate crystals)
6 Trichomonas - Present / Absent It is motile parasite
7 Spermatozoa - present /absent Present in contamination with semen
8 Bacilli - present / absent UTI
10. Detection of Malaria

10.2. Interpretation:
Parasite by Malarial Antigen In case of positive test, band for respective kind of
test (RDK) malaria is visible.
Malaria is serious, sometimes fatal, parasitic disease In case of negative test, band is absent.
characterized by fever, chills and anemia caused by a
parasite that is transmitted from one human to another 10.3. Peripheral blood smear for
by the bite of infected female Anopheles mosquitoes.
There are four kind of malaria that can infect humans:
Malaria Parasite
Plasmodium Falciparum, Plasmodium Vivax,
Plasmodium Ovale and Plasmodium Malaria. Specimen collection by using Lancet-
Pierce tip of finger with sterile lancet & take one drop
10.1. Principle: of blood on clean glass slide & spread it with the help
Malaria antigen kit contain a membrane strip which is of spreader to make thin blood smear
pre-coated with one monoclonal antibody and one
polyclonal antibody as two separate lines across Fixation- Fix the blood smear by alcohol spray or spirit
attached strip. One monoclonal antibody (test line PF) Staining of Smear-Staining of blood smear by field A
are specific to the HRP-II (Histidine Rich Protein- II, & B stain.
Specific to Plasmodium Falciparum) and other
polyclonal antibody (Test Line PAN) are PAN specific Microscopic Examination of peripheral smear: - After
to the Lactate dehydrogenase of plasmodium species applying oil on smear with the help of oil emulsion
(P. Falciparum, P. Vivax, P. Malariae and P.Ovale). lens screen the morphology of RBC's & any of the
following form of malaria parasite.
Malaria Thick & thin smear Ring form Ring form - multiple small rings - Falciparum,
Detection under oil emulsion Trophozoite / schizont single large ring - vivax
form, Gametocyte form Trophozoite / schizont form
Commonly present Gametocyte form – in
Falciparum.
Page 607
Plasmodium falciparum
Maurer’s Dots
Trophozoites
Gametocytes
Plasmodium vivax
Schuffner’s Dots
Trophozoites
Gametocytes
Schizonts
Fig. 4: Different forms of Malaria Parasite
Page 608
11. Rapid test for Leptospirosis 12.1 Collection of Sample: -
Take approximately 5-10gm of stool passed by the
11.1. Principle: Qualitative and differential patient at the end of defecation, it is usually semi
definition of IgG and /or IgM antibody to Leptospira in solid with the half of wooden spatula (Ice cream
human serum or plasma. It is only a screening test. stick) into a plastic container with cap (Urine
collection cup). Morning sample is preferred and
11.2. Method: Rapid test is solid phase is transported to laboratory immediately.
immunochromatographic assay.
12.2 Preservation of Faecal Sample: -
11.3. Sample: Serum or plasma. This is done when sample cannot be examined
immediately or it has to be transported. The
11.4. Procedure: Remove test device from sample of stool is made into thin paste with tap
sealed pouch and place horizontally. Add 5 micro liter water. To this add equal part of steaming 10%
of plasma or serum in sample well(s), odd 4 drops of formalin and left for a few hours. The supernatant
diluents in another well provided. Read interpretation is discarded. It should be noted that formalin
in 20 minutes. preserved ova become in a ratio of 30:1 to stool
sample. Ova can be examined for about one
11.5. Interpretation: month.
1) Negative- Only one color line at control © in 12.3 Examination of Stool for Ova and
result window.
cyst:
2) Positive-
Methods
 IgM positive- Two color lines at control (c) and
at Ig M (M) i. Direct Smear
 IgG Positive- Two color lines at control (c) & at ii. Concentration by floatation method
IgG.
iii. Direct Centrifugal floatation.
 IgM and Ig G Positive -Three color lines at
control (c), IgM (M) &IgG.
3) Invalid Test- No control © line in result
window.
- No color line in (c) & also in Ig M (M) and / or G.
result window
12. Stool Examination:

Finding Interpretation
A Routine Examination
1 Physical Examination
1.1 Colour - Black, White, Red 1. Black in Occult blood in upper G.I. bleed. 2. Reddish in lower G.I.
bleed, 3. White in biliary obstruction
1.2 Consistency - soft, loose, hard, Loose in Diarrhea & Dysentery, Hard in chronic constipation
semisolid
1.3 Worms Adult worm – Ascaris Lumbricoides, Pin worm (small round worm)
2 Chemical Test
2.1 Reducing substance For Lactose intolerance in infants
2.2 Occult blood Upper G.I. bleed

B Microscopic exam
1 PUS cells +/- / HPF Diarrhea & Dysentery
Page 609
2 RBCS +/- /HPF Lower G.I. bleed
3 OVA & Cyst Cyst of 1. Entamoeba histolytica, Giardia Lamblia 2. Enterobius
vermicularis (Pinworm) 3. Ancylostoma duodenale (Hook worm) 4.
Taenia solium (Tape Worm)
4 Mucous +/- Amoebic Dysentery
13. Sputum for AFB 13.3 Direct Examination of Sputum

 Work safely with the sputum as it is
13.1 Introduction: infectious.
Sputum should be obtained from the lower
 If possible bleach the specimen with 5%
respiratory tract (Bronchi of the lung). Saliva
sodium hypochlorite or bleach (1:1)
produced by the salivary gland in the mouth is not
sputum, but is frequently and mistakenly sent to the 13.4 Acid fast staining (Ziehl-Nelson
laboratory instead of sputum.
method)
Note: -Purity of the specimen should be checked.
True sputum should contain fewer than 10
Result:
squamous epithelial cells and more than 25
 All acid fast bacilli are not pathogenic. So the
leucocytes/ low power field.
result should be reported as-
13.2 Specimen Collection: o AF organism present or positive.
The patient should be instructed properly as to the o AF organism absent or negative.
type of the specimen required. Specimen is
collected in the early morning. It must be coughed  Technician should examine 10 microscopic fields
up from deep down in the chest. Apply the aerosol under oil immersion and then report.
technique if the patient is unable to produce the
required specimen.
Bibliography
1. Godkar PB. The Book of Medical Laboratory Technology. 2nd Ed. Mumbai: Bhalani Publishing House;
2008. Chapter 39, Hemostasis, Coagulation and routine coagulation tests.
2008. Chapter 37, Hematological Diseases.
2008. Chapter 41, Routine Urine Examination.
2008. Chapter 38, Special Hematological Tests.
2008. Chapter 33, Diagnostic Serology.
2008. Chapter 44, Parasitology and Examination of Feces.
2008. Chapter 47, Routine Examination of Sputum.
8. Godkar PB. The Book of Medical Laboratory Technology. 2 nd Ed. Mumbai: Bhalani Publishing House;
2008. Chapter 36, Routine Hematological Tests.
Further reading
1. Sood R. Textbook of Medical Laboratory Technology. New Delhi: Jaypee Brothers Publishers; 2006.


Page 610
3. SEROLOGY SECTION
Serological tests usually done in laboratory are pneumonia. Any positive result must be confirmed by
broadly classified into following two groups. other serological assay (e.g. TPHA).
 Agglutination Tests: This group includes tests like
Widal test, VDRL test, RA factor test, Blood
2. HBsAg Test
Group test, ASO test, CRP test, HBsAg test etc.
 Rapid Tests (Also known as Spot/ Line Tests):
2.1. Principle:
This group includes tests like, HBsAg test, HIV The HBsAg one-step Hepatitis B surface antigen test
test, Dengue test, Malaria test, Hepatitis C test etc. device (serum/plasma) is a qualitative, solid phase,
Serological Tests: two-site sandwich immunoassay for the detection of
HBsAg in serum or plasma.
Various serological tests are done for diagnosis of
diseases. Here we are discussing common serological 2.2. Interpretation:
tests like VDRL, HBsAg, HIV, Widal, RA factor,
dengue antibody test. Double line- Positive
Single line with control - Negative
1. RPR Test for Syphilis
(VDRL) 3. Rheumatoid factor test
The RPR carbon reagent is a stabilized suspension of Principle
cholesterol crystals coated with cardiolipin. Lecithin is
The RF reagent is a suspension of polystyrene latex
added to adjust the sensitivity and charcoal particles to
particle sensitized with specially prepared Human IgG.
improve the reading of the reaction. The reagent act as
When serum containing RF is mixed with the latex
antigen against antibodies present in person suffering
reagent visible agglutination occurs. When serum
from syphilis caused by Treponema pallidum.
containing greater than 0.8mg/dl RF is mixed with the
Reagents are a group of antibodies against some
latex reagent, visible agglutination occurs.
components of the damaged tissue from patient
infected by Treponema pallidum. Result: In positive case agglutination occurs.
This test is rapid method for diagnosis of syphilis,
macroscopic agglutination indicates positive result.
4. ASO titer
1.1. Storage: Principle
It is an immunological reaction between streptococcal
Kit should be stored at 2-8˚C and protected from light.
exoenzyme bound to biologically inert latex particles
1.2. Patient Sample: and streptococcal antibodies in the test specimen.
When serum containing greater than 200 IU/ml of
Fresh serum (Free of Haemolysis) ASO titre is mixed with the latex reagent, visible
agglutination occurs.
1.3. Interpretation of Result: Result: In positive cases agglutination occurs.
Medium & Large aggregates against white back
ground – Reactive
5. Widal test
Finely dispersed aggregates against white back ground Principle
– Weak Reactive Widal kit contains killed bacterial suspension of
No aggregates, even grey back ground - Non Reactive. Salmonella which carries specific ‘O’ and ‘H’ antigen.
This reacts with immunospecific antibodies present in
False positive results can be seen in diseases like the sample resulting in agglutination.
leprosy, SLE, infectious mononucleosis, malaria, viral
Page 611
6. HIV – Tridot spot test Glass slide covers tip, pipettes, Neubauer counting
chamber, pH paper, semen diluting fluid, wide mouth
Confirmation with ELISA test container for semen collection.
7. Dengue – 9.3. Specimen-

Spot test ELISA test
Freshly Collected Semen
8. Urine Pregnancy Test (UPT) 9.4. Physical Examination:

Colour, volume, viscosity of semen.
8.1. Principle: -
9.5. Chemical Examination-
Qualitative detection of human chorionic gonadotropin
(HCG) in urine in early detection of pregnancy. pH, Detection of fructose in semen.
8.2. Method: 9.6. Microscopic Examination:
Pregnancy test device (Urine) is rapid chromatography Under low and high power
immunoassay for qualitative detection of HCG.
 Study of sperm motility & its percentage
8.3. Sample:  Morphology's Abnormal forms & its percentage
 Pus cells, RBC or epithelial cells / HPF
Early morning sample for early detection of pregnancy.  Determination of sperm count with help of
Neubauer chamber & semen diluting fluid.
8.4. Interpretation
Note: It is necessary to note while reporting for routine
Negative: - semen examination
One coloured line appears in control line region and no  Abstinence days
any coloured line appears in test region (+)  Method of sample collection
 Time & place of Sample collection.
Positive: -
One coloured line in control and other coloured line in

10. Swine Flu Diagnosis /
test. Sample collection
Invalid test: -
10.1. Principle - Detection of H1N1 (Swine Flu)
No coloured line in control (c). Virus by polymerase chain reaction (PCR) method.
9. Semen Analysis/Examination. 10.2. Sample- Throat & nasal swab

9.1. Indication: 10.3. Reagent- Sterile swab, Viral transport
media (VTM)
(a) To rule out male infertility
10.4. Procedure- One throat swab & nasal swab
(b) Post vasectomy by sterile swab should be taken & place in one VTM
with universal precaution.
9.2. To perform routine examination
of semen VTM is kept at 2 to 8ºC & transported to virology lab
by maintaining temperature with icepack in thermocol
container or vaccine carrier.
9.2.1. Requirement: -
Detail history sheet should be provided with sample.
Page 612
11. Common Rapid Test:
1 Leptospirosis RDK card method Positive/Negative IgM indicates recent infection
detected for of Leptospirosis; IgG
Leptospirosis indicates old infection of
Leptospirosis
2 Dengue RDK card method Dengue NS1, IgG & IgM Dengue NS1 present in 1st 5
can be detected for days of infection, IgM
Dengue indicates recent infection of
Dengue, IgG indicates old
infection of Dengue
3 HIV RDK card method HIV I & II can be HIV I or II can be detected.
detected
4 HBsAg RDK card method Positive/ Negative Hepatitis B viral infection
detected for Hepatitis B
5 Malaria RDK card method Pl Vivax & PL Pl. Vivax & Pl. Falciparum is
Falciparum can be detected
detected
6 UPT RDK card method Positive / negative Pregnancy can be detected
detected for pregnancy
7 Widal Test Rapid Agglutination Positive /Negative to Enteric /Typhoid Fever can
Method detect Enteric /Typhoid be detected
Fever
8 CRP Test Rapid Agglutination Positive/Negative to Detected in infection &
Method detect infection & septicemia
septicemia
9 RA Test Rapid Agglutination Positive / Negative to Detected in Rheumatoid
Method detect Rheumatoid Arthritis
Arthritis
10 VDRL Rapid Agglutination Positive/ Negative to Detected in Syphilis infection
Method detect Syphilis infection
Bibliography
1. Godkar PB. The Book of Medical Laboratory Technology. 2 nd Ed. Mumbai: Bhalani Publishing House; 2008.
Chapter 33, Diagnostic Serology.
2. Godkar PB. The Book of Medical Laboratory Technology. 2 nd Ed. Mumbai: Bhalani Publishing House; 2008.
Chapter 46, Semen Examination.
Further reading

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Page 613
4. BIOCHEMISTRY SECTION
Biochemistry tests usually done in laboratory include 6) SGPT
following tests. These tests are done with available 7) Alkaline Phosphatase
standard biochemical kits on semi-automatic / fully 8) Serum Total Proteins
automated auto-analyzer. Procedure, method and 9) Serum Albumin
interpretation varies as per available kit. 10) Serum Na/K/Cl
11) Serum LDH
1) Blood Sugar
12) Serum Cholesterol
2) Blood Urea/ Blood Urea Nitrogen
13) Serum HDL Cholesterol
3) Serum Creatinine
14) Serum Triglycerides
4) Serum Bilirubin
5) SGOT
Further reading

Page 614
5. HISTOPATHOLOGY
1. Definition: 3. Fixation
It is a branch of pathology, which deals with the study 3.1. Definition:
of disease in a tissue section.
The tissue undergoes a series of steps before it reaches It is a complex series of chemical events, which brings
the examiners desk to be thoroughly examined about changes in the various chemical constituents of
microscopically to arrive at a particular diagnosis. cell like hardening, however the cell morphology and
structural detail is preserved.
To achieve this, it is important that the tissue must be
prepared in such a manner that it is sufficiently thick or Unless a tissue is fixed soon after the removal from the
thin to be examined microscopically and all the body, it will undergo degenerative changes due to
structures in a tissue may be differentiated. autolysis and putrefaction so that the morphology of
the individual cell will be lost.
The objective of the subsequent discussions will be to
acquaint the staff with their responsibility; the basic 3.2. Principle of fixation:
details of tissue handling, processing and staining.
The fixative brings about cross linking of proteins
The term histochemistry means study of chemical
which produces denaturation or coagulation of proteins
nature of the tissue components by histological
so that the semifluid state is converted into semisolid
methods.
state; so that it maintains everything in vivo in relation
The cell is the single structural unit of all tissues. The to each other. Thus semisolid state facilitates easy
study of cell is called cytology. manipulation of tissue.
A tissue is a group of cells specialized and 3.3. Tissue Processing
differentiated to perform a specialized function.
Collection of different type of cells forms an organ. The tissue processing is the heart of any tissue section,
which will be cut adequately only if the tissue is
2. Type of material obtained in properly preserved and processed. The study of this
laboratory: topic is to understand the coarse and fine details of
tissue processing so that excellent sections are
The human tissue comes from the surgery and the
obtained.
autopsy room.
From surgery two types of tissue are obtained. 4. Staining
i. As biopsy- A small piece of lesions or tumor The sections, as they are prepared, are colourless and
which in sent for diagnosis before final removal different components cannot be appreciated. Staining
of the lesion or the tumor (Incisional biopsy). them by different coloured dyes, having affinities of
specific components of tissues makes identification
ii. If the whole of the tumor or lesion is sent for
and study of their morphology possible.
examination and diagnosis by the surgeon, it is
called excisional biopsy. Tissues from the
autopsy are sent for the study of disease and its
course, for the advancement of medicine.
Bibliography
2008. Chapter 50, Basic Histopathology Techniques and Laboratory requirements.
Further reading

Page 615
6. CYTOLOGY STUDY
Cytology is divided into four groups - are fixed by bio fixatives and are stained with
PAP stain.
1) Fine needle aspiration Results
cytology (FNAC)– Nucleus - blue
Cytoplasm and background – pink
It is done for diagnosis of any lump/mass in
body. With the help of 20 bore needle fine
aspiration from any lump or mass in the body is
3) Body fluid cytology–
done and smear made from aspirated material is It is done on CSF / Pleural fluid / Ascitic fluid /
fixed with bio fixative and stained with Synovial fluid etc. All the body fluids are
Hematoxylin and Eosin staining (H & E). examined for physical / chemical examination.
Cell count is done on Neubauer chamber. The
Results smear of the deposited material is stained with
Nucleus - blue Leishman stain, Gram stain and ZN stain.
Cytoplasm and background – pink
4) Bronchial lavage cytology–
2) Exfoliative cytology – Smears are stained with H&E, Gram stain, and
ZN stain.
It is done in the female patients to diagnose
gynecological pathology. The cervical smears
Bibliography
2008. Chapter 52, Cytology Techniques.
Further reading

Page 616
7. BLOOD BANK
Blood Grouping (ABO & Rh 1.3. Methods for ABO Grouping:
system) The two main methods of ABO grouping for a routine
blood bank are:
There are more than 300 blood group systems but
ABO and Rhesus (Rh) systems are of importance from i. Slide method: The slide test is not recommended
clinical point of view. These are inherited characters as it is not reliable. It is less sensitive than the
which give rise to antigen-antibody reactions. tube test. The slide is prone to drying effect that
may be wrongly interpreted as agglutination.
1. ABO system: ii. Tube method: The tube method is recommended
It was discovered by Landsteiner in 1900. The red cells
because:
contain different types of antigens (Agglutinogen),
while plasma contains antibodies (Agglutinins). In  It allows longer incubation of antigen-antibody
order to determine the blood group of a subject, the red mixture without drying.
cells are allowed to react with a sera containing known
antibody (Agglutinin).  Tubes can be centrifuged which enhance
antigen-antibody reactions.
1.1. Practical aspects of ABO  Both cell and serum grouping can be performed.
grouping:  Weaker antigens and antibodies can be
detected.
 Routine ABO grouping must include both cell and
serum grouping as each test serves as a check on  Less reagents are required.
the other.
 Results can be read comfortably as there is no
 ABO grouping test should be done at room drying.
temperature. Testing at 37 °C weakens the
reaction. 2. Rh blood group system:
 Tubes, slides, reagents and microplates should be Rh blood group system was first reported Landsteiner
labelled properly. and Weiner in 1940.
 Serum should be added before adding cells and In contrast to ABO system, Rh antigens are present on
examine each tube after serum has been added. red blood cells only and Rh antibodies develop only in
response to a known stimulus. Rh factor is present in
 Tubes or slides should be clean and dry and 85-95% of human beings.
disposable plastic tubes may be used.
2.1. Methods of Rh Grouping:
 Microscope should be used to examine reactions
that appear negative by naked eye. The two main methods of Rh grouping for a routine
 Results should be recorded immediately after blood bank are:
observation. i. Slide method: The slide test is not recommended
as it is not reliable. It is less sensitive than the
1.2. Blood sample tube test. The slide is prone to drying effect that
may be wrongly interpreted as agglutination.
 Clearly labelled samples of blood in plain tubes.
No sign of haemolysis should be there. ii. Tube method: The tube method is recommended
because:
 If serum has not completely separated or become
clear, centrifuge the blood sample at 1000-3000  It allows longer incubation of antigen-antibody
rpm for 3 minutes. mixture without drying.
 Take one to two millilitres of serum in pipette and  Tubes can be centrifuged which enhance
place into a relabelled tube for serum grouping and antigen-antibody reactions.
other tests.  Both cell and serum grouping can be performed.
Page 617
 Weaker antigens and antibodies can be After the testing is complete, the blood bag is labelled
detected. and then taken on stock and used for crossmatch and
issue to the patients.
 Less reagents are required
 Results can be read comfortably as there is no 4. Procedure of blood
drying.
TRANSFUSSION:
2.2. Interpretation: Important aspects:
The blood bag received in the ward for transfusion to
i. Agglutination in the tube ‘test’ and in the tube the patient is to be maintained at room temperature for
‘positive control’ and smooth suspension of one hour, so that it will come to the body temperature.
cells in the tube ‘negative control’: This is Pre-transfusion medication to patient is done half-hour
interpreted as test cells Rh (D) positive. before blood transfusion.
The blood bag should not be warmed in hot water
ii. A smooth suspension of red cells in tubes of otherwise hemolysis may take place.
‘test’ and ‘negative controls’ and agglutination Do not transfuse the blood bag immediately after
in the tube labelled as ‘positive control’: This is receiving because at that time the blood bag is at 4 to 6
interpreted as test cells Rh (D) negative. degree centigrade. Transfusion of cold blood may get
iii. Blood Donor red cells found negative should be transfusion reaction.
further tested by AHG test for weak D. Rate of blood transfusion should be such that it will
take 4 hours to transfuse the bag. In emergency the
iv. If in any test ‘negative control’ gives clinician will take decision.
agglutination or ‘positive control’ does not give During transfusion the patient is monitored for body
agglutination, the results are invalid. temperature/ pulse/blood pressure/respiratory rate and
watch for transfusion reaction.
3. Cross Match
4.1. Blood transfusion reaction:
 Major crossmatch: Recipient’s serum is cross
matched with donor red cells for IgM and IgG 1) Fever
antibodies compatibility. 2) Pain
 Minor crossmatch: Donor’ serum is cross 3) Jaundice
matched with recipient’s red cells for IgM and 4) Allergic
IgG antibodies compatibility. If donor’s serum 5) Other
is tested negative for unexpected or irregular In case of blood transfusion reaction, BTO should be
antibodies, minor crossmatch can be avoided. informed immediately after stopping blood transfusion
 If incompatibility is not detected in cross and blood bag along with blood transfusion reaction
matching, then it is likely that the donor blood card duly filled should also be returned to blood bank.
transfused into patient will survive normally.
4.2. Complication of blood
 Finding of incompatibility indicates that transfusion reactions-
transfusion of such blood is potentially
dangerous and further steps should be taken to i. Haemolytic transfusion reactions which could be
identify the antibody.
immediate or delayed.
Note: It is mandatory to test the blood for the ii. Allergic reactions like 1) Fever 2) Anaphylactic
following transfusion transmissible infections before it reaction 3) Allergic reactions 4) Graft versus-
is taken on stock and issued to the patient. host diseases
i. HIV antibody screening by ELISA iii. Circulatory overload leading to pulmonary
ii. Hepatitis B surface antigen (HBsAg) by ELISA congestion and acute Heart failure,
iii. Hepatitis C antibody by ELISA thrombocytopenia & dilution of coagulation
iv. Syphilis by RPR test factors.
v. Malaria by thick and thin blood smear or iv. Transmission of infections e.g. Hepatitis B & C,
malaria antigen. malaria, HIV Infection, syphilis, infectious
mononucleosis, toxoplasmosis.
Page 618
In case of blood transfusion reaction, for carrying out with blood transfusion reaction card duly filled should
investigations pre and post-blood transfusion patient’s also be returned to blood bank by the medical officer.
blood and urine sample is needed. Blood bag along
Bibliography
1. Director General of Health services. Manual for Blood Banks. Health and Family Welfare, GoI, New
Delhi. [ Last updated on 2012 July 26] [Citied 2016 July 5]
Available at: http://www.cdsco.nic.in/forms/list.aspx?lid=1642&Id=1
Further reading
1. National AIDS Control Organization. Standards for Blood Banks & Blood Transfusion Services. Ministry
of Health and Family Welfare, GoI, New Delhi; 2007
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Page 619
8. NORMAL LAB VALUES
Hematology
Hemoglobin
: 13.5-17.5 g/dl
: 12.0-16.0 g/dl
Hematocrit : 39-49%
: 35-45%
Red Blood Corpuscles
: 4.3-5.7 ×108/µl
: 3.8-5.1 ×108/µl
Platelet 150-450 × 103/ µl
White Blood Cells (differential below) 4.5-11.0× 103/ µl

Neutrophils 57-67%
Lymphocytes 22-33%
Monocytes 3-7%
Eosinophils 1-3%
Basophils 0-1%
Erythrocyte Sedimentation Rate (ESR) : <15mm/hr
: <20mm/hr
Ferritin : 20-250 ng/ml
: 10-120 ng/ml
Fibrinogen 150-350 mg/dl
Haptoglobin 26-185 mg/dl
Hb A1c 5.0-7.5%
Mean Corpuscular Hemoglobin 26-34 pg
Mean Corpuscular Hemoglobin Concentration 33-37%
Mean Corpuscular Volume 80-100fl
Prothrombin Time 10-14 sec
Activated Partial Prothrombin Time 20-40 sec
Reticulocytes 0.5-1.5%
Total Iron Binding Capacity 250-400 µg/dl
Transferrin 200-400 mg/dl
Chemistry
Sodium 135-145 mEq/l
Potassium 3.5-5.3 mEq/l
Page 620
Chloride 95-105 mEq/l
Bicarbonate 22-29 mEq/l
Blood Urea Nitrogen 10-26 mg/dl
Creatinine 0.6-1.3 mg/dl
Glucose 70-115 mg/dl
Anion Gap 7-16 mEq/l
Osmolality 275-300 mOsm/kg
Calcium Total 8.5-10.5 mg/dl
Calcium Ionized 4.65-5.28 mg/dl
Magnesium 1.3-2.4 mEq/l
Phosphate 2.5-4.5 mg/dl
Alfa Fetoprotein <10 ng/mol
Albumin 3.5-5.5 g/dl
IgA 70-312 mg/dl
IgG 640-1350 mg/dl
IgM 56-350 mg/dl
Lactate 0.5-1.3 mEq/l
Protein (Total) 6.0-8.0 g/dl
Uric Acid : 3.0-7.4 mg/dl
: 2.1-6.3 mg/dl
Zinc 55-135 µg/dl
Liver/Pancreas
SGOT/ALT 0-40 IU/l
Alkaline Phosphatase : 38-126 U/l
: 70-230 U/l
Ammonia 10-50 µmol/l

AST/SGPT 7-40 IU/l
Bilirubin (Total) 0.2-1.0 mg/dl
Bilirubin (Conjugated) 0-0.2 mg/dl
Lecithin dehydrogenase 90-190 U/l
Amylase 25-125 U/l
C Peptide 0.7-1.89 ng/ml
Lipase 10-140
>60 years: 10-180
Page 621
Lipids
Total Cholesterol <200 mg/dl
Low density Lipoproteins <130 mg/dl
High density Lipoproteins : >29 mg/dl
: >35 mg/dl
Triglycerides : 40-160 mg/dl
: 35-135 mg/dl
Other
Phosphokinase : 38-174 U/l
: 26-140 U/l
Phosphokinase MB <5%
Acid Phosphatase <0.8 IU/ml
B12 100-700 pg/ml
CA-125 <35 U/ml
Copper (Cu) : 70-140 µg /dl
: 80-155 µg /dl
Folate 3-15 ng/ml
Lead (Pb) <10 µg /dl
Zinc (Ionized) 70-150 µg /dl

Blood Gases
Arterial Venous
Ph 7.35-7.45 7.32-7.42
pCO2 35-45 41-51
pO2 80-100 25-40
HCO3 21-27 24-28
Oxygen Saturation 95-99%
Urine
Ph 5-9
Minimal Volume 0.5-1.0 mg/kg/hr
Specific Gravity 1.015-1.030
Osmolarity 600-1400 mOsm/kg
Page 622
Creatinine : 14-26 mg/kg/day
: 11-20 mg/kg/day
Creatinine Clearance : 100-150 ml/min
: 90-140 ml/min
* Rough estimate only varies with BMI
Urea Nitrogen 12-20 g/day
Calcium (Ionized) 100-300 mg/day
Potassium (Ionized) 25-125 mEq/day
Sodium (Ionized) 40-220 mEq/day
Phosphate 0.4-1.3 g/day
Uric Acid 250-750 mg/day
Albumin 10-100 mg/day
Amylase 1-17 U/hr
Glucose <0.5 g/day
Protein 10-100 mg/day
CSF
Pressure 60-180 mmH2O
White Blood Cell 0-5 /ul
Protein 15-45 mg/dl
Glucose 40-80 mg/dl
Synovial Fluid
White Blood Cell <200 /ul
Trauma, OA, SLE <3,000/ul
Gout. RA >4,000/ul
Septic >60,000/ul
Protein <3.0 g/dl
Glucose >50 mg/dl
Uric Acid <8.0 mg/dl
Endocrine
Aldosterone Supine: 3-10 ng/dl
Upright: 5-30
Cortisol 0800h: 6-23 µg/dl
1600h: 3-15 µg/dl
2200h: ≤50% of 0800h value
Gastrin <100 pg/ml
Page 623
Growth Hormone (<60yr) : <2 ng/ml
: <10 ng/ml
Growth Hormone (>60yr) : <10 ng/ml
: <14 ng/ml
Estrogen Follicular: 60-200 pg/ml
Luteal: 160-400 pg/ml
Menopause: ≤130 pg/ml
Follicle stimulating Hormone Follicular: 1-9 mU/ml
Ovulation: 6-26 mU/ml
Luteal: 1-9 mU/ml
Menopause: 30-118 mU/ml
Luteinizing Hormone Follicular: 1-12 mU/ml
Mid-Cycle: 16-104 mU/ml
Luteal: 1-12 mU/ml
Menopause: 16-66 mU/ml
Progesterone Follicular: 0.15-0.7 ng/ml
Luteal: 2.0-25 ng/ml
Prolactin <20 ng/ml
Para Thyroid Hormone 10-65 pg/ml
Sperm 20-200 million/ml
Testosterone Free 52-280 pg/ml
Total 300-1000 ng/dl
T3 Uptake 0.82-1.18
Total 100-200 ng/dl
T4 Total 5.0-12.0 µg/dl
Free 0.3-2.3 ng/dl
Thyroid stimulating Hormone <10 µU/ml
>60 years : 2-7.3 µU/ml
>60 years : 2-16.8 µU/ml
Toxic Levels
Acetaminophen >200 µg/ml
Ethyl Alcohol (in a non-alcoholic patient) Intoxicated >100 mg/ml
Lethargic >200 mg/ml
Coma >300 mg/ml
Page 624
Resp. Distress Death >500 mg/ml
Ethylene Glycol >20 mg/dl

Lead >100 µg/dl
Salicylate >300 µg/ml
Normal of Cerebral Spinal Fluid
Opening
Glucose Protein
Color Pressure Cells (#mm3)
(mg/100ml) (mg/100ml)
(mmH2O)
Adult clear 70-180 45-80 0-5 WBCs 15-45
Newborn clear 70-180 2/3 of serum 40-60 WBCs 20-120
Bibliography
2008.

Page 625
9. LABORATORY TESTS PERFORMED
Clinical Services Rural / Sub-district District Hospitals and all
PHC
Related to: hospital 100 bedded hospitals
Viral infection Blood smear Blood smear Blood smear, serology test
Bacterial Infection Urine exam, blood smear, Urine exam, blood smear, Urine exam, blood smear,
sputum examination, Widal test, CSF exam, Widal test, CSF exam,
Gram stain, ZN stain Gram stain, ZN stain serology, Gram stain, ZN
stain
Protozoal Urine exam, Stool, Urine exam, Stool, Urine exam, Stool, Filaria,
Malarial parasite, Filarial Malarial parasite, Rapid Blood smear
Blood smear malaria test, Filaria,
Blood smear,
STD Urine exam, Blood smear Urine exam, Blood Urine exam, Blood smear,
smear, HIV& VDRL tests HIV& VDRL tests,
serology
Poisoning cases Urine exam, Blood smear Urine exam, Blood Plasma Cholinesterase, Sr.
smear, Creatinine in aluminum
phosphide poisoning
Animal Bites Urine exam, Blood smear Urine exam, Blood smear Urine exam, Blood smear
Environmental disorders Urine exam Urine exam, Blood Urine exam, Blood smear,
smear,
Sr Creatinine & urea
Sr Creatinine & urea
Gastro-intestinal Tract Stool exam, Blood smear Stool exam, Blood smear, Stool exam, Blood smear
Disorder Total Eosinophilic count
Total Eosinophilic count
Respiratory disorder Sputum Gram & AFB Sputum Gram & AFB Sputum Gram & AFB stain
stain exam, Blood smear stain exam, Blood smear exam, Blood smear
Cardio-vascular Disorder Urine exam, Blood smear Urine exam, Blood Urine exam, Blood smear,
smear, SGOT Sr CMB, Troponin
Hematological Disorder Hb %, Blood smear Hb %, Blood smear, Hb %, Blood smear,
sickling tests, BT & CT sickling tests, RBC indices,
BT, PT, APTT
Bibliography
2008.

Page 626
Dentistry
12. Dentistry
1 Dental Caries 627

2 Diseases of Dental Pulp & Periapical Tissues 629
3 Periodontal Diseases 634
4 Spread of Oral Infection 639
5 Oral Mucosal Diseases 642
6 Premalignant lesions and conditions 645
7 Orofacial Pain 650
8 Traumatic injuries to teeth 651
9 Discolouration of Teeth 653
10 Maxillofacial Injuries 654
11 Temporomandibular Joint disorders 657
12 Dental Impactions 660
1. DENTAL CARIES
Dental caries is a microbial disease of the calcified 2.3 Radiographic investigation:
tissues of the teeth characterized by Radiograph shows dental caries and its extent as
demineralization of the inorganic portion and radiolucent lesion due to demineralization of tooth
destruction of the organic substance of the tooth. structure.
1. Signs and Symptoms:
Grayish black discolouration of tooth in pit and fissure
areas.
 Cavity formation and food lodgment.
 Sensitivity if caries reaches to the dentin.
 Pain and swelling in vicinity area if pulp is Figure 1.3: Stages of Dental Caries
involved due to caries.
 Periapical abscess & draining sinus in advanced 3. Treatment:
stages.
Avoid extreme hot and cold beverages.
Restoration of cavitated lesions if limited to enamel and
dentin.
Endodontic therapy for pulp involvement due to caries.
Abscess drainage followed by endodontic therapy.
Tooth extraction may be performed in advanced cases
when conservation of tooth structure is critical.
4. Prevention of Dental Caries

Figure 1.1. Dental Caries 4.1 Diet modification / Dietary counseling
4.2 Maintenance of oral hygiene
2. Diagnosis:
 Daily removal of plaque by tooth-
2.1 Visual Examination: brushing/flossing/rinsing is the best measure for
preventing caries and periodontal disease.
For visual examination – teeth should be cleaned,  Proper brushing technique.
dried with compressed air and illuminated under
 Flossing should be done in the interdental areas to
adequate light source and observe for cavitation,
maintain the proximal surface clean.
surface roughness, opacity of marginal ridge or
occlusal area, discolouration.
Figure 1.2 IOPA X-Ray Showing Radiolucent Carious lesion
2.2 Tactile Examination: Figure 1.4: Proper brushing technique
Includes determining roughness or softness of tooth

surface/discontinuity of enamel with a sharp explorer.
Discolouration of pits and fissures may be a universal
finding in normal healthy adult teeth-may be mistaken
for presence of caries.
Page 627
4.3 Antimicrobial Agents:
i) Use of APF gel 1.23%.
a) Antimicrobial agents like Chlorhexidine, Fluoride and
antibiotics available to help prevent caries. ii) Use of 2% Sodium Fluoride.
b) 0.12 – 0.2% Chlorhexidine mouth rinse prescribed for 5. Pit & fissure sealants:
home use at bedtime as a 30-second rinse.
 Sealants mechanically fill pits and fissures with an
4.4 Fluorides: acid resistant resin.
 Renders pits and fissures easier to clean by tooth
To reduce caries risk primarily achieved by systemic and
brushing and mastication.
topical fluoridation.
Use of Fluoride: KEY MESSAGE:
a) Systemic use: Systemic fluoridation can be achieved by  Avoid sticky and food with rich sugar content.
community water fluoridation (1ppm) in the areas of low  Brush the teeth twice a day with proper
fluoride content (below 1ppm).
brushing technique.
b) Topical use:
 Visit your doctor every six months for regular
Self-application: Daily use of fluoridated toothpastes and dental check up and get the treatment done at
mouthwashes.
early stages.
Professional application: application on tooth surfaces.
Bibliography
1. Robinson M, Heymann H, Swift E. Conservative: Stuedevant’s Art and science of operative dentistry. 5th
ed. Elsevier publication.
2. Dean J, Avery D, McDonald R. McDonald and Avery Dentistry for The Child and Adolescent. 9th ed.
Mosby Elsevier.
3. Peter S. Essentials of Preventive And Community Dentistry. 3rd ed. Oscar publication.
Further reading
1. Anusavice KJ. Management of dental caries as a chronic infectious disease. J Dent Education. 1998; 62:
791-802.
2. Brown LJ. Indicators for caries management from the patient history. J Dent Education. 1997; 61:855-860.
3. Emlson CG. Potential efficacy of chlorhexidine against mutans streptococci and human dental caries. J
Dental Research 1994. 73:682-691.
4. Charbeneau GT. Principles and Practice of Operative Dentistry. 3rd ed. Varghese Publishing House.

Page 628
2. DISEASES OF DENTAL PULP AND
PERIAPICAL TISSUES
Diseases of the dental pulp initiate dental pain of pulpal  Inspection generally discloses a deep cavity
origin, which can be due to pulpitis, apical periodontitis extending to the pulp or decay under filling.
and periapical abscess. The pulp may be already exposed.
1. Pulpitis is an inflammation  Radiograph may disclose an interproximal
cavity, or may suggest involvement or exposure
of pulp which may be acute of pulp, caries under filling.
or chronic.  Vitality Test.
1.1. Acute Reversible Pulpitis: - 1.2.3 Treatment:

Mild to moderate inflammatory conditions of pulp  Removal of inflamed pulp tissues with
caused by noxious stimuli in which pulp is capable of endodontic therapy.
returning to the uninflamed state following removal of  Cap. Amoxicillin 250/500mg 3 times a
the stimuli. day for 3 to 5 days.
 Tab. Diclofenac 50mg 1BD for 3 days.
1.1.1 Clinical features:
 Sharp momentary pain on exposure to sweet or 1.3. Chronic Pulpitis:
thermal stimuli (cold). 1.3.1 Clinical features:
 It does not occur spontaneously and does not  It occurs as the chronic type of pulpal disease
continue when the cause has been removed. from its onset.
 Reacts normally to percussion, palpation and  Dull pain is present which is more often
mobility and the periapical tissue is normal on intermittent and there is a delayed response in
radiograph. vitality testing.
1.1.2 Treatment: 1.3.2 Treatment:
 Removal of etiology and restoration of the  Endodontic treatment.
tooth.
 Cap. Amoxicillin 250/500 mg 3 times a day for
3 to 5 days.
1.4. Chronic Hyperplastic Pulpitis
 Tab. Diclofenac 50mg 1BD for 3 days. (Pulp Polyp):
It is a productive pulp inflammation due to an
extensive carious exposure of a young pulp.
1.2. Acute Irreversible Pulpitis: -
A persistent inflammatory condition of pulp
symptomatic or asymptomatic caused by a noxious
stimulus.

 Sharp pain usually caused by thermal
stimuli and can occur spontaneously.
 The pain persists for several minutes to hours,
lingering after removal of the thermal
stimulus.
 In early stages the pain is sharp shooting,
piercing while in later stages pain is more Figure 2.1: Chronic hyperplastic pulpitis
severe and is generally described as boring,
gnawing or throbbing and may be more
intense.
Page 629
There is pain on mastication and tooth is tender on
percussion.
Radiographic examination may show a thickened
periodontal ligament or a small area of rarefaction if a
pulpless tooth is involved and it may show normal
Figure 2.2: Chronic hyperplastic pulpitis periradicular structures if a vital pulp is present.
1.4.1 Clinical features: 2.1.3 Treatment:

 Occurs generally in children and young adults. If the inflammation is caused by occlusal trauma it should
 Involved teeth with large, open carious lesions. be relieved by selective grinding. If it is due to spread of
pulpal infection RCT is indicated.
1.4.2 Signs & Symptoms:
Cap. Amoxicillin 250/500 mg 3 times a day for 3 to
 Chronic hyperplastic pulpitis is symptomless, 5 days.
except during mastication, when pressure of the Tab. Metronidazole 200/400 mg 1BD for 3 days.
food bolus may cause discomfort. Tab. Diclofenac 50mg 1BD for 3 days.
 Pulp appears as a pinkish red globule of tissue
protruding, from the pulp chamber.
2.2 Acute Alveolar Abscess:
Acute alveolar abscess is a localized collection of
Radiograph shows large open cavity with direct pus in the alveolar bone at the apex of a tooth
access to the pulp chamber. following death of pulp with extension of the
1.4.4 Treatment: infection through the apical foramen into
periradicular tissue.
 Elimination of the polypoid tissue followed by
RCT, provided the tooth can be restored 2.2.1 Clinical features:
otherwise extraction is needed.  The patient has severe throbbing pain with
 Cap. Amoxicillin 250/500 mg 3 times a day for 3 swelling of the overlying soft tissue.
to 5 days.  Pus may exude through tiny openings.
2.2.2 Treatment:
2. Diseases of Periapical tissues:  Establishing drainage and completion of RCT
after subsidence of symptom is done.
 Cap. Amoxicillin 250/500 mg 3 times a day for 3
2.1 Apical Periodontitis: to 5 days.
Apical Periodontitis is a painful inflammation of the  Tab. Metronidazole 200/400 mg 1BD for 3 days.
periodontium as a result of trauma, irritation or infection  Tab. Diclofenac 50mg 1BD for 3 days.
around the root apex regardless of whether the pulp is
vital or non- vital.
Page 630
2.3 Chronic Apical Periodontitis: 2.5 Osteomyelitis:
(Periapical granuloma): Inflammation of bone and its marrow contents.
Localized mass of chronic granulation tissue formed 2.5.1 Acute Suppurative Osteomyelitis:
in response to infection.
It is a serious sequel of periapical infection that often
2.3.1 Clinical features: results in a diffuse spread of infection throughout
The involved tooth is non- vital and slightly tender to medullary space, with subsequent necrosis of variable
percussion. Patient may complaint about mild pain on amount of bone.
biting. The patient feels tooth is slightly elongated in 2.5.1.1. Clinical features:
its socket.  Severe pain, trismus and paraesthesia of lips in
case of mandibular involvement and manifests
2.3.2 Radiographic examination:
an elevation of temperature with regional
Periapical granuloma appears as a radiolucent area of lymphadenopathy.
variable size attached to root apex.  The teeth in the area of involvement are loose.
 Pus exudes from gingival margin.
2.3.3 Treatment:
 In the maxilla the disease is well localized to
 Root canal treatment with or without the area of initial infection and in mandible
subsequent apicoectomy. bone involvement is more diffuse &
 Cap. Amoxicillin 250/500mg 3 times a day widespread.
for 3 to 5 days.  Radiographically: Little evidence of its
 Tab. Metronidazole 200/400mg 1BD for 3 presence until the disease has developed for at
days. least one to two weeks. At this time diffuse lytic
 Tab. Diclofenac 50mg 1BD for 3 days. changes in the bone, radiolucent areas begin to
appear, ill-defined margins and have moth-eaten
2.4 Radicular Cyst: appearance.
It is slowly growing epithelial cyst at the apex of the 2.5.1.2. Treatment:
tooth. Radicular cyst presupposes physical, chemical
General principles of management include
or bacterial injury resulting in death of pulp.
 Debridement
 Drainage
The majority of cases are asymptomatic. The  Cap. Amoxicillin 250/500 mg 3 times a day
associated tooth is non-vital or shows deep carious for 3 to 5 days.
lesion or a restoration which is seldom painful or even  Tab. Metronidazole 200/400 mg 1BD for 3
sensitive to percussion. days.
If sequestrum is small, it gradually exfoliates through
Roentgenographic features: - Radiolucent area
the mucosa. If large, surgical removal may be
surrounded by radio-opaque border attached to root
necessary. Acute suppurative osteomyelitis may
apex.
proceed to development of periostitis, soft tissue
2.4.3 Treatment: - abscess or cellulitis.
Involved tooth is extracted and periapical tissue is
carefully curetted.
Page 631
2.5.2 Chronic Suppurative Osteomyelitis: 2.5.4.1 Clinical features:
 Occur at any age but is most common in
It may develop in inadequately treated acute
older person especially in edentulous areas.
osteomyelitis or may arise from dental infection
 Vague pain, unpleasant taste and mild
without preceding acute stage.
suppuration with the spontaneous formation
of fistula when acute exacerbation of dormant
chronic infections.
2.5.4.2 Investigation:
 Radiographic features: - Diffuse patchy,
sclerosis of bone often described as cotton
wool appearance. Radiopaque lesion may be
extensive and is sometimes bilateral. The
border between sclerosis and normal bone is
indistinct.
Figure 2.3: Chronic Suppurative Osteomyelitis 2.5.4.3 Treatment:
 Conservative treatment of acute episodes by
2.5.2.1. Clinical features: antibiotic administration. If the tooth is
Similar to acute suppurative osteomyelitis present in one of these sclerotic areas, then it
except all signs and symptoms are milder. The must be extracted.
suppuration may perforate the bone and overlying  Cap. Amoxicillin 250/500mg 3 times a day
skin or mucosa to form fistulous tract and empty on for 3 to 5 days.
surface.  Tab. Metronidazole 200/400mg 1BD for 3
2.5.3 Chronic Focal Sclerosing Osteomyelitis: days.
A reaction to mild bacterial infection entering the  Tab. Diclofenac 50mg 1BD for 3 days.
bone through a carious tooth in persons who have a 2.5.5 Chronic Osteomyelitis with
high degree of tissue resistance and tissue reactivity. Proliferative Periostitis:
2.5.3.1. Clinical features: There is focal gross thickening of periosteum with
peripheral reactive bone formation resulting from
 Most common in children and young adults. mild irritation or infection.
 Commonly involve mandibular first molar. 2.5.5.1 Clinical features:
 Mild pain associated with an infected pulp.  Occurs exclusively in the mandible, in
2.5.3.2. Investigation: children and young adults and most cases
 Radiographic features show well occur in the bicuspid and molar region.
circumscribed radiopaque mass of sclerotic  The patient complains of toothache or pain in
bone surrounding and extending below the the jaw and a bony hard swelling on outer
apex of carious tooth involving one or both surface of jaw.
roots. Intact lamina dura. Periodontal ligament 2.5.5.2 Radiographic examination:
space is widened.  Intra oral periapical X- ray will reveal a
2.5.3.2. Treatment: carious tooth.
 Extraction of carious tooth. The sclerotic bone  Occlusal roentgenogram shows a focal
constituting the osteomyelitis is not attached overgrowth of bone on the outer surface of
to the tooth and remains after the tooth is the cortex which may be described as
removed. Surgical removal of sclerotic lesion duplication of cortical layer of bone. This
is not indicated unless symptomatic. mass of bone is smooth and well calcified
 Cap. Amoxicillin 250/500mg 3 times a day and may itself show a thin but definite
for 3 to 5 days. cortical layer.
 Tab. Metronidazole 200/400mg 1BD for 3 2.5.5.3Treatment:
days.  Extraction of carious tooth.
 Tab. Diclofenac 50mg 1BD for 3 days.  Cap. Amoxicillin 250/500mg 3 times a day
for 3 to 5 days.
2.5.4 Chronic Diffuse Sclerosing  Tab. Metronidazole 200/400mg 1BD for
Osteomyelitis: 3days. Tab. Diclofenac 50mg 1BD for 3
It is a proliferative reaction of the bone days.
to low- grade infection. Portal of entry
for the infection is through diffuse
periodontal disease.
Page 632
Bibliography
1. Suresh Chandra B, Gopi Krishna V. Grossman's Endodontic Practice 12th ed. Publisher Wolters Kluwer
Health.
2. Ingle J, Bakland, Baumgartner. Endodontics. 6th ed. USA: PMPH.
3. Dean J, Avery D, McDonald R. McDonald and Avery Dentistry for the Child and Adolescent. 9th ed.
Mosby Elsevier.
4. Malik AN. Text book of Oral and Maxillofacial surgery. 2nd ed. Jaypee Brothers Publishers.
5. Rajendran A, Sivapathasundharam B, editors. Shafer's Textbook of Oral Pathology. 6 th ed. Elsevier Health
sciences.
Further reading
1. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and Maxillofacial Pathology. Saunders, an imprint
of Elsevier Inc.
2. Matthews DC, Sutherland S, Basrani B, Emergency management of acute apical abscesses in the
permanent dentition: a systemic review of the literature. J Can Dent Association. 2003; 69: 660, 661.
3. Marx RF. Chronic Osteomyelitis of the Jaws, Oral Maxillofacial Clinics. 1991; 3: 367-381.
4. Van Merkesteyn JR, Groot RH, Vander Akker HP. Treatment of Chronic suppurative osteomyelitis of the
mandible, Int J Oral Maxillofacial Surg. 1997; 26: 450-454.
5. Jacobsan HLJ, Baumgartner JC, Marshall JG. Proliferative periostitis of Garre: report of a case, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2002; 94: 111-114.

Page 633
3. PERIODONTAL DISEASES
Periodontium is the anatomical structure surrounding
tooth which involves gingival periodontal ligament,
2. Acute Gingival Infections:
cementum, alveolar bone.
2.1 Necrotizing Ulcerative Gingivitis:
It is microbial disease of gingiva characterized by death
and sloughing of gingival tissue.
2.1.1 Clinical Features:
 Sudden onset sometime with respiratory tract
infection.
Figure 3.1: Periodontal Diseases  Lesions are punched out crater like depressions
on crest of interdental papilla.
1. Gingivitis  Ulcers are covered with grey
Inflammation of gingiva is called gingivitis. pseudomembranous slough.
 Spontaneous gingival hemorrhage and also
bleeding on slightest provocation.
 Constant radiating, gnawing pain of gingiva.
 Metallic foul taste.
 Excessive amount of pasty salivary secretions.
 Local lymphadenopathy.
 In severe and acute cases high grade fever, loss
of appetite, generalized lassitude, insomnia,
constipation, headache, mental depression may
be seen.
Figure 3.2: Gingivitis  Necrotizing ulcerative gingivitis is caused by
fusiform bacilli and spirochetes.
1.1 Clinical features: 2.1.2 Treatment of Acute Necrotizing Ulcerative

1.1.1 Acute Gingivitis: Gingivitis (ANUG)
 Diffuse puffiness and softening of gingiva. With moist cotton and lignocaine jelly gently remove
 Redness of gingiva, presence of exudates. pseudo membrane.
 Plaque usually present and calculus is often  Antibiotic and Analgesic – Cap. Amoxicillin
seen. 500mg 8 hourly 10 days for patient sensitive to
 Sloughing with grayish debris adhering to Amoxicillin.
eroded surface.  Cap. Erythromycin 500mg x 8 hourly.
 Vesicle formation.  Tab. Diclofenac 50mg 1BD for five days
1.1.2 Chronic Gingivitis:  Rinsing with 3% H202 + equal quantity of
water 2-3 hourly and/or 0.12% Chlorohexidine
 Soggy puffiness that pits on pressure, marked
mouth wash BD.
softness and friability with fragmentation on
exploration with probe.  After 2 days if pseudo membrane is absent and
erythematous gingiva are present, evaluate for
 Firm, leathery consistency.
scaling if sensitivity permits.
1.2 Treatment:  After 5 days discontinue Hydrogen Peroxide
Scaling and polishing gargles but continue with Chlorhexidine
gargles.
 Vitamin B complex 1 OD for ten days.
2.2 Pericoronitis:
Inflammation of the gingiva in relation to the crown of
an incompletely erupted tooth is called Pericoronitis.
Figure 3.3: ANUG
Page 634
2.2.1 Clinical features: 3.1.2 Chronic inflammatory enlargement
3.1.2.1 Clinical Features
 Partially erupted or impacted mandibular third
 Ballooning of marginal gingiva and interdental
molar is common site of Pericoronitis.
papilla or both.
 Pericoronitis is exacerbated by trauma, or
 Progresses slowly and painlessly.
foreign body trapped under tissue flap.
 Appears like pedunculated mass on gingival.
 Trismus may or may not be present.
 Painful ulcerations may occur.
 Pericoronitis presents as a red swollen
 Exposed gingival surface appears red
sometimes suppurating lesion with tenderness,
edematous and shiny in mouth breathers.
and pain radiating towards ear, nose or floor of
mouth. 3.1.3 Treatment
 Fever and malaise may be present.  Scaling and root planning.
 Difficulty in swallowing may be present.  If the shrinkage of fibrotic tissue doesn’t occur,
 Many a times infection may spread to different then surgical therapy is the treatment of choice.
tissue spaces leading to tonsillar abscess
formation, cellulitis or Ludwig’s angina.
2.2.2 Treatment:
 Area should be anesthetized.
 Drainage is established by gently lifting the soft
tissue operculum.
 Area should be irrigated by normal saline to
remove debris. Figure 3.4: Drug Induced Gingival Enlargement
 Cap. Amoxycillin 250/500 mg 3 times a day for
3 to 5 days. 3.2 Drug Induced Gingival
 Advice warm saline gargles every 2 hours. Enlargement
 Once swelling subsides, partially erupted tooth 3.2.1 Clinical features
should be treated by excision of pericoronal  Painless bead like enlargement.
flap or by extractions.  May enlarge to cover crown portions.
 Enlargement is generalized.
3. Gingival Enlargement:  Enlargement more in anterior teeth.
 Recurs after surgical excision.
Increase in size of gingiva is a common feature called as
 Patient gives history of taking medicines like
gingival enlargement or gingival hyperplasia or gingival
anticonvulsants, immunosuppressant, and
hypertrophy.
calcium channel blockers.
3.1 Inflammatory Enlargements:
3.1.1 Acute Inflammatory enlargements: 3.2.2 Treatment
 Possibility of discontinuing the drug or
3.1.1.1 Clinical Features: changing the drug should be assessed by
consulting the physician.
 Gingival abscess, localized, painful, sudden
onset, rapidly expanding.  Plaque control helps to limit the enlargement
and subsequent periodontal diseases.
 Usually on marginal gingival or interdental
papilla.  If required by assessing the periodontal status
go for periodontal surgical procedures like
 Appears as a red swelling with a smooth shiny
gingivectomy or flap as indicated.
surface.
 Purulent exudates may be present.
 Tooth sensitive to percussion.
Page 635
3.3 Gingival Enlargement  Radiograph shows periodontal angular bone loss
and furcation radiolucency.
Associated with Systemic
Diseases: 5.2 Treatment:
 Drainage through pocket retraction or incision.
3.3.1 Pregnancy Gingivitis  Scaling and root planning.
 Gingival enlargement may be marginal or  Required periodontal surgery.
generalized, single or multiple tumor like  Systemic antibiotics –
masses.  Cap. Amoxicillin 250/500 mg 3 times a day for
 It occurs due to increased progesterone and 3 to 5 days.
estrogen levels in pregnancy especially in third  Tab. Metronidazole 200/400 mg 1BD for 3
trimester. days.
3.3.1.1 Treatment of Pregnancy Gingivitis:
 Tooth removal if required.
Removal of local irritants in early stages of
pregnancy and emphasis should be given on
preventing gingival diseases. 6. Periodontitis:
3.3.2 Gingival Enlargement in Vitamin C 6.1 Chronic Periodontitis:
Deficiency (SCURVY): An infectious disease resulting in inflammation
within the supporting tissues of the teeth, leading to
 Acute vitamin C deficiency itself does not cause
inflammation. But it does cause hemorrhage, progressive attachment loss and bone loss.
collagen degeneration, oedema of gingival
tissue. 6.1.1 Clinical Features:
 These changes are in response to plaque.  Supragingival and subgingival accumulation
 Regular intake of vitamin C and maintenance of with calculus formation.
oral hygiene prevents scurvy.  Gingival inflammation and pocket formation.
 Loss of periodontal attachment and alveolar
4. Pyogenic Granuloma: bone.
 Occasional pus discharge and poor oral hygiene.
4.1 Clinical features:  Moderate swelling of gingiva with pale red to
 It is a tumor like gingival swelling that is magenta colors.
considered as exaggerated conditioned response  Blunt or rolled gingival margins.
to minor trauma.  Bleeding on probing may be present.
 It presents as a pedunculated spherical tumor  Sometimes tooth may be mobile.
like mass.  It may be localized or generalized.
 It is red or purple.
 It can be firm or friable. Sometimes surface may
be ulcerated and purulent.
6.2 Necrotizing Ulcerative
Periodontitis:
4.2 Treatment:
Excision of mass and removal of local irritating Necrotizing ulcerative periodontitis is an extension of
factors. necrotizing ulcerative gingivitis. Historically it is
described as Vincent’s infection or trench mouth.
5. Periodontal Abscess:
5.1 Clinical features: 6.2.1 Clinical features
 Mild to severe discomfort.
 Localized red, ovoid swelling.  Areas of ulceration and necrosis of interdental
 Periodontal pocket, exudation. papilla with yellowish white soft layer of
 Mobility. pseudo membrane is present.
 Tooth elevation in socket.  Lesions are painful.
 Tenderness to percussion or biting  Bleed without provocation.
 Elevated temperature, regional  Punched out lesions present.
lymphadenopathy.
Page 636
 Associated with malodor, localized  Quantity of amount of plaque seems
lymphadenopathy, fever and malaise. inconsistent with the amount of periodontal
 Destructive progression of disease includes destruction.
destruction of periodontal attachment and bone  Deep pockets and suppuration.
loss.  Systemic manifestation may be seen such as
 Deep interdental osseous craters are very typical weight loss, mental depression and general
with necrotizing ulcerative periodontitis. malaise.
 Tooth mobility with untimely loss of tooth 6.3.3 Treatment:
is a common feature.  Conventional periodontal therapies for
aggressive periodontitis consist of patient
6.3Aggressive Periodontitis education, oral hygiene improvement, scaling
and root planing and recall maintenance.
6.3.1 Localized Aggressive Periodontitis:  Resective periodontal surgery can be effective
(Juvenile Periodontitis): to reduce pocket depth.
 Anti-microbial therapy consists of Cap
 Usually first molar or incisor is affected Tetracycline (500 mg 1BD for 14 days every 8
with interproximal bone loss. weeks).
 There is lack of inflammation despite loss of
deep periodontal pocket. 7. Oral Malodor (HALITOSIS)
 Rate of bone loss is four fold as compared to
chronic periodontitis. Breath odor is defined as subjective perception after
 Mobility of teeth increases fast. smelling someone’s breath. If unpleasant, the term
 Sensitivity to root surfaces. breath mal odor, halitosis or bad breath can be
 Deep dull, radiating pain during mastication. applied.
 Usually disease starts around beginning of
puberty. 7.1 Etiological factors:
 Radiological vertical bone loss is seen.  Deep caries with infection, candidial
infections, Pericoronitis, periodontitis, oral
ulcerations, xerostomia, tongue and tongue
coating especially in fissured tongue and hairy
tongue.
 Infections like pharyngitis, sinusitis, and chronic
purulent tonsillitis, chronic bronchitis,
bronchiectasis, bronchial carcinoma, gastric
hernia, regurgitation, esophagitis, and intestinal
gas production, chronic glomerular nephritis,
Figure 3.5: Generalized Aggressive diabetes.
Periodontitis  Trimethylaminuria hereditary metabolic
disorder causes typical fishy odor.
6.3.2 Generalized Aggressive Periodontitis
 Affects individuals below the age of 30. 7.2 Treatment:

The treatment of malodor is cause related.
 Gives very poor response to antibiotics.
 Mechanical reduction of plaque and
 Characterized by generalized interproximal
microorganisms by cleaning dorsum of the
attachment loss affecting at least 3 permanent
tongue by tongue scrapper and interdental
teeth other than first molar and incisor.
spaces by interdental brush and proper cleaning
 Periods of advanced destruction is followed by
of oral cavity. If required professional
stages of quiescence of variable length (weeks
periodontal treatment is to be done
to months to years).
Page 637
 Reduction of oral microbial load by mouth
rinsing with Chlorhexidine 0.12% mouthwash
twice a day for 15 days.
 Masking the malodor with rinses and mouth
sprays.
KEY MESSAGE
 Maintenance of proper oral hygiene by using correct teeth brushing technique and rinsing the
mouth to avoid food lodgement.
 Local etiological factors like accumulation of dental plaque, calculus must be eliminated in the
dental clinic.
 Rule out and manage systemic disorders leading to periodontal diseases.
Bibliography
1. Newman MG, Takei HH, Klokkevold PR. Carranza's Clinical Periodontology. 11th ed. Elsevier Health
Sciences.
2. Rajendran A, Sivapathasundharam B, editors. Shafer's Textbook of Oral Pathology. 6th ed. Elsevier Health
sciences.
Mosby Elsevier.
Further reading
1. Genco RJ, Goldman HM, Cohan DW. Contemporary Periodontics. the C. V. Mosby Company.
2. Suzuki JB. Diagnosis and classification of the periodontal diseases. Dental clinics North America, 1998;
32: 195-216.
3. Horning GM, Cohen ME. Necrotizing ulcerative gingivitis, periodontitis and stomatitis. Clinical factors, J
Periodontal 1995; 66: 990-998.
4. American Academy of Periodontology Informational paper, Drug associated gingival enlargement, J
Periodontology. 2004; 75:1424-1431.
5. Schatzle M, Loe H, Lang N P. The Clinical course of Chronic Periodontitis IV Gingival inflammation as a
risk factor in tooth mortality, J Clinical Periodontalogy. 2004; 31: 1122-1127.
6. Suzuki, Diagnosis and Classification of the Periodontal diseases Dental clinics of North America. 1998
Apr; 32(2).
7. Botha PJ. Drug induced gingival hyperplasia and its management- a literature review, J Dent Assoc. S.
Africa. 1997; 52: 659-664.
8. Greenstein G. Periodontal response to mechanical nonsurgical therapy: a review, J Periodontal. 1992; 63:
118-130.
9. Tatkis DN, Kumar PS: Etiology and Pathogenesis of Periodontal Diseases. Dental Clinics North America.
2005; 49: 491-561.
10. Donly KJ, Ashkenazi M. Juvenile Periodontitis: a review of pathogenesis, diagnosis and treatment, J Clin
Pediatric Dent. 1992; 16:73-78.
11. Guerrero A, Griffiths GS, Nibali L. Adjunctive benefits of systemic amoxicillin and metronidazole in
nonsurgical treatment of generalized aggressive periodontitis: a randomized placebo – controlled clinical
trial. J Clin Periodontology. 2005; 32:1096-1107.
12. Botha PJ. Drug induced gingival hyperplasia and its management- a literature review, J Dent Assoc. S.
Africa. 1997; 52: 659-664.

Page 638
4. SPREAD OF ORAL INFECTION
Many of the fascial spaces of head and neck  Severe trismus.
communicate either directly or indirectly with each  Extreme radiating pain.
other, thus infection in the oral cavity spread from one  No evident extraoral swelling.
region to another through these spaces.  Dysphagia is present.
 The spaces that get first infected are called primary  Difficulty in breathing
spaces.  Midline of palate is displaced to unaffected side
 Spaces, which get infected later, are called as and uvula is swollen.
secondary spaces.  Medial displacement of the lateral wall of the
pharynx.
The fascial spaces in head and neck are the potential  Redness and edema of the area around the third
spaces between the various layers of the fascia normally molar.
filled with loose connective tissue and bounded by
anatomical barrier usually bone, muscle and fascial 1.4.2 Differential diagnosis:
layer.
The Pterygomandibular space abscess must be
distinguished from peritonsillar abscess. In peritonsillar
1. Important space infections abscess there is no dental involvement and less trismus.
1.1 Canine Space: -
 Swelling of cheek and upper lip. 1.5 Submandibular Space:
 Obliteration of nasolabial fold. 1.5.1 Clinical features:
 Drooping of angle of the mouth.
 Edema of lower eyelid it indicates pointing of  Firm swelling in submandibular region, below the
abscess below medial corner. inferior border of mandible.
 Redness of overlying skin, dysphagia, moderate
1.2 Buccal Space Abscess: - trismus.
 Space infection is dome shaped and periorbital
edema develops due to impaired venous and 1.6 Submental Space
lymphatic drainage.
 Swelling begins at the lower border of the 1.6.1 Clinical features:
mandible and extends upwards to the level of the
 Distinct, firm swelling in midline beneath the chin.
zygomatic arch.
 Dysphagia.
 Trismus is not usually present.
1.7 Sub lingual Space
1.3 Submasseteric Space: -
 Swelling in the floor of the mouth.
 Swelling over the masseter muscle i.e. the swelling  Dyspnea.
is seen extending from lower border of the  Dysphagia.
mandible to zygomatic arch and anteriorly to
anterior border of the masseter and posteriorly to 1.8 Treatment:
posterior border of the mandible.
All space infections need antibiotics & analgesics,
 Pain over the region.
incision & drainage depending upon severity.
 Severe trismus is present.
 Tenderness over the angle of the mandible  Cap. amoxicillin 250/500mg 3 times a day for 3 to
 Pyrexia and malaise. 5 days.
 Tab. Metronidazole 200/400mg BD for 3 days.
1.4 Pterygomandibular Space:  Tab. Diclofenac 50mg 1BD for 3 days.
Page 639
 Swelling is firm painful and diffuse.
2. Cellulitis  Trismus, dysphagia.
Cellulitis is a diffuse inflammation of soft tissues,  Difficulty in breathing.
tends to spread through tissue spaces and along  High fever, rapid pulse and fast respiration
fascial planes.  Tongue may be raised against palate.
Cellulitis of face and neck most commonly results  As the disease continues, the swelling
from dental infection either as sequel of apical involves the neck, and edema of the glottis
abscess or osteomyelitis or following periodontal may occur. This carries the serious risk of
infection or pericoronitis. death by acute respiratory failure or
septicemia.
 Painful swelling of the soft tissues involved
that are firm and brawny.
 Patient is moderately ill and has raised
temperature and leukocytosis.
 If the facial cellulitis persists the infection
frequently tends to become localized and a
facial abscess may form. When this happens
the suppurative material present seeks to
point or discharge upon a free surface. If
Figure 4.1: Ludwigs Angina
early treatment is instituted a resolution
usually occurs without drainage through a
break in the skin.
3.2 Antibiotic therapy:
2.2 Treatment: Usually IV antibiotics with proper dosage and frequency
Administration of antibiotics and removal of the are necessary according to age and severity.
cause of infection.
 Injection Ampicillin 250/500mg 6 hourly for3 days
 Cap. Amoxicillin + Clavulanic acid 375/625 Injection Gentamycin 40/80mg BD for 3 days
mg 1BD for 5 days  Injection Metronidazole 50 mg (100ml bottle IV)
 Tab. Diclofenac 50mg 1BD for 5 days. TID for 3 days
 Injection Diclofenac sodium 3CC for 3 days
To avoid the further spread of infection or
 Injection Ranitidine 2ml BD for 3 days
solidification of abscess the patient should be
 Magnesium Sulphate dressing till the swelling
advised not to massage the affected area with any
subsides
medication.
 I.V fluids to maintain the electrolyte balance.
3. Ludwig's Angina:  Refer to higher center for further management
immediately.
Massive, firm, brawny cellulitis, beginning usually in
submaxillary space and secondarily involving the KEY MESSAGE:
sublingual and submental space bilaterally.
 Avoid hot fomentation or application of any
3.1 Clinical feature: counter irritants locally.
 A rapidly developing board like swelling of  Perform incision and drainage of abscess at
the floor of mouth and subsequent elevation earliest to avoid further spread of infection
of the tongue.
Bibliography
sciences.
Page 640
Further reading
1. Baqain ZH, Newman L, Hyde N. How serious are oral infections? J Laryngeal Otol. 2004; 118:561-565.
2. Busch RF, Shah D. Ludwigs angina: improved treatment, Otolaryngol Head Neck Surg, 1997; 117:172-175.
3. Hutchinson IL, James DR. New treatment for Ludwigs angina. Br. J Oral Maxillofacial surg. 1987; 27:83–
84.
4. Pynn BR, Sands T, Pharoah MJ. Odontogenic infections: Part I. Anatony & Radiology, oral health 1995; 85
:7–21.
5. Sands T, Pynn BT, Katsi KN. Odontogenic infection: Part 2. Microbiology, antibiotics and management.
Oral health. 1995; 85:11-28.

Page 641
5. ORAL MUCOSAL LESIONS
1. Chronic Cheek or Lip Biting 2.1.1 Symptoms:

Burning sensation and rapid onset of bad taste.
Superficial lesions produced by frequent and repeated
rubbing, sucking or chewing movements that abrade 2.1.2. Clinical features-
the surface of a wide area of lip, buccal mucosa, Common sites are roof of the mouth, retromolar area and
lateral border of tongue without producing discrete mucobuccal fold.
ulceration. Clinically pearly white or bluish white plaques are
present on oral mucosa. Patches are loosely adherent to
1.1 Clinical feature: oral mucosa. Mucosa adjacent to it appears red and
 It can occur at any age, common sites are buccal moderately swollen. White patches are easily wiped out
mucosa at the level of occlusion, lip and lateral with wet gauze leaving a bright red raw bleeding
border of tongue. surface. In some cases, it may present as a brightly
erythematous mucosa with only scattered white patches.
 Clinically it appears as a linear or diffuse lesion
irregular opaque white. In some cases, lacerated 2.1.3 Treatment:
and reddened area usually with patch of partly 2.1.3.1 Topical treatment
detached surface epithelium.  Clotrimazole: One oral Troche (10 mg tablet)
 It is rough on palpation as area becomes dissolves in the mouth 5 times daily.
thickened and scaled.  Nystatin oral pastille, 1 or 2 pastilles dissolves
slowly in the mouth 5 times a day.
1.2 Treatment:  Clotrimazole 1 % mouth paint topically 1 to 2
Recommendation to stop the habit, smoothening of times/day till lesion subsides.
sharp edges of teeth. Acrylic shields can be fabricated  Nystatin suspension 100,000 units (1 ml of
to cover the facial surface of teeth and there by suspension held in the mouth before swallowing).
restricting access to buccal and labial mucosa. 2.1.3.2 Systemic treatment
 Nystatin -250 mg TID for 2 weeks.
 Supplemental therapy by Vit B12. Tab Vit B
Complex 1OD for 10 days.
2.2 Denture Stomatitis: -
Denture stomatitis is a common form of oral candidiasis
that manifests as a diffuse inflammation of the denture
bearing areas and often associated with angular cheilitis.
Traumatic Lesion involving buccal mucosa and 2.2.1 Treatment:
lateral border of tongue Troches containing Clotrimazole and Nystatin 4-5 times
Figure 5.1 Figure 5.2 should be applied on the denture after meals. Antifungal
therapy and cessation of denture wearing till elimination
of mucosal inflammation. Rinsing the denture and
2. Oral Candidiasis: applying antifungal cream before inserting the denture.
Candidiasis is the disease caused by infection with 2.3 Angular Cheilitis:
yeast like fungus Candida albicans. It can occur either Angular cheilitis is the term used for an infection
solely confined to the oral mucosa or as a part of any involving the lip commissures. The majority of cases is
of the several mucocutaneous candidiasis syndromes. candida associated and respond promptly to antifungal
therapy. Other possible etiologic cofactors include
2.1 Oral Thrushes or reduced vertical dimension, nutritional deficiency (Iron
Pseudomembranous Oral deficiency anemia and Vitamin-B or Folic acid
Candidiasis deficiency) and rarely Diabetes, neutropenia and AIDS.
Candidiasis is the disease caused by infection with Treatment includes correction of primary cause.
yeast like fungus Candida albicans.
Page 642
3. Ulcerative lesions of oral 3.1.2 Treatment: -
Medication prescribe treatment should relate to the
cavity severity of the disease.
Ulcerative lesions are a group of common oral mucosal i. Anaesthetic cream - topical protective emollient
lesions. The most common causes of these lesions are base in mild cases with two or three small lesions.
mechanical and reactive factors, infectious diseases and Pain relief can be obtained with use of topical
neoplasms as well as autoimmune and hematological anaesthetic agent.
disorders. The main clinical feature in all these ii. Topical Corticosteroid - Triamcinolone Acetonide
conditions is an ulcer. Ulcer consists of margins, edges, 3 to 4 times daily. Nutritional supplements with
floor and base. Site, size, shape of the ulcer should be Tab. B Complex 1 BD for 10 days.
examined. iii. Maintenance of oral hygiene: - Chlorhexidine
0.12 % mouth wash twice a day for 10 days to
3.1. Recurrent Aphthous Stomatitis maintain oral hygiene.
(RAS)
RAS is a disorder characterized by recurring ulcers
confined to the oral mucosa in patients with no other
signs of disease. Precipitating factors are trauma,
endocrine conditions, stress, allergy, immunological
abnormalities and nutritional deficiency.
Herpetic Gingivo stomatitis

Figure 5.4 Figure 5.5
4. Viral Infection
4.1 Herpetic Gingivo-stomatitis:
Herpes simplex, an acute viral infectious disease caused
by Herpes simplex virus.
Figure-5.3: Aphthous Ulcer
3.1.1 Clinical features: The disease occurring in children is frequently primary
Sites: Occurs most commonly on buccal & labial attack and is characterized by development of fever,
mucosa, buccal & lingual sulci, tongue and soft palate. It irritability, headache, pain upon swallowing, regional
begins with prodromal stage of tingling, burning or lymphadenopathy. Within few days mouth becomes
itching for 1 to 2 days before the ulcer occur. Lesions painful and the gingiva become intensely inflamed
are round to oval in shape, symmetric, single or which appear erythematous and edematous. The lips,
multiple. Superficial ulcers covered by grey membrane. tongue, buccal mucosa, palate may be involved. Shortly
It is surrounded by localized area of erythema. yellow fluid filled vesicles develops. These rupture and
a) Minor aphthae: Minor aphthae are less than 1 cm in form shallow, ragged extremely painful ulcers covered
diameter and heal completely in 7 to 10 days by an erythematous halo. They heal spontaneously with
b) Major aphthae: Size of the lesion is larger than 1 cm 7 to 14 days and leave no scar.
and may reach up to 5 cm in diameter. They interfere
with speech and eating. The lesions heal slowly and 4.2 Recurrent or Secondary Herpetic
leave scars. Labialis and Stomatitis:
c) Herpetiform ulcers: Multiple small ulcers often upto
100 in number. It is found on any intra oral mucosal It is usually seen in adult patients and manifests itself
surface. It begins as small pinhead size erosion that clinically as an attenuated form of primary disease. The
gradually enlarges and coalesces. Lesions are more recurrent form of disease is often associated with
painful. Patient gets relief immediately with 2% trauma, fatigue, menstruation, pregnancy, upper
Tetracycline mouth wash. respiratory tract infection, emotional upset etc.
Page 643
4.2.1 Clinical feature: 4.2.2 Treatment:
Recurrent herpes simplex infection may occur at widely i. Acyclovir: Acyclovir cream for lips to be
varying intervals, from nearly every month in some applied 4 hourly for 5 days.
patients to only once a year or even less in others. Tab Acyclovir 200 mg 5times /day for 3 to 5
Lesion may either at the site of primary inoculation or in days.
adjacent area supplied by the involved ganglion. In may ii. Chlorhexidine 0.12% mouthwash twice a day
develop on lips (recurrent herpes labialis) or intra-orally. for 10 days
The lesions are preceded by burning or tingling iii. Avoid stress.
sensation and a feeling of tautness, swelling or slight
soreness at the location in which vesicle are small 1mm
or less in diameter, tend to occur in cluster and coalesce
to form large ulcer. These gray or gray-white vesicles
rupture quickly leaving a small red erythematous halo.
Bibliography
sciences.
2. Burket LW, Greenberg MS, Glick M, Ship JA. Burket's Oral Medicine. 11 th ed. USA: PMPH.
Further reading
1. Akintoye SO, Greenberg MS. Recurrent aphthous stomatitis, Dental clinics of North America. 49:31-47.
2. Amir J. Clinical aspects and antiviral therapy in primary herpetic gingivostomatitis. Paediatric drugs. 2001;
3: 593-597.
3. Raborn GW, Grace MGA. Recurrent herpes simplex labialis: selected therapeutic options. J Can Dent
Assoc. 2003; 69: 498-503.
4. Stopper ET, Greenberg MS. Update on herpes virus infections, Dental clinics of North America. 2003;
47:517-532.
5. Akpan A, Morgan R. Oral Candidiasis. Postgrad Med J. 2002; 78:455-459.
6. Fotos PG, Vincent SD, Hellstein JW. Oral candidiasis: clinical, historical and therapeutic features of 100
cases. Oral Surg Oral Med Oral Pathol. 1992; 74:41- 49.
7. Scully C, Gorsky M, Lozada-NurF. The diagnosis and management of recurrent aphthous stomatitis. J Am
Dent Assoc. 2003; 134:200-207.

Page 644
6. PREMALIGNANT AND MALIGNANT
LESIONS
1. Oral Leukoplakia: - 1.6 Treatment:
It is a whitish patch or plaque that cannot be  Patient should be asked to cease tobacco related
characterized clinically or pathologically as any habits immediately.
other diseases and which is not associated with  Removal of chronic irritant like sharp, broken
any other physical or chemical causative agent teeth dissimilar metal restorations and other
except the use of tobacco. predisposing factors like syphilis, alcohol, etc
1.1 Homogenous Leukoplakia: should be controlled and eliminated.
It is also called as leukoplakia simplex; uniform 1.6.1 Conservative treatment: -
raised white plaque formation, varying in size,  Vitamin A: It is given orally, parentally or
with regular edges. topically. Therapeutic dose -75000-300000. IU
for 3months.
1.2 Nodular or speckled  Antioxidant therapy: -β-Carotene
leukoplakia: supplementation can be beneficial for treatment
Also called as leukoplakia erosiva. It is a mixed of leukoplakia.
red white lesion in which small keratotic nodules  Vitamin B: complex: It is given as supplement
are scattered over an atrophic patch of oral in cases of commissural and lingual lesions.
mucosa. Nodules may be pinhead sized or even 1.6.2 Surgical management: -
larger. It has got a high malignant potential. Conventional surgery, Cryo surgery, Fulguration
(electro cautery and electro surgery), Laser treatment.
Biopsy may be carried out if there is no change in
leukoplakia after cessation of stimulus and may require
conservative or surgical treatment.
2. Erythroplakia:
Erythroplakia is bright red velvety plaque or patch
Figure 6.1: Oral leukoplakia which cannot be characterized clinically or
pathologically as being due to any other condition.
1.3 Ulcerated Leukoplakia: “Erythroplakia” is premalignant lesion with frequency
less than leukoplakia but more malignant potential.
It is characterized by red area, which at times
exhibit yellowish area of fibrin giving the 2.1 Clinical features:
appearance of ulceration white patches are present
at the periphery of the lesions. Erythroplakia occurs predominantly in older men, in the
sixth and seventh decades of life. Erythroplakia is more
commonly seen on the floor of the mouth, the ventral
1.4 Verrucous Leukoplakia: tongue, soft palate and tonsillar fauces. Although the
It is also called as ‘leukoplakia verrucosa’. It is etiology is uncertain, most cases are associated with
characterized by verrucous proliferation above the heavy smoking. Erythroplakia is asymptomatic.
mucosal surface. These lesions demonstrate sharp
and blunt projection.
2.2 Diagnosis:
Red velvety patch with no sign of infection and
1.5 Erythroleukoplakia: inflammation.
In some lesions of leukoplakia red component is 2.3 Treatment:

present. This intermixed lesion is called as
erythroleukoplakia. Removal of cause: elimination of suspected irritant and
observation for one to two weeks. Prompt biopsy if
lesions persist. If biopsy shows dysplasia or carcinoma
total excision is indicated.
Page 645
3. Oral Submucous Fibrosis patients who discontinue the habit.
(OSMF):
Etiological factors are chilly and spicy food, betel nut,
3.2.2 Medicinal therapy
Administration of Vitamin B complex and
tobacco & lime, nutritional deficiency etc.
antioxidants as supportive therapy.
3.1 Clinical features:  Vitamin rich diet along with iron preparation is
helpful to some extent.
 It affects both sexes, majority of patients are  B-Complex preparation – Intramuscular
between 20 to 40 years of age. injection starts with small doses and continuing
 The most frequent location of OSMF is buccal with larger doses (2ml ampule daily). The
mucosa and retromolar area. It also commonly course of 5 injections is repeated after 7days.
involves palate, palatal fauces, uvula, tongue and  Steroids –
labial mucosa. Local – Injection Hydrocortisone 1.5 ml (25
mg/ml) locally in the area of fibrosis twice a
week for four weeks or more as per conditions
Systemic – A therapy with Hydrocortisone
25mg tablet in doses of 100mg per day for 7
days is useful in relieving burning sensation
without untoward effects.
Placental extract – 2 ml biweekly or weekly for
three to four weeks locally injected around
Figure 6.3: Oral submucous fibrosis fibrous bands.
 Sometimes floor of mouth and gingival.
 The onset of condition is insidious and is often of 2
3.2.3 Surgical treatment like Conventional
to 5 years of duration. surgery, Laser, Cryosurgery
 Initial symptom commonly seen as burning 3.2.4 Oral Physiotherapy –
sensation of oral mucosa aggravated by spicy food This includes mouth opening and ballooning of
followed by either hyper salivation or dryness of mouth.
mouth. Vesiculation, ulceration, recurrent 3.2.5 Diathermy
stomatitis. 4. Oral Lichen Planus:
 Late symptoms are trismus, difficulty in tongue
protrusion, swallowing. It is a chronic immunologic inflammatory
 The most common and earliest sign is blanching of mucocutaneous disorder that varies in appearance from
mucosa. keratotic (reticular or plaque like) to erythematous and
 As disease progresses the mucosa becomes stiff ulcerative lichen planus.
and vertical fibrous band appears. These bands can
be palpable easily.
 The mobility of soft palate is restricted. Uvula
when involved is shrunken.
 Tongue becomes smooth and its mobility is
limited.
3.2 Treatment:
The treatment of patients with OSMF depends on the
Figure 6.4 Figure 6.5
degree of clinical involvement.
Oral Lichen Planus
3.2.1 Restriction of habit/behavioural therapy – 4.1 Clinical features:
The preventive measure should be in the form of It may occur in adulthood with age range for male
stoppage of habit, through health education. 35- 44 years and for female 45-54 years. It has
Affected patients should be explained about the more predilections for females.
disease and its malignant potential. Improvement 4.1.1 Sites: Common are buccal mucosa and to lesser
in clinical features like- gradual increase in inter- extent tongue, lips, gingiva, floor of mouth and palate.
incisal opening has been observed in most of
Page 646
4.1.2 Symptoms: Patients may report with burning 6.1 Clinical features: -
sensation of oral mucosa. 6.1.1 Benign Tumors: -
 Encapsulated tumor
4.1.3 Clinical features: Oral lesion is characterized  Base of tumor is of two types sessile and
by radiating white and gray velvety thread like papules pedunculated.
in a linear, annular or retiform arrangement forming
 Not involving the adjacent tissue.
typical lacy, reticular patterns, rings and streaks over
 Painless and slowly growing.
the buccal mucosa to a lesser extent on lip, tongue and
palate. Tiny white elevated dots are present at the
intersection of white lines called as Wickham’s straie. 6.1.2 Malignant Tumors: -
Types are reticular, papular, plaque, atrophic, bullous,  Ulcero-proliferative lesion
hypertrophic, annular and erosive.  Invading into adjacent structures
 Pain, paraesthesia
 Trismus
4.2 Treatment:
 Bony erosion
 Small and moderately sized either erosive or
 Mobility of teeth
ulcerative painful lesions can be treated with
Triamcinolone Acetonide cream base. Systemic  Not encapsulated
steroid Tab. Prednisolone (5 mg tab.) in tapering  Palpable Lymph nodes
doses of 30 mg per day for the first of the three  Pathological Fracture of the bone
weeks, 15 mg per day for 2nd week and 5 mg per
day for 3rd and final week. 6.1.3 Investigation:
 Symptomatic treatment with topical analgesic, Lateral oblique X-ray, OPG.
topical anesthetic and antihistaminic rinse.
 Psychotherapy 6.2 Common Cancers
6.2.1 Squamous Cell Carcinoma
5. Cyst of Jaws: A malignant epithelial neoplasm exhibiting squamous
differentiation as characterized by formation of keratin
It may be epithelial or non-epithelial. Epithelial cyst may
be odontogenic or non-odontogenic. Clinically and/or presence of intercellular bridges. The most
presenting as smooth, hard, painless prominence. important task is to establish an early diagnosis at the
Dentigerous cysts are mainly associated with impacted first stages of the disease. Risk factors include use of
molars and canines. Odontogenic keratocyst are seen in tobacco in its various forms, alcohol, ultraviolet light,
the lower third molar area extending into ramus. chronic irritation to oral mucosa, human papilloma virus
Radiographically cyst appears as well defined round or infection.
oval areas of radiolucency circumscribed by a sharp
radiopaque margin.
5.1 Treatment:
1. Marsupialization.
2. Enucleation of cyst.
6. Tumors:
Presenting as intra oral swelling may be odontogenic or
non-odontogenic variety, may be central or peripheral, Figure-6.6: Carcinoma of buccal mucosa
epithelial or connective tissue origin. The most common
tumor occurring in oral cavity is squamous cell 6.2.1 Clinical features: -
carcinoma. Tobacco, alcohol, smoking are the 6.2.1.1 Symptoms: -
predisposing factors. The patient may present with a  Ulcerative lesion in the oral cavity that does not
swelling, ulcero-proliferative growth with involvement heal.
of lymph nodes. Pain may accompany if it involves the  A persistent red or white patch
adjacent structures or superadded with infections.  Loosening of the teeth or pain around the teeth or
Radiographically it may show bone erosion. jaw.
 Voice changes.
Page 647
6.2.1.2 Site: Tongue, floor of mouth, lower alveolus, 6.2.5 Treatment:
buccal mucosa, upper alveolar / hard palate, Treatment includes surgical intervention, radiation
retromolar area, lip, floor of mouth. therapy and chemotherapy.
6.2.1.3 Signs: Clinically almost all oral cancers, except
those in earliest stages have two characterized
features in the form of ulceration and indurated
7. Tobacco Cessation Centers
margin. (TCC):
6.2.2 Diagnosis:
History and detail clinical examination, lymph Setting up TCC facilities at district hospital level. At the
node examination. district hospital Tobacco cessation centers are combined
It is important for early detection to decrease with dental units.
mortality rate.
6.2.3 Prevention: - KEY MESSAGE:
 Oral cancers can be prevented by /sensible
attitude towards maintenance of oral care and Any discolouration or grayish white patch in the oral
regular checkups. cavity must be properly evaluated and managed at
 Proper education regarding the adverse effect of early stage considering possibility of oral
the dreaded habits. malignancies. Cessation of tobacco consumption and
 Successful persuasion to quit the bad habits
self-examination by patients should be promoted.
(smoking, alcohol consumption, gutkha).
 The presence of persistent grayish white patches
developing in people who smoke or chew tobacco
needs to be investigated.
 Maintenance of good oral hygiene.
 Any faulty restoration or a sharp tooth needs to
be corrected.
Bibliography
1. Lumerman H, Freedman P, Kerpel S. Oral Epithelial dysplasia and the development of invasive squamous
cell carcinoma. Oral Surgery Oral Medicine Oral Pathology Oral Radiology Endodontics. 1995; 79: 321-
329.
2. Hazarey VK, Erlewad DM, Mundhe KA. Oral submucous fibrosis: Study of 1000 cases from central India,
J oral Pathol Med. 2007; 36:12-17.
3. Massano J, Regateiro FS, Januario G. Oral squamous cell carcinoma: review of prognostic and predictive
factors, Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006; 102: 67-76.
4. Burket LW, Greenberg MS, Glick M, Ship JA. Burket's Oral Medicine. 11 TH ed. USA: PMPH.
sciences.
Further reading
1. Reichart PA, Philipsen HP. Oral Erythroplakia – a review, Oral Oncology. 2005; 41: 551 -61.
2. Van der Wal I, Schepman KP, Van der Meij EH. Oral Leukoplakia: a clinicopathological review oral
oncology. 1997; 33: 291-301.
3. Lodi G, Scully C, Carrozzo M. Current controversies in oral lichen Planus: report of an international
consensus meeting. Part 2 clinical management and malignant transformation. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2005; 100: 164-78.
4. Kalmar JR. Advances in the detection and diagnosis of oral precancerous and cancerous lesions Oral and
maxillofacial surgery clinics of North America. 2006 Nov; 18 (4).
5. Alaxander RE, Wright JM, Thiebaud S. Evaluating, documenting and following up oral pathological
conditions. A suggested protocol. J Am Dent Assoc. 2001; 132: 329- 335.
Page 648
6. Martin IC, Kerawala CJ, Reed M. The applications of toluidine blue as a diagnostic adjunct in the detection
of epithelial dysplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998; 85: 444-446.
7. Van der Waal I, Shepman KP, Van der Meij EH. Oral Leukoplakia: a clinicopathologic review, Oral
Oncology. 1998; 33: 291-301.
8. Van der Waal I, Axell T. Oral leukoplakia: a proposal for uniform reporting, Oral Oncol. 2002; 38:521-
526.
9. Regezi JA, Sciubba JJ, Richard CK. Jordan Oral Pathology clinical Pathologic correlation 5 th ed. Elsevier,
Health Sciences Education.
10. Hancock PJ, Epstein JB, Sadler GR. Oral and dental management therapy for head and neck cancer. J. Can
Dent association. 2003; 69: 585-590.
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Page 649
7. OROFACIAL PAIN
An unpleasant sensory and emotional experience Carbamazepine: - Effective therapy for greater
associated with actual or potential tissue damage, or than 85% of newly diagnosed cases. Tab.
described in terms of such damage associated with Carbamazepine as an initial dose, 100 mg is
oral lesions. given twice daily until relief is established.
Baclofen: - Patient who do not respond to
1. Trigeminal Neuralgia Carbamazepine alone may obtain relief from
(TIC DOULOUREUX) Baclofen (5 to 10 mg 3 times a day) or by
combining Carbamazepine with Baclofen.
Refer to higher centre for further management
 Age – Middle and old age group
 Episodes of intense shooting stabbing, pain 2. Glossopharyngeal
that lasts for a few seconds and then Neuralgia
completely disappears.
 Quality of pain – Electric shock like, (Ninth cranial nerve neuralgia)
unilateral along the course of the affected
nerve. 2.1 Clinical features:
 Maxillary branch is most commonly
affected followed by the mandibular branch  Characterized by severe paroxysmal pain in
and (rarely) the ophthalmic branch. the tonsils and ear.
 Involvement of more than one branch occurs  Less intense than trigeminal neuralgia.
in some cases.  Similar clinical features as trigeminal
 Trigger zones precipitated by light touch on neuralgia.
a “trigger zone” present on the skin or  Precipitating factors Yawning, talking,
mucosa within distribution of the involved chewing and swallowing.
nerve branch. Common sites for trigger  Trigger zone: pain sensation following the
zones include nasolabial fold and the corner distribution of glossopharyngeal nerve
of the lip namely, the pharynx, posterior tongue, ear
 Pain aggravated by: - Shaving, showering, and intraarticular retromandibular area.
eating, speaking or even exposure to wind.
 Number of attacks – varies from 1-2 per day 2.2 Treatment:
to several per minute
 Similar to trigeminal neuralgia.
1.2 Treatment:  Good response to Carbamazepine and
Baclofen.
Drug therapy
Bibliography
sciences.
Further reading
1. David G. Austin special consideration in orofacial pain Dental clinics of North America. 1991 Jan; (35) 1.
2. Richard A. Pertes chronic orofacial pain, a practical approach to differential diagnosis. Dental Clinics of
North America. 1991 Jan; (35)1.

Page 650
8. TRAUMATIC INJURIES TO TEETH
1. Classification: 2.1.1 Enamel dentin fracture:
Radiograph is mandatory to determine the full extent of
Traumatic injuries are classified as the injury.
Class Simple fracture of the crown, involving
2.1.2 Fracture Crown without pulp exposure:
Objective in treating a fractured crown without pulp
I little or no dentin.
exposure is three fold.
Class Extensive fracture of the crown,  Elimination of discomfort.
II involving considerable dentin but not  Preservation of vital pulp.
dental pulp.  Restoration of fracture crown.
Class Extensive fracture of the crown, The tooth should be tested with electric pulp tester or
III involving considerable dentin and with ice or ethyl chloride spray. If the pulp test is vital
exposing the dental pulp. and tooth is comfortable it should be checked again after
a week, 3 weeks, 3 months, 6 months and 1 year.
Class Traumatized tooth that become non-
IV vital, with or without a loss of crown 2.1.3 Fracture with pulp involvement:
structure.
Class Teeth lost as a result of trauma.
V
Class Fracture of the root, with or without loss
VI of the crown structure.
Class Displacement of a tooth, without fracture Figure 8.2: Crown fracture with pulp exposure
VII of the crown or root. If there is involvement of pulp (Complicated Fracture)
vital pulp therapy can be done for which optimal time is
Class Fracture of crown en mass and its
first 24 hours.
VIII replacement.
 In traumatic exposure after 72 hours in immature
Class Traumatic injuries to primary teeth teeth, full pulpotomy can be considered for
IX apexogenesis. In mature teeth, pulpectomy should
be done.
 In non-vital teeth with the open apex, apexification
is indicated to create an apical stop.
2.1.3 Treatment
Crown with pulp exposure: Following treatments are
possible:
 Pulpotomy (Pulp is vital).
 Endodontic treatment.
2.2 Root fracture:
Figure-8.1: Crown fracture without pulp In this coronal segment is reduced quickly and
exposure functional splint is placed for 2 to 4 weeks. When
attended in time, pulp necrosis is remarkably low. It will
occur only 25% of the time and in majority of cases,
2. The various effect of trauma to necrosis will occur only in the coronal segment and only
that is root canal treated.
teeth are  If in the middle 1/3 of root: If tooth is restorable
stabilize, RCT, Resect fracture portion, restoration.
2.1 Crown Fracture:  If tooth is not restorable or unable to stabilize,
If it involves only enamel and dentin (Uncomplicated extraction is needed.
fracture) aesthetic restoration of the teeth is sufficient.
Page 651
2.3 Displacement injuries:
Lateral Luxation and avulsion: Lateral Luxation,
extrusion, and avulsion need emergency splinting &
later RCT if required.
Figure 8.3: Splinting of traumatically displaced upper

anterior teeth

Bibliography
Health.
2. Ingle J, Bakland, Baumgartner. Endodontics. 6th ed. USA: PMPH.
Mosby Elsevier.
Further reading
1. Sturdevant’s Art and Science of operative dentistry fifth ed. Roberson TM. Heymann HO, Swift EJ.
Mosby An imprint of Elsevier.
2. Turner EG, Ferratti GA. Management of minor dentoalveolar trauma to the anterior dentition Oral and
Maxillofacial surgery clinics of North America 1999 May; 11(2):225-240.
3. Trope M: Clinical management of the avulsed tooth. Present strategies and future direction. Int. Endod J.
2002; 18:1–11.
4. Finn SB. Clinical Periodontics. 4th ed. W.B. Saunders Company.
5. Flores MT. Traumatic injuries in the primary dentition, Dent Traumatic. 2002; 18:287–298.
6. Laskin DM. Oral and Maxillofacial Surgery, Oral Surgery, AITBS publishers India. 2012.
7. Ingle JI, Bakland L, Baumgartner JC. Ingle’s Endodontics 6 TH ed., B.C Decker Inc. 2008.

Page 652
9. DISCOLOURATION OF TEETH
1. Introduction:
Discoloration of teeth is a cosmetic problem that is
often the patient’s primary concern. Although
restorative procedures are available, discoloration can
often be corrected totally or partially by a more
conservative approach.
2. Etiology of Tooth Discolouration:
Extrinsic stains Intrinsic stains
 Diet related  Dental Fluorosis

 Bacterial strains  Tetracycline staining
 Medications  Amelogenesis imperfecta
 Erythroblastosis foetalis
 Tobacco related Habits
 Porphyria
 Poor oral hygiene  Jaundice
 Pulpal necrosis
 Intrapulpal haemorrhage due to trauma
 Dentin hyper-calcification
3. Treatment:
Discolouration can be minimized by oral prophylaxis,
bleaching techniques, composite resin, laminates.
Bibliography
Health.
2. Ingle J, Bakland, Baumgartner. Endodontics. 6th ed. USA: PMPH
3. Newman MG, Takei HH, Klokkevold PR. Carranza's Clinical Periodontology. 11th ed. Elsevier Health
Sciences.
4. Robinson M, Heymann H, Swift E. Conservative: Stuedevant’s Art and science of operative dentistry. 5th
ed. Elsevier publication.
Further reading
1. Attin T, Paque F, Lenon AM. Review of the current status of tooth whitening with the walking bleach
technique. International Endodotics Jour. 2003; 36:313.
2. Joiner A. The bleaching oh teeth: a review of literature. J Dent 2006; 25:101.
3. Greenwall L. Bleaching techniques in restorative dentistry, an illustrated guide. Martin Dernitz ltd. 2001.

Page 653
10. MAXILLO-FACIAL INJURIES
Any injury to either a soft tissue or hard tissue of
face caused by an assault, road traffic accidents,
sharp instruments, fall, sports injuries or
violence can cause loss of soft tissue and hard
tissue which has to be handled by an oral or
dental surgeon meticulously at the time of
casualty.
1. Soft tissue injuries:

Abrasion, contusion, ecchymosis, haematoma,
avulsion or degloving injury
2. Hard tissue injuries:

Fracture: External force beyond the modulus of Figure 10.1. Le Fort fracture
elasticity of the bone.
4. Mandibular fractures
2.1. Simple fracture: 4.1 Classification:
Closed linear fractures of bone. Fractures of mandible are more common than the fracture of
middle third.
2.2. Compound fracture: 4.1.1 Mandibular fractures are classified by the anatomic areas
Fractures which communicate to the exterior involved. These areas are as follows: symphysis, body,
through skin or mucous membrane. angle, ramus, condylar process, coronoid process and
alveolar process.
2.3. Greenstick fracture: 4.1.2 Mandibular fractures are also classified into simple,
It occurs in immature bone where one surface is compound, and comminuted.
compressed and opposing surface is stretched
leads to fracture.
2.4. Dentoalveolar fracture:

 Fracture of dentate alveolus may occur as
a separate clinical entity or in conjugation
with other
 Facial bone fractures are usually
associated with injury to teeth like
fracture, subluxation or avulsion.
Figure 10.2: Mandibular Fracture
 Fractures of maxillary tuberosity and
antral floor are relatively common
complications which occur during 4.1.3 An important classification of mandibular angle and body
exodontia. fractures relates to the direction of the fracture line and the
effect of muscle action on the fracture fragments.
3. Le Fort fracture:
Page 654
Angle fractures may be classified as
i. Vertically favorable or unfavorable and
ii. Horizontally favorable or unfavorable.
4.2. Diagnosis of mandibular fractures:

The patient’s health history may reveal pre-existing
systemic bone disease,
The type and direction of traumatic force can be extremely
Figure 10.3: Orthopantomogram (OPG)
helpful in diagnosis. Fractures sustained in vehicular
accidents are usually far different from those sustained in
personal alterations.
4.3. Clinical Examination

The signs and symptoms of mandibular fractures are as
follows.
 Change in occlusion
 Any change in occlusion is highly suggestive of
mandibular fracture.
 Anesthesia, paresthesia, or dysesthesia of the Figure 10.4: 3D Computed tomography
lower Lip. (CBCT) scan
 Abnormal mandibular movements, limited opening 4.5. Management of mandibular
and trismus, deviation on opening toward the side of a fractures
mandibular condylar fracture, Inability to close the
jaw. 4.5.1 Closed reduction basic methods
 Direct interdental wiring
 Change in facial contour and mandibular arch form
 Indirect interdental wiring
 Lacerations, hematoma, and ecchymosis.  Continuous or multiple loop wiring
 Arch bars
 The diagnostic sign of ecchymosis in the floor of the
 Gunning type splints
mouth indicates mandibular body or symphyseal fracture.
4.5.2 Open reduction with direct skeletal
 Loose teeth and crepitation on palpation. fixation:
Allows the bones to be directly manipulated through
 Dolor, Tumor, Rubor, and Color.
an incision so that the fractured ends meet, then they
 Tenderness on palpation. can be secured together either rigidly (with screws or
plates and screws) or non-rigidly (with trans osseous
4.4 Radiology wires).
 Panoramic radiograph
 Lateral oblique radiograph
 Posteroanterior radiograph
 Occlusal view
 Periapical view
 Reverse Towne's view
 Temporomandibular joint, including tomograms
 Computed tomography (CT) scan, CBCT
Figure 10.5 Close Figure 10.6 Open
Reduction Reduction
Page 655
4.6 Post-operative care:
 Soft diet and liquids
 Control of infection
 Oral hygiene maintenance by using mouth rinses.
Bibliography
1. Kruger GO. Textbook of Oral and Maxillofacial Surgery. 6 th ed. Mosby.
2. Williams JL. Rowe and Williams' maxillofacial injuries. 2nd ed. Churchill Livingstone.
3. Killey HC. Bank P. Killey’s Fracture of the mandible. 3 rd ed. Bristol-John wright & sons limited.
4. Malik AN. Text book of Oral and Maxillofacial surgery. 2 nd ed. Jaypee Brothers Publishers.
5. White SC. Pharoah MJ. Oral radiology Principles & Interpretation. 7th ed. Mosby Elsevier.
6. Burket LW, Greenberg MS, Glick M, Ship JA. Burket's Oral Medicine. 11 th ed. USA: PMPH.
Further reading
1. Assael LA, Atlas of facial fracture, Oral and Maxillofacial surgery. Clinics of North America.
Maxillofacial trauma. 2:281-371.

Page 656
11. TEMPOROMANDIBULAR
JOINT DISORDERS
1. Trismus: 1.3. Investigation:

OPG, CT scan, MRI
Restriction of normal oral opening or inability to open the
mouth fully. Trismus is also defined as a condition in which
muscle spasm on contracture prevents opening of the mouth 1.4. Management:
(due to infection or other condition which alter muscle). i. Before starting treatment reassure the
patient.
1.1. Causes of trismus ii. Anti-inflammatory drugs and analgesics.
1.1.1 Articular: - iii. Antibiotics in case of infection.
i. Ankylosis: - Fibrous, Bony iv. Space infection: Antibiotics, incision and
ii. Arthritis: - Stills disease (children), Rheumatoid (adults) drainage.
iii. Pyogenic arthritis v. Muscle relaxants and mouth gags followed
iv. Osteoarthritis by physiotherapy.
v. Psoriatic vi. Tetanus- IM Immunoglobulin followed by
vi. Reiter Syndrome antibiotics.
vii. Gout vii. Tetany- IV Calcium Gluconate 10mg.
viii. Marie Strumpell disease viii. Splints (soft as well as anterior bite planes).
ix. Congenital syphilis ix. Fracture: - Reduction and fixation either
x. Fracture Condyle closed or open under LA or GA.
x. Surgical intervention.
1.1.2 Extra Articular
i. Myositis Ossificans: - following trauma to the 2. Dislocation, Subluxation,
masticatory muscles especially masseter. Hypermobility of
ii. Infection:-Orofacial infection around the TMJ area can
bring about trismus or limitation of oral opening. Temporomandibular Joint
Odontogenic infection like pericoronitis, Ludwig’s (TMJ):
angina, Submasseteric space Infection, Mumps,
Tuberculosis osteomyelitis, Parotid infection 2.1 The dislocation can be
iii. Oral Submucous fibrosis
iv. Systemic causes: -Tetanus, Tetany. unilateral or bilateral
v. Trauma: -Fractures involving zygomatic arch, fracture of Anterior mandibular dislocation
mandible also causes trismus, pain and tenderness or
muscle spasm. i. Acute
vi. Malignancies of oral cavity: Either due to infiltration or ii. Chronic recurrent (habitual) subluxation
due to pain iii. Long standing
vii. Osteomyelitis The term luxation is used for complete
viii. Coronoid hyperplasia dislocation. Subluxation or hypermobility is a
ix. Scarring of the temporalis partial or incomplete dislocation.
x. Fibrosis of Pterygomandibular raphae due to cleft palate
surgery. 2.2. Causes:
1.2. Clinical examination: Extrinsic or Iatrogenic causes: -
Detailed clinical history. Inspection, Palpation, Auscultation in i. Blow on the chin while mouth is open
an around the temporomandibular joint and muscles of ii. Injudicious use of mouth gags during
mastication. general anaesthesia.
iii. Excessive pressure on mandible during
dental extraction.
iv. Post traumatic
Page 657
Intrinsic or Self -induced causes: - 2.4.1 Manipulation:
i. Excessive yawning, Remains the same irrespective of type of
ii. Vomiting, anesthesia.
iii. Opening mouth too wide for eating
iv. Hysterical fits. First of all, patient should be given assurance
about procedure and asked to relax completely.
2.3 Clinical feature: Operator has to stand in front of the patient; he
2.3.1 Unilateral acute dislocation. has to grasp the mandible with both the hand one
on each side.
 Difficulty in mastication and swallowing.
The thumb of operator should be covered with
 Difficulty in speaking.
gauze to prevent injury during manipulation. The
 Profuse drooling of saliva. thumbs are placed on occlusal surfaces of lower
 Deviation of the chin toward contralateral side. molars and finger tips are placed below the chin.
 Deviation produces a lateral cross and open bite on the Operator has to exert full body pressure on
contralateral side. posterior teeth to depress the jaw and at same
 The mouth is partly open and the affected condyle time the finger tips are placed below the chin to
cannot be palpable. elevate it by giving upward pressure. The
downward pressure overcome spasm of muscle,
2.3.2 Bilateral acute dislocation: - plus it brings the locked condylar head below the
level of articular eminence and then backward
 Pain, inability to close the mouth, tense masticatory
pressure is given to push the entire mandible
muscles.
posteriorly.
 Difficulty in speech.
 Profuse drooling of saliva After this reduction procedure, the mouth is
 Protruding chin closed and patient is asked to keep the mouth
 Mandible is protruded and movements are restricted. opening restricted.
 Patients complain of pain in temporal region rather Immobilization can be carried out by giving
than the joint. barrel bandage for 10 to 14 days' period. Patient is
 Distinct hollowness can be felt in both preauricular kept on semisolid diet. Anti-inflammatory
regions. analgesics prescribed for 3to 5 days.
Long standing acute dislocation which do not
4. Treatment: respond to above procedure can be reduced by
administering General Anesthesia. If manual
 Reassuring the patient. reduction fails than open surgical procedure as
 Tranquilizer or sedative drugs. last resort.
 Pressure and massage of the area.
 Manipulation with or without anesthesia.
3. Temporomandibular
disorder (TMD):
Temporomandibular joint syndrome or
temporomandibular disorder (TMD) is the most
common cause of facial pain after toothache.
TMD can be classified broadly as TMD
secondary to myofascial pain and dysfunction
(MPD) and TMD secondary to true articular
disease.
MPD form is associated with pain without
Figure 11.1: apparent destructive changes of the TMJ on x-ray.
It is frequently associated with bruxism and
Press his premolar teeth downwards at the same time press daytime jaw clenching in a stressed and anxious
3.2. Etiology:
the underneath of his chin upwards and backwards person.
3.1 Etiology:
The etiology of TMD is multifactorial and
Page 658
includes malocclusion, jaw clenching, bruxism, personality  Cryotherapy with Ice packs application to
disorders, increased pain sensitivity and stress and anxiety. the painful area 4 times a day for 20
minutes for relief of pain followed by an
3.2 Clinical features: acute injury superimposed over a chronic
i. Pain TMD.
ii. Muscle tenderness  Mild analgesic Tab. Diclofenac 50 mg 1
iii. A clicking or popping noise in the temporomandibular BD.
joint.  Anti-anxiety agents for short duration in
iv. Limitation of jaw motion unilaterally or bilaterally. acute pain like. Tab Diazepam 2 to 5 mg a
bed time for 10 days.
 Physiotherapy and active stretch exercise.
3.3 Differential Diagnosis:  Intraoral appliances: Use of Splints,
Cluster headache, Migraine headache, Post herpetic Neuralgia, orthopedic appliances, bite guards, night
Temporal or Giant Cell Arteritis,Ttrigeminal Neuralgia. guards or bruxism guards.
3.4 Treatment:  Stress management
Counselling regarding self-care and reversal of parafunctional
habits.
 Heat application to increase local circulation which acts
as a sedatives and lowers muscle tension to be given for
15 to 20 minutes 4 times a day.
Bibliography
sciences.
3. Malik AN. Text book of Oral and Maxillofacial surgery. 2 nd ed. Jaypee Brothers Publishers.
Further reading
1. Dworkin S, Le Resche L. Research Diagnostic criteria for temporomandibular disorders: review, criteria,
examinations and specifications, critique. J Craniomandibular disorder 1992; 6:301-335.
2. List T, Axelssons S, Leijon G. Pharmacologic Interventions in the treatment of Temporomandibular
disorders, atypical facial pain and burning mouth syndrome. A Qualitative systematic review Journal of
Orofacial pain. 2003; 17:301-310.
3. Fricton JR. Clinical care for myofacial pain. Dental clinics of North America. 1991 Jan; 35(1).
4. Gibilisco JA. Management of temporomandibular joint disorders associated with systematic disease. Dental
clinics of North America. 1983 Jul; 27(3).

Page 659
12. DENTAL IMPACTION
An impacted tooth is one that is erupted, partially
1. Introduction: erupted or unerupted and will not eventually assume
Impaction is cessation of eruption of tooth caused by normal arch relationship with other teeth and tissue
physical barrier or ectopic positioning of tooth. commonly seen with third molar and sometimes
maxillary canine teeth.
sss
Figure 12.1: Pericoronitis
Figure 12.2: Impacted Wisdom Teeth
 Vertical
2. Types of Impaction:  Buccoangular
 Soft tissue impaction.
 Linguoangular
 Bony impaction.
3. Third molar impaction: 4. Clinical Features:

This can be classified by angulation in relation to  Difficulty in opening the mouth and deglutition.
long axis of second molar  Localized tenderness and swelling.
 Mesioangular  Radiating pain towards ear and sometimes
 Distoangular headache.
 Horizontal
Page 660
 Purulent discharge may be present from the site
of infection.
6. Treatment:
 Advice antibiotics and analgesics.
5. Investigations: Cap. Amoxicillin 500mg 1 BD for 5 days.
IOPA X-Ray, lateral oblique x-ray, OPG, Tab. Diclofenac 50mg 1 BD for 5 days.
Complete haemogram  Surgical removal of impacted tooth.

Bibliography
2. White SC. Pharoah MJ. Oral radiology Principles & Interpretation. 7th ed. Mosby Elsevier.
3. Kruger GO. Textbook of Oral and Maxillofacial Surgery. 6th ed. Mosby.
Further reading
1. Seward GR, Harris M, Mcgowon DA. Dental Practitioner Handbook 2 nd ed. Varghese publishing house.


Page 661

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STANDARD TREATMENT

Public Health Department

demands rational and efficient utilisation of the limited resources.

approaches for diagnosis, management and prevention of the health issues.

quality health services.

treatment regimen suitable for the disease.

(STP) for all diseases of public health importance in the State.

their vision for developing this STP.

making and in day to day working of the Healthcare providers.

Team No.2 National Health Programme, NRHM

1 Dr. Dodwad Ex. Addl.DHS Pune 9421014106

Team No.3 General Surgery, Ortho., Burn & Trauma

4 Dr. Piyush P. Jakkal Ortho. Surgeon, Cl.I D.H. Bhandara 8888865848

Team No.4 Pediatric & Neonatology

2 Dr. Havle Abhay D. Prof. ENT KIMS, Karad 9423263164

3 Dr. Sanjana Nemade Asso. Prof.ENT Pune 9923730525

4 Dr. Sarika Dhoot Asst. Prof.ENT Bharati Vidyapeeth Medical 9326349006

5 Dr. N. B. Patel M.S. (ENT) RMO (OR) DH Beed 9370066114

6 Dr. Manoj Deshmukh M.S. (ENT) YCMH Pimpri 9922501564

7 Dr. S. M. Mahalle Class-I, ENT Surgeon C.H. Amravati 9423124812

8 Dr. Kamble A.G. (Team Leader) MO ENT C.H. Pune 9823174647

9 Dr. Vikram Oak DMH Consultant Dinanath Mangeshkar 9822031070

10 Dr. Yadav Physician VSS Hospital, Amravati 8308667603

11 Dr. Kamble Physician Civil Hospital Thane 9823776442

13 Dr. M.V. Karnataki UNICEF SFWB, Pune 9324341580

Team No.7 Anesthesiology

1 Dr. Kharat (Team Leader) Dental Surgeon D.H. Beed 9423450077

2 Dr. Supriya Mahajan Dental Surgeon UH-3 Thane 8108715475

3 Dr. Dinesh Ashok Dhole Dental Surgeon D.H. Nashik 9923551519

1 Dr. Ramkrishnan V. Ghubde Asso. Professor Smt. Kashibai Navale 9822462536

2 Dr. Ramesh L. Pawar M.O. RRH Nashik 9420335958

3 Dr. Anita Kharat Dental Surgeon D.H. Jalna 9423450077

4 Dr. Zapkar Dental Surgeon D.H. Thane 9029083693

5 Dr. Shegavkar Dental Surgeon RH, Igatpuri, Nashik 9890317834

Team No.9 Psychiatry

1 Dr. Sharmishta S. Deshpande Prof. (Psychiatry) Smt. Kashibai Navale 9890381144

2 Dr. Jyoti Shetty Prof. (Psychiatry) Bharati Vidyapeeth 9822326019

3 Dr. Khandekar (Team NRHM Psychiatrist Thane 9821351712

4 Dr. Amit Nagarkar Class I, Psychiatrist Regional Mental Hospital, 9579591936

5 Dr. Hemant Sonanis Psychiatrist D.H. Nashik 9922069966

6 Dr. Amol Gulhane Psychiatrist GH Amravati 9881424080

7 Dr. Divekar Psychiatrist D.H. Thane 9619388012

8 Dr. M. Bahale Psychiatrist D.H. Thane 9850411911

9 Dr. Shirsath Med. Superintendent D.H. Thane 9096726700

Team No.11 Dermatology

1 Dr. Archana Patil Addl Director SFWB, Pune 9869394115

2 Dr. Tanaji Mane DDHS SBHIVS 9422746567

4 Dr Madhusudan Karnataki UNICEF Consultant SFWB, Pune 9324341580

5 Dr Chandrakala Jaiswal UNICEF Consultant SFWB, Pune 9822496233

7 Dr Aparna Deshpande UNICEF Consultant SFWB, Pune 9373089938

9 Dr Neha Wagh UNICEF Consultant Aurangabad 9673527421

10 Dr Vinay Koparde UNICEF Consultant Nanded 9168849555

11 Dr Vaibhav Mahatme UNICEF Consultant Beed 9096309076

12 Dr Prashant Hingankar UNICEF Consultant Nandurbar 8879597487

3 Obstetrics and Gynaecology 270-335

The concept of essential medicines

Common types of irrational medicines use are:

• The use of too many medicines per patient (poly-pharmacy);

Reasons for irrational use of medicines are: